DOCSLIB.ORG

Higher Offspring Birth Weight Predicts the Metabolic Syndrome in Mothers but Not Fathers 8 Years After Delivery the Pune Children’S Study Chittaranjan S

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Higher Offspring Birth Weight Predicts the Metabolic Syndrome in Mothers but Not Fathers 8 Years After Delivery the Pune Children’S Study Chittaranjan S Higher Offspring Birth Weight Predicts the Metabolic Syndrome in Mothers but Not Fathers 8 Years After Delivery The Pune Children’s Study Chittaranjan S. Yajnik,1 Charu V. Joglekar,1 Anand N. Pandit,2 Ashish R. Bavdekar,2 Swati A. Bapat,2 Sheila A. Bhave,2 Samantha D. Leary,3 and Caroline H.D. Fall3 In Europid populations, low birth weight of offspring predicts insulin resistance in the mother and cardiovas- cular disease in both parents. We investigated the asso- here is growing interest in the association be- ciation between birth weight of offspring and obesity tween size at birth and the risk of diabetes and and cardiovascular risk in the parents of 477 8-year-old cardiovascular disease in later life (1). Size at children born at the King Edward Memorial Hospital, Tbirth reflects intrauterine growth, which is deter- Pune, India. Eight years after the birth of the child, mined by intrauterine environment as well as genetic of heavier babies factors. Diabetes is more common in those who are small (459 ؍ mothers (33 years of age, n were taller and more obese (BMI, fat mass, and waist or large at birth (2,3). Studies that show an inverse relation circumference, all P < 0.001) than mothers of lighter between birth weight and insulin resistance syndrome babies. Increasing offspring birth weight predicted (metabolic syndrome) have been interpreted to mean that higher homeostasis model assessment for insulin resis- “fetal undernutrition” is the causative factor (the “thrifty tance (P < 0.01) and metabolic syndrome in mothers phenotype” hypothesis) (4). The “fetal insulin hypothesis” (P < 0.001) (adjusted for offspring sex and birth order, offers an alternative genetic explanation for the relation- maternal age, and socioeconomic status) but not hyper- ship (5). Davey-Smith et al. (6) have explored another ؍ glycemia. Fathers (39 years of age, n 398) of heavier aspect of this relationship. They showed that offspring low babies were taller and heavier, independent of maternal birth weight is associated with increased cardiovascular size (P < 0.01, both), but were not more insulin resis- risk in parents (6–8), increased maternal insulin resis- tant. Unlike other reports, lower offspring birth weight tance during late adulthood (9), and diabetes in fathers did not predict insulin resistance in fathers. Thus, urban Indian parents have a higher risk of being obese 8 years (10). They favor a genetic explanation for their findings. after delivery of a heavier child. Mothers but not fathers On the other hand, large babies born to mothers with of heavier babies also have a higher risk of being insulin gestational diabetes mellitus (GDM) have an increased resistant and developing the metabolic syndrome. Our risk of diabetes (11,12), and mothers also have an in- findings highlight the need for a better understanding of creased risk of diabetes (13). Maternal insulin resistance the relation between fetal growth and future health during (late) gestation is an important mechanism to before contemplating public health interventions to divert nutrients (glucose, amino acids, and triglycerides/ improve fetal growth. Diabetes 52:2090–2096, 2003 fatty acids) to the fetus to promote growth (14). Offspring birth weight could be used as a useful surrogate for maternal metabolism in pregnancy. In recent years there has been a growing recognition that pregnant metabolic state and events provide a window into future maternal risk of disease (15). In the Pune Children’s Study, we investigated the deter- minants of insulin resistance in 8-year-old urban children (16). At the same time, we measured body size, insulin From the 1Diabetes Unit, King Edward Memorial Hospital and Research Centre, Pune, India; the 2Department of Pediatrics, King Edward Memorial resistance, and other cardiovascular risk factors in their Hospital and Research Centre, Pune, India; and the 3Medical Research parents. We report the relationship between the child’s Council, Environmental Epidemiology Unit, Southampton, U.K. birth weight and parental measurements. Address correspondence and reprint requests to Dr. C.S. Yajnik, Director, Diabetes Unit, King Edward Memorial Hospital and Research Centre, Pune, India 400 011. E-mail: [email protected]. Received for publication 6 November 2002 and accepted in revised form12 RESEARCH DESIGN AND METHODS May 2003. Details of our methods have been