Thrifty Phenotype Research Articles

Shared genetic architecture links energy metabolism, behavior and starvation resistance along a power-endurance axis

Abstract Shared developmental, physiological, and molecular mechanisms can generate strong genetic covariances across suites of traits, constraining genetic variability, and evolvability to certain axes in multivariate trait space (“variational modules” or “syndromes”). Such trait suites will not only respond jointly to selection; they will also covary across populations that diverged from one another by genetic drift. We report evidence for such a genetically correlated trait suite that links traits related to energy metabolism along a “power-endurance” axis in Drosophila melanogaster. The “power” pole of the axis is characterized by high potential for energy generation and expenditure—high expression of glycolysis and TCA cycle genes, high abundance of mitochondria, and high spontaneous locomotor activity. The opposite “endurance” pole is characterized by high triglyceride (fat) reserves, locomotor endurance, and starvation resistance (and low values of traits associated with the “power” pole). This trait suite also aligns with the first principal component of metabolome; the “power” direction is characterized by low levels of trehalose (blood sugar) and high levels of some amino acids and their derivatives, including creatine, a compound known to facilitate energy production in muscles. Our evidence comes from six replicate “Selected” populations adapted to a nutrient-poor larval diet regime during 250 generations of experimental evolution and six “Control” populations evolved in parallel on a standard diet regime. We found that, within each of these experimental evolutionary regimes, the above traits strongly covaried along this “power-endurance” axis across replicate populations which diversified by drift, indicating a shared genetic architecture. The two evolutionary regimes also drove divergence along this axis, with Selected populations on average displaced towards the “power” direction compared to Controls. Aspects of this “power-endurance” axis resemble the “pace of life” syndrome and the “thrifty phenotype”; it may have evolved as part of a coordinated organismal response to nutritional conditions.

Cardiovascular Health Starts in the Womb.

Hypertension has largely been viewed as a disorder of adulthood. Historically, blood pressure (BP) was not routinely measured in children because hypertension was considered uncommon in childhood. It was not until the 1970s that it was apparent that in childhood BP levels were normally lower compared with those in adults, were related to age and growth, and that abnormal BP in children needed different definitions. Based on the distribution of BP levels in available child cohorts, the 95th percentile of BP levels became the definition of hypertension in children and adolescents-an epidemiological definition. Subsequent clinical and epidemiological research identified associated risk factors in childhood that linked abnormal BP in youth with hypertension in adulthood. In the 1980s, the Barker hypothesis, based on observations that low birth weight could be linked to cardiovascular disease in adulthood, promoted further research spanning epidemiological, clinical, and basic science on the childhood origins of hypertension. This review focuses on recent findings from both longitudinal maternal-child cohorts and experimental models that examine both maternal and offspring conditions associated with risks of subsequent cardiovascular disease.

Childhood growth of singletons conceived following intracytoplasmic sperm injection - irrelevance of gonadotropin stimulation.

