life course and wellbeing Flashcards
epidemiological transition
during 20th centm populations experienced an epidemiological transition with morbidity and mortality increasingly being due to NCDs
as countries undergo transitions, mortality from communicable diseases declines and from NCDs increases
more developed countries are further through the transition
aetiological model
emphasises adulthood risk factors becuase NCDs normally manifest for the first time in adulthood and are modifiable by lifestyle or environmental factors such as diet, PA and smoking
communicable disease rates decline due to improved sanitiation + hygien, discovery of antibiotics and childhood vaccination
NCD rates increase, lifestyle factors as above
birth weight
risk of CVD was greatest in individuals who were lightest at birth - BW being a conveniantly availably proxy marker for growth and nutrition in utero
barker hypothesis
foetal origins of health and disease- thought to be due to changes in conc of foetal and placenta hormones, persititng changes in the levels of hormone secretion or in the sensitivity of tissues to them
now known that BW reflected all the biological changes made in utero in response to adverse environment, biological adaptations- eventually leading to disease
biological programming
hypertension is initiated by the reduced number of nephrons found in people who were small at birth
number of nephrons is decided in utero and remains unchanged
smaller babies= less nephrons, less ability to filter blood + regulate blood pressue so increased risk of hypertension
BW is not cause of disease but an indicator of the biological changes that occur later in life
low BW linked with many diseases + general motrality
developmental plasticity
capacity of cells, organs and systems to change function or state- often in response to environmental stimulus
infant growth
children who later develop CHD and type 2 diabetes grow slowly during foetal life and infance but after that, increase BMIs
poor intrauterine growth followed by rapid postnatal growth is associated with increased risk of diabetes
poor intrauterine- not enough nutrients for fetal development- rapid postnatal= abundacne of food and energy so big mismatch between pre and postnatal environment
DOHaD
development of origins of health and disease paradigm describes how, during early life, the environment induces changes in development that have long term impact on health and disease risk
not just about birth weight but named chnages to developmental origins
problems with DOHaD is what happens later in life is also important- not just about early life
adulthood risk factors are still important
life course epidemiology
study of long term effects on later health or disease risk of physical or social exposures during gestation, childhood, adolescence amd later adult life
idea developed by scientists who recognised disease development was a lifelong process
mixture of feotus/ childhood development aswell as adult life
DOHaD and LCE cross same areas
conceptual models
shows how a child with a critical risk factor at birth can have different outcomes due to exposure to certain risk factors later in life
(in notes)
trajectories
life course approach requires undertsanding of normal biological trajectory
if we know normal trajectory- can hypothesise how different exposures or events across life can affect impact your trajectory
intergenerational effects
how diseases can operate across generations
nutritional enviornment that a pregant women was exposed impacted on the long term health of the offspring
figure (in notes) shows cycle of malnutrution
secular trends
changes over the life course will change the likelihood of disease even if the children in the past had the same issues
eg low BW 50 years ago linked to CHD but as lifestyle changes, the link between these issues will also be different
different cohorts of people are born at different times and experience different things across their lives