reported previously (16). Of 477 families, 6 CHD, coronary heart disease; GDM, gestational diabetes mellitus; HOMA, homeostasis model assessment; HOMA-IR, HOMA for insulin resistance; IGT, mothers and 12 fathers had died, and 459 (nonpregnant) mothers and 398 impaired glucose tolerance; OGTT, oral glucose tolerance test; SES, socio- fathers agreed to be studied. Standardized anthropometric measurements economic status; WHR, waist-to-hip ratio. were made by one of two trained observers. Fat mass was calculated from © 2003 by the American Diabetes Association. four skinfold-thickness measurements using Durnin’s formula (17). Blood 2090 DIABETES, VOL. 52, AUGUST 2003 CS YAJNIK AND ASSOCIATES TABLE 1 Anthropometric and biochemical measurements in parents of 8-year-old children Mothers Fathers n 456 398 Age (years) 33 (30–35) 39 (36–42) Anthropometry Height (cm) 153.0 (150.0–157.0) 165.8 (162.3–170.3) Weight (kg) 52.0 (44.5–59.8) 63.0 (55.8–70.0) BMI (kg/m2) 22.1 (18.9–25.3) 22.8 (20.7–25.4) WHR 0.76 (0.71–0.81) 0.91 (0.86–0.94) Body fat (%) 33.6 (27.6–37.6) 25.3 (21.3–28.2) Glucose-insulin Fasting plasma glucose (mmol/l) 4.8 (4.4–5.4) 5.0 (4.4–5.6) 30-min plasma glucose (mmol/l) 7.8 (6.7–8.8) 8.2 (6.9–9.3) 120-min plasma glucose (OGTT) (mmol/l) 5.5 (4.7–6.7) 6.1 (5.0–7.7) Fasting plasma insulin (pmol/l) 34.0 (22.0–50.0) 35.0 (21.0–51.0) 30-min plasma insulin (pmol/l) 199.0 (123.0–308.5) 195.0 (103.5–319.0) 120-min plasma insulin (pmol/l) 176.5 (102.7–308.2) 214.0 (107.0–425.0) Plasma split 32-33 insulin (pmol/l) 6.3 (3.9–9.8) 12.0 (7.6–22.0) Plasma proinsulin (pmol/l) 4.1 (3.0–5.8) 7.8 (4.9–13.0) HOMA-IR 1.42 (0.96–2.13) 1.94 (1.15–3.10) Lipids Total cholesterol (mmol/l) 3.8 (3.3–4.4) 4.2 (3.6–5.0) HDL cholesterol (mmol/l) 1.0 (0.8–1.2) 0.9 (0.7–1.1) Triglycerides (mmol/l) 0.8 (0.6–1.2) 1.2 (0.9–1.9) Blood pressure Systolic (mmHg) 120 (113–127) 129 (122–137) Diastolic (mmHg) 71 (65–78) 77 (71–84) Data are median (interquartile range). pressure was measured using a digital automated device (Dinamap; Criticon, RESULTS Tampa, FL) after 10-min rest in the supine position. The mean birth weights of the children were 2.8 kg (boys) A 75-g anhydrous oral glucose tolerance test (OGTT) was performed on subjects not on antidiabetic treatment. Three venous blood samples (fasting and 2.6 kg (girls). Their birth weight distribution was and at 30 and 120 min after oral glucose) were collected for measurement of similar to that for all babies born in the hospital during the plasma glucose and insulin concentrations. Plasma cholesterol, HDL choles- same time period. There was no significant difference in terol, triglycerides, proinsulin, and 32-33 split proinsulin were measured in the birth weight of children whose parents were studied or not fasting sample by standard methods. Insulin resistance was calculated using studied. Birth weight increased with the birth order of the the homeostasis model assessment (HOMA) (18), and the 30-min insulin Ͻ ␤ child (P 0.001), but was not related to the SES of the increment was used as an estimate of -cell function (19). Metabolic syn- ϭ drome was defined following World Health Organization guidelines (20), family (P 0.42). except that the BMI cutoff point for obesity was 25 kg/m2 rather than 30 kg/m2 Parents. Table 1 shows the characteristics of the parents. because of the recent recognition of a need to revise BMI criteria for Asian Tables 2 and 3 show maternal and paternal size and populations (21). Those in the highest quartile of HOMA for insulin resistance cardiovascular risk factors by thirds of their child’s birth (HOMA-IR) were diagnosed as insulin resistant. Metabolic syndrome was weight. diagnosed if a subject had a fasting plasma glucose concentration Ն6.1 mmol/l or a 120-min concentration Ն7.8 mmol/l and/or were insulin resistant and in Mothers. One mother was known to be diabetic before addition had two or more of the following: 1) BMI Ն25 kg/m2 and/or waist-hip pregnancy and died 5 years after delivery. Her child and ratio Ն0.90 for men and Ն0.85 for women, 2) plasma triglyceride concentra- his father are excluded from the analysis. tion Ն1.7 mmol/l and/or HDL cholesterol Ͻ0.9 mmol/l for men and Ͻ1.0 The OGTT was not routinely performed during preg- mmol/l for women, and 3) blood pressure Ն140/90 mmHg. nancy, but 13 mothers were diagnosed as having GDM by Socioeconomic status (SES) was assessed using the Kuppuswamy score the treating obstetrician on clinical indications; none of (22), a standardized scoring system based on a questionnaire asking for details of occupation, education, income, and size and type of housing. Each aspect them were on antidiabetic treatment at the time of this is separately scored, and the scores are added to get a total socioeconomic study.