In conventional, gonadotropin stimulated, in vitro fertilization or intracytoplasmic sperm injection (c-IVF/ICSI) growth and development of multiple follicles is induced by gonadotropins, combined with gonadotropin-releasing hormone agonist or antagonist. In recent studies, singletons conceived after c-IVF/ICSI cycles had lower birth weight not only than spontaneously conceived children but also children born after unstimulated natural IVF/ICSI cycles (NC-IVF/ICSI). Lower birth weight is associated with a catch-up growth within the first years of life. Following the Barker hypothesis accelerated growth has been associated with a higher risk of cardiovascular diseases later in life. The aim of the study is to assess, if children conceived with NC-IVF/ICSI have a higher birthweight and therefore do not show a catch-up growth within the first two years. Therefore, we assume that children born after NC-IVF/ICSI have a better long-term cardiometabolic risk profile. Whether the weight- and height gain is comparable to spontaneously conceived children is unknown, since to our knowledge we are the first study to investigate the longitudinal growth of children born after unstimulated natural cycle ICSI (NC-ICSI). We conducted a single-center, prospective cohort study (2010-2017) including children (n = 139) born after NC-ICSI or c-ICSI treatment. Growth parameters up to 24 months were collected. Standard deviation scores based on growth references were calculated. The study included 98 children in the NC-ICSI and 41 children in the c-ICSI group. The median birth weight in NC-ICSI children was 3.4 kg [0.1 standard deviation score (SDS)] compared to 3.3 kg (-0.3 SDS) in c-ICSI children (p = 0.61). Median length at birth was 50 cm in both groups (NC-ICSI (-0.5 SDS), c-ICSI children (-0.8 SDS), p = 0.48). At age 24 months, median weight in NC-ICSI children was 12.2 kg (0.3 SDS) versus 12.2 kg (0.2 SDS) in c-ICSI children (p = 0.82) and median length 87.5 cm (0.1 SDS) versus 88.0 cm (0.4 SDS) (p = 0.43). We found no difference in growth between children conceived after stimulated and unstimulated ICSI. Growth parameters of both treatment groups did not differ from Swiss national growth references (N = 8500). One of the main limitations of our study was the small sample size (N = 139) of complete data sets over time and the high drop-out rate of 49% (68/139). Nevertheless, with the increasing number of children born after IVF/ICSI every year it is of immense importance to search for possibilities to reduce their long-term cardiometabolic risk and we want our data to contribute to this discussion.

SPAG7 deletion causes intrauterine growth restriction, resulting in adulthood obesity and metabolic dysfunction.

From a forward mutagenetic screen to discover mutations associated with obesity, we identified mutations in the Spag7 gene linked to metabolic dysfunction in mice. Here, we show that SPAG7 KO mice are born smaller and develop obesity and glucose intolerance in adulthood. This obesity does not stem from hyperphagia, but a decrease in energy expenditure. The KO animals also display reduced exercise tolerance and muscle function due to impaired mitochondrial function. Furthermore, SPAG7-deficiency in developing embryos leads to intrauterine growth restriction, brought on by placental insufficiency, likely due to abnormal development of the placental junctional zone. This insufficiency leads to loss of SPAG7-deficient fetuses in utero and reduced birth weights of those that survive. We hypothesize that a 'thrifty phenotype' is ingrained in SPAG7 KO animals during development that leads to adult obesity. Collectively, these results indicate that SPAG7 is essential for embryonic development and energy homeostasis later in life.

Seasonal changes in body composition in children from Maya agriculturalists in central Yucatán, Mexico.

Development policies have aimed to substitute subsistence agriculture for cash crops or other cash generating activities to encourage local farmers to depend on store-bought groceries available year-round instead of seasonal subsistence crops. In this paper, we test the hypothesis that increased dependence on store bought foods has decreased seasonal changes in nutritional status and fat mass in Maya Children from Yucatan, Mexico. Weight for age (W/A), body mass index (BMI), and tricipital Skinfold z scores in children under the age of 10 years from 14 Maya rural towns with different degrees of development were compared longitudinally between scarcity and abundance seasons using a repeated measures analysis of variance. Height for age (H/A) z scores were also estimated. Origin of food consumed corresponded to the town's degree of development. Nutritional status (W/Az) and adiposity, BMI, and tricipital z scores were significantly lower during the scarcity season in every community. W/Az, tricipital skinfold z, and H/Az scores were significantly higher in developed than in traditional towns, yet in both types of town W/Az and H/Az scores were below the WHO standard mean. Tricipital skinfold z score was only below the WHO standard amongst traditional towns during the scarcity season. Increased dependence on store foods failed to eliminate significant losses in body fat during the scarcity season. This failure may be affecting linear growth and promoting a thrifty phenotype that is seen in short and stocky individuals with a tendency to accumulate fat during abundance seasons.

Relation Between Obesity and Type 2 Diabetes: Evolutionary Insights, Perspectives and Controversies.

