Developmental Origins of Health and Disease

Background: Undernutrition in early life (UELife) is a condition associated with greater occurrence of chronic diseases in adulthood. Some studies on this relationship have used short stature as indicator of UELife. However, other non-nutritional factors can also determine short stature. Depending on the severity of UELife, the human body reacts primarily compromising weight and length gain, but prioritizing brain growth, resulting in disproportionate individuals. Based on this premise, this study aimed to validate a new anthropometric indicator of UELife. Design: Using stature and head circumference data from a probabilistic sample of 3,109 women, the Head-to-Height Index was calculated: HHI = (head × 2.898)/height. A HHI >1.028 (75th percentile) was the best cutoff for predicting obesity (best balance between sensitivity/ specificity, largest area under the receiver operating characteristic curve, and highest correlation coefficient) and was used to define the condition of body disproportionality. The strength of associations with several outcomes was tested for both disproportionality and short stature (height ≤25th percentile: 153.1 cm). Results: In adjusted analysis for confounding factors (age, smoking, and education level), the strength of the associations between body disproportionality and the analyzed outcomes was greater than that observed when short stature was used. Respectively, the observed prevalence ratios (95% CI) were (P<0.05 for all comparisons): obesity

The typical classification of prevention into primary, secondary, and tertiary categories has encountered various criticisms. We review the history and limitations of this and other classifications, and offer a substitute paradigm: five Stages of Prevention, which address consecutive steps in the development of chronic and gradually developing diseases, and corresponding stages for prevention: 1) avoiding exposure to causative agents, 2) reducing acquisition of disease resulting from exposure, 3) interrupting advancement of acquired disease, 4) preventing complications from advanced disease, and 5) delay (or palliation) of death, or rehabilitation of disability, from complications. This new model can serve as a tool for health planning, including calculation of costs vs. benefits for investment of resources. It can also be applied to counseling patients on personal options for prevention.

This slide presentation was first developed at Loma Linda University 2006-2009, with resident Melody Law).  In various versions, it has had over 20,000 online views, 14,537 on Academia.edu by over 10,000 unique viewers, and about 10,000 on Researchgate.net. This 2022 version has replaced previous versions posted on Academia, and adds references at the end, which were not included in early versions.

Early growth cessation and reproduction are predicted to maximize fitness under conditions of high adult mortality, factors that could explain the pygmy phenotype of many rainforest hunter-gatherers. This life-history hypothesis is elegant but contentious in part because it lacks a clear biological mechanism. One mechanism stems from the field of human immunological ecology and the concept of inflammation “memory” across the life cycle and into subsequent generations. Maternal exposures to disease can influence immunological cues present in breast milk; because maternal provisioning via lactation occurs during critical periods of development, it is plausible that these cues can also mediate early growth cessation and small body size. Such epigenetic hypotheses are difficult to test, but the concept of developmental programming is attractive because it could explain how the stature of a population can change over time, in terms of both secular increases and rapid intergenerational decreases. Here we explore this concept by focusing on the Aeta, a population of former hunter-gatherers, and the Ilocano, a population of rice farmers. We predicted that Aeta mothers would produce breast milk with higher concentrations of four bioactive factors due to high infectious burdens. Further, we predicted that the concentrations of these factors would be highest in the cohort of women born in the early 1990s, when exposure to infectious disease was acute following the eruption of Mount Pinatubo in June 1991. We analyzed levels of adiponectin, C-reactive protein, and epidermal growth factor in the milk of 24 Aeta and 31 Ilocano women and found no detectable differences, whereas levels of transforming growth factor-􏰇2 were elevated among the Aeta, particularly as a function of maternal age. We found no difference between cohorts divided by the volcanic eruption (n = 43 born before, n = 12 born after). We discuss the implications of our findings for the terminal investment hypothesis and we suggest that the historical ecology of the Aeta is a promising model system for testing epigenetic hypotheses focused on the evolution of small body size.