Load more

Recommended publications
  • Genetics of Types 2 Diabetes Mellitus
    Genetics of type 2 diabetes mellitus Genetics of type 2 diabetes mellitus WY So, MCY Ng, SC Lee, T Sanke, HK Lee, JCN Chan Type 2 diabetes mellitus is a heterogeneous disease that is caused by both genetic and environmental factors. Only a minority of cases of type 2 diabetes are caused by a single-gene defect, such as maturity- onset diabetes of youth (mutated MODY gene), syndrome of insulin resistance (insulin receptor defect), and maternally inherited diabetes and deafness (mitochondrial gene defect). The genetic component of the more common form of type 2 diabetes is probably complex and involves the interactions of multiple genes and environmental factors. The candidate gene approach has identified several genes that regulate insulin signalling and secretion, but their contributions to diabetes are small. Recent genome scan studies have been conducted to identify major susceptibility loci that are linked with type 2 diabetes. This information would provide new insights into the identification of novel genes and pathways that lead to this complex disease. HKMJ 2000;6:69-76 Key words: Amyloid metabolism; Diabetes mellitus, non-insulin-dependent/genetics; DNA, mitochondrial; Insulin/ deficiency; Insulin resistance/genetic; Mutation Introduction Insulin Growth hormone, The maintenance of the blood glucose concentration cortisol, within a narrow range (between 3 and 7 mmol/L) ↑ Glycogen synthesis catecholamines, ↑ Lipogenesis glucagon irrespective of the pathophysiological circumstances, ↑ Glucose transport depends on the intricate relationships between the ↓ Lipolysis ↑ Glycogen breakdown actions of insulin—the only hormone that reduces ↓ Gluconeogenesis ↑ Lipolysis ↓ ↑ blood glucose level—and those of counter-regulatory Glycogenolysis Gluconeogenesis hormones. The latter group of hormones comprises growth hormone, catecholamines, cortisol, and gluca- gon, all of which tend to elevate blood glucose levels Glucose homeostasis (Fig 1).
    [Show full text]
  • Type 2 (Non-Insulin-Dependent) Diabetes Mellitus: the Thrifty Phenotype Hypothesis*
    Diabetologia (1992) 35:595~601 Diabetologia © Spfinger-Verlag 1992 Review Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis* C. N. Hales 1 and D. J. P. Barker 2 1Department of Clinical Biochemistry, Addenbrooke's Hospital, Cambridge, and 2MRC Environmental EpidemiologyUnit, University of Southampton, Southampton General Hospital, UK In this contribution we put forward a novel hypothesis con- rises in plasma insulin concentration were those most like- cerning the aetiology of Type 2 (non-insulin-dependent) ly to develop diabetes. Unfortunately the relatively small diabetes mellitus. The concept underlying our hypothesis numbers of subjects who could be studied in those days is that poor fetal and early post-natal nutrition imposes meant that this finding could only be taken as suggestive mechanisms of nutritional thrift upon the growing individ- rather than definitive. ual. We propose that one of the major long-term conse- Whilst this work was in progress the discovery ofproin- quences of inadequate early nutrition is impaired develop- sulin [4], the later demonstration of its presence in plasma ment of the endocrine pancreas and a greatly increased [5, 6] and of its elevation in the plasma of Type 2 diabetic susceptibility to the development of Type 2 diabetes. In the subjects [7-9] raised a question concerning the specificity first section we outline our research which has led to this of insulin measurements in plasma. It was apparent from hypothesis. We will then review the relevant literature. early days that proinsulin cross-reacted strongly in many Finally we show that the hypothesis suggests a reinter- insulin radioimmunoassays.
