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normal & abnormal foetal development > Developmental Origins of Health and Disease > Flashcards

Developmental Origins of Health and Disease Flashcards

1
Q

can the rapid increases in rates of non-communicable diseases be explained by genetics

A

no

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2
Q

non-communicable diseases in developed countries are increasing rapidly which is not in correlation to ____ that is not changing much

A

changes in genetic makeup of the population

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3
Q

what was the relationship found between average income and CHD (coronary heart disease)

A

high income had lower rates of CHD

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4
Q

what was the relationship between REGIONAL infant mortality rates and heart disease 50yrs later & why

A
  • strong correlation
  • ie/ babies who were undernourished before or after birth were more likely to have poor health much later
  • high infant mortality rate reflects poor maternal health and nutrition -> suggest adverse pregnancy and infant conditions that impact later health (IN REGIONAL)
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5
Q

what factor strongly predicted whether someone died of CVD before reached 65 years of age

A

birth weight

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6
Q

what does the hook like pattern (non-linear) of birth weight to CVD related death <65yo indicate

A
  • increasing risk of CVD with decreasing birth weight
  • but also increasing risk of CVD at the highest birthweight groups
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7
Q

what does gestational diabetes do to foetus

A
  • can cause foetal overgrowth
  • increases risk of later disease
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8
Q

relationship between birth weight and current health (alive)

A
  • low birth weight had higher rates non-communicable disease
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9
Q

what is the Barker hypothesis

A
  • adverse nutrition in early life, including prenatally - as measured by low birth weight -> increases susceptibility to cardiometabolic diseases
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10
Q

what has the Barker hypothesis evolved into

A

DOHaD paradigm

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11
Q

what was Barker’s suggestion (which is supported by many studies) & what was the suggestion that opposed it

A
  • that adult disease was affected by events before birth
  • adult disease attributed to genetics and adult lifestyle
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12
Q

list some cardiovascular and metabolic diseases that are increased risk later in life from lower birth weight

A
  • diabetes, insulin resistance, insulin deficiency
  • hypertension
  • CVD
  • stroke
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13
Q

list some neurological and mental diseases that are increased risk later in life from lower birth weight

A
  • schizophrenia
  • impaired neuromotor function
  • poor cognition
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14
Q

list some other diseases (repro, bone, respiratory, immune) that are increased risk later in life from lower birth weight

A
  • polycystic ovary syndrome
  • osteoporosis
  • chronic obstructive lung disease
  • asthma (overall, mostly not allergic)
  • early life susceptible to infection
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15
Q

list some diseases that are increased risk later in life from very high birth weight

A
  • some cancers (breast, ovarian, prostate cancers)
  • allergy (eczema /allergic dermatitis, food allergy)
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16
Q

a change from nutrient-poor to nutrient-rich environments were associated with increase or decrease in disease risk
this is referred to as the ______ _______ hypothesis

A
  • increase risk
  • thrifty phenotype hypothesis
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17
Q

(Hales and Barker) proposed what as the thrifty phenotype hypothesis
(concerns foetal nutrition)

A
  • low availability of nutrients prenatally
  • followed by improvement in nutritional availability in early childhood
  • caused increased risk metabolic disorders
  • due to permanent changes in metabolic processing of glucose-insulin determined in utero
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18
Q

explain the ‘set points’ of hales & barker thrifty phenotype hypothesis
(concerns foetal nutrition)

A
  • undernourished foetus has set points -> saves energy possible
  • if more nutrients are available after birth, a thrifty response results in obesity and metabolic poor health
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19
Q

what is low birth weight a marker of for research purposes

A
  • foetal nutrition
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20
Q

what is Foetal Origins of Adult Disease (FOAD) hypothesis

A
  • that low birth weight (a marker of foetal nutrition) not the only exposure that affects later health (broadening of thrifty phenotype hypothesis)
  • the environment a foetus is exposed to affects foetal development, which in turn alters the individual’s risks of later disease
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21
Q

what is the refinement of the thrifty phenotype

A
  • ‘predictive adaptation’
  • not by barker
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22
Q

what is the concept of predictive adaptation

A
  • foetuses adapt to environment they expect to enter into once outside womb -> increase likelihood of survival (short-term benefit)
  • results in adverse consequences for long-term health when prenatal and postnatal environments don’t align
  • adult disease risk was increased by this ‘developmental mismatch’
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23
Q

developmental origins of health and disease paradigm (DOHaD) reflects what & not what about disease risk