Harsh conditions during development may alter the human adult phenotype in ways that affect vulnerability to disease and death. This study’s objectives are A) to explore the utility of neural canal size and appendicular osteoarthritis as prospective indicators of developmental stress; B) to test for developmental stress effects in a foraging population with no significant socioeconomic stratification; and C) to explore temporal variation in neuroskeletal size and joint degeneration. The study sample consists of 143 Later Stone Age foragers (M=75, F=64, I=4) from the Cape Floristic Region of southern Africa. 135 cases have radiocarbon dates between 9100 and 560 uncalibrated years BP. Osteoarthritis was quantified with an ordinal scoring procedure. Relationships among radiocarbon date, measures of body and neural canal size, OA, and age at death were explored using logistic and ordinary least squares regression, independence tests, and means contrasts. Age, sex, and body size were controlled where appropriate. A positive relationship is observed between age at death and both body size and ML NC diameter, but reaches statistical significance only in the latter case (OR=1.74, 95% CI=1.08–2.82). The effect is detected in both sexes but odds ratios are greater and p values smaller in females (Male OR=1.50, 95% CI=0.82–2.73; Female OR=2.14, 95% CI=1.02–4.50). Age at death is the only significant predictor for both presence and severity of osteoarthritis. No significant relationship is observed between age and anteroposterior diameter. Average mediolateral diameter of the neural canal declines between 3000–2000BP and increases slightly afterwards (β 1 = −0.83, β 2 = 0.68, adjusted R 2 = 0.06, SEE=0.99). This quadratic curve is consistent with published accounts of temporal change in average body size. No temporal pattern is identified in osteoarthritis.

We propose a transdisciplinary, life span framework for examining the underlying cause of the observed intergenerational decline in health among Hispanic Americans. We focus on acculturation, and we posit that acculturation- related processes in first-generation Hispanic immigrant mothers may affect the intrauterine development of an unborn child, via the process of fetal pro- gramming, to produce phenotypic effects that may alter the susceptibility for noncommunicable chronic diseases. In this manner, an intergenerational cascade of perpetuation may become established. Our framework may shed light on the biological, behavioral, and social causes of intergenerational cycles of vulnerability among immigrant minority groups, with public health and policy implications for primary prevention and intervention.

Environmentally-induced epigenetic changes of gene regulation could result from chronic, lifelong exposure, to low doses of environmental toxicants, such as chemicals including, tobacco smoking and endocrine disrupting compounds, or to other environmental factors such as nutritional changes, and lifestyle-related conditions. These environmentally-acquired epigenetic marks may influence the control of gene regulation through DNA methylation, histone modification, or through a large set of non-coding RNAs (ncRNAs). These epigenetic effects might be passed on to the developing embryo and child as inheritable non-genetic marks, which recapitulate previous lifelong history of exposure to environmental influences that start from the stage of primordial germ cell, passing through the maturing germ cell, and ending by the zygote stage. This involves the paternally transmitted information on the sperm that contribute to modulating embryogenesis functions and later childhood development, in concert with, the maternally transmitted information encountered by the exposure to a large milieu of environmental factors either periconceptionally or during lactation period.

In lieu of an abstract: Introduction:

Bioarchaeologists have been investigating diverse features of past lives, particularly health and disease relative to identity, for several decades. Identity can be defined in a number of ways across disciplines and fields, but within the social sciences it is generally understood as the features that comprise an individual or group. It is fluid, a process, and composed of multiple aspects, such as gender, social race, religion, ancestry, ethnicity , occupation, sexual orientation, socioeconomic status, and class. Any of these may be more or less significant in some situations (Weinreich and Saunderson 2003). In bioarchaeology, most work on identity, health, and disease has been investigated at the population level within the context of exploring group identity (Larsen 2015). This chapter focuses on this analytical level as well. Prior to the early 2000s, most of this research analyzed one or two aspects of identity, such as socioeconomic status, relative to health. But over the ensuing years, spurred in large part by Knudson and Stojanowski’s (2008, 2009) influential works, bioarchaeological research on the topic has greatly increased in number, scope, theoretical sophistication , and attention to the complexity of identity and its equally complex , compounding effects on health and the production of disease. As part of this, bioarchaeologists have recently begun to employ intersectionality (Zuckerman and Crandall 2019), which originated within third-wave Black feminist theoretical work on identity (Collins 1990; hooks 1984). Intersectionality conceptualizes simultaneous intersections among aspects of social difference and identity, such as race, ethnicity, sex, age and 164 · Molly K. Zuckerman religion, and forms of systemic oppression, like racism and classism. It has become a commonly used theoretical framework across diverse fields in the social and natural sciences, humanities, and medical sciences (e.g., Bowleg 2012; Rosenthal 2016). Perhaps most influentially and informatively, over the past decade bioarchaeologists have begun to meaningfully engage with theory, methods, and data from public health and clinical medicine on how identity, often conceptualized through intersectionality, relates to health and disease in modern populations (Klaus 2014). Much of this work deals with how chronic or episodic lifelong experiences of physiological stress can affect health and susceptibility to disease, particularly chronic and degenerative disease, over the life course. Importantly, these experiences are intractably enmeshed with individual-level and group-level identity (Berkman, Kawachi, and Glymour 2014). This work is especially valuable to bioarchaeology because experiences of chronic stress can generate suites of skeletal stress indicators, such as porotic hyperostosis (PH) and periosteal reactions, as well as oral pathologies, such as linear enamel hypoplasias (LEH), dental caries, and periodontal disease (PD). Also, as these indicators form over the life course, experiences of stress over the life course— and the cumulative effects of such experiences—can be empirically reconstructed from skeletal material (Larsen 2015). In addition, many forms of chronic disease, ranging from osteoarthritis to acquired syphilis, leave discernible traces within human remains at the macroscopic to biomolecular level (Ortner 2003). This means that bioarchaeologists can reconstruct the downstream effects of stress relative to disease and identity as well. Rather than superficially engaging with research in public health and clinical medicine on stress, such as through use of a single theory, bioarchaeologists are using it to generate robust hypotheses. They then test these hypotheses using bioarchaeological data, and interpret their findings within frameworks informed not only by public health and clinical medical research but also by highly specific and contextualized archaeological as well as historical and/or ethnographic data (e.g., Crespo et al. 2016; Marklein, Leahy, and Crews 2016). Importantly, this approach aims to produce a more holistic understanding of health, disease, and stress in the past (Marklein et al. 2016; Reitsema and McIlvaine 2014), while generating inferences about how these biological processes relate to diverse aspects of identity. Within this vein, bioarchaeological research on Exploring Relationships among Health, Disease, and Identity in Past Populations · 165 stress aims to uncover the interplay between stress, behavior, underlying biology, diet, ecology and sociopolitical structures, and how they disrupt biological functioning, leading to disease (Klaus 2014). The approach also enables productive, empirical comparisons between states of health and stress observed in the dead with those observed in the living (Klaus 2014; Marklein et al. 2016; Temple and Goodman 2014; Reitsema and McIlvaine 2014). Here, I highlight several recent advances in bioarchaeological work on identity, health, and disease, with an emphasis on the role of stress within this dynamic. I also discuss how discrimination...