Since the mid-twentieth century, obesity and its related comorbidities, notably insulin resistance (IR) and type 2 diabetes (T2D), have surged. Nevertheless, their underlying mechanisms remain elusive. Evolutionary medicine (EM) sheds light on these issues by examining how evolutionary processes shape traits and diseases, offering insights for medical practice. This review summarizes the pathogenesis and genetics of obesity-related IR and T2D. Subsequently, delving into their evolutionary connections. Addressing limitations and proposing future research directions aims to enhance our understanding of these conditions, paving the way for improved treatments and prevention strategies. Several evolutionary hypotheses have been proposed to unmask the origin of obesity-related IR and T2D, e.g., the "thrifty genotype" hypothesis suggests that certain "thrifty genes" that helped hunter-gatherer populations efficiently store energy as fat during feast-famine cycles are now maladaptive in our modern obesogenic environment. The "drifty genotype" theory suggests that if thrifty genes were advantageous, they would have spread widely, but proposes genetic drift instead. The "behavioral switch" and "carnivore connection" hypotheses propose insulin resistance as an adaptation for a brain-dependent, low-carbohydrate lifestyle. The thrifty phenotype theory suggests various metabolic outcomes shaped by genes and environment during development. However, the majority of these hypotheses lack experimental validation. Understanding why ancestral advantages now predispose us to diseases may aid in drug development and prevention of disease. EM helps us to understand the evolutionary relation between obesity-related IR and T2D. But still gaps and contradictions persist. Further interdisciplinary research is required to elucidate complete mechanisms.

Pre-eclampsia and barker's hypothesis: are we beginning to see the trees within the forest?

Pre-eclampsia and barker's hypothesis: are we beginning to see the trees within the forest?

The interplay of maternal and offspring obesogenic diets: the impact on offspring metabolism and muscle mitochondria in an outbred mouse model.

Consumption of obesogenic (OB) diets increases the prevalence of maternal obesity worldwide, causing major psychological and social burdens in women. Obesity not only impacts the mother's health and fertility but also elevates the risk of obesity and metabolic disorders in the offspring. Family lifestyle is mostly persistent through generations, possibly contributing to the growing prevalence of obesity. We hypothesized that offspring metabolic health is dependent on both maternal and offspring diet and their interaction. We also hypothesized that the sensitivity of the offspring to the diet may be influenced by the match or mismatch between offspring and maternal diets. To test these hypotheses, outbred Swiss mice were fed a control (C, 10% fat, 7% sugar, and n = 14) or OB diet (60% fat, 20% sugar, and n = 15) for 7 weeks and then mated with the same control males. Mice were maintained on the same corresponding diet during pregnancy and lactation, and the offspring were kept with their mothers until weaning. The study focused only on female offspring, which were equally distributed at weaning and fed C or OB diets for 7 weeks, resulting in four treatment groups: C-born offspring fed C or OB diets (C » C and C » OB) and OB-born offspring fed C or OB diets (OB » C and OB » OB). Adult offspring's systemic blood profile (lipid and glucose metabolism) and muscle mitochondrial features were assessed. We confirmed that the offspring's OB diet majorly impacted the offspring's health by impairing the offspring's serum glucose and lipid profiles, which are associated with abnormal muscle mitochondrial ultrastructure. Contrarily, maternal OB diet was associated with increased expression of mitochondrial complex markers and mitochondrial morphology in offspring muscle, but no additive effects of (increased sensitivity to) an offspring OB diet were observed in pups born to obese mothers. In contrast, their metabolic profile appeared to be healthier compared to those born to lean mothers and fed an OB diet. These results are in line with the thrifty phenotype hypothesis, suggesting that OB-born offspring are better adapted to an environment with high energy availability later in life. Thus, using a murine outbred model, we could not confirm that maternal obesogenic diets contribute to female familial obesity in the following generations.

