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B1 > Biology, Health, and Disease > Flashcards

Biology, Health, and Disease Flashcards

1
Q

Outline the trade off organisms experience, and different strategies used to overcome this

A
  • Energy source- tradeoff between growth, maintenance, and reproduction
  • fast life history strategy- more energy for reproduction (large litters, low investment per offspring in hope that half survive e.g.)
  • slow life history strategy- more energy into growth and reproduction- produce single offspring and greta investment into them
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2
Q

Outline the relationship between different life history traits

A

Jones, 2011:
- larger size relates to older age at first reproduction, longer lifespan, and lower annual fertility rates
- suggests life history traits may come as package
- standard patterns across species, but primates have slightly slower reproduction and live slightly longer

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3
Q

Definitions of life history

A

Hutchings, 2021: a solution that natural selection has produced to solve the problem of how to persist in a given environment
Reznik, 2010: predicts how natural selection should shape the way organisms parcel their resources into making babies

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4
Q

List life history traits

A
  • size at birth
  • growth pattern
  • age and size at maturity
  • number, size, and sex of offspring
  • age-, stage- or size-specific reproductive effort
  • age-, stage- or size-specific survival
  • lifespan
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5
Q

Outline different types of mortality, and their relationship with life history strategy

A
  • Extrinsic mortality = death caused by some factor largely outside of an organisms control such as disease, starvation, predation
  • Intrinsic mortality = death due to bodily deterioration/senescence

Life history strongly associated with degree of extrinsic mortality- high associated with live fast/have lots of small offspring/die young life strategy

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6
Q

Compare life history of humans and other primates

A

Zimmerman et al, 2015:
- longer post-reproductive lifespan
- slightly longer gestation (270 days vs 26- in others)- but amount of growth achieved in those 9 months is much larger

  • DeSilva, 2011: larger brains, larger babies
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7
Q

Outline human feral growth

A
  • first trimester- organogenesis- formation of organs and physiological systems of the body
  • second trimester- skeletal growth
  • third trimester- fat build ups, physiological preparedness for extra-uterine life
  • 12-26 weeks- 5/6 fold increase in weight
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8
Q

Outline human growth and development during infancy

A

Growth:
- 0-3 years- rapid growth velocity (10-20cm/year increase in height)
- steep deceleration with age

Milestones:
- Transition from breast-feeding to solid foods (weaning)
- Full set of deciduous teeth before third birthday: two incisors, one canine, two molars
- Bipedal walking by ~15mo
- Learning motors skills, language, social relationships
- Shared intentionality and theory of mind developed by 3yo

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9
Q

Compare weaning in humans and other mammals

A
  • processes rather than single event in all
    -non-industrial societies- mean age of breastfeeidng termination 36 months (much earlier than other apes)
  • generally a fast life history strategy
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10
Q

Outline the human juvenile period

A
  • In a general mammalian content, the juvenile period often includes everything after weaning and sexual maturity
  • In humans, split this period into childhood, juvenility, and adolescence

Important features:
* Brain growth finishes much earlier than overall body growth
* We are energetically dependent for much longer than other primates
* The adolescent growth-spurt is derived in humans
* We could reach adult body size much more rapidly than we do

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11
Q

Compare brain and body growth in humans

A

Kuzaqa et al, 2014:
- brain growth finishes much earlier
- brains hugely energetically demanding to grow/maintain- estimated proportion of basal metabolic rate in children is ~60% in 5yo
- growth concentrated in childhood- by end of childhood (~8yo)- body size is ~70% adult hight, brain size >95% adult size

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12
Q

Outline energetic dependency in humans compared to other primates

A
  • Kaplan et al (2000)- energetically dependent for much longer than other primates
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13
Q

Outline the adolescent growth spurt in humans and Peter primates

A
  • A body weight growth spurt is seen in chimpanzees and many other Old World monkeys (often just for males, not females)- sexual dimorphism not seen in same way in humans- Hamada et al, 2002
  • However, evidence for a spurt in skeletal growth (as we see in humans) is less clear- spurt in skeletal growth not seen in chimpanzees
  • skeletal growth spurt is evolutionarily novel
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14
Q

Outline catch-up growth

A
  • A rapid increase in growth velocity following a short-term period of starvation or illness which slowed or stopped growth (Bogin, 2020)
  • suggests rate of growth slower than could be- extends period for brain and technical skill development- rely on parent provisions- suggest spreading out costs helps parents to invest in own reproduction, increases time for socialisation, play, and the development of complex social and cultural behaviour
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15
Q

Outline. study of catch-up growth

A

Hermanussen et al, 2018:
- Case study of severe malnutrition in German school-age children toward the end of WWI
- Children grew between 3-5cm in 8 weeks of supplementary feeding
- however, only if came from in-tact social background

Bogin et al, 2018:
- celiac child- at 11, was below 3rd percentile for age- caused by celiac as couldn’t get energy from diet
- catch up growth by 17- reached 50th percentile- rate of growth 2-3x faster than typical for age

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16
Q

Compare the adult reproductive period in humans and other primates

A

Wells et al, 2007:
- duration not unusual, but rate of reproduction is
- humans have shorter inter-birth interval- higher fertility- 3yrs average vs 4-7 in some primates
- not possible to get pregnant while breastfeeding- lactational amonhorea