A
  • disease risk reflects cumulative effect of events across a person’s lifespan that changes an individual’s health trajectory
  • disease risk does not reflect a once-off exposure
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24
Q

according to the developmental origins of health and disease paradigm (DOHaD), individual’s health trajectory have greatest effect from events when

A
  • events that occur early on have greatest effects on health trajectories
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25
Q

according to the developmental origins of health and disease paradigm (DOHaD), does early or late intervention provide greater potential benefit for life-long health

A
  • earlier intervention
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26
Q

define DOHaD

A
  • a disturbance of the environment in early life, occurring at critical stages of the development of regulatory systems and their target tissues, that alters functional developmental and capacity, therefore predisposing to impaired function and disease in alter life
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27
Q

(3) main types of early life exposures that program later health and disease risk

A
  • maternal
  • paternal
  • placental
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28
Q

examples of maternal factors of exposure

A
  • diseases like diabetes
  • smoking during pregnancy
  • maternal stress
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29
Q

how do maternal factors of exposure affect foetus

A
  • affect foetal nutrition
  • result in foetal exposure to chemicals that cross placenta
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30
Q

examples of paternal factors that of exposure

A
  • obesity and poor diet quality which affect sperm
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31
Q

what is one of the most common reasons for poor foetal growth in developed countries?

A
  • poor placental function
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32
Q

function of the placenta

A
  • transport nutrients from mother to foetus, including: oxygen, glucose, amino acids, methyl donors
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33
Q

by what process / mode are nutrients (including most amino acids) transported across placenta against conc gradient

A
  • active process
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34
Q

how is foetal exposure to active corticosteroids (cortisol in humans) reduced

A
  • deactivates maternal stress hormones as they pass across placenta
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35
Q

list 2 roles of placenta

A
  • actively metabolises many nutrients
  • important source of hormones that regulate maternal adaptation to pregnancy
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36
Q

what is excess foetal corticosteroid exposure a well-established risk factor of

A
  • poor progeny (foetus) health
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37
Q

can non-maternal factors developmentally program individuals

A

yes

38
Q

what are some exposures independent of the mother that can program later health

A
  • during ART, gamete and embryo exposures
39
Q

which exposure type is more likely to affect most of us

A

paternal factors

40
Q

what can occur form paternal factors that affects us as an exposure

A
  • paternal factors can affect sperm and later expression of paternally derived genes
  • can affect way sperm and semen exposure induce maternal immune tolerance of pregnancy
41
Q

examples of a paternal factor that affects later disease risk

A
  • paternal age (ie/ more likely to have a child w autism if older father)
  • paternal BMI (for childhood obesity)
42
Q

define multigenerational effects vs transgenerational effects

A

exposures in one generation (F0 generation) may affect:
- subsequent generations directly (multigenerational effects)
- or be inherited (transgenerational effects)

43
Q

explain exposure in multigenerational effects

A
  • individuals or gametes that will contribute to subsequent generations are exposed
44
Q

how many generations do multigenerational effects occur for females & why

A
  • woman pregnant with a female foetus is exposed to under nutrition
    -> pregnant woman (F0)
    -> her female foetus (F1)
    -> oocytes developing inside female foetus that will contribute genetic material to next generation (F2)
45
Q

how many generations do multigenerational effects occur for males & why

A
  • two male generations
  • as male gametes develop postnatally
46
Q

what changes are passed from an exposed to unexposed generation in transgenerational effects

A

persistent epigenetic changes pass

47
Q

in who would changes from transgenerational effects be seen in (male and female)