Influence of maternal stress during pregnancy and child outcomes

Prenatal stress is an overwhelming concern in pregnancy-related care. The mother exposed to prenatal stress poses the fetus at the risk of developing many adverse health conditions. It is estimated that around 10%–20% of pregnant women suffer from mental health concerns during the perinatal period. History dates back to the tragic 1961 Thalidomide tragedy which cautions both the individual and the health professionals about pregnancy-related care. Multiple mechanisms have been put forth to link the relationship between the indwelling fetus and the carrying mother. Of them, the “Barker hypothesis” suggests the role of perinatal conditions in influencing the development of diseases in the later life of the child. Mental health issues are a growing concern during pregnancy. In recent years, there has been an increasing trend of smoking, alcohol abuse, and illicit drug use among pregnant women, which has been shown to adversely affect the fetus. In the 21st century, environmental stressors are a looming threat that has now been shown to affect the pregnant population. These data emphasize the need to consider early environmental life events as etiological factors for adverse child outcomes. This review summarizes the history, background, causes of maternal stress, and the ways to improve them.

Comparative study of pluripotency-related gene expression in Umbilical Cord Mesenchymal Stem Cells (UC-MSC) from IUGR, SGA and normally grown fetuses

Background and Objectives: Intrauterine growth restriction (IUGR) is worldwide a public health problem. IUGR-born individuals acquire epigenetic “thrifty-phenotype” gene adaptations, according to the “Barker hypothesis” and are more susceptible to develop metabolic related diseases. Small for Gestational Age (SGA) fetuses consist of a transitional group between IUGR and normally grown fetuses (Appropriate for Gestational Age, AGA). Currently, there is limited information in the literature whether IUGR or SGA status affects the pluripotency of the Umbilical Cord Mesenchymal Stem Cell (UC-MSC) with respect to gene expression at various stages of cell culture. Materials and Methods: In this study, we investigated stemness marker expression in UC-MSCs derived from twenty-one AGA, IUGR, and SGA fetuses. The relative expression of key genes involved in stemness, pluripotency, and cell proliferation, namely IGF2BP1, CMYC, GLI1, P21, NANOG, OCT4, and SOX2, was assessed in UC-MSCs at passages P0 and P1 using flow cytometry and quantitative PCR. Results: We found lower median expression levels of IGF2BP1 in IUGR group (P=0.044) and P21 in SGA group (P=0.024) at P0 compared to control group. GLI1 and OCT4 exhibited reduced expression at P1 in the IUGR group (P=0.0434 and P=0.0343 respectively) compared to AGA. NANOG median expression differed statistically between CONTROL and IUGR group in P0 (P=0.034) and P1 (P=0.0205). No significant changes were noted for SOX2 and CMYC median expression among the various groups in P0 and P1. Conclusion: The comparative analysis of stemness marker expression among UC-MSCs from these three different sources is a novel descriptive aspect of our study, adding a new perspective to the existing literature.

Gestational exposure to the great Chinese famine: early life undernutrition impact on prostatic hyperplasia in adulthood.

Benign prostatic hyperplasia (BPH) is a frequent illness in aged men that impacts their quality of life; early childhood exposure to famines may have long-term effects on the chance of developing BPH. The aim of this study is to investigate the relationship between early-life famine exposure and benign prostatic hyperplasia (BPH) risk in Chinese men born during 1959-1961. We used medical records from a large, comprehensive hospital to screen people born in China during the years of famine (1959-1961). Birthplaces were identified as indicators of famine exposure status. In the time window between 2017 and 2022, people born during the famine years who had prostatic ultrasonic examinations were selected, and their medical records were retrieved from the database. Univariate and multivariate logistic regression analyses investigated the relationship between famine exposure and BPH risk. A total of 3,009 subjects were included in this study. Patients with heavy famine exposure had older age, shorter height, lighter weight, lower cholesterol, lower uric acid (UA), lower aspartate aminotransferase (ALT), and a higher incidence of BPH than those with light famine exposure (all p < 0.05). Univariate logistic regression showed that BPH was positively related to famine exposure, age, height, weight, and body mass index (BMI) but negatively related to UA (all p < 0.05). Multivariate logistic regression showed that age and famine exposure were still independent risk factors (p < 0.05), while UA was an independent protective factor for BPH (p < 0.05). Heavy famine exposure increased the risk of BPH (adjusted OR = 1.214, 95% CI = 1.05-1.467, p = 0.045). Famine and malnutrition exposure during early life may be independent risk factors for BPH in Chinese adults. This relationship provides additional evidence to support the fetal origins of adult diseases and offers clues for the pathological mechanisms of BPH.