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17
Q

Compare maternal investment strategies in humans and other primates

A
  • humans- more offspring in same amount of time- chimpanzees have one at a time investment, whereas humans have several dependent off spring at once- newborn stacking- affects energetic demand on parents
  • this is feature of fast life history strategy
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18
Q

Categorise human life history strategies as part of either slow or fast life history strategy

A
  • pregnancy duration- long- slow
  • birth size- high- slow
  • lactation period- short- fast
  • pre-reproductive period- slow
  • pregnancy duration- between
  • shorter inter-birth intervals and high fertility- fast
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19
Q

Outline factors needing to balance in human offspring/life history’s nd the solution to this

A
  • question how to increase quantity of offspring an divestment in each
  • potential answer- energetic interdependence (Kaplan et al, 2000)
  • shift to calorie-dense, large-package, skill-intensive food resources is responsible for the unique evolutionary trajectory
  • shift produced co-evolutionary selection pressures, which, in turn, operated to produce the extreme intelligence, long developmental period, three-generational system of resource flows, and exceptionally long adult life characteristic of our species
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20
Q

Distinctive features of human growth and life-history summary

A
  • Large relative birth weight
  • Shorter period of lactation, followed by extended period of energetic dependence on adults
  • A relatively slow period of growth during childhood but with adult brain size achieved at ~8years.
  • An adolescent spurt in skeletal growth not seen in other primates
  • Shorter inter-birth intervals
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21
Q

Outline figures highlighting human energetic inefficiency

A
  • Adult body: ~125,000 kcals
  • 1,500 kcals/day for 20years = ~11 million kcals
  • means have ‘lost’ ~99% of the energy you have consumed
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22
Q

What is energetics

A

the study of the use and transfer of energy
- energy is the common currency for everything in human evolution- studying human energetics allows us to better understand the evolutionary causes, consequences, and relationships that exist between key human traits such as large brains, hunter-gathering niche, large babies, bipedalism, meat eating, long childhood, cooperative social behaviour etc; helps us to understand differences in health, growth, reproduction, and body size across human populations

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23
Q

Outline parts of total energy expenditure

A

Snodgrass (2012):

Basic survival costs (costs of somatic maintenance):
- basal metabolic rate
- thermic effect of food
- thermoregulation
- immune activity
- physical activity

Productive costs:
- growth (including muscular)
- reproduction
- fat storage

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24
Q

Summarise energetics and transfers between species

A
  • 1st law of thermodynamics (conservation of energy): energy cannot be created nor destroyed, only transferred or changed from one form to another
  • Energy used for somatic maintenance and physical activity rather than growth of tissues is ‘lost’ from the food chain
  • only ~10% of energy transferred between adjacent trophic levels, limiting the length of food chains- limited by energetic inefficiency
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25
Q

Outline calories

A
  • calorie is the amount of energy required to raise the temperature of exactly one gram of water by one degree Celsius at one atmospheric pressure
  • not all calories equal- e.g. milk has most of energy in form of lactose, whereas Jerusalem artichoke has most in form of inulin (largely indigestible by humans)- different values despite having similar calories per 100g (66/73)
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26
Q

Outline the additive model of energy expenditure

A

Pontzer, 2015:
- suggests TEE composed of baseline running cost for non-physical activity expenditure (BMR-fixed), and any additional costs depending on physical activity

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27
Q

Outline an example of an energetically unusual pophulatopmn- background

A

The Hadza/Hadzabe (Raichlen et al, 2016):
population ~1,200 people, ~300 still primarily foragers
* Northern Tanzania, S of Lake Eyasi
* Serengeti plateau (and Olduvai gorge) to the north
* Language isolate
* Encroachment from pastoralists (and tourism)
* Interest in their lives motivated (rightly or wrongly) by assumption of savannah foraging as the key environment in human evolutionary history

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28
Q

Outline physical activity in hunter-gatherers

A

248-90 min/day across different populations- highest Bayaka men, lowest Tismane women (Pontzer et al, 2018)
- WHO recommendations 150/week

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29
Q

Outline physical activity in HAzda populations

A
  • Racihlen et al (2016) - men 114, women 150 min/day exercise
  • Wood et al, 2021- men 10-20,000 steps per dat, women >10,000- higher Han average smartphone users across 11,000 countries
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30
Q

Link increased physical exercise and total energy expenditure

A

Pontzer et al (2012)- compared total energy expenditure (kCal/day) across (USA), hunter-gatherer (Hadza, Tanzania), and farming (Bolivia) populations using doubly labelled water
- Physical activity significantly higher in the hunter-gather and farming populations than the Western one
- Overall, higher fat free mass = higher TEE
- no difference between populations in this relationship- average daily energy expenditure of traditional Hadza foragers was no different than that of Westerners after controlling for body size- higher physical activity didn’t result in higher TEE for hunter-gatheres/farmers

  • similar results in adults in Ghana, South Africa, Seychelles, Jamaica, and USA- increase from inactive to moderately active, but then flatlines- not linear like additive model would suggests- only possible if BMR dynamics,ically responds (Pontzer et al, 206)
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31
Q

Outline an improves model of energy expenditure

A

Constrained model (Pontxer et al, 2015):
- There is an upper limit to TEE
- non-physical activity energy
expenditure responds dynamically to physical activity
- metabolic trade-offs- humans adapt dynamically to changes in daily physical activity, maintaining total energy expenditure within a narrow range
- Chronic exercise thus suppresses other physiological activity, including immunity, reproduction, and stress response
- exercise-induced downregulation improves health at moderate levels of physical activity but can be detrimental at extreme workloads

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32
Q

Negative energy balance response diagram

A
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33
Q

Outline the Minnesota starvation study

A

wells, 2010:
- Starvation and how to treat it as a major concern towards end of WWII- 6 young men; conscientious objectors
- Halving of dietary intake for 6 months, tightly controlled (~3000 kcal - ~1500 kcal/day)
- 24% decrease in body mass
- Controlled and then ad libitum refeeding
- Monitoring of weight, body composition, physiological performance
- unrestricted food intake caused overshoot in fat mass (weight returned but most of gain it fat mass)- may be result of appetite dysregulation and metabolic changes

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34
Q

Compare TEE of humans to other apes, list potential reasons for this

A

Pontzer et al (2016):
- 400 more than chimpanzees, 635 than gorillas, 820 than bonobos
- reasons- energetic demands of human life history, expensive tissue hypothesis, changing energetic costs and benefits of human subsistence

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35
Q

Outline the effects of human life history on energetic demands

A
  • part of reproductive strategy- high investment in offpspring- Dunsworth et al, 2012
  • birth stacking- Pavard et al, 2019
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36
Q

Outline the expensive tissue hypothesis

A
  • brain- expensive- 20% BMR to brain but only makes up 2% of weight (Aiello & Wheeler, 1995)
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37
Q

Outline changing energetic costs and benefits of human subsistence

A

Kraft et al, 2021:
- elevated energy capture
- shift from great ape foraging to hunter-gathering, and then adoption of subsistence farming during Neolithic revolution- involved changes in behaviour and technology to access novel food resources
- meant humans paid higher energiy costs to acquire more calories in less time- minimises time costs but not energy costs- improved return Raes but efficiency similar to that of other great apes

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38
Q

Outline brain size and growth in humans

A
  • primates- ranges 1g-1400g; apes- 275-750g- no overlap with other groups
  • great apes 400-700 cm3 capacity; humans 1100-1700cm3 (Dean, 2014)
  • human brain larger at birth than any other primates, smaller at birth in relation to adult brain size than any other primate (Neuubauer et al, 2012)
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39
Q

Outline brain energy use

A

Kuzawa et al, 2014:
Estimated proportion of BMR dedicated to the brain:
* ~50% at birth
* ~20% in adulthood (vs. 8-10% non-
human primates; 3-5% non-primate mammals)
- however, not most energetically menacing by weight- similar energetic demanding level as liver (Wang, 2010)

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40
Q

Compare gestational length in humans and other primates

A

Dufour et al (2002):
- Human gestation length is (relative to our body size) typical for primates
- However human are babies are much larger relative to adult body size than is typical for primates

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41
Q

Outline energy costs of pregnancy

A

Dufour et al (2002:
- capital gains- increased issue mass, fetus and associated tissues, maternal tissue hyperplasia, maternal fat gain
- sunning costs- increased BMR, increased cost of physical activity
- eating changes- only increased demand of 277kcal/day
- however, 277kcal/day is difficult to detect without a very
large sample
- Reduced physical activity could make up for the difference: additional intake not necessarily required

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42
Q

Outline energetic costs of lactation

A

Dufour et al, 2002:
* Lactation (during the period of exclusive breastfeeding) is more energetically demanding per day than pregnancy
* Duration of lactation may be greater than duration of gestation
* Costs, as estimated for the first 3 months by Dewey (1997): ~750g/day, 0.67kcal/gram = ~ 500kcal/day- almost twice as demanding per day as pregnancy ~25% increase in energy expenditure
- assumption that this additional energy expenditure is paid for partly by the catabolism of fat stores set down during pregnancy
- ‘maternal fat gain’ component of the estimated costs of pregnancy were ~40% of the pregnancy estimate
- Without these advanced costs of lactation, pregnancy is <200kcal/day

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43
Q

Definitions of aging

A

Physiological- López-Otín et al (2013)- characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death

Evolutionary- Ackermann and Pletcher (2003)- decline in condition with increasing age that manifests itself as a reduction in the rate of survival and fecundity

Aging and senescence used synonymously, though aging could be more broadly defined as a simple chronological increase in age

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44
Q

Outline patterns of human ageing

A

Ackemann & Pletcher, 2008:
- age specific mortality- early spike (infant mortality)
- exponential increase with age after (10 fold between 20 and 6)
- chnace of death doubles every 7-8 years after 35 yrs
- fertility rate falls post 35

Austad & Finch, 2010- age related increase in mortality is substantial- If humans did not age and could preserve their pristine physiological peak (typically near the age of puberty) then life expectancy in the US in 2000 would have been ~5,000 years

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45
Q

Outline human lifespan length

A
  • humans have longer lifespan than other primates (Zimmerman et al, 2015)- particular increase in post-reproductive lifespan
  • the extreme- Jeanne Calment- dies 1997 aged 122- role of exercise
46
Q

Outline secular trends in life expectancy

A
  • 29 years average in 1800, 46 in 1950, 21 in 2015
  • large inequality globally
  • shortest today higher than previous highest
  • often drive by infant mortality- e.g. even if average 20, many may live longer but high infant mortality pulls average down
  • UK will likely plague,less than 2012 based predictions, but considerably higher than 1970s based predictions (ONS)
  • Hobbesian view- short life- harsh conditions old age proiveledge of few (Ackermann & Pletcher, 2008)
47
Q

Outline hunter-gatherer longevity

A

Kaplan et al, 2007:
- large variation between HG communities
- 50% born still alive art 40
- similar to trends seen in early-modern Europe
- modal age at death 71-78 e.g. Hiwi, !Kung (US 85)- living two 7-s robust feature of species (not just artefact of modern medicine etc (given survival to 15 yrs)

48
Q

Summarise patterns in human longevity

A
  • Among foragers, mortality is stable & fairly low (1-2% annually) from maturity to age 40 years
  • After 40, mortality rates increase exponentially with doubling time of 6-9 years
  • Post-reproductive longevity is a robust feature of H. sapiens
49
Q

List evolutionary theories of ageing

A

Kirkwood et al, 2000:
(1) Mutation accumulation
(2) Antagonistic pleiotropy
(3) ‘Disposable soma’ theory

50
Q

Outline the mutation accumulation hypothesis of aging

A
  • harmful mutations that occur past the reproductive age will not be affected by natural selection
  • those before reproduction will not be passed on as to reproduced
  • selection shadow- accumulation of deleterious mutation that happen at later age e.g. Huntingtons disease has effect in late 40s when already reproduced
  • Ageing does not have a function; it exists because it is ignored by natural selection
51
Q

Outline the antagonistic pleiotropy hypothesis

A
  • Pleiotropy: when a gene has two or more separate effects
  • Antagonistic pleiotropy: when those effects work against each other or where one effect is beneficial and the other harmful.
  • Williams (1957): senescence could be driven by genes that are beneficial in early life but lead to senescence in later life
  • Scrable et al, 1957- Tumor protein P53: suppresses cancer but also suppresses stem cell function, impairing cellular maintenance
  • suggests aging is inevitable consequence of later life being ignored by natural selection
52
Q

Outline the disposable soma theory of ageing

A
  • senescence is a consequence of investment in reproduction rather than maintenance
  • Genes-eye view: selection acts on genes that survive, not on individuals that survive. Reproduction > somatic maintenance.
  • Dawkins (The Selfish Gene): survival machines – robot vehicles blindly programmed to preserve the selfish molecules known as genes
53
Q

Outline the shared idea of the three theories of ageing

A

ageing does not have a function; it exists either because it is ignored by natural selection or is the cost of something beneficial to fitness earlier in life

54
Q

Outline female post-reproductive life

A
  • refers to period after which reproduction is physiologically possible (rather than actual reproduction)
  • Menopause: cessation of menstrual periods (clinically: 12 months without a menstrual period)
  • mean menopause age in UK is 51 (range typically 44-55)
  • often preceded by irregularity I periods leading to menopause
  • proximately caused by decline in oestrogen and progesterone production by the ovaries
55
Q

Name explanations for extended post-reproductive life in humans

A

Non-adaptive hypotheses:
- physiological trade off
- selective shadow
- by-product of increased longevity

Adaptive hypotheses:
* The mother hypothesis
* The grandmother hypothesis * Reproductive conflict model

56
Q

Outline the physiological trade-off hypothesis for extended post-reproductive life in humans

A
  • extension of the disposable soma hypothesis (consequence of investment in reproduction rather than maintenance- selection acts on genes not individuals)
  • Selection for ‘front-loaded’ fertility
  • across populations, fertility declines
    significantly between 40-50- supports
56
Q

Outline the selective shadow hypothesis for extended post-reproductive life in humans

A
  • later in life so not affected by natural selection
  • ISSUE- Doesn’t explain why reproductive senescence occurs before
    other functions
57
Q

Outline the by-product of increased longevity hypothesis for extended post-reproductive life in humans

A
  • assumes long post-reproductive lives are evolutionarily novel
  • not the case for foragers, as shown earlier
  • Humans have enough oocytes to last 70 years
58
Q

Outline the mother hypothesis for extended post-reproductive life in humans

A
  • menopause evolved to avoid higher reproductive mediated mortality risk
    in late-life and improve survival and outcomes of existing offspring
  • costs of continued reproduction to existing children
  • HOWEVER, lost benefits of reproduction in later life are not possible to observe
59
Q

Outline evidence for the mother hypothesis for extended post-reproductive life in humans

A

Lahdenperä et al (2011):
- data from pre-industrial Finland and Canada
- Maternal mortality increases with age (but not dramatically)
- Child mortality risk is increased by maternal mortality (but only for the first 2-3 years of life)

