Fetal Origins of Adult Diseases Flashcards
(34 cards)
What is the fetal origins of adult disease (FOAD) hypothesis?
The idea that environmental and nutritional factors during fetal development can influence the risk of chronic diseases in adulthood.
What does the Barker Hypothesis propose?
Fetal undernutrition, leading to disproportionate fetal growth, programs an increased risk of coronary heart disease in later life.
What evidence supports the FOAD hypothesis?
Individuals with lower birth weights have a higher risk of dying from heart disease in adulthood.
What are the risks associated with low birth weight (LBW)?
Increased risk of infection, learning disabilities, impaired physical development, and death in the first year of life.
Why is maternal nutrition one of the most important modifiable factors in fetal health?
It influences birth weight and reduces the risk of chronic diseases in adulthood.
How does poor maternal nutrition affect offspring?
It increases the risk of low birth weight, which in turn raises the likelihood of long-term health challenges.
What did the Dutch Hunger Winter study reveal about fetal nutrition?
Exposure to famine at different gestational stages led to different health outcomes in adulthood, such as glucose intolerance, cardiovascular disease, and obesity.
How can maternal obesity affect offspring health?
It can lead to fetal overnutrition, increasing the risk of metabolic disorders like type 2 diabetes.
What is developmental plasticity?
The ability of a single genotype to produce different phenotypes depending on environmental exposures.
What is fetal programming?
The process by which stimuli during early development lead to permanent changes in physiology and metabolism.
What is epigenetics?
The study of heritable changes in gene expression that do not involve changes to the DNA sequence.
How does fetal programming contribute to chronic disease risk?
Poor maternal nutrition and stress can alter fetal development in ways that persist throughout life, increasing disease susceptibility.
What is the mismatch paradigm of metabolic disease?
When the prenatal and postnatal environments differ significantly, it can increase the risk of metabolic diseases.
How does the thrifty phenotype hypothesis explain chronic disease risk?
Fetal undernutrition programs the body for survival in a nutrient-poor environment, but if postnatal nutrition is abundant, it leads to obesity and metabolic disease.
What was observed in the maternal undernutrition study with rats?
Offspring from undernourished mothers who were fed a hypercaloric diet post-weaning gained more fat and had higher blood pressure and insulin resistance.
What is a critical period in fetal development?
A specific timeframe when tissues and organs are genetically and epigenetically programmed to develop properly.
What happens if an organ does not develop properly during its critical period?
The deficiency cannot be fully compensated for later in life, leading to long-term health consequences.
How can malnutrition during fetal development structurally affect organs?
Reduced kidney development can lead to hypertension, while reduced pancreatic beta cells can impair insulin secretion.
What role do methyl groups play in epigenetic modifications?
They silence or activate genes by altering DNA methylation patterns.
How did the Agouti mouse study demonstrate epigenetic effects?
Supplementing pregnant mice with methyl donors (like folate and B12) altered coat color and obesity risk in offspring by modifying DNA methylation.
How does prenatal malnutrition affect the risk of type 2 diabetes?
It can silence the Pdx1 gene in the pancreas, impairing insulin production.
How does gestational diabetes affect offspring through epigenetic changes?
It can lead to hypermethylation of the leptin gene, reducing leptin secretion and increasing obesity and diabetes risk.
What were the findings of the Motherwell cohort study?
An unbalanced maternal diet increased methylation in the HSD2 region, leading to higher cortisol levels and increased cardiovascular disease risk in offspring.
What did the Pune maternal nutrition study reveal about vitamin B12 and folate?
Low maternal B12 combined with high folate levels was linked to increased insulin resistance in children.