    [Show full text]
  • Early Life Lessons: the Lasting Effects of Germline Epigenetic Information on Organismal Development
    University of Massachusetts Medical School eScholarship@UMMS Open Access Articles Open Access Publications by UMMS Authors 2020-08-01 Early life lessons: The lasting effects of germline epigenetic information on organismal development Carolina Galan University of Massachusetts Medical School Et al. Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/oapubs Part of the Biochemical Phenomena, Metabolism, and Nutrition Commons, Cellular and Molecular Physiology Commons, Comparative and Evolutionary Physiology Commons, Developmental Biology Commons, Embryonic Structures Commons, and the Genetics and Genomics Commons Repository Citation Galan C, Krykbaeva M, Rando OJ. (2020). Early life lessons: The lasting effects of germline epigenetic information on organismal development. Open Access Articles. https://doi.org/10.1016/ j.molmet.2019.12.004. Retrieved from https://escholarship.umassmed.edu/oapubs/4335 Creative Commons License This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License. This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in Open Access Articles by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. Review Early life lessons: The lasting effects of germline epigenetic information on organismal development Carolina Galan 1, Marina Krykbaeva 1, Oliver J. Rando* ABSTRACT Background: An organism’s metabolic phenotype is primarily affected by its genotype, its lifestyle, and the nutritional composition of its food supply. In addition, it is now clear from studies in many different species that ancestral environments can also modulate metabolism in at least one to two generations of offspring.
    [Show full text]
  • Genne-Bacon Thinking Evolutionarily About Obesity
    YALE JOURNAL OF BIOLOGY AND MEDICINE 87 (2014), pp.99-112. Copyright © 2014. FOCUS: OBESITY Thinking Evolutionarily About Obesity Elizabeth A. Genné-Bacon Department of Genetics, Yale University, Connecticut Mental Health Center, New Haven, Connecticut Obesity, diabetes, and metabolic syndrome are growing worldwide health concerns, yet their causes are not fully understood. Research into the etiology of the obesity epidemic is highly influenced by our understanding of the evolutionary roots of metabolic control. For half a cen- tury, the thrifty gene hypothesis, which argues that obesity is an evolutionary adaptation for surviving periods of famine, has dominated the thinking on this topic. Obesity researchers are often not aware that there is, in fact, limited evidence to support the thrifty gene hy- pothesis and that alternative hypotheses have been suggested. This review presents evi- dence for and against the thrifty gene hypothesis and introduces readers to additional hypotheses for the evolutionary origins of the obesity epidemic. Because these alternate hypotheses imply significantly different strategies for research and clinical management of obesity, their consideration is critical to halting the spread of this epidemic. INTRODUCTION drome,” which strongly predisposes suffers to type 2 diabetes, cardiovascular disease, The incidence of obesity worldwide and early mortality [2]. Metabolic syn- has risen dramatically in the past century, drome affects 34 percent of Americans, 53 enough to be formally declared a global percent of whom are obese [3]. Obesity is a epidemic by the World Health Organization growing concern in developing nations in 1997 [1]. Obesity (defined by a body [4,5] and is now one of the leading causes mass index exceeding 30 kg/m), together of preventable death worldwide [6].