60
Q

Outline the grandmother hypothesis for extended post-reproductive life in humans

A

Gurven & Kaplan, 2007:
- kin selection model (the process by which a trait can be positively selected because it increases the fitness of genetic relatives, even if it decreases individual fitnes)
- menopause is bad for individual fitness but could be selected because the post- reproductive women increases the fertility of their daughters
- only works (in theory) because of the genetic relatedness between the post-reproductive grandmother and reproductive-age mother- reproducing by proxy- NS favours behaviour that improves fertility of children

61
Q

Outline evidence for the grandmother hypothesis

A

Lahdenperä et al, (2004):
- women with prolonged postreproductive lifespan have more grandchildren, and hence greater fitness, in pre-modern populations of both Finns and Canadians
- arises because post-reproductive mothers enhance the lifetime reproductive success of their offspring by allowing them to breed earlier, more frequently and more successfully
- fitness benefits of prolonged lifespan diminish as the reproductive output of offspring declines- in female humans, selection for deferred ageing should wane when one’s own offspring become post-reproductive and, correspondingly, we show that rates of female mortality accelerate as their offspring terminate reproduction

62
Q

Outline methodological issues when testing the grandmother hypothesis, and counter-evidence overcoming these

A
  • unable to determine whether grandmother increases fertility of daughter and survival off offspring, or whether the sae things increasing teh longevity of the grandmother also improve the survival of the of the grandchildren (e.g. health/wealth/genetic effects)

Counter-evidence:
- Sear and Mace (2000)- Rural Gambia- controlled for these effects (height/weight/wealth etc)- 25 year longitudinal, N>2000- found that children living with maternal grandmothers had higher survival and were better nourished
- stronger evidence as looked at co-residtence with grandmother (not just them being alive), and provided a plausible proximate explanation- nutritional status
- Sear & Mace (2008)- meta analysis- Broad (though not universal) positive effect of MGM and PGM on child outcomes, more mixed effects for father, MGF, and PGF, positive effects of older siblings

63
Q

Outline the reproductive conflict hypothesis for extended post-reproductive life in humans

A

Cant & Rufus, 2008:
- assumption of a patrilocal context (where men stay and women disperse)
- older women will be genetically related to their son’s wives children, but younger women won’t be genetically related to their husband’s mother’s children
- low reproductive overlap in humans- mother cares about daughter in laws children- genetic stake in fitness of incoming women
- In the event of competition for resources, older females will sooner ‘give way’ to the younger females as still get genetic benefit
- competition (as well as cooperation) could play a role in selection for early menopause
- not mutually exclusive to M or GM hypotheses
- problem- most contemporary hunter-gatherers are bilocal, not patrilocal

64
Q

Outline findings on post-reproductive life in chimpanzees, and implications for explanations in humans

A

Wood et al, 2023:
- Ngogo community of Kibale National Park, Uganda.
- Post-reproductive representation was 0.195- indicating that a female who reached adulthood could expect to live about one-fifth of her adult life in a post-reproductive state (around half as long as human hunter- gatherers)
- Post-reproductive females exhibited hormonal signatures of menopause, including sharply increasing gonadotropins after age 50

  • mother hypothesis unchanged, grandmother hypothesis conflicts (as model assumes grandmothers help- don’t in chimpanzees), supports reproductive conflict model (as assumes female dispersal, which is seen in chimpanzees)
65
Q

What are pathogens, name categories/diseases caused examples

A
  • invading organisms/agents that cause diseas
  • paraistes (e.g. tapeworm), protozo (e.g. Malaria), Fungi (e.g. athletes foot), prokaryote (e.g. Leprosy), Virus (e.g. AIDS), Prion (e.g. CJD)
66
Q

Outline changes in impact of infectious disease over time

A
  • rapid decline in mortality caused by them un western world in 20th century
  • now, more non-communicable-70% of deaths in 2019 (WHO)
67
Q

Outline host-pathogen coevolution

A
  • Throughout evolution, disease has exerted selective pressures on human populations
  • In turn, human responses to disease have promoted evolutionary changes in pathogens
  • means need to compete with pathogens to maintain position- no absolute increase
  • Pathogen alleles that evade defences of larger proportion of hosts do better
    Host alleles that evade attacks of larger proportion of pathogens do better
    -negative frequency dependent selection
68
Q

name an origin of new infectious diseases

A

Zoonoses- transmission from non-human animal to humans

69
Q

Outline the stages of zoonoses, including examples

A

Wolfe et al, 2007:
Stage 1:
- A microbe that is present in animals but that has not been detected in humans under natural conditions
- e.g. most malarial plasmodia- largely specific to 1 host species

Stage 2:
- A pathogen of animals that, under natural conditions, has been transmitted from animals to humans (‘primary infection’) but has not been transmitted between humans (‘secondary infection’)
- e.g. anthrax, rabies

Stage 3:
- Animal pathogens that can undergo only a few cycles of secondary transmission between humans, so that occasional human outbreaks triggered by a primary infection soon die out
- e.g. Ebola, monkeypox

Stage 4:
- A disease that exists in animals, but that also undergoes long sequences of secondary transmission between humans
- e.g. cholera, influenza A

Stage 5:
- A pathogen exclusive to humans
- e.g. meals, mumps, rubella, syphillis, agents causing falciparum malaria, smallpox

70
Q

Outline factors which may increase likelihood of disease advancing through stages of zoonoses