The fascinating theory of fetal programming of adult diseases: A review of the fundamentals of the Barker hypothesis.

The theory of fetal programming of adult diseases was first proposed by David J.P. Barker in the eighties of the previous century, to explain the higher susceptibility of some people toward the development of ischemic heart disease. According to his hypothesis, poor maternal living conditions during gestation represent an important risk factor for the onset of atherosclerotic heart disease later in life. The analysis of the early phases of fetal development is a fundamental tool for the risk stratification of children and adults, allowing the identification of susceptible or resistant subjects to multiple diseases later in life. Here, we provide a narrative summary of the most relevant evidence supporting the Barker hypothesis in multiple fields of medicine, including neuropsychiatric disorders, such as Parkinson disease and Alzheimer disease, kidney failure, atherosclerosis, coronary heart disease, stroke, diabetes, cancer onset and progression, metabolic syndrome, and infectious diseases including COVID-19. Given the consensus on the role of body weight at birth as a practical indicator of the fetal nutritional status during gestation, every subject with a low birth weight should be considered an "at risk" subject for the development of multiple diseases later in life. The hypothesis of the "physiological regenerative medicine," able to improve fetal organs' development in the perinatal period is discussed, in the light of recent experimental data indicating Thymosin Beta-4 as a powerful growth promoter when administered to pregnant mothers before birth.

Starvation resistance in planarians: multiple strategies to get a thrifty phenotype.

Starvation resistance is a life-saving mechanism for many organisms facing food availability fluctuation in the natural environment. Different strategies have been episodically identified for some model organisms, the first of which was the ability to suppress metabolic rate. Among the identified strategies, the ability of planarians to shrink their body under fasting conditions and revert the process after feeding (the growth-degrowth process) represents a fascinating mechanism to face long periods of fasting. The growth-degrowth process is strictly related to the capability of planarians to continuously maintain tissue homeostasis and body proportions even in challenging conditions, thanks to the presence of a population of pluripotent stem cells. Here, we take advantage of several previous studies describing the growth-degrowth process and of recent progress in the understanding of planarian homeostasis mechanisms, to identify tissue-selective transcriptional downregulation as a driving strategy for the development of a thrifty phenotype, and the p53 transcription factor as a player in adjusting tissue homeostasis in accordance with food availability.

YTHDF3 modulates the Cbln1 level by recruiting BTG2 and is implicated in the impaired cognition of prenatal hypoxia offspring

The "Fetal Origins of Adult Disease (FOAD)" hypothesis holds that adverse factors during pregnancy can increase the risk of chronic diseases in offspring. Here, we investigated the effects of prenatal hypoxia (PH) on brain structure and function in adult offspring and explored the role of the N6-methyladenosine (m6A) pathway. The results suggest that abnormal cognition in PH offspring may be related to the dysregulation of the m6A pathway, specifically increased levels of YTHDF3 in the hippocampus. YTHDF3 interacts with BTG2 and is involved in the decay of Cbln1 mRNA, leading to the down-regulation of Cbln1 expression. Deficiency of Cbln1 may contribute to abnormal synaptic function, which in turn causes cognitive impairment in PH offspring. This study provides a scientific clues for understanding the mechanisms of impaired cognition in PH offspring and provides a theoretical basis for the treatment of cognitive impairment in offspring exposed to PH.

A fetus in the world: Physiology, epidemiology, and the making of fetal origins of adult disease

