169 Topic 1, Intro-Overview '15

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IB 169 Introduction/Overview Evolutionary Medicine

Lecture Topic #1 (Text pp. xiii-xvi; pp. 257-268, 272-275,

17/Box 1.7, Science Ellison pdf; PNAS Nesse pdf; PRSB Stearns pdf)

Instructor: Tom Carlson Department of Integrative Biology University of California, Berkeley

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IB 169 Syllabus Instructor: Tom Carlson [email protected] Office Hours: Tuesday 3:40-4:00 PM, Wednesday

11:10-12:00, Thursday 12:40-1:30 in VLSB 1098 Lectures: 11:00-12:30 Tuesdays and Thursdays in

in 145 Dwinelle Discussion section one hour a week GSIs: Dena Block [email protected] (Friday

sections) Charlotte Jennings [email protected]

(Wednesday sections) Katya Mack [email protected] (Monday

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IB 169 Required textbook

Gluckman, Peter; Alan Beedle; and Mark Hanson. 2009. Principles of Evolutionary Medicine, Oxford University Press."

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Lecture material Lectures are based on information in

required text as well as other sources. Additional PDFs of key articles from sources

other than the required text will be made available on IB 169 bspace site.

PDFs of lecture powerpoint slides will be downloaded onto IB 169 course website at bspace.berkeley.edu before each lecture.

Midterms & Final Exam material will be based only on material presented in the lectures.

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Midterm & Final Exams

Midterm #1 on 2/19/15 at 11:00 AM (30% of grade)

Midterm #2 on 4/2/15 at 11:00 AM (30% of grade)

Final Exam: 5/14/15 at 8:00 AM (30% of grade)

Discussion section: 10% of grade

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IB 169 Lecture Topics

Overview of evolutionary medicine & evolutionary pathways to disease

Primate evolution & diversity Ape evolution & diversity Hominin evolution & diversity Human migration & evolution

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Evolutionary Theory Genetics: Molecular Basis of

Variation & Inheritance Evolution, Development &

Phenotypes Epigenetics

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Life histories Puberty & Menarche Menopause Reproduction

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Culture, Psychology, Stress and HPA & HPG axes

Diet and Metabolism Host-Pathogen Interactions Cancer

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Human Clinical Case Presentations

Human Clinical Case Presentations on a spectrum of different disease pathophysiological states will be presented throughout the course

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Evo-Devo Interaction of evolution with embryonic

and other developmental processes Role of genes regulating embryonic

development. Epigenetic influences on development. The role of developmental plasticity in

evolution.

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Life history

The traits that affect an organisms life cycle, especially the schedule of reproduction and survival.

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Stress and endocrine and autonomic systems

Evolution of human endocrine system and autonomic nervous system and responses to stress.

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Nutrition and metabolism

Evolution of human diet. Emergence of obesity, insulin

resistance, and metabolic syndrome, and the integrative understanding of genetic, developmental, environmental, and behavioral risk factors for these diseases.

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Infectious diseases Host-pathogen interaction Pathogen resistance Pathogen virulence Human host immune response Vaccinations Antimicrobial medications Emerging infectious diseases

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Human defense

Hygiene theory. Autoimmune diseases.

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Cancer

Different evolutionary perspectives on development of different types of cancers.

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Medical terminology

Hx = history PE = physical exam Dx = diagnosis Tx = treatment Rx = prescription

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Medical abbreviations CV = cardiovascular GI = gastrointestinal GU = genitourinary DM = diabetes mellitus ID = infectious disease OB = obstetrics GYN = gynecology OB/GYN = obstetrics & gynecology

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History of evolution of evolutionary thought

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Evolution of evolutionary thought Linnaeus 1758: hierarchical classification of organisms;

(Systema Naturae book by Linnaeus) Jean-Baptiste Lamarck early 1800s: proposed the

concept of evolution Darwin & Wallace 1858-1859: natural selection and

evolution (Origin of Species 1859 by Darwin) Mendel 1866: inheritance in peas ("Experiments in plant

hybridization". Journal Royal Horticultural Society 26: 132, 1866)

Ronald A. Fisher, Julian Huxley and others 1936-1947: modern synthesis (Evolution: The Modern Synthesis, 1942 by Julian Huxley)

Watson & Crick 1953: double helix of DNA (Nature 171, 738-740, 1953)

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Linnaeus classification system of organisms in 1758

Carl Linnaeus in 1758, published his Systema Naturae book describing thousands of plants, fungi, and animals in a hierarchical classification system of taxonomy with species, genera, families, orders, classes, phyla, & kingdoms.

Binomial system of species names e.g., Homo sapiens

His underlying definition of a species was the ability of individuals within the species to interbreed and produce viable offspring.

However, Linnaeus thought that species were fixed and immutable.

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Jