https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(07)61692-4.pdf

Maternal and child undernutrition: consequences for adult health and human capital.

https://www.bmj.com/content/bmj/301/6761/1111.full.pdf

The fetal and infant origins of adult disease.

The last systematic review on the health consequences of child and adolescent obesity found little evidence on consequences for adult health. The present study aimed to summarize evidence on the long-term impact of child and adolescent obesity for premature mortality and physical morbidity in adulthood. Systematic review with evidence searched from January 2002 to June 2010. Studies were included if they contained a measure of overweight and/or obesity between birth and 18 years (exposure measure) and premature mortality and physical morbidity (outcome) in adulthood. Five eligible studies examined associations between overweight and/or obesity, and premature mortality: 4/5 found significantly increased risk of premature mortality with child and adolescent overweight or obesity. All 11 studies with cardiometabolic morbidity as outcomes reported that overweight and obesity were associated with significantly increased risk of later cardiometabolic morbidity (diabetes, hypertension, ischaemic heart disease, and stroke) in adult life, with hazard ratios ranging from 1.1–5.1. Nine studies examined associations of child or adolescent overweight and obesity with other adult morbidity: studies of cancer morbidity were inconsistent; child and adolescent overweight and obesity were associated with significantly increased risk of later disability pension, asthma, and polycystic ovary syndrome symptoms. A relatively large and fairly consistent body of evidence now demonstrates that overweight and obesity in childhood and adolescence have adverse consequences on premature mortality and physical morbidity in adulthood.

Long-term impact of overweight and obesity in childhood and adolescence on morbidity and premature mortality in adulthood: systematic review

The "fetal" or "early" origins of adult disease hypothesis was originally put forward by David Barker and colleagues and stated that environmental factors, particularly nutrition, act in early life to program the risks for adverse health outcomes in adult life. This hypothesis has been supported by a worldwide series of epidemiological studies that have provided evidence for the association between the perturbation of the early nutritional environment and the major risk factors (hypertension, insulin resistance, and obesity) for cardiovascular disease, diabetes, and the metabolic syndrome in adult life. It is also clear from experimental studies that a range of molecular, cellular, metabolic, neuroendocrine, and physiological adaptations to changes in the early nutritional environment result in a permanent alteration of the developmental pattern of cellular proliferation and differentiation in key tissue and organ systems that result in pathological consequences in adult life. This review focuses on those experimental studies that have investigated the critical windows during which perturbations of the intrauterine environment have major effects, the nature of the epigenetic, structural, and functional adaptive responses which result in a permanent programming of cardiovascular and metabolic function, and the role of the interaction between the pre- and postnatal environment in determining final health outcomes.

https://www.physiology.org/doi/pdf/10.1152/physrev.00053.2003

Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming

Low birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and non-insulin dependent diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. A new vision of optimal early human development is emerging which takes account of both short and long-term outcomes.

The Developmental Origins of Adult Disease

AIM: To determine the relationship of birth weight to later glucose and insulin metabolism. METHODS: Systematic review of the published literature. Data sources were Medline and Embase. Included studies were papers reporting the relationship of birth weight with a measure of glucose or insulin metabolism after 1 year of age, including the prevalence of Type 2 diabetes mellitus (DM). Three reviewers abstracted information from each paper according to specified criteria. RESULTS: Forty-eight papers fulfilled the criteria for inclusion, mostly of adults in developed countries. Most studies reported an inverse relationship between birth weight and fasting plasma glucose concentrations (15 of 25 papers), fasting plasma insulin concentrations (20 of 26), plasma glucose concentrations 2 h after a glucose load (20 of 25), the prevalence of Type 2 DM (13 of 16), measures of insulin resistance (17 of 22), and measures of insulin secretion (16 of 24). The predominance of these inverse relationships and the demonstration in a minority of studies of other directions of the relationships could not generally be explained by differences between studies in the sex, age, or current size of the subjects. However, the relationship of birth weight with insulin secretion was inconsistent in studies of adults. CONCLUSIONS: The published literature shows that, generally, people who were light at birth have an adverse profile of later glucose and insulin metabolism. This is related to higher insulin resistance, but the relationship to insulin secretion in adults is less clear.

Is birth weight related to later glucose and insulin metabolism?--A systematic review.

The 'thrifty phenotype' hypothesis states that impaired glucose tolerance (IGT) and non-insulin-dependent diabetes mellitus (NIDDM) are the result of adaptation to undernutrition in the fetal and infant environment. In adapting the fetus and infant have to be nutritionally 'thrifty'. If poor nutrition continues throughout life these adaptations are not detrimental. However, if adult nutrition is better, the ability of the pancreas to maintain homeostasis is exceeded, with resulting diabetes. The hypothesis has been tested by a series of longitudinal studies which relate early growth with IGT and NIDDM in adult life. The studies show that babies who are small at birth or during infancy have increased rates of IGT and NIDDM. These relations are independent of social class and are seen at all levels of current body mass. More detailed anthropometric measurements at birth show that the baby at risk of glucose intolerance is characterized by disproportionate fetal growth, particularly relative thinness. Direct measurements have shown that this is a function of insulin resistance rather than deficiency. Reduced fetal growth is also associated with higher levels of plasma glucose in children. The aetiology of IGT and NIDDM may lie in undernutrition in utero or during infancy. This has major implications for their prevention.

Fetal and infant influences on non-insulin-dependent diabetes mellitus (NIDDM).

ObjectiveTo assess the strength of evidence for an inverse relationship between blood pressure and birth weight.DesignA systematic review of the published literature.SettingPublished studies describing the relationship between blood pressure and birth weight since 1956.SubjectsMore than 66 000 subje

Is blood pressure inversely related to birth weight? The strength of evidence from a systematic review of the literature

Background— People who are small at birth tend to have higher blood pressure in later life. However, it is not clear whether it is fetal growth restriction or the accelerated postnatal growth that often follows it that leads to higher blood pressure. Methods and Results— We studied blood pressure in 346 British men and women aged 22 years whose size had been measured at birth and for the first 10 years of life. Their childhood growth was characterized using a conditional method that, free from the effect of regression to the mean, estimated catch-up growth. People who had been small at birth but who gained weight rapidly during early childhood (1 to 5 years) had the highest adult blood pressures. Systolic pressure increased by 1.3 mm Hg (95% CI, 0.3 to 2.3) for every standard deviation score decrease in birth weight and, independently, increased by 1.6 mm Hg (95% CI, 0.6 to 2.7) for every standard deviation score increase in early childhood weight gain. Adjustment for adult body mass index attenuated the ...

/pdf/fetal-infant-and-childhood-growth-and-adult-blood-pressure-a-qjuw5psvob.pdf

Fetal, Infant, and Childhood Growth and Adult Blood Pressure A Longitudinal Study From Birth to 22 Years of Age

Fetal and Infant Influences on Non-insulin-dependent Diabetes Mellitus (NIDDM)

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

C. M. Law

Author Tools

Chat about Author