A

Changes to chances of the initial zoonotic infection, and changes that increase potential for human-human transmission

  • note- may also be transmission from humans to animas
71
Q

Outline the ‘one health’ approach

A
  • approach to public health that recognises that human health cannot be considered in isolation from the health of our environment or the wild and domesticated animals around us
  • Developed in response to the increased threat of novel zoonotic disease
72
Q

Outline the effect of population increase (agriculture) on pathogens

A
  • leads to the emergence of new “crowd diseases” that couldn’t have been be sustained in small and low-density populations
  • Grenfell & Booker (1998)- meals requires population 300,000+ to maintain transmission
73
Q

List parts of agriculture that effects pathogens, and what may increase these effects

A
  • population increase
  • sedentism
  • domesticated animal contact

Effect may be exacerbated in those populations by limited diets and nutritional deficiencies

74
Q

Outline the effect of sedentism (agriculture) on pathogens

A
  • increased parasitic diseases spread through contact with human waste
  • Page et al (2015)- Agta foraggers/farmers in Phillipines- People residing in camps with permanent and semipermanent houses had significantly higher eosinophil concentrations than individuals residing in temporary camps- indicative of extreme helminth infestations and found only in sedentarised camps
75
Q

Outline the effect of domestic animal contact (agriculture) on pathogens

A
  • Frequent contact with domesticated animals who themselves are crowded
  • Harper and Armelagos (2013)- estimated that domesticated and peri-domesticated animals are the source of at least 184 different zoonotic diseases
76
Q

Distinguish between heirloom and souvenir pathogens, including examples

A

Sprent (1969):
- heirloom- infected anthropoid ancestors- e.g. lice, leprosy, whooping cough, tapeworms, human pappilomavorus
- souvenir- acquired more recently in human history- e.g. rotavirus A, measles, hepatitis C, dysentery, malaria, HIV1

77
Q

Outline issues with the heirloom and souvenir pathogen distinction

A

Smith et al, 2009:
- -genomic evidence for human pathogen evolution- suggests story not simple- e.g. Tuberculosis- similar to bovine TN- initially assumed to be be product of cattle to human transmission- but genomic evidence now suggests was more likely a human to non-human transmission

78
Q

Outline an example of divergence of a pathogen in humans and apes

A

Read et al (2004):
- Human and chimpanzee body lice diverged around 5-6mya
- Human head lice (Pediculus humanus) are composed of two ancient lineages- one had population bottleneck 100,000 years ago, along with humans- other lineage had no bottleneck
- 2 liniafes diverged over 1mya (before humans appeared)
- ancient divergence- suggests split between homo species and subsequent host switch from archaic to modern humans (requiring direct physical context)- may be that caught lice of neanderthals

79
Q

Outline an example of a link between pathogens and human population histories

A

Crellen et al (2016):
- Schistosoma mansoni- parasitic fluke that infects millions of people
- Similar to Schistosoma rodhaini, which infects rodents
- Zoonotic jump to humans with exploitation of aquatic environments 100-200kya?
- Spread across Africa during the Holocene (last ~10ky)
- Spread to the New World via Atlantic slave trade

80
Q

Outline HIV

A
  • retrovirus- infects a host cell cytoplasm with viral RNA and reverse transcriptase- produces double-stranded DNA which gets integrated into the host’s nuclear DNA- gets transcribed into viral RNA- some gets translated into virus proteins- reconstructed into new viruses
  • largely sexually transmitted, but can be through blood (needle sharing e.g.), and may occur mother –> infancy during pregnancy, childbirth or breastfeeding
81
Q

Outline the consequences of HIV/AIDS

A
  • HIV infects cells in the human immune system that have a particular receptor protein (CD4) on their surface inc. some T helper cells (that signal pathogens) and macrophages (that engulf and destroy pathogens).
  • Leads to progressive failure of the immune system (AIDS, acquired immunodeficiency syndrome) that open the door to opportunistic infections and cancers.
  • Antiretroviral drugs successful in managing infection by keeping viral load low. Also reducing probability of transmission
  • Without medication, HIV advances to AIDS in ~10years.
    *2022- 39 million people living with HIV, of which ~30million accessing antiretroviral drugs
82
Q

Outline what makes HIV difficult to tackle

A
  • High mutation rate, short lifecycle (retroviruses particularly susceptible to copying errors)
  • Infection by multiple strains
  • Attack the immune cells themselves
  • Viral reservoir and latency: never cured. Viral DNA hides in host DNA as ‘provirus’ → chronic low-grade inflammation
  • No natural recovery (unlike e.g. smallpox, chicken pox) – lack of natural immunity to use as model
  • Lack of biomarkers/correlates of effective immunity
  • Lack of animal models predicting vaccine efficacy in humans
83
Q

Outline natural HIV immunity

A

Gupta et al, 2019:
* CCR5-Δ32 mutation
* Affects expression of receptors onto which HIV binds on CD4 cells
* Bone marrow transplant to the “Berlin patient” in 1998 from CCR5- Δ32 mutation carrier led to disappearance of virus
* Similar for the “London patient” in 2016 (treated by Prof Ravindra Gupta)
* Failed in subsequent 6 individuals (mutation?)
* CCR5-Δ32 mutation found in 1% of Europeans, possibly gave resistance to smallpox/plague, gives HIV protection when homozygous- therefore not likely to be evolutionary repose to HIV