Since the late 1980s, the fetal origins of adult disease, from 2003 developmental origins of health and disease (DOHaD), has stimulated significant interest in and an efflorescence of research on the long-term effects of the intrauterine environment. From the start, this field has been interdisciplinary, using experimental animal, clinical and epidemiological tools. As the influence of DOHaD on public health and policy expanded, it has drawn criticism for reducing the complex social and physical world of early life to women’s reproductive bodies as drivers of intergenerational ills. This paper explains this narrowing of focus in terms of a formative and consequential exchange between David Barker, the British epidemiologist whose work is credited with establishing the field, and the discipline of fetal physiology. We suggest that fetal physiologists were a crucial constituency of support for Barker’s hypothesis about early life origins of disease. Their collaborations with Barker helped secure and sustain the theory amid considerable controversy. The trajectory of DOHaD and its focus on the maternal body can be understood, we argue, as a consequence of this alliance, which brought together two distinct conceptualizations of the intrauterine environment, one from epidemiology and the other from fetal physiology. Along the way, we trace the histories of these conceptualizations, both of which were products of mid-to-late twentieth century British science, and show how Barker’s early emphasis on social and economic conditions was superseded by a narrower focus on physiological mechanisms acting upon the autonomous fetus.

Barker's Hypothesis Among the Global Poor: Positive Long-Term Cardiovascular Effects of in Utero Famine Exposure

An influential literature on the Developmental Origins of Health and Disease (DOHaD) has documented that poor conditions in utero lead to higher risk of cardiovascular disease at older ages. Evidence from low-income countries (LICs) has hitherto been missing, despite the fact that adverse in utero conditions are far more common in LICs. We find that Malawians exposed in utero to the 1949 Nyasaland famine have better cardiovascular health 70 years later. These findings highlight the potential context specificity of the DOHaD hypothesis, with in utero adversity having different health implications among aging LIC individuals who were exposed to persistent poverty.

Современные трактовки эволюционных и антропоэкологических аспектов гипотезы «экономного генотипа»

Introduction. There are a number of genes, individual alleles of which or their combinations make the carrier susceptible to the disease. In the case of type 2 diabetes, obesity, and metabolic syndrome, the hypothesis of a “thrifty genotype” was put forward as a combination of gene alleles that provided their carriers with advantages in the prehistoric and historical past, but provoked morbidity now. Such a genotype should have previously been under the positive selection, whereas in the modern world it may play a negative role. It is also obvious that the expression of the thrifty genotype as well as the genes that form it and their alleles, should depend on anthropological and ecological conditions: the ecology of the region where the human population lives and their traditional subsistence and farming systems. The aim of the proposed review is to systematize modern views on the problem of thrifty genotype with special attention to the evolutionary anthropological, and ecological aspects of the problem. Materials and methods. Herein we represent a review of current data regarding the thrifty genotype hypothesis. The paper reviews the main theses of the hypothesis, its basis, and the arguments of supporters and critics. The evolutionary, anthropological, and ecological aspects of the thrifty genotype hypothesis are discussed. Results. A significant number of experimental studies and reviews give an idea of the distribution of thrifty genotypes in populations of different origins and anthropological affiliations. However, the coverage of material and inclusion of population data in the analysis is uneven. The genetic geography of thrifty genotypes remains poor and, commonly, insufficiently studied. The most complete and methodologically correct systematization of primary materials on the prevalence of thrifty genotypes, their connection with the ecological conditions of the natural environment, and anthropogenic factors, including traditional subsistence and farming systems and the nature of nutrition, remains still relevant. Conclusion. We consider the integrated ecological approach to be the most promising direction of theoretical research on the problem of “thrifty genotype”. The approach from the standpoint of the concept of “niche construction” removes the seeming contradictions between the main hypotheses considered in our review – the thrifty genotype, the drifty genotype and the thrifty phenotype. @ 2023. This work is licensed under a CC BY 4.0 license

Prenatal caloric restriction adjusts the energy homeostasis and behavior in response to acute and chronic variations in food availability in adulthood.