    [Show full text]
  • Hormonal Biomarkers for Evaluating the Impact of Fetal Growth
    Published online: 2019-04-02 THIEME 256 Review Article Hormonal Biomarkers for Evaluating the Impact of Fetal Growth Restriction on the Development of Chronic Adult Disease Biomarcadores hormonais para avaliar o impacto da restrição do crescimento fetal no desenvolvimento de doenças crônicas em adultos Elizabeth Soares da Silva Magalhães1 Maria Dalva Barbosa Baker Méio1 Maria Elisabeth Lopes Moreira1 1 Clinical Research Unit, Fundação Oswaldo Cruz, Rio de Janeiro, RJ, Address for correspondence Maria Dalva Barbosa Baker Méio, MD, Av. Brazil Rui Barbosa, 716, Flamengo, 22250-020, Rio de Janeiro, RJ, Brazil (e-mail: [email protected]). Rev Bras Ginecol Obstet 2019;41:256–263. Abstract The hypothesis of fetal origins to adult diseases proposes that metabolic chronic disorders, including cardiovascular diseases, diabetes, and hypertension originate in the developmental plasticity due to intrauterine insults. These processes involve an adaptative response by the fetus to changes in the environmental signals, which can promote the reset of hormones and of the metabolism to establish a “thrifty phenotype”. Metabolic alterations during intrauterine growth restriction can modify Keywords the fetal programming. The present nonsystematic review intended to summarize ► fetal growth historical and current references that indicated that developmental origins of health restriction and disease (DOHaD) occur as a consequence of altered maternal and fetal metabolic ► developmental pathways. The purpose is to highlight the potential implications of growth factors and origins of health and adipokines in “developmental programming”, which could interfere in the develop- disease ment by controlling fetal growth patterns. These changes affect the structure and the ► growth functional capacity of various organs, including the brain, the kidneys, and the ► development pancreas.
    [Show full text]
  • Early Programming of Adult Diseases in Resource Poor Countries
    429 GLOBAL CHILD HEALTH Arch Dis Child: first published as 10.1136/adc.2004.059030 on 21 March 2005. Downloaded from Early programming of adult diseases in resource poor countries A M Prentice, S E Moore ............................................................................................................................... Arch Dis Child 2005;90:429–432. doi: 10.1136/adc.2004.059030 Considerable evidence now exists to suggest that early particularly vulnerable to nutritional insults, and that certain organs such as the brain tend to be exposure to nutritional deprivation can have long term spared at the expense of others.3 consequences to health, with low birth weight now At the current time Barker’s theories still considered a risk factor for later health outcomes such as remain the subject of intense scrutiny and not inconsiderable controversy,4 but few would now coronary heart disease, stroke, type 2 diabetes, and the deny the underlying tenet that early exposure to metabolic syndrome. Of importance, such effects are most nutritional deprivation can have long term exaggerated when faced with over-nutrition in later life, consequences to health. In summary, there is considerable evidence that fetal and early post- forming the basis for the ‘‘thrifty phenotype’’ hypothesis. natal undernutrition can invoke the following The evidence in support of these associations comes largely changes: metabolic adaptations that affect variables from retrospective cohort studies in which adult outcomes such as hepatic enzyme profiles,5 lipoprotein 6 7 were correlated with birth weight records. Relatively little profiles, and clotting factor production; anato- mical adaptations that affect processes such as end data is available from developing countries, where long organ glucose uptake8 and renal solute hand- term record keeping of birth weight data has not been a ling;9 and endocrine adaptations that affect the high priority.
    [Show full text]
  • Intrauterine Growth Restriction: New Insight from the Metabolomic Approach
    H OH metabolites OH Review Intrauterine Growth Restriction: New Insight from the Metabolomic Approach Elena Priante 1,*, Giovanna Verlato 1, Giuseppe Giordano 2,3, Matteo Stocchero 2 , Silvia Visentin 4, Veronica Mardegan 1 and Eugenio Baraldi 1,3 1 Neonatal Intensive Care Unit, Department of Women’s and Children’s Health, University of Padua, 35128 Padua, Italy; [email protected] (G.V.); [email protected] (V.M.); [email protected] (E.B.) 2 Department of Women’s and Children’s Health, University of Padua, 35128 Padua, Italy; [email protected] (G.G.); [email protected] (M.S.) 3 Institute of Pediatric Research, “Città della Speranza” Foundation, 35129 Padua, Italy 4 Gynecology and Obstetrics Unit, Department of Women’s and Children’s Health, University of Padua, 35128 Padua, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-049-8213545 Received: 17 September 2019; Accepted: 4 November 2019; Published: 6 November 2019 Abstract: Recognizing intrauterine growth restriction (IUGR) is a matter of great concern because this condition can significantly affect the newborn’s short- and long-term health. Ever since the first suggestion of the “thrifty phenotype hypothesis” in the last decade of the 20th century, a number of studies have confirmed the association between low birth weight and cardiometabolic syndrome later in life. During intrauterine life, the growth-restricted fetus makes a number of hemodynamic, metabolic, and hormonal adjustments to cope with the adverse uterine environment, and these changes may become permanent and irreversible. Despite advances in our knowledge of IUGR newborns, biomarkers capable of identifying this condition early on, and stratifying its severity both pre- and postnatally, are still lacking.
