Chronic Diseases In Adult Life Research Articles

Birth size, growth trajectory and later cardio-metabolic risk.

There is increasing evidence of a strong association between intrauterine growth and subsequent development of chronic disease in adult life. Birth size and growth trajectory have been demonstrated to have an impact on cardio-metabolic health, both in childhood and adult life. Hence, careful observation of the children's growth pattern, starting from the intrauterine period and the first years of life, should be emphasized to detect the possible onset of cardio-metabolic sequelae. This allows to intervene on them as soon as they are detected, first of all through lifestyle interventions, whose efficacy seems to be higher when they are started early. Recent papers suggest that prematurity may constitute an independent risk factor for the development of cardiovascular disease and metabolic syndrome, regardless of birth weight. The purpose of the present review is to examine and summarize the available knowledge about the dynamic association between intrauterine and postnatal growth and cardio-metabolic risk, from childhood to adulthood.

Pooled prevalence of stunting and associated factors among children aged 6-59 months in Sub-Saharan Africa countries: A Bayesian multilevel approach.

Over 155 million children under five suffer from stunting, and it is responsible for over one million deaths and 54.9 million Disability Adjusted Life Years (DALYS) of under-five children worldwide. These predominantly occurred in low-and middle-income countries like sub-Saharan Africa. Stunted children begin their lives at a marked disadvantage. Some of these are; poor cognition and educational performance, low adult wages, lost productivity and, when accompanied by excessive weight gain later in childhood, an increased risk of nutrition-related chronic diseases in adult life and the devastating effects of stunting can last a lifetime and even affect the next generation. Despite this, its magnitude rises in the past 25 years in sub-Saharan Africa. Studies that capture the pooled prevalence and associated factors of stunting among children aged 6-59 months in sub-Saharan Africa are limited. Therefore, this study was carried out on the basis of the Bayesian approach to determine the pooled prevalence and predictors of stunting among children aged 6-59 months in Sub-Saharan Africa. To assess the pooled prevalence of stunting and associated factors among children aged 6-59 months in Sub-Saharan Africa. For this study a total of 173,483 weighted samples from the demography and health survey data set of 35 sub-Saharan African countries from 2008 to 2020 were used. After checking Variation between cluster by computing Intraclass Correlation Coefficient, binary logistic regression model was conducted based on hierarchical Bayesian statistical approach to account the hierarchical nature of demography and health survey data and to get reliable estimates by using additional information from the prior distribution. Adjusted odds ratio with 95% credible interval of the best fitted model was used to ascertain the predictors. The pooled prevalence of stunting in Sub-Saharan Africa was about 35% (95%CI: 34.87, 35.31). Of the sub-regions, the highest prevalence of stunting was in East Africa, 37% (95%, CI: 36.96, 37.63) followed by Central Africa, 35% (95%CI: (34.93, 35.94). Being male (AOR = 1.27, 95% CrI 1.25, 1.30), small birth size (AOR = 1.29, CrI 1.25, 1.32), home delivery (AOR = 1.17, CrI 1.14, 1.20), and no education of mothers (AOR = 3.07, CrI 2.79, 3.39) were some of the significant predictors of stunting of children. The prevalence of stunting of children in sub-Saharan Africa is among the highest in the world. Predictors such as being male, being small at birth, a child delivered at home, and, low level of maternal education were some of the predictors of childhood stunting. Stakeholders and non-governmental organizations should consider those contributing factors of stunting when they plan and design nutritional improvement programs.

Metabolomic profiles and microbiota of GDM offspring: The key for future perspective?

Gestational diabetes mellitus (GDM), or any degree of glucose intolerance recognized for the first time during pregnancy, is one of the diseases that most frequently aggravates the course of gestation. Missed or late diagnosis and inadequate treatment are associated with high maternal and fetal morbidity, with possible short- and long-term repercussions. Estimates on the prevalence of GDM are alarming and increasing by about 30% in the last 10–20 years. In addition, there is the negative influence of the SARS-CoV-2 emergency on the glycemic control of pregnant women, making the matter increasingly topical. To date, knowledge on the metabolic maturation of newborns is still incomplete. However, in light of the considerable progress of the theory of “developmental origins of health and disease,” the relevant role of the intrauterine environment cannot be overlooked. In fact, due to the high plasticity of the early stages of development, some detrimental metabolic alterations during fetal growth, including maternal hyperglycemia, are associated with a higher incidence of chronic diseases in adult life. In this context, metabolomic analysis which allows to obtain a detailed phenotypic portrait through the dynamic detection of all metabolites in cells, tissues and different biological fluids could be very useful for the early diagnosis and prevention of complications. Indeed, if the diagnostic timing is optimized through the identification of specific metabolites, the detailed understanding of the altered metabolic pathway could also allow better management and more careful monitoring, also from a nutritional profile, of the more fragile children. In this context, a further contribution derives from the analysis of the intestinal microbiota, the main responsible for the fecal metabolome, given its alteration in pregnancies complicated by GDM and the possibility of transmission to offspring. The purpose of this review is to analyze the available data regarding the alterations in the metabolomic profile and microbiota of the offspring of mothers with GDM in order to highlight future prospects for reducing GDM-related complications in children of mothers affected by this disorder.

Does the intrauterine condition dictate chronic metabolic disorders in the adult life?

Foetal development has dictated by maternal gestational diet and intrinsic factors, physical activity, and environmental stimulations. Many studies provided evidence for metabolic disorders in adult life who underwent under nutrition during their foetal life. This review is an effort to use the published data to know the effect of the intrauterine environment on chronic metabolic disorders. Here, we discuss the impact of foetal under nutrition on the development of chronic metabolic diseases. Intrauterine under nutrition negatively influences health after birth. In adults, under-nutrition in utero results in metabolic impairments and cognitive impairments. Under nutrition during foetal/embryonic development influences human physiology and has a lifelong effect, often called foetal programming. This review concludes that the intrauterine environment and foetal nutrition play a significant role in developing chronic metabolic disorders. Therefore, this study provides the necessary insight into target timely interventions in the earliest possible time to prevent offspring from developing chronic diseases in adult life.

Adverse effects of perinatal protein restriction on glucose homeostasis in offspring of Sprague-Dawley rats

Adequate evidence suggests that poor in-utero environment produced by early life dietary disturbance may predispose offspring to chronic diseases in adult life. It remains to be defined the adverse effect of early exposure due to perinatal protein restriction (PPR) (gestation, lactation and/or both) on the regulators of glucose homeostasis of the male offspring in later life. Hence, the present study investigated the role of perinatal protein restriction on the regulators of glucose homeostasis in adult offspring. Twenty-four pregnant and twelve male Sprague-Dawley rats were used. They were fed either a normal diet containing 20% protein or protein-restricted (PR) diet with 8% protein. The dams were given PR diet up to parturition (in-utero group, IUPR), or from birth to postnatal day 21 (lactation group, LPR) or for a period covering both groups (combined group, CPR). Control dams with control diet was run in parallel for comparison. At day 120, oral glucose tolerance, insulin tolerance, fasting blood glucose, fasting insulin level were determined. Hepatic and myocytic glycogen contents, GLUT-4 protein abundance, alpha amylase and alpha glucosidase activities were also assessed. The results revealed that glucose tolerance was unchanged, insulin sensitivity was significantly decreased in IUPR and CPR offspring. HOMA-IR elicited a significant elevation (p<0.01) in IUPR and CPR offspring compared with CONT. Hepatic and myocytic glycogen contents in all PPR offspring significantly decreased compared with CONT. GLUT-4 protein was significantly (p<0.01) reduced in all PPR offspring compared with CONT. Alpha amylase activity decreased significantly (p<0.01) in IUPR and CPR offspring with a significant increase (p<0.01) in LPR offspring compared with CONT. However, alpha glucosidase activity showed no significant difference (p>0.01) in all PPR offspring compared with CONT. In conclusion, the data described in the present investigation provides ample evidence that PPR remarkably malprogram the offspring to impairment of glucose homeostasis with blunted insulin action in the tissues of the periphery which eventually reduces uptake of glucose, utilization and absorption as well as deposition of glycogen in liver and skeletal muscle leading to insulin resistance in PPR offspring.

Effects of early-life stress and sex on blood-brain barrier permeability and integrity in juvenile and adult rats.

