Midterm 1 Flashcards
Describe the epidemiological and experimental evidence that links early life environments to pregnancy outcomes, adverse development and disease
- Malnutrition: Too much or too little nutrient intake is tied to chronic disease risk.
(Nutrition is one of many environmental influences) - Obesity: increased exposure to energy dense, nutrient poor foods, and lack of physical activity
- low birth weight is a surrogate
Define developmental plasticity
Ability of an organism to develop in various ways,
depending on the particular environment or setting
* Multiple phenotypes can arise during development from a
single genotype
* Different phenotypes are based on the nature of the gene –
environment interactions (GXE)
* Normal aspect of development
Identify critical windows of plasticity across the lifespan
Define Evolutionary and Developmental
Mismatch: between the environment in uterine vs adult
Evolutionary Mismatch = environments experienced by
contemporary humans are markedly different from those
encountered throughout most of our evolutionary history
* Changes in our nutritional environment appetite-rewarding energy-
dense foods;
* Replacement of human breast milk with bottle feeding using cow’s milk-
based formula
* In vitro fertilization
Developmental Mismatch = later life environment is different
from that predicted in early life maladaptation
* Maternal illness
* Placental disease
* Unbalanced maternal diet
* Significant change in the post-natal environment
Can provide false in utero cues
Describe and identify common surrogates of the intrauterine environment
low birth weight???
both animal and human research is now that phenotypes can be induced in offspring without necessarily being accompanied by …
low birthweight, it is clear that reduction of fetal growth per se does not lie on a causal pathway to later disease.
Rather, low birthweight is a surrogate marker of the effects of the prenatal environment on the fetus, and one aspect of the fetal ‘coping’ responses to that environment
‘Barker hypothesis’
“exposure to environmental factors during specific sensitive periods of development might predispose an organism to diseases in adult life.”
Chronic disease is more than just ____ and _____ adult lifestyles.
- bad genes
- unhealthy
Ischaemic heart disease is strongly correlated with both neonatal and postneonatal mortality. It is suggested that poor nutrition in ____ increases susceptibility to the effects of an affluent diet
early life
neonatal vs post-neonatal
___ birth weight was also found to be associated with disorders characterized by insulin resistance, such as type 2 diabetes (T2D), hypertension, and dyslipidemia (abnormaly high levels of lipids in the blood).
LOW
Hertfordshire Cohort Study
The Hertfordshire Cohort Study is a nationally unique study of men and women born in the English county of Hertfordshire in the early part of the 20thcentury. Records that detail their health in infancy and childhood have been preserved, their sociodemographic, lifestyle, medical and biological attributes have been characterised in later life, and routinely collected data on their hospital use and mortality have been acquired.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6381804/
intrauterine
within the uterus
Helsinki Birth Cohort (1924-1933; 1934-1944)
There is now clear evidence that the pace and pathway of early growth is a major risk factor for the development of a group of chronic diseases that include coronary heart disease, stroke, type 2 diabetes and hypertension. This has led to a new ‘developmental’ model for these disorders. The so-called ‘fetal origins hypothesis’ proposes that the disorders originate through developmental plasticity, whereby malnutrition during fetal life, infancy and early childhood permanently change the structure and function of the body, a phenomenon known as ‘programming’. This paper reviews recent findings in the Helsinki Birth Cohort, which comprises 13 345 men and women born in the city during 1934-1944. There is also an older cohort comprising 7086 people born during 1924-1933. We review the paths of pre- and postnatal growth that lead to later disease. Children who later develop coronary heart disease and type 2 diabetes grow slowly during fetal life and infancy but thereafter increase their body mass indices rapidly. Those who later develop stroke grow slowly in fetal life, infancy and during childhood. We also review how the growth of girls during infancy, childhood and at puberty influences chronic disease in the next generation.
Standardized Mortality Ratio(SMR)
is aratiobetween the observed number of deaths in an study population and the number of deaths would be expected, based on the age- and sex-specific rates in astandardpopulation and the population size of the study population by the same age/sex groups.
Dutch Hunger Winter (1944-1945)
intrauterine environment.
A baby grows inside the mother’s womb or uterus.
Barkers Hypothesis
Inadequate nutrition
in utero poor fetal growth/low birthweight metabolic and cardiovascular disease in later life
Fetal Origins of Adult Disease (FOAD)
Intrauterine environmental (not just nutrition) exposures affect thefetus’ development during sensitive periods increases the risk of specificdiseasesinadultlife
(CVD and type 2 diabetes)
3 characteristics of Developmental Plasticity:
- the nature of the response will in part be dependent on the nature of
the environmental cue. - there are critical windows for plasticity in different systems – when
system is most vulnerable to change. - the duration of developmental plasticity is time-limited: once
organogenesis is complete (structure & function), plasticity is no
longer possible (limited).