84
Q

Outline success of antiretroviral therapy

A
  • > 30 antiretrovirals available to treat HIV
  • Work on disrupting various phases of the viral life-cycle
  • Often given in combinations of 3 or more: highly active antiretroviral therapy (HAART)
  • now in a single combined daily pill
  • Successful: progression from HIV to AIDS rare with HAART
  • Similar treatment can be used as a pre-exposure prophylaxis (PrEP)
85
Q

Outline resistance to antiretroviral therapy

A
  • evolutionary theory predicts intensive antiretroviral treatment (ART) may reduce efficiency and select for higher HIV virulence
  • Possible support for this with HIV virulence increasing in Europe (Pantazis et al. 2014) and decreasing in Africa (Payne et al. 2014)
  • Antiretrovirals (ARVs) becoming increasingly ineffective: in Africa: failure rate up to 31% after 12 months and 38% beyond 48 months of treatment
  • Pre‐exposure prophylaxis (PrEP): Meta-analysis suggests decreases risk of infection in high risk groups by 51% (but data variable and good adherence essential)
86
Q

Outline non-communicable disease including definition, prevalence, examples, risk factors

A
  • disease that is not directly transmissible from one person to another
  • The leading cause of death globally (~7 of 10 deaths)
  • Includes heart disease, cancer, chronic respiratory disease, diabetes, dementia, chronic kidney disease, osteoarthritis etc
  • Risk factors: genetics, obesity, environment, lifestyle, diet, tobacco use
87
Q

Name the 4 main non-communicable diseases

A
  • Cardiovascular disease
  • diabetes
  • chronic respiratory disease
  • cancer
88
Q

Outline cardiovascular disease

A
  • group of diseases involving the heart/blood vessels
  • usually related to poor blood supply due to a diseased vascular supply
  • May lead to heart attack, stroke, heart failure
  • ~30% of deaths worldwide
  • > 80% of CVD risk explained by physical inactivity, tobacco use and unhealthy diet
89
Q

Outline diabetes

A
  • Metabolic disorder: body unable to effectively regulate blood sugar levels because of either insufficient insulin production or insensitivity to it
  • Major risk factor for other NCDs
90
Q

Outline chronic respiratory disease

A
  • Diseases of the lung (e.g. asthma, emphysema, respiratory allergies, occupational lung disease)
  • ~7% of deaths worldwide
91
Q

Online cancer

A
  • Rapid growth and division of abnormal cells in a part of the body
  • > 100 types of cancer, each with different/differently predictive risk factors.
  • ~13% of deaths worldwide
92
Q

Name the 4 major shared risk factors for non-communicable disease

A

Yi et al, 2020:
- Poor diet
- Physical inactivity
- Tobacco
- Alcohol

93
Q

Outline scurvy as an example of mismatch

A
  • disease caused by serious dietary vitamin C deficiency (humans cannot synthesise vitamin C- need to consume it in our diet)
  • Symptoms: gum disease, easy bleeding, low red blood cell count
  • Common among sailors in early modern era: estimated to have killed 2 million
  • Rare on land
  • Recognition in 18th century Royal Navy that scurvy was caused by the inavailability of fresh fruit and vegetable: a mismatch between what we need in our diets and what was available on long voyages
  • Recommendation of limes as part of ship rations
94
Q

Outline the idea of mismatch (non-communicable disease)

A

Williams and Nesse (1991):
- idea that much of disease today is teh consequence of a mismatch between the environment in which we evolved, and the environment in which we now live
- suggested human biology designed for Stone Age conditions- physical environment of evolutionary
adaptiveness is probably that of Pleistocene savannah
- human developmental system was selected to make optimum use of the range of dietary abundance under Stone Age conditions

95
Q

Outline maladaptation in relation to health and disease in the human past

A

Up to <10,000 years ago:
- Hunter-gatherers
- Low population density
- Active
- Mobile
- Diet high in fibre, vegetables and tubers, lean meat, eggs (no dairy, processed grains etc.)

96
Q

Outline the transition to food production

A
  • Limited dietary variation, domesticates
  • Risk of resource failure
  • Increased fertility
  • Increased population density (greater infectious disease reservoir)
  • Living in close proximity with animals
  • Sedentary
  • Need for sanitation
  • Still relatively active
  • Increased opportunity for parasites, zoonoses, acute infections that need a reservoir
97
Q

Outline effects of urbanisation/industrialisation on health and disease

A
  • Recurrent pandemics
  • Poor nutrition
  • Crowding
  • Poverty
  • Poor sanitation
  • Pollution
98
Q

Outline post-industrial health/disease

A
  • Dietary excess
  • Inactivity
  • Longevity
  • Public health intervention
  • Treatment and prevention
  • Emerging infections
99
Q

epidemiological transitions over time graph

A
100
Q

Outline examples of hypothesised mismatches causing specific nn-communicable diseases today