Early-life stress (ELS) is considered a relevant etiological factor for neurodegenerative and mental disorders. In the present study, we hypothesized that ELS may persistently and sex dependently influence blood-brain barrier (BBB) integrity and function during critical periods of brain development and consequently determine susceptibility to and sex-related prevalence of chronic diseases in adult life. We used the maternal separation (MS) procedure in rats to model ELS and evaluated BBB permeability and gene expression of selected tight junction (TJ) proteins, glucose transporter type 1 (Slc2a1) and aquaporin 4 (Aqp4) in the medial prefrontal cortex (mPFC), dorsal striatum (dSTR) and hippocampus of juvenile and adult rats. Serum concentrations of a peripheral marker of BBB function (S100β) and proinflammatory cytokines were also assessed. We observed developmental sealing of the BBB and sex differences in the permeability of the BBB and the mRNA expression of TJ proteins and Slc2a1. Adult females showed lower BBB permeability and higher levels of Cldn3, Cldn5, Ocln, and Slc2a1 in the mPFC and dSTR than males. MS temporarily increased BBB permeability in the dSTR of juvenile males and affected mRNA expression of the majority of studied proteins related to BBB function in age-, region- and sex-dependent manners. Additionally, MS sex dependently decreased serum S100β levels and did not affect proinflammatory cytokine concentrations. In general, our study did not reveal a clear or strong negative effect of MS on BBB integrity. However, the results suggest that ELS may induce adaptive/maladaptive changes or compensatory mechanisms within the BBB of unknown yet consequences.

Nutritional knowledge among a large cohort of Italian students: a cross-sectional study.

Healthy food behavior among adolescents represents a prevention factor for the onset of chronic diseases in adult life and is influenced by the familiar, socio-cultural and physical environment. Good nutritional knowledge plays a key role in ensuring healthy eating, that is adequate food choice and intake. This study aimed to assess the nutritional knowledge of Italian students from three Italian provinces of the Lazio Region (i.e., Rome, Frosinone, Latina) and to investigate its interrelationship with some socio-demographic characteristics (physical activity, parental education, school district city, BMI) of the surveyed subjects. Students (n = 2573) were surveyed for their nutritional knowledge through the Italian version of the Moynihan questionnaire and for their socio-demographic characteristics. The relationship between their nutritional knowledge and their socio-demographic characteristics was investigated by univariate and multivariate statistical analyses. Most participants displayed a normal weight (84%), followed by overweight (14%) and underweight (2%) subjects. Most students (44%) practiced physical activity at least twice a week. Most students (75%) reported a high family education level. Sixty percent of the subjects showed inadequate knowledge about healthy nutrition. A significant association (p<0.001) was observed between nutritional knowledge and school district city. Educational nutrition programs should be promoted to improve nutritional knowledge among young people and reduce the risk of chronic disease development.

Parents’ body mass index and/or maternal gestational weight gain associations with offspring body compartments in young adults

Rationale: Intrauterine environment can induce metabolic programming that predisposes to adiposity-related chronic diseases in adult life. We examined how parents’ BMI and gestational weight gain could be associated with offspring muscle and adipose body compartments in early adulthood.

LEVELS OF FECAL CALPROTECTIN AND ALPHA ONE ANTITRYPSIN IN CHILDREN WITH STUNTING

Stunting is the impaired growth and development that children experience from poor nutrition, repeated infection, and inadequate psychosocial stimulation. Children are defined as stunted if their height-for-age is more than two standard deviations below the WHO Child Growth Standards median.Stunting in early life -- particularly in the first 1000 days from conception until the age of two - impaired growth has adverse functional consequences on the child. Some of those consequences include poor cognition and educational performance, low adult wages, lost productivity and, when accompanied by excessive weight gain later in childhood, an increased risk of nutrition-related chronic diseases in adult life. Childhood stunting is considered the best overall indicator of children’s well-being and an accurate reflection of social inequalities in communitie.In 2010, it was found that 171 million child was stunted compared to 167 million in developing countries. Globally, childhood stunting decreased from 39.7% in 1990 to 26.7% in 2010. This trend is expected to reach 21•8 %, or 142 million, in 2020.In Egypt: the incidence of children with stunting is 21.4%.-

Programming of Renal Development and Chronic Disease in Adult Life.