A
  • great-granddaughter (F3) and subsequent generations in female line
  • grandson (F2) in male line
48
Q

why would changes in these people transgenerationally be seen

A

because cells and gametes contributing to these generations were not subject to the original exposure

49
Q

identify who is F0, F1, F2, F3

A

F0 - grandmother or grandfather
F1 - daughter / mother or son / father
F2 - granddaughter or grandson
F3 - great granddaughter

50
Q

which body systems can be programmed by early life exposures

A

any body system

51
Q

how do we usually deduce which system is altered

A

phenotype (eg/ growth patterns, behavioural changes, disease susceptibilities)

52
Q

what is the concept of critical windows for programming

A
  • different systems are more or less susceptible at different times, usually during periods of rapid development
53
Q

what are the underlying signals that change development

A

foetal development changes in response to:
- altered supply of substrates (O2, macronutrients, micronutrients)
- altered hormones
when these occur at critical stages of deevelopment

54
Q

foetal hormone production changes in response to ______

A

nutrition

55
Q

foetal development can be ______ without changes in birth weight

A

altered

56
Q

list some mechanisms for developmental programming that have been identified for DOHaD

A
  • epigenetic modifications
  • altered cell kinetics
  • clonal selection
57
Q

(mechanisms DOHad) describe epigenetics in regards to cells, genes, expression

A
  • all cells in an individual have the same genes
  • epigenetics describes processes that result in particular genes being expressed in some cells but not others
  • thru different processes
58
Q

(mechanisms DOHad) define epigenetics

A

heritable changes in gene expression without a change in DNA sequence

59
Q

(mechanisms DOHad) epigenetic processes alter _______ __________ not the ________ _______

A
  • gene expression
  • gene production
60
Q

(mechanisms DOHad) do epigenetic changes occur thru mitosis or meiosis

A
  • mostly transmitted thru mitosis (cell division)
  • some can be partially inherited thru meiosis
61
Q

(mechanisms DOHad) name ways epigenetic processes occur

A
  • by changing amount of a gene that is transcribed by altering chromatin structure
  • or changing turnover of transcript - if mRNA is broken down rapidly then less of the protein product of that gene will be made
62
Q

list epigenetic mechanisms that developmentally program later health & which process (2) they affect:

A
  • DNA methylation of cytosines (affect chromatin) ie/ epigenetic changes
  • chemical modifications to histones (affect chromatin) ie/ epigenetic changes
  • expression of non-coding RNAs (affect mRNA transcript turnover) ie/ epigenetic changes
  • altered cell kinetics
  • clonal selection
63
Q

[epigenetic mechanisms that developmentally program] is DNA methylation associated with higher or lower gene expression & what happens to chromatin

A
  • associated with lower gene expression
  • with more tightly packaged chromatin
64
Q

[epigenetic mechanisms that developmentally program] how do chemical modifications to histones

A
  • how tightly DNA is packed around histones in chromatin
  • including histone methylation and histone acetylation
65
Q

what is histone methylation associated with

A

increased gene expression

66
Q

what is histone acetylation associated with

A
  • can increase or decrease gene expression depending on position
67
Q

[epigenetic mechanisms that developmentally program] what does expression of non-coding RNAs to do mRNA

A
  • non-coding RNAs such as microRNA
  • target mRNA for degradation
  • generally leads to lower gene expression
68
Q

[epigenetic mechanisms that developmentally program] in altered cell kinetics, what do glucocorticoids trigger

A
  • a switch from cell division (proliferation) to cell specialisation (differentiation)
69
Q

[epigenetic mechanisms that developmentally program] what can early exposure to elevated glucocorticoids result in

A
  • fewer cells in the mature organ
70
Q

[epigenetic mechanisms that developmentally program] describe clonal selection

A
  • if a specific foetal environment is more suited to daughters of one cell over another
  • the final tissue will be made up of cells with slightly different function
71
Q

list the types of changes in development [type: changes to numbers, types, or proportions of cells in a tissue] and examples of consequences from it in later health

