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216 > Lecture 9/10 > Flashcards

Lecture 9/10 Flashcards

1
Q

are all characteristics developed

A

yes

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2
Q

what are types of environments

A
  • unconstrained
  • patterned
  • constrained
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3
Q

What are unconstrained environments

A
  • environment is supportive
  • individual achieves full potential
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4
Q

What are patterned/channeled environments

A
  • growth is shaped by environmental pressures leading to developmental adaptations in response to challenges
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5
Q

what are constrained environments

A
  • phenotypic plasticity does not allow for a complete adaptation
  • growth is constrained and the full impact of the challenges depend on timing and severity of the insult
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6
Q

What is the baby’s first environment

A

mother

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7
Q

what marks the relationship between mother and unborn offspring

A
  1. constraints in quality of mother’s environment = quality of fetus’ environment
  2. conflict of interests between players involved
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8
Q

______ and _____ will depend on the ______ and ______ of the constraint

A

adaption, survival, nature, intensity

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9
Q

True or false: prenatal constraints tend to affect post-natal phenotypes

A

true

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10
Q

What do post natal phenotypes from constraints may represent?

A
  1. unavoidable costs of prenatal constraints
  2. the costs of prenatal adaptations to those prenatal challenges
  3. predictive adaptive responses
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11
Q

What does it mean when unavoidable costs have unavoidable results

A
  • no benefits associated - the result of not having enough resources
  • ex: small phenotype could be because of scarce energetic resources
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12
Q

What does the costs of prenatal adaptations mean

A
  • surviving in utero require changes in developmental trajectories - trade offs such as lower quality post natal phenotype
  • ex: prioritize development of brain rather than body
  • (may be mediated by phenotypic plasticity)
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13
Q

What are predictive adaptive responses

A
  • phenotypic changes that do not provide immediate advantages but may aid with predictable future challenges
  • (can be mediated by phenotypic plasticity_
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14
Q

What is plasticity ?

A

change phenotype according to environment

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15
Q

explain Daphnia helmets/water fleas

A
  • grows head and spokes with exposure to pheromones that it is developing near predators
  • Less energy in belly, more to the spike = smaller belly
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16
Q

What is the intra-genomic conflict hypothesis

A
  • predicts different replication strategies by individual genes within a genome leading to conflicts that affect the phenotype
  • could result from different transmission strategies within parent or competition between genes of different parental origin
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17
Q

What is meiotic drive

A
  • segregation distortion during meiosis - some alleles overrepresented in oocytes
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18
Q

describe segregation distortion

A

…..

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19
Q

true or false: genes are not part of other genes’ environment… if false explain

A

FALSE
- the presence of particular alleles on the genome can affect transmission of other alleles
- the presence of particular alleles on the genome can affect expression of other alleles

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20
Q

What would benefit maternal genes

A
  • maximize inclusive fitness of mother
  • modulate investment according to offspring quality
  • sensitive to tradeoffs between offspring quantity and quality
  • sensitive to tradeoffs between current and future offspring
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21
Q

What would benefit paternal genes

A
  • survive at almost all costs
  • take as much from mom as possible (despite costs to siblings)
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22
Q

What does a promiscuous mating system lead to

A

lower genetic relatedness to father in a mother’s brood

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23
Q

Selection in a promiscuous mating system should favour…..

A

paternal genes that either
1. favour maternal investment
2. silence maternal genes that down regulate maternal investment

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24
Q

selective pressure on maternal genes should favour

A
  • genes that aid in regulation of maternal investment
  • genes that silence paternally expressed genes that increase demands on mother
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25
Q

serial monogamy =

A

polygamy
(divorce)

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26
Q

Homo sapiens is a species with a ______ degree of polygamy

A

moderate

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27
Q

When are potential times for conflict

A
  1. conception
  2. early survival of embryo
  3. placentation
  4. intrauterine growth
  5. gestational length
  6. early post partum
  7. post natal development
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28
Q

How can conflict at conception and early survival of embryo arise

A
  • deteriorating environments ==> mechanisms preventing conception (anovulatory cycles, hostile vaginal environment)
  • prevent implantation (change uterine chemical or physical environment)
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29
Q

How is a potential mechanism a mom can assess ability of embryo to develop

A

by the levels of cytokines or human chorionic gonadotropin (hCG) the embryos produce

(these are the same hormones pregnancy tests measure)

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30
Q

How do fetuses try to gain more blood

A
  • change diameter of maternal spiral arteries and increase blood volume to placenta
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31
Q

What are consequences to the mother by the fetus trying to gain more blood

A
  • vasoconstriction (reduce diameter of blood vessels)
  • high BP
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32
Q

What is preeclampsia

A
  • decreased blood flow to placenta = premature brith and LBW
  • decreased blood flow to mother’s kidneys, brain, liver, retina
  • can lead to eclampsia = maternal cerebral hemorrhage, seizures, death, fetal stillbirths
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33
Q

the risk of pre-eclampsia _______ with changes in sexual partner

A

increases

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34
Q

What is the role of the male partner in pre-eclampsia

A
  • may be mediated by immunological interaction between male and female tissues
  • some men linked to higher risks
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35
Q

true or false - preeclampsia may have had some effect in evolution of human mating system

A

true

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36
Q

what are health implications of viewing pre-eclampsia as a paternal/fetal strategy

A
  • strengthen maternal counter-adaptations to limit fetal manipulation
  • preventing nutritional conditions that trigger it
  • develop preventative tests for men with partners who experienced it / women who change partners
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37
Q

What does the placenta releasing human placental lactose do?