Chronic kidney disease (CKD) can have an insidious onset because there is a gradual decline in nephron number throughout life. There may be no overt symptoms of renal dysfunction until about two thirds or more of the nephrons have been destroyed and glomerular filtration rate (GFR) falls to below 25% of normal (often in mid-late life) (Martinez-Maldonaldo et al., 1992). Once End Stage Renal Disease (ESRD) has been reached, survival depends on renal replacement therapy (RRT). CKD causes hypertension and cardiovascular disease; and hypertension causes CKD. Albuminuria is also a risk factor for cardiovascular disease. The age of onset of CKD is partly determined during fetal life. This review describes the mechanisms underlying the development of CKD in adult life that results from abnormal renal development caused by an adverse intrauterine environment. The basis of this form of CKD is thought to be mainly due to a reduction in the number of nephrons formed in utero which impacts on the age dependent decline in glomerular function. Factors that affect the risk of reduced nephron formation during intrauterine life are discussed and include maternal nutrition (malnutrition and obesity, micronutrients), smoking and alcohol, use of drugs that block the maternal renin-angiotensin system, glucocorticoid excess and maternal renal dysfunction and prematurity. Since CKD, hypertension and cardiovascular disease add to the disease burden in the community we recommend that kidney size at birth should be recorded using ultrasound and those individuals who are born premature or who have small kidneys at this time should be monitored regularly by determining GFR and albumin:creatinine clearance ratio. Furthermore, public health measures aimed at limiting the prevalence of obesity and diabetes mellitus as well as providing advice on limiting the amount of protein ingested during a single meal, because they are all associated with increased glomerular hyperfiltration and subsequent glomerulosclerosis would be beneficial.

Protective effect of maternal exercise against amyloid-β neurotoxicity in the male rat offspring's cerebellum.

The Developmental Origins of Health and Disease (DOHaD) states that intrauterine maternal environment influences postnatal life by programming offspring's metabolism. Intrauterine milieu induced by exercise during pregnancy promotes long-lasting benefits to the offspring's health and seems to offer some resistance against chronic diseases in adult life. Alzheimer's disease is a public health concern with limited treatment options. In the present study, we assessed the potential of maternal exercise during pregnancy in long-term programming of young adult male rat offspring's cerebellar metabolism in conferring neuroprotection against amyloid-β (Aβ) neurotoxicity. Female Wistar rats were submitted to a swimming protocol 1 week prior mating and throughout pregnancy (five sessions/a week lasting 30 min). Aβ oligomers were infused bilaterally in the brain ventricles of 60-day-old male offspring. Fourteen days after surgery, we measured parameters related to redox state, mitochondrial function, and the immunocontent of proteins related to synaptic function. We found that maternal exercise during pregnancy attenuated several parameters in the offspring's male rat cerebellum, such as the reactive species rise, the increase of inducible nitric oxide synthase immunocontent and tau phosphorylation induced by Aβ oligomers, increased mitochondrial fission indicated by dynamin-related protein 1 (DRP1), and protein oxidation identified by carbonylation. Strikingly, we find that maternal exercise promotes changes in the rat offspring's cerebellum that are still evident in young adult life. These favorable neurochemical changes in offspring's cerebellum induced by maternal exercise may contribute to a protective phenotype against Aβ-induced neurotoxicity in young adult male rat offspring.

What is the evidence for beneficial effects of growth hormone treatment beyond height in short children born small for gestational age? A review of published literature

Background An increasing body of evidence supports the view that both an adverse intrauterine milieu and rapid postnatal weight gain in children born small for gestational age (SGA) contribute towards the risk for the development of chronic diseases in adult life. Content The aim of this review was to identify and summarize the published evidence on metabolic and cardiovascular risk, as well as risk of impaired cardiac function, intellectual capacity, quality of life, pubertal development and bone strength among children born SGA. The review will then address whether growth hormone (GH) therapy, commonly prescribed to reduce the height deficit in children born SGA who do not catch up in height, increases or decreases these risks over time. Summary Overall, there are limited data in support of a modest beneficial effect of GH therapy on the adverse metabolic and cardiovascular risk observed in short children born SGA. Evidence to support a positive effect of GH on bone strength and psychosocial outcomes is less convincing. Outlook Further evaluation into the clinical relevance of any potential long-term benefits of GH therapy on metabolic and cardiovascular endpoints is warranted.

The International Federation of Gynecology and Obstetrics (FIGO) initiative on pre-eclampsia: A pragmatic guide for first-trimester screening and prevention.

The International Federation of Gynecology and Obstetrics (FIGO) initiative on pre-eclampsia: A pragmatic guide for first-trimester screening and prevention.

425. How does programming work – Animal models of placental dysfunction and their epigenetic outcome

An adverse intrauterine environment belongs to the well-known roots of chronic disease in adult life. This is often coined the ’Developmental Origins of Health and Disease’ (DOHaD) paradigm. One of the key factors transmitting environmental information along the lifespan of an organism is epigenetic programming. Classical rodent models used in research on the Developmental Origins of Health and Disease are based on dietary interventions during pregnancy. Simulation of human hunger periods by caloric or protein restriction are examples. Similarly, placental dysfunction is often simulated by clamping of the uterine artery, which requires surgical procedures. I will here compare several novel mouse models of placental dysfunction and their benefits for research. These models are based on the genetic deletion of the transcription factor TFAP2C in the placenta, or on a combination of virus-mediated overexpression of sFlt1, with or without low-grade inflammation. The former model leads to growth restriction in the offspring, whereas the latter model is furthermore accompanied by signs of preeclampsia. Interestingly, in both cases also the sex of the offspring matters for the outcome. These new models, especially when compared to each other, will in future allow us to specifically differentiate between different forms of placental dysfunction, which might contribute to personalized care strategies.