A

type: changes to numbers, types, or proportions of cells in a tissue
consequences:
- fewer glomeruli in kidney of progeny when rat mothers fed low protein diet -> offspring more susceptible to kidney failure after kidney damage or ageing
- fewer muscle fibres following maternal undernutrition in pigs -> muscle can’t grow as much, more fat is deposited
- altered proportions of different muscle fibres -> altered muscle strength

72
Q

list the types of changes in development [type: altered structure within a tissue] and examples of consequences from it in later health

A

type: altered structure within a tissue
change:
- lower density of blood vessels in muscle of intrauterine growth restriction progeny -> worse fuel supply to these cells & poorer muscle strength after birth
- increased collagen in blood vessels -> less elastic vessels & incr bp with ageing

73
Q

list the types of changes in development [type: altered function and capacity of particular cells, via changes in gene expression] and examples of consequences from it in later health

A

type: altered function and capacity of particular cells, via changes in gene expression
changes:
- lower expression of nutrient transporters -> reduced nutrient uptake & therefore lower substrate storage

74
Q

the same exposure at _____ times before birth can have ___ effects because different systems are _____ at different times

A
  • different
  • different
  • vulnerable
75
Q

can one event in foetal life affect multiple systems given they are each developing rapidly

A

yes

76
Q

for organs that develop over a longer period does this mean they are vulnerable for shorter or longer period eg/ brain

A

longer

77
Q

define critical windows

A

body systems are susceptible to environmental exposures at different stages of development
because of this, same exposure will have different outcomes in individuals who are exposed to same insult at different times

78
Q

main human evidence for critical windows for programming

A

Dutch Winter hunger

79
Q

what exposure was in Dutch Winter hunger

A

undernutrition

80
Q

pregnancy outcomes of Dutch Winter hunger

A
  • babies born after famine exposure during mid or late gestation were lighter and smaller than those exposed during early gestation or not-exposed (born before famine or conceived after)
81
Q

during the Dutch Winter hunger did those exposed during early gestation have lower birth weights

A

no

82
Q

long-term effects of exposure onto the offspring depended on what

A

effects of famine exposure depended on:
- timing of famine exposure during gestation

83
Q

can developmental programming occur without birth weight being affected

A

yes

84
Q

explain this in relation to the Dutch Winter hunger: developmental programming can occur without birth weight being affected

A
  • those exposed to famine in early gestation did not have lower birth weight but still had increased risk of multiple health outcomes
85
Q

3 main intervention approaches to adverse exposures in early life

A
  • removing or reducing adverse exposures
  • aiming to reverse effects
  • amelioration (make better) or prevention of the long-term effects
86
Q

[3 main intervention approaches to adverse exposures in early life] example of removing or reducing adverse exposures

A
  • providing iodine supplements during pregnancy to avoid (remove) adverse effects of iodine deficiency (exposure) on brain development
87
Q

[3 main intervention approaches to adverse exposures in early life] example of aiming to reverse effects

A
  • providing environmental enrichment after preterm birth to promote brain development
87
Q

[3 main intervention approaches to adverse exposures in early life] example of amelioration or prevention of long-term effects

A
  • more frequent or earlier monitoring in a group at increased risk of diabetes
  • so that medications to improve glucose control can be started as soon as disease begins to develop
  • and side effects of elevated glucose are avoided
87
Q

in developmental programming, does the first adverse exposure lead to disease why or why not

A
  • it does not
  • unless a second adverse exposure to homeostasis also occurs - ‘second hit’
88
Q

provide an example of a first adverse exposure followed by a second hit for a problem with glucose control

A
  • first adverse exposure: intrauterine growth restriction -> may reduce number of insulin-producing beta cells in pancreas
    => not a problem for glucose control unless followed by second hit
  • second hit: high fat intake postnatally
    => exposing a limited capacity for insulin secretion when that individual becomes glucose resistant
88
Q

how can a vulnerable group avoid disease after developmental programming has them exposed to an adverse exposure

A

avoid secondary challenges

88
Q

can developmental programming have an effect on susceptibility of secondary exposure later on

A

yes

normal & abnormal foetal development (7 decks)

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