Fetal metabolic programming produced by unfavorable prenatal nutritional conditions leads to the development of a disorder called "thrifty phenotype", which is associated with pathologies such as diabetes and obesity in adulthood. However, from an ecophysiological approach, few studies have addressed the development of thrifty phenotypes in terms of energy. This might represent an adaptive advantage against caloric deficiency conditions extending into adulthood. The objective of this study is to investigate the potential adaptive value of the thrifty phenotype expression through prenatal programming in a rodent model experiencing varying dietary conditions in different temporal contexts. To fill this gap, adult males of Mus musculus (BALB/C) from two maternal pregnancy groups were analyzed: control (ad libitum feeding) and caloric restriction from day 10 of gestation (70% restriction). Adult offspring of these groups were split further for two experiments: acute food deprivation and chronic caloric restriction at 60%. The acute food deprivation was performed for 24, 48 or 72h while the caloric restriction regime was sustained for 20days. For each experiment, morphological variables, such as body and organ mass, and gene expression related to lipid and carbohydrate metabolism from the liver and brain, were evaluated. In chronic caloric restriction, behavioral tests (open-field test and home-cage behavior) were performed. Our results indicate that under acute deprivation, the liver mass and triglyceride content remained unchanged in individuals subjected to prenatal restriction, in contrast to the reduction experienced by the control group. The latter is associated with the expression of the key genes involved in energy homeostasis (Pepck, Pparα/Pparγ), indicating a differential use of nutritional resources. In addition, thrifty animals, subjected to chronic caloric restriction, showed a severe reduction in locomotor and gluconeogenic activity, which is consistent with the regulatory role of Sirt1 and its downstream targetsMaoandPepck. Our results reveal that prenatal caloric restriction translates into a sparing metabolism in response to acute and chronic lack of food in adulthood.

Comparison of Body Measurements and Adiposity Between Small and Appropriate for Gestational Age Term Neonates: An Observational Study

Background Small for gestational age (SGA) infants have preserved adipose tissue compared to appropriate for gestational age (AGA) infants. This forms the basis of the fetal origin of adult disease. Studies show that Indian babies are ‘thin’ but ‘fat’ compared to babies born in high-income countries. Skin fold thickness (SFT) is a measure of adiposity. Objective To compare the newborn adiposity by SFT in term moderate SGA infants and term AGA infants. Methods We included 222 term newborns, 62 moderate SGA, and 160 AGA with no fetal growth restriction. Babies born to mothers with obesity, abnormal weight gain, pregnancy-related illnesses, and severe SGA were excluded. Weight, length, head circumference, and other circumferences (mid-upper-arm, abdominal, and mid-thigh) and SFT (Anterior abdomen, quadriceps or mid-thigh, triceps, and subscapular) were measured. The mean SD scores were calculated for each of the measurements. Comparisons were made using independent sample t-test. Results Weight, length, circumferences, and SFT were significantly lower ( p &lt; .001) in the SGA infants compared to AGA. Among AGA, the mean standard deviation (SD) scores of all measures ranged between 0.1 and 0.5. However, in the SGA group, the mean SD scores for SFT showed minimal deviation (–0.3 to –0.5) compared to anthropometry (–0.7 to –1.2) and circumferences (–0.5 and –0.7), demonstrating the preservation of newborn adiposity. All the SFTs showed a moderate correlation ( r = 0.4) with the newborn weight and circumferences. There was no correlation to the anthropometry of non-obese mothers. Conclusion Term SGA newborns showed preservation of adiposity compared to AGA newborns.

A maladaptive parental effect: offspring survival decreases with maternal over-condition in an amphibian

Abstract Parental effects are often considered an evolved response, in which parents transmit information about the environment to enhance offspring fitness. However, these effects need not be adaptive. Here, we provide a striking example by presenting evidence that overfeeding of adult Mexican spadefoot toads, Spea multiplicata, is associated with decreased offspring survival. After a temporary change to their standard feeding regimen, S. multiplicata in our captive colony developed a much higher body condition (i.e. body mass for a given body length) than those in the wild. We analysed data from three subsequent experiments and found that although the body condition of a father was positively correlated with tadpole survival, mothers with a higher condition had lower tadpole survival. Our study highlights how obesity can negatively impact future generations via maladaptive maternal effects. Such effects could be especially likely for animals living in variable environments (such as spadefoots) that have evolved ‘thrifty phenotypes’ that make them prone to obesity. Our study also illustrates how husbandry conditions typically regarded as beneficial might be harmful. Given that captive breeding programmes are increasingly used to combat worldwide amphibian declines, these programmes must consider the ecology and evolutionary history of the focal species to minimize any maladaptive parental effects.