A

increase insulin resistance, keeping blood glucose circulating for a longer time after meal = more glucose for fetus

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38
Q

How do mothers’ bodies counter effects of human placental lactogen

A

increase insulin secretion
- which can result in gestational diabetes

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39
Q

What are health risks of gestational diabetes

A
  • really large babies
  • increased risk of maternal non-gestational diabetes
  • newborn problems regulating circulating glucose, increased risk of diabetes and obesity
40
Q

What can the adrenal glands trigger

A

parnurtition/pre-mature —> maturation of the lungs

41
Q

How are babies and tadpoles similar

A
  • adrenal glands signal metamorphosis in tadpoles when environment is not too good
  • adrenal glands in baby can trigger premature birth because of environment
42
Q

What is low birth weight and influenced by?

A

<2500 g
- influenced by maternal nutrition and disease

43
Q

What is intrauterine growth retardation

A
  • fetal weight < 10th percentile = smaller than expected for gestational age
  • thin, pale, loose, dry skin, thin and dull umbilical cords
44
Q

What are maternal proximate factors associated with IUGR

A
  • high BP
  • chronic kidney disease
  • diabetes
  • CVD
  • malnutrition
  • anemia
  • infections
  • substance use
45
Q

What are proximate factors involving the uterus and placenta associated with IUGR

A
  • decreased blood flow
  • placental abruption (detachment from uterus)
  • placenta previa (attaches low in uterus)
46
Q

What are proximate factors associated with IUGR related to the fetus

A
  • multiple gestations
  • chromosomal and birth anomalies
  • organ growth limitation
  • low fetal heart rate
47
Q

what conditions linked with IUGR

A
  • still birth
  • low Apgar scores (reflex?)
  • meconium aspiration (inhaler fecal ish matter)
  • hypoglycemia
  • body temp regulation problems
  • polycythemia
  • shouldn’t treat these independently
48
Q

What are interventions for IUGR

A
  • maternal nutrition (fetal growth?)
  • maternal bedrest (circulation to fetus)
  • delivery (may be necessary)
49
Q

What could post partum depression, psychosis, infanticide be?

A
  • evolved mechanisms for maternal investment avoidance?
  • contributing factors - lack of support, low self esteem, inadequacy, isolation, financial, life changes
50
Q

is there one gene for one behaviour

A

NOOOOOOO

51
Q

What are factors affecting growth trajectories

A
  • pre and perinatal problems
  • nutrition
  • high altitude hypoxia
  • pollutants
  • maternal health conditions
  • psychosocial environment
  • social and economic status
52
Q

growth problems in utero/childhood can lead to

A

fetal programming and chronic diseases in adulthood

  • psychosocial consequences
53
Q

what is growth canalization

A

a tendency to keep to a narrow and predictable track of growth, usually along a centile line

54
Q

When is the biggest growth spurt one will ever have

A

in utero, between 20-30 weeks of gestation fetus grows at rate 120 cm/year

55
Q

Why are growth spurts a time of increased vulnerability

A
  • If one cell is exposed to a toxicant -> mutation or effects epigenome then the cells will carry that affect - organs and tissues affected, the younger you are and faster you develop the higher the impact of the exposure will be
56
Q

What is the thrift phenotype hypothesis

A

poor prenatal nutrition leads to small postnatal phenotypes, a decrease in basal metabolic rates, efficient fat metabolism which ultimately lead to an increased risk for metabolic syndrome

57
Q

Infant nutrition

A
  • early nutrition crucial for healthy growth
  • breast fed infants grow differently from formula fed infants
58
Q

What is the most vulnerable period for growth and development

A
  • weaning period
59
Q

What is protein energy malnutrition

A
  • typically when weaning
  • thin limbs, enlarged belly
  • severe growth faltering
  • overall health and mental impairment
60
Q

PEM + caloric deficiences/dehydration =

A

increased risk of infections and circulatory disorders like marasmus

61
Q

how is over nutrition a modern mismatch

A
  • low levels of physical activity
  • hyper caloric diet
62
Q

What are possible causes of the association between SES and height

A
  • nutritional status
  • disease load
  • access to medical care
  • psychosocial stress
63
Q

What is psychosocial short stature/dwarfism/kaspar houser syndrome

A

growth failure/delayed development in association w emotional deprivation

64
Q

Why do low SES and high SES seem more even in Sweden than other countries

A
  • welfare state - social programs and support
65
Q

are children born in restricted environments doomed?

A

no! if they are placed in a more advantageous environment they can grow up and catch up with those who enjoyed a more nourishing environment

66
Q

What is catch up growth

A
  • an unusually rapid height increase, considering age and/or maturity of an individual, following a transient period of growth inhibition
67
Q

canalization makes it possible to…..

A

identify a period of catch up growth

68
Q

what is puberty

A

onset of reproductive, physical and behavioural changes leading to adulthood

69
Q

why do sex differences in heigh exist

A
70
Q

the timing and pace of transition of puberty are sensitive to …….. factors

A

internal(development) and external(ecological) factors

71
Q

The hypothalamus regulates

A

growth, cardiac function, body temperature, hunger, sleep, reproductive function via the pituitary gland

72
Q

What does the hypothalamus release by the median eminence

A

gonadotropin releasing hormone/GnRH to anterior pituitary

73
Q

What does GnRH stimulate

A

production and release of the gonadotropins
1. follicle stimulating hormone
2. luteinizing hormone
from anterior pituitary

74
Q

what do FSH and LH do

A

stimulate the gonads (testes/ovaries)

75
Q

What does FSH do in women

A

stimulate recruitment and development of ovarian follicles (egg) for ovulation

76
Q

What does the luteinizing hormone do in women

A

triggers ovulation and formation of corpus luteum

77
Q

Maturation of follicle triggers…

A

estrogen - stimulates proliferation of the endometrium

78
Q

formation of the corpus luteum results in….

A

an increase in luteal progesterone
- maintains the endometrium

79
Q

what does LH do for men

A

stimulate production and release of testosterone

80
Q

what does FSH do for men

A

with testosterone, stimulate sperm production

81
Q

how often is GnRH released

A

in pulses, once an hour

82
Q

what is the circhoral rhythm

A

once an hour - crucial for function of HPGA

83
Q

What affects GnRH cir choral rhythm of secretion

A

environment (auditory, olfactory, visual, tactile stimuli, changes in photoperiod)

84
Q

What are two theories of the maturation of HPGA axis during puberty

A
  1. Gonadostat hypothesis
  2. Hypophysiotropic hypothesis
85
Q

What is Gonadostat hypothesis

A

pre puberty GnRH pulse generator highly sensitive to gonadotropin levels and during puberty that decreases, resulting in an increase in gonadal steroids

86
Q

what is the hypophysiotropic hypothesis

A

puberty associated with an increase in positive feedback by stimulatory factors

87
Q

what are the 5 correlates of HPGA maturation

A
  1. somatotropin axis
  2. adrenarche
  3. insulin sensitivity
  4. body composition
  5. skeletal maturation
88
Q

Somatotropin (GROWTH) axis

A
  • regulated by the hypothalamus via growth hormone releasing hormone and somatostatin
  • acts on pituitary to regulate release of growth hormone
  • GH stimulates release of insulin like growth factors from liver and other tissues
  • GH and IGF1 stimulate skeletal growth and protein anabolism
  • increase in somatotropin activity appears to be a consequence of gonadal steroid production
  • both estradiol and testosterone affect GH production by augmenting the amplitude of GHRH pulses
89
Q

adrenarche

A
  • adrenal cortex and medulla
  • during adrenarche adrenal cortex develops third layer - zone reticular and begins producing large amounts of adrenal androgens (DHEA and androstenedione) which increase in pre-pubertal children
  • changes occur before detectable increases in gonadotropins and gonadal steroids
  • suggested WEAK ANDROGENS MAY CONTRIBUTE TO MATURATION OF HPGA
90
Q

insulin sensitivity

A
  • controls energy metabolism
  • produced by islet cells in pancreas
  • stimulates cellular uptake of glucose
  • insulin and growth hormone up regulate each other
  • elevated insulin -> increased IGF1
  • more insulin = more gonadal steroid hormone levels
91
Q

How does insulin relate to puberty

A

during puberty = a decrease in insulin sensitivity -> insulin resistance -> increase in insulin levels -> increases in gonadal steroid -> pubertal development

92
Q

body composition

A
  • fatness threshold hypothesis = criticized
  • increase in fat mass as a consequence of HPGA maturation and not cause
  • skeletal dimensions ???
93
Q

skeletal maturation hypothesis

A

timing of puberty is coordinated with attainment of appropriate physical size for reproduction

94
Q

Why is the HPGA so sensitive to the rhythm hypothalamus releases GnRH pulses

A

allows us to
- adjust reproductive maturation and function to the quality of environment
- as long as development is not complete, reproduction comes second to growth and survival

95
Q

What do we need to develop well

A
  1. to be wanted
  2. tranquil parents
  3. social support group
  4. clean environment
  5. appropriate nutrition
  6. appropriate stimulation
  7. to be loved

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