    [Show full text]
  • Preliminary Evidence for an Impulsivity-Based Thrifty Eating Phenotype
    nature publishing group Clinical Investigation Articles Preliminary evidence for an impulsivity-based thrifty eating phenotype Patrícia P. Silveira1, Marilyn Agranonik1, Hadeel Faras2, André K. Portella1, Michael J. Meaney3,4, Robert D. Levitan5; on behalf of the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) Study Team INTRODUCTiON: Low birth weight is associated with obesity malnutrition passing across the placenta to the developing and an increased risk for metabolic/cardiovascular diseases in fetus, providing the fetus with a forecast of a sparse nutritional later life. environment. If the prediction proves inaccurate and food sup- RESULTS: The results of the snack delay test, which encom- plies become abundant, the thrifty phenotype becomes a risk passed four distinct trials, indicated that the gender × intrauter- factor for obesity, diabetes, and cardiovascular disease. ine growth restriction (IUGR) × trial interaction was a predictor of Although the thrifty phenotype hypothesis focuses on pro- the ability to delay the food reward (P = 0.002). Among children gramming of metabolism during fetal development, it is entirely with normal birth weights, girls showed a greater ability to delay plausible that obesogenic patterns of eating behavior per se are food rewards than did boys (P = 0.014).In contrast, among chil- also programmed by early fetal adversity and low birth weights. dren with IUGR, there was no such differential ability between In support of this hypothesis, we found that young adult women girls and boys. Furthermore, in girls, impulsive responding pre- who have experienced IUGR prefer carbohydrates over protein dicted both increased consumption of palatable fat (P = 0.007) and have larger waist-to-hip ratios, despite having no signs of and higher BMIs (P = 0.020) at 48 mo of age, although there was insulin resistance or diabetes mellitus (14).
    [Show full text]
  • Short Life Expectancy and Metabolic Syndrome in Romanies (Gypsies) in Slovakia
    Cent Eur J Public Health 2010; 18 (1): 16–18 SHORT LIFE EXPECTANCY AND METABOLIC SYNDROME IN ROMANIES (GYPSIES) IN SLOVAKIA Vlado Simko1, Emil Ginter2 1State University New York, Downstate Medical Center at Brooklyn, USA 2Institute of Preventive and Clinical Medicine, Bratislava, Slovakia SUMMARY The aim of this review is to explain short life expectancy in Romanies. Romanies represent the second largest minority in Slovakia (about 7%). Most of them exist on the fringes of the majority society. Their general situation worsened after the fall of communism in 1989. In a market oriented society the unemployment of Romanies further increased due to their poor education and lack of skills. Romany general health substantially is worse than that of the majority population: They have high prevalence of communicable diseases due to poor sanitary and living conditions. Furthermore, epidemiological and metabolic studies revealed in Romanies high prevalence of obesity associated with increased cardiovascular risk. There is no explanation for this seemingly paradoxical phenomenon, in a population living in poor economic conditions. It is possible that in the course of the many generation-long migration from India to Europe, pregnant Romanies and their fetuses suf ferred excessive nutritional deficiency. This might have induced adaptive metabolic and genetic changes aimed at optimum utilization of scarce food supply. There is a hypothetical possibility that in them “thrifty gene” was formed. Arrival of Romanies to Europe resulted in somewhat better nutrition, along with sharply reduced physical expenditure. The consequence is a metabolic syndrome with type 2 diabetes and increased cardiovascular mortality. Such unique metabolic feature in Romanies will undoubtedly stimulate further research in molecular biology that may ultimately clarify the role of “thrifty genes”.