The exposure to uteroplacental insufficiency is associated with activation of unfolded protein response in postnatal life.

Early life events are associated with the susceptibility to chronic diseases in adult life. Perturbations of endoplasmic reticulum (ER) homeostasis activate the unfolded protein response (UPR), which contributes to the development of metabolic alterations. Our aim was to evaluate liver UPR in an animal model of intrauterine growth restriction (IUGR). A significantly increased expression of X-box binding protein-1 spliced (XBP1s) mRNA (p<0.01), Endoplasmic Reticulum-localized DnaJ homologue (Erdj4) mRNA (p<0.05) and Bip/GRP78-glucose-regulated protein 78 (Bip) mRNA (p<0.05) was observed in the liver of IUGR rats at birth. Furthermore, the expression of gluconeogenesis genes and lipogenesis genes were significantly upregulated (p<0.05) in IUGR pups. At 105 d, IUGR male rats showed significantly reduced glucose tolerance (p<0.01). A significant decreased expression of XBP1s mRNA (p<0.01) and increased expression of double-stranded RNA-dependent protein kinase-like ER kinase (PERK) and Asparagine synthetase (ASNS) (p<0.05) was observed in the liver of IUGR male adult rats. Liver focal steatosis and periportal fibrosis were observed in IUGR rats. These findings show for the first time that fetal exposure to uteroplacental insufficiency is associated with the activation of hepatic UPR and suggest that UPR signaling may play a role in the metabolic risk.

Bioactive lipids are altered in the kidney of chronic undernourished rats: is there any correlation with the progression of prevalent nephropathies?

BackgroundUndernutrition during childhood leads to chronic diseases in adult life including hypertension, diabetes and chronic kidney disease. Here we explore the hypothesis that physiological alterations in the bioactive lipids pattern within kidney tissue might be involved in the progression of chronic kidney disease.MethodsMembrane fractions from kidney homogenates of undernourished rats (RBD) were submitted to lipid extraction and analysis by thin layer chromatography and cholesterol determination.ResultsKidneys from RBD rats had 25% lower cholesterol content, which disturb membrane microdomains, affecting Ca2+ homeostasis and the enzymes responsible for important lipid mediators such as phosphatidylinositol-4 kinase, sphingosine kinase, diacylglicerol kinase and phospholipase A2. We observed a decrease in phosphatidylinositol(4)-phosphate (8.8 ± 0.9 vs. 3.6 ± 0.7 pmol.mg−1.mim−1), and an increase in phosphatidic acid (2.2 ± 0.8 vs. 3.8 ± 1.3 pmol.mg−1.mim−1), being these lipid mediators involved in the regulation of key renal functions. Ceramide levels are augmented in kidney tissue from RBD rats (18.7 ± 1.4 vs. 21.7 ± 1.5 fmol.mg−1.min−1) indicating an ongoing renal lesion.ConclusionResults point to an imbalance in the bioactive lipid generation with further consequences to key events related to kidney function, thus contributing to the establishment of chronic kidney disease.

Central Hematocrit Levels in Fetal Malnourished Term Infants.

Fetal malnutrition is especially important for common chronic diseases in adult life. They could potentially be prevented by achieving optimal fetal nutrition. The aim of this study was to investigate hematocrit levels of malnourished, term, appropriate for gestational age (AGA) neonates. A total of 80 AGA neonates (between 10% and 90% percentiles interval according to birth week), born with spontaneous vaginal delivery between 37 and 42 weeks of gestation, detected by both last menstrual period and ultrasonography measurements, were included in the study. Neonates with fetal malnutrition constituted the study group and the control group consisted of well-nourished neonates. We analyzed central venous hematocrit levels obtained 4 hours after birth and maternal risk factors for both groups. Although there were no differences in gestational age, head circumference, maternal factors (gravidity, parity, abortions and curettage counts, maternal tobacco use, preeclampsia, hypertension, diabetes mellitus, gestational diabetes mellitus, and history of urinary tract infections), first minute APGAR scores, and sex, Clinical Assessment of Nutritional Status score was lower (29.91±2.87 vs. 21.25±1.65) and hematocrit levels were higher (51.33±2.740 vs. 59.53±5.094) in the fetal malnutrition group (P<0.0001). Central hematocrit levels in malnourished term AGA neonates were found significantly higher than well-nourished term AGA newborns.