Building on early animal studies, 20th-century researchers increasingly explored the fact that early events – ranging from conception to childhood – affect a child’s health trajectory in the long-term. By the 21st century, a wide body of research had emerged, incorporating the original ‘Fetal Origins Hypothesis’ into the ‘Developmental Origins of Health and Disease’. Evidence from OECD countries suggests that health inequalities are strongly correlated with many dimensions of socio-economic status, such as educational attainment; and that they tend to increase with age and carry stark intergenerational implications. Different economic theories have been developed to rationalize this evidence, with an overarching comprehensive framework still lacking. Existing models widely rely on human capital theory, which has given rise to separate dynamic models of adult and child health capital, within a production function framework. A large body of empirical evidence has also found support for the developmental origins of inequalities in health. On the one hand, studies exploiting quasi-random exposure to adverse events have shown long-term physical and mental health impacts of exposure to early shocks, including pandemics or maternal illness, famine, malnutrition, stress, vitamin deficiencies, maltreatment, pollution and economic recessions. On the other hand, studies from the 20th century have shown that early interventions of various content and delivery format improve life course health. Further, given that the most socioeconomically disadvantaged groups show the greatest gains, such measures can potentially reduce health inequalities. However, studies of long-term impacts, as well as the mechanisms via which shocks or policies affect health, and the dynamic interaction amongst them, are still lacking. Mapping the complexities of those early event dynamics is an important avenue for future research.

The long term impact of being born premature has received limited scientific investigation. Studies that have been carried out, focus on outcomes in childhood, with very few considering the impact on adult physical health. Three case studies are presented here, investigating differences in adult minor illness and psychological variables between adult participants born preterm, fullterm but small and fullterm with normal birthweight. This is a retrospective design using questionnaires and checklist to gather relevant information. Minor illness symptoms, daily hassles, anxiety, depression and general self-efficacy were measured. The participant born preterm scored higher on all measures. Data were applied to the Equilibrium Model for Minor Illness. Being born early appears to have a greater impact on later adult outcomes measured than being born fullterm but small or fullterm but of normal weight. In this article the authors reflect upon possible explanations for the different outcome...

Resilience and adaptation in past populations are increasingly studied through the lens of childhood stress. Neural canal size (NC) in the thoracic and lumbar spine shows potential as a marker of stress because it reaches adult size relatively early in development and is therefore
less amenable to catch-up growth.

Research has linked smaller canals to earlier adult
mortality, but confounding by socioeconomic factors is a potential concern. This study tests the hypothesis that a smaller neural canal is associated with lower adulthood
survival in Later Stone Age KhoeSan foragers, a population with little evidence of social inequality.

Anteroposterior (AP) and mediolateral (ML) diameters were measured at T1, T6, L1, and L5 (n=143). Preservation varied, so missing values were imputed in 5 iterative datasets, giving a
final n=105 (F=49; M=56). Femur length and head diameter served as proxies for body size. Individuals were categorized as “young” (<35 years) or “mature” (35≤ years) based on conventional indicators. Logistic regression was used to test the hypothesis.

An increase in ML equal to 1 standard deviation was associated with, on average, 60% greater odds of surviving to mature adulthood (p<0.05), while AP diameter showed no effect. The effect was strong in females, but weak in males. Body size was not a significant confounder. Although confounding by heterogeneous environmental stressors cannot be ruled out, these results suggest that childhood outcomes and adulthood survival are linked even when social stratification is minimal. Early-life growth effects may be a long-standing feature of human life history.

This work has been supported by the Canadian
Social Sciences and Humanities Research
Council

Intrauterine factors important for cognitive development, such as birth weight, chorionicity and umbilical cord characteristics were investigated. A total of 663 twin pairs completed the Wechsler Intelligence Scale for Children-Revised and scores were available for Performance, Verbal and Total Intelligence Quotient (IQ). The intrauterine factors examined were birth weight, placental weight and morphology, cord knots, cord length and cord insertion. IQ scores for the varying levels of the intrauterine markers adjusting for gender and gestational age were calculated. The heritability of IQ and the association between IQ and intrauterine environment were examined. Twins with lower birth weight and cord knots had lower IQ scores. The aetiology of IQ is largely distinct from that of birth weight and cord knots, and non-shared environment may influence the observed relationships.