A
  • Obesity as (partly) a product of dietary preferences that were adaptive in our evolutionary history but now, not (e.g. sugar preference)
  • Cardiovascular disease as (partly) a product of sedentary modern lifestyles
  • Autoimmune disease (e.g. multiple sclerosis) as a consequence of inappropriate reactions to the loss of ancestral microbiota and intestinal parasites
  • Breast cancer as a consequence of evolutionary novel fertility regimes and oral contraception
101
Q

Outline drugs/toxins in relation to evolutionary mismatch

A
  • Drug addition as a product of evolutionarily novel substances ‘hijacking’ otherwise adaptive reward mechanisms in the brain?
  • Williams & Nesse (1991)- not evolved to resist substances [such as opiates] that directly stimulate reward mechanisms in the brain
  • Alcohol not evolutionarily novel- most mammals will consume, especially frugivores eating overripe fruit → alcohol dehydrogenases as an adaptation to process dietary alcohol
  • Technology of distillation (first evidence ~1200 BC) produces alcohol at evolutionarily novel strengths: possible mismatch?
  • note- exposure to a toxin in evolutionary history does not necessarily mean adaptations exist to counter this
102
Q

Outline an example of a hunter-gatherer population of interest regarding non-communicable disease, at what was measured

A
  • The Agta
  • hunter-gatherers from the northern Philippines
  • activities include hunting, gathering, fishing, honey collecting

Measured:
- Lymphocytes: proxy for viral infection
- Neutrophils: proxy for bacterial infection
- Eosinophils: proxy for helminth infection

103
Q

Outline health consequences of transitions in Agta populations

A

Page et al, 2016:
* people in large camps with low out-of-camp mobility had a 2.8x higher chance of presenting with lymphocytosis than people residing in mobile camps
* People residing in camps with permanent and semipermanent houses had significantly higher eosinophil concentrations than individuals residing in temporary camps
* Severe eosinophilia is indicative of extreme helminth infestations and is found only in sedentarized camps
* In contrast, people residing in sedentarized camps with some form of infrastructure (i.e., church or water pump) had lower odds (by 80%) of neutrophilia

Sample form thsioe presented with eosinophilia:
- All 30 samples tested positive for helminth ova
- mean number of species detected- 1.6- included: roundworm (Ascaris lumbricoides, 83.3%), hookworm (Ancylostoma duodenale or Necator americanus; 46.7%), whipworm (Trichuris trichiura; 30%)

104
Q

Outline an example of a health project

A
  • Tsimane health and life and history project
105
Q

Outline the Tsimane health and life and history project

A

Gurven et al, 2017:
- Started in 2002
- Tsimane horticulturalists/foragers, Bolivia, N>5,000

Project aims to understand:
- the bidirectional connections between life history and social behaviour in a high‐fertility, kin‐based context lacking amenities of modern urban life (e.g. sanitation, banks, electricity)
- how a high pathogen burden influences health and well‐being during development and adulthood
- how modernization shapes human life histories and sociality

106
Q

Outline coronary atherosclerosis in the Tsimane population

A

Kaplan et al, 2017:
- refers to build-up of fatty substances in the blood vessels supplying the heart, reducing blood flow
- Causes coronary heart disease
- Classic set of risk factors for a “Western Disease”: poor diet, inactivity, smoking- account for >90% of risk in USA
- Measured by scoring coronary artery calcium (CAC)
- Tsimane- lowest reported levels of coronary artery disease of any population recorded to date
- suggests can be avoided in most people by having lifetime with very low LDL, low blood pressure, low glucose, normal body-mass index, no smoking, and plenty of physical activity

107
Q

name non-communcibale diseases/health complications with unusual prevalence in Tsimane populations

A
  • coronary atherosclerosis
  • increasing blood pressure with age
108
Q

Outline increasing blood pressure with age in the Tsimane populations

A

Gruven et al, 2012:
- Hypertension (high blood pressure) is major risk factor for most NCDs, especially cardiovascular and renal disease, stroke, and type 2 diabetes mellitus
- Typical pattern in is of age-related increase in blood pressure
- measured blood pressure longitudinally on 2248 adults age ≥20 years (n=6468 observations over 8 years)
- In England 31% men, 26% women (>140/90mmHg)
- Among Tsimane, systolic, diastolic, and pulse blood pressure all increase with age but the age-related increase is substantially lower than rates found elsewhere

109
Q

Compare Hadza diets to UK recommendations

A

Pontzer et al, 2021:
» Fibre- H 90, UK 30g/d
» Protein- H150, UK50g/d
< Fat-H50, UK80g/d
== Carbohydrate- H340, UK 300g/d

110
Q

Outline contributions to diet in hunter-gatherer populations

A

Cordian et al, 2002 :
- mean subsistence dependence upon gathered plant foods = 32% mean subsistence dependence upon animal foods = 68%
- 13 studies average - 65% from animals

111
Q

Outline dietary adaptations at high altitudes

A
  • Pontzer et al (2018)- More meat at high latitudes
  • Inuit (Alaska natives)- quintisential carnivores

Generic adaptation to extreme diet:
- Fumagalli et al. (2015): Greenland Inuit rich diet is rich in omega-3 polyunsaturated fatty acids (PUFAs) ‘fish oil’
- signal of positive selection on a cluster of fatty acid desaturases that determine PUFA levels (FADS1-3)

B1 (8 decks)

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