Placental Origins of Chronic Disease.

Epidemiological evidence links an individual's susceptibility to chronic disease in adult life to events during their intrauterine phase of development. Biologically this should not be unexpected, for organ systems are at their most plastic when progenitor cells are proliferating and differentiating. Influences operating at this time can permanently affect their structure and functional capacity, and the activity of enzyme systems and endocrine axes. It is now appreciated that such effects lay the foundations for a diverse array of diseases that become manifest many years later, often in response to secondary environmental stressors. Fetal development is underpinned by the placenta, the organ that forms the interface between the fetus and its mother. All nutrients and oxygen reaching the fetus must pass through this organ. The placenta also has major endocrine functions, orchestrating maternal adaptations to pregnancy and mobilizing resources for fetal use. In addition, it acts as a selective barrier, creating a protective milieu by minimizing exposure of the fetus to maternal hormones, such as glucocorticoids, xenobiotics, pathogens, and parasites. The placenta shows a remarkable capacity to adapt to adverse environmental cues and lessen their impact on the fetus. However, if placental function is impaired, or its capacity to adapt is exceeded, then fetal development may be compromised. Here, we explore the complex relationships between the placental phenotype and developmental programming of chronic disease in the offspring. Ensuring optimal placentation offers a new approach to the prevention of disorders such as cardiovascular disease, diabetes, and obesity, which are reaching epidemic proportions.

Prevalence of overweight and obesity among children aged 5-15 years in a rural school in Coimbatore

Background: Childhood obesity is a fast emerging problem in developing countries such as India because of lifestyle changes and economic transition.[1] Childhood overweight and obesity are major risk factors for many chronic diseases such as diabetes, hypertension, cardiovascular diseases, and cancer.[1–4] Effective preventive measures will prevent the risk of developing chronic diseases in adult life. Objective: To study the prevalence of overweight and obesity among school children in a rural school in Coimbatore using the WHO standard reference for age 5–19 years. Materials and Methods: A cross-sectional study was conducted along with annual school health check up for the children studying in a rural matriculation school located in Neelambur village, Coimbatore district. A total of 890 school children in the age group 5–15 years enrolled in the study were examined for height and weight, and BMI was calculated. The WHO standard reference for age 5–19 years was used to define overweight (> 2SD) and obesity (> 3SD). Result: In our study, prevalence of overweight was 8.32% and prevalence of obesity was 4.72%. Among boys, prevalence of overweight and obesity was 8.43% and 6.43%, respectively. Among girls, prevalence of overweight and obesity was 8.20% and 2.96%, respectively. There is no statistical significant difference in the prevalence of overweight/obesity among boys and girls. Conclusion: A high proportion of Rural School children in our study are having weight more than their normal weight, indicating the need for public awareness and preventive measures on childhood obesity. Intervention in the form of health education should be initiated at all levels of society to stop the progression of the problem.

Long-Term Effects of Maternal Nutrition and Childhood Growth on Later Health

Objectives: This paper reviews the importance of maternal nutrition and weight gain with birthweigh and neonatal/childhood growth, and highlights the r isk of chronic diseases in later life. Methods: The data was sourced based on the result of original and review articles relating to the life exposures, pregnancy weight gain, birth weight, childhood growth and the risk of chronic diseases in adult life. Findings: Experimental studies have suggested that both maternal undernutrition and overnutrition are involved in later disease risk. Maternal macronutrient deficiency leads to LBW and subsequently insulin resistance and adiposity in later life. It seems that micronutrient deficiencies contribute to long-term negative effects such as metabolic syndrome and related disorders. As well as fetal life, early infancy, the adiposity rebound period and puberty also account as critical periods for the development of obesity in adulthood. Conclusion: It is now widely accepted that the risks of adult chronic diseases may have their developmental origins in fetal life. Maternal under-nutrition or over-nutrition affect the infant’s health . Both macro- and micro-nutrients are critical for appropriate pregnancy outcomes. Understanding their precise patho-physiological mechanism are critical to apply new strategies to prevent the adverse effects of maternal dietary restriction and environmental factors in early stages of life.