Health/disease indicators may reveal information on cultural, social, and economic aspects of a population. This study aims to: estimate the frequency of child stress in a peri-urban sample of adult individuals from the Roman era (Moinho do Castelinho, Amadora, Portugal, III-V centuries); investigate the relationship between childhood stress and age-at-death; and understand whether individuals who suffered childhood stress were more likely to present higher degrees of morbidity in adulthood. Non-specific stress markers, namely dental enamel hypoplasia (DEH), were recorded in the individuals' anterior teeth and the age at which each defect occurred was estimated. Other stress markers, like porotic hyperostosis (PH) and orbital cribra (OC), were also observed and the stature estimated. Most individuals experienced childhood stress (DEH: 84.6%, n=22 individuals, 49.3%, n=104 teeth). However, adult age morbidity indicators are relatively moderate (OC: 7.7%, n=2; PH: 23.1%, n=6; Mean Stature=159cm, S.D. 3.99-5.45). These results point to more punctual than systemic episodes of stress with a mild effect in the individuals' development and adults' morbidity. The comparisons with medieval samples from Soure, Leiria and Coimbra show that, in the Roman period, health indicators were relatively positive.

Recent advances in epigenetics have enhanced our knowledge of how environmental factors (UV radiation, drugs, infections, etc.) contribute to the development of autoimmune diseases (AID) in genetically predisposed individuals. Studies conducted in monozygotic twins discordant for AID and spontaneous autoimmune animal models have highlighted the importance of DNA methylation changes and histone modifications. Alterations in the epigenetic pattern seem to be cell specific, as CD4+ T cells and B cells are dysregulated in systemic lupus erythematosus, synovial fibroblasts in rheumatoid arthritis and cerebral cells in multiple sclerosis. With regard to lymphocytes, the control of tolerance is affected, leading to the development of autoreactive cells. Other epigenetic processes, such as the newly described miRNAs, and post-translational protein modifications may also be suspected. Altogether, a conceptual revolution is in progress, in AID, with potential new therapeutic strategies target...

The mini-review is presented about the evolution of stress hormones (the components of hypothalamo-pituitary-adrenal axis) and stress proteins (heat shock proteins
and others), as related to the concept of developmental origins of health and disease. The data on somatic growth retardation by glucocorticoids as mediators and
targets of programming / imprinting phenomena are discussed in evolutionary aspect. Finally, two theoretical constructs are briefly introduced, the onto- and
phylopatogenic model, with the last one having some perspectives of elaboration, as referred to biological evolution.

Early nutrition is critical for later health and sustainable development. We determined potential effectiveness of the Kenyan Community Health Strategy in promoting exclusive breastfeeding (EBF) in urban poor settings in Nairobi, Kenya. We used a quasi-experimental study design, based on three studies [Pre-intervention (2007–2011;n=5824), Intervention (2012–2015;n=1110) and Comparison (2012–2014;n=487)], which followed mother–child pairs longitudinally to establish EBF rates from 0 to 6 months. The Maternal, Infant and Young Child Nutrition (MIYCN) study was a cluster randomized trial; the control arm (MIYCN-Control) received standard care involving community health workers (CHWs) visits for counselling on antenatal and postnatal care. The intervention arm (MIYCN-Intervention) received standard care and regular MIYCN counselling by trained CHWs. Both groups received MIYCN information materials. We tested differences in EBF rates from 0 to 6 months among four study groups (Pre-interv...

Objective: To study the food pattern of stunted and nonstunted, obese and nonobese individuals in a very-low-income population. Design: A household survey. Setting: Slum set up by the 'Homeless Movement', city of Maceió (Alagoas), Brazil. Subjects and methods: A total of 532 adults classified by sex, stature (Zr and Z 4 À2s.d. of the NCHS curves), and body mass index (BMI) were compared using the following variables: waist circumference, waist-hip circumference ratio (W/H), percentage body fat (skinfold thickness and bioelectrical impedance), and food intake (24-h recall). Results: The prevalence of stunting was 22.6%. In all, 30% of the stunted subjects were overweight or obese, compared with 23% for the nonstunted individuals (Po0.05). In women, logistic regression analysis showed a strong association among weight, abdominal fat, and stunting (r ¼ 0.81). No significant differences were observed in the values of W/H or in the qualitative menu of the different categories. Energy intake was below the RDA figures (about 63%). There was similarity among the groups regarding the proportion of macronutrients, except for the fact that stunted obese women ingested less fat and protein than nonstunted obese women. Stunted obese individuals consumed less energy (5962 kJ) than the population as a whole (6213 kJ), an amount far lower than their average needs, which were calculated on the basis of their shorter stature (8109 kJ). Conclusion: The observed energy consumption seems compatible with the panorama of undernutrition present in the population, but it does not explain the high prevalence of obesity detected.

Sunlight exposure during pregnancy could be implicated in the physiological development and growth of the fetus, as well as long-term health after birth. Although several studies suggest the involvement of ultraviolet radiation-mediated vitamin D synthesis, current knowledge regarding the effects of sunlight exposure during pregnancy remains limited. We aimed to (i) summarize the existing body of research studying the influence of sunlight exposure on fetal growth-related birth outcomes and longterm health outcomes and (ii) determine its implications for therapeutics and public health policy. Of the studies identified on birth outcomes, the majority (5/8) demonstrated an association between sunlight exposure and reduced adverse birth outcomes (e.g., low birth weight, preterm births, small for gestational age, etc.), 2/8 studies showed no association, and 1/8 suggested a negative association between sunlight exposure and reduction of these adverse birth outcomes. Of the studies examining long-term health outcomes, sunlight exposure during pregnancy was shown to promote skeletal growth and development (2/6), and reduce the incidence of multiple sclerosis (2/6), asthma (2/6) and pneumonia (1/6). However, several of these studies used different methodologies and populations making it difficult to compare and integrate findings. Based on these results, we examined: the importance of exposure at different stages of pregnancy, proposed mechanisms by which sunlight exposure could lead to optimal outcomes, epidemiological differences influencing the findings, and necessary practical considerations prior to the implementation of public health policy recommendations. While these findings are promising, more rigorous research is warranted to support these recommendations. Sunlight consists of infrared, visible, and ultraviolet (UV) radiation and plays a critical role in regulating normal physiological functions, including vitamin D production and synthesis of hormones such as serotonin in the brain [1,2]; however, little is understood about its effects during pregnancy on offspring. Exposure to environmental stressors during critical periods of growth and development of the offspring could have severe consequences on its short-and long-term health [3], suggesting that differences in level of exposure to sunlight during pregnancy could considerably impact immediate and long-term outcomes. This is highly relevant in both developing regions with abundant sunlight exposure, as well as in regions, such as Canada, where greater seasonal differences result in a lower amount of exposure to sunlight for several months of the year. Overexposure to UV rays during pregnancy is associated with increased adverse risks in mothers including skin damage and cancers [4]. At the same time, exposure to UV is essential for chemical reactions involved in conversion

The endocannabinoid system (ECS), modulated by metabolites of linoleic acid (LA), is important in regulating cardiovascular function. In pregnancy, LA is vital for foetal development. We investigated the effects of elevated LA in H9c2 cardiomyoblasts in vitro and of a high linoleic acid (HLA, 6.21%) or low linoleic acid (LLA, 1.44%) diet during pregnancy in maternal and offspring hearts. H9c2 cell viability was reduced following LA exposure at concentrations between 300 and 1000 µM. HLA diet decreased cannabinoid receptor type 2 (CB2) mRNA expression in foetal hearts from both sexes. However, HLA diet increased CB2 expression in maternal hearts. The mRNA expression of fatty acid amide hydrolase (FAAH) in foetal hearts was higher in females than in males irrespective of diet and N-acyl phosphatidylethanolamine-specific phospholipase D (NAPE-PLD) mRNA expression showed an interaction between diet and sex. Data indicate that a high LA diet alters cell viability and CB2 expression, pote...

Environmental exposures have a significant influence on the chronic health conditions plaguing children and adults. Although the Developmental Origins of Health and Disease (DOHaD) paradigm historically has focused on nutrition, an expanding body of research specifically communicates the effects of chemical exposures on early-life development and the propagation of non-communicable disease across the lifespan. This paper provides an overview of 20 years of research efforts aimed at identifying critical windows of susceptibility to environmental exposures and the signaling changes and epigenetic influences associated with disease progression. DOHaD grants funded by the National Institute of Environmental Health Sciences (NIEHS) in 1991, 2001 and 2011 are identified by grant-analysis software, and each portfolio is analyzed for exposures, disease endpoints, windows of exposure, study design and impact on the field based on publication data. Results show that the 1991 and 2001 portfoli...

The long term impact of being born premature has received limited scientific investigation. Studies that have been carried out, focus on outcomes in childhood, with very few considering the impact on adult physical health. Three case studies are presented here, investigating differences in adult minor illness and psychological variables between adult participants born preterm, fullterm but small and fullterm with normal birthweight. This is a retrospective design using questionnaires and checklist to gather relevant information. Minor illness symptoms, daily hassles, anxiety, depression and general self-efficacy were measured. The participant born preterm scored higher on all measures. Data were applied to the Equilibrium Model for Minor Illness. Being born early appears to have a greater impact on later adult outcomes measured than being born fullterm but small or fullterm but of normal weight. In this article the authors reflect upon possible explanations for the different outcome...

Initiatives to optimise preconception health are emerging following growing recognition that this may improve the health and well-being of women and men of reproductive age and optimise health in their children. To inform and evaluate such initiatives, guidance is required on indicators that describe and monitor population-level preconception health. We searched relevant databases and websites (March 2021) to identify national and international preconception guidelines, recommendations and policy reports. These were reviewed to identify preconception indicators. Indicators were aligned with a measure describing the prevalence of the indicator as recorded in national population-based data sources in England. From 22 documents reviewed, we identified 66 indicators across 12 domains. Domains included wider (social/economic) determinants of health; health care; reproductive health and family planning; health behaviours; environmental exposures; cervical screening; immunisation and infec...

OBJECTIVE Foetal origins theory has suggested that early environment can affect vulnerability to major diseases in later life. Recent research also suggests that foetal hormonal programming may influence neurotransmitter and hormone levels affecting adult psychological states (i.e. depression and general self-efficacy). However, investigations into early environment and depression have focused on hospitalised or elderly participants, using non-standard measures. This study investigates links between birthweight and depression in a non clinical adult population, as well as links with general self-efficacy and depression. METHODS This is a retrospective design. 100 participants mean age 25.9 self reported birthweight, current height and weight to allow computation of BMI. A General Self-Efficacy Scale and the Hospital Anxiety and Depression Scale were also completed. The official classification of low birthweight (2.5 kg) and the median weight for the group (3.26 kg) were used to iden...

Prenatal insults during fetal development result in increased likelihood of developing chronic disease. Obesity, the biggest risk factor for the development of metabolic disease, is affected by several genetic and environmental factors. High-fat diet (HFD) consumption is usually linked with the development of obesity. The main goal of this study was to analyze the impact of the exposure to a HFD in prenatally stressed animals. For this purpose, we subjected pregnant BALB/c mice to restraint stress for 2 h a day between gestational day (GD) 14 and GD 21. Prenatally stressed and control offspring of both sexes were postnatally exposed to a HFD for 24 weeks. We found that prenatal stress (PS) per se produced disturbances in males such as increased total blood cholesterol and triglycerides, with a decrease in mRNA expression of sirtuin-1. When these animals were fed a HFD, we observed a rise in glucose and insulin levels and an increase in visceral adipose tissue gene expression of lept...