    [Show full text]
  • Famine and the Thrifty Phenotype: Implications for Long-Term Health
    In: Early Life Nutrition and Adult Health and Development ISBN: 978-1-62417-129-1 Editors: L. H. Lumey and Alexander Vaiserman © 2013 Nova Science Publishers, Inc. No part of this digital document may be reproduced, stored in a retrieval system or transmitted commercially in any form or by any means. The publisher has taken reasonable care in the preparation of this digital document, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained herein. This digital document is sold with the clear understanding that the publisher is not engaged in rendering legal, medical or any other professional services. Chapter II Famine and the Thrifty Phenotype: Implications for Long-Term Health Jonathan C. K. Wells Childhood Nutrition Research Centre, UCL Institute of Child Health, London, UK Abstract Famines have been common in human history, but their effects on human biology remain only partially understood. Recent studies have highlighted how these effects may propagate through the life-course into subsequent generations. An evolutionary approach helps understand how these multiple effects are distributed. Generically, undernutrition in early life constrains early growth, increasing the short-term risk of morbidity and mortality. However, the long-term health effects of early undernutrition are mediated by catch-up growth, which improves early survival, but potentially at the expense of later metabolic penalties. The long-term effects of early undernutrition vary in relation to several factors: whether the undernutrition comprises a brief sharp shock (maternal famine) or chronic malnutrition of the lineage; how much catch-up occurs and when; and what environment is encountered from childhood onwards.
    [Show full text]
  • Evolutionary, Developmental and Transgenerational Influences
    Hornstra G, Uauy R, Yang X (eds): The Impact of Maternal Nutrition on the Offspring. Nestlé Nutrition Workshop Series Pediatric Program, vol 55, pp 17–27, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2005. Metabolic Disease: Evolutionary, Developmental and Transgenerational Influences Peter D. Gluckmana and Mark A. Hansonb aLiggins Institute, University of Auckland and National Research Centre for Growth and Development, Grafton, New Zealand, and bCentre for Developmental Origins of Health and Disease, University of Southampton, Princess Anne Hospital, Southampton, UK Introduction There is a rising incidence of metabolic syndrome (non-insulin-dependent or type-2 diabetes, obesity and cardiovascular disease) in both the developed and developing worlds. It is generally assumed that this rapid increase is simply a reflection of the marked change in dietary and exercise behaviors of children, adolescents and adults. These factors play a dominant role, but other factors must be involved to explain the changing pattern of disease. This chapter reviews the growing evidence that the developmental and environmental history of both the individual and his/her population are important factors. The first suggestion that there may be early life determinants of later disease came from Forsdahl [1] who reported that the risk of arteriosclerotic heart disease was enhanced in those who had experienced a poorer environ- ment as infants. However, it was the retrospective epidemiological studies of Barker [2] and his colleagues that suggested that the intrauterine and infant environments might have major influences on the later risk of disease. They proposed that certain events in prenatal life ‘programmed’ postnatal physi- ology in such a way that adult type-2 diabetes (T2D), cardiovascular heart disease, and central obesity were more likely.
    [Show full text]
  • Impact of Early Nutrition, Physical Activity and Sleep on the Fetal Programming of Disease in the Pregnancy: a Narrative Review
    nutrients Review Impact of Early Nutrition, Physical Activity and Sleep on the Fetal Programming of Disease in the Pregnancy: A Narrative Review Jorge Moreno-Fernandez 1,2 , Julio J. Ochoa 1,2,* , Magdalena Lopez-Frias 1,2 and Javier Diaz-Castro 1,2 1 Department of Physiology, Faculty of Pharmacy, Campus Universitario de Cartuja, E-18071 Granada, Spain; [email protected] (J.M.-F.); [email protected] (M.L.-F.); [email protected] (J.D.-C.) 2 Institute of Nutrition and Food Technology “José Mataix Verdú”, University of Granada, E-18071 Granada, Spain * Correspondence: [email protected]; Tel.: +34-958-241-000 (ext. 20317) Received: 21 November 2020; Accepted: 18 December 2020; Published: 20 December 2020 Abstract: Early programming is the adaptation process by which nutrition and environmental factors alter development pathways during prenatal growth, inducing changes in postnatal metabolism and diseases. The aim of this narrative review, is evaluating the current knowledge in the scientific literature on the effects of nutrition, environmental factors, physical activity and sleep on development pathways. If in utero adaptations were incorrect, this would cause a mismatch between prenatal programming and adulthood. Adequate caloric intake, protein, mineral, vitamin, and long-chain fatty acids, have been noted for their relevance in the offspring brain functions and behavior. Fetus undernutrition/malnutrition causes a delay in growth and have detrimental effects on the development and subsequent functioning of the organs. Pregnancy is a particularly vulnerable period for the development of food preferences and for modifications in the emotional response. Maternal obesity increases the risk of developing perinatal complications and delivery by cesarean section and has long-term implications in the development of metabolic diseases.
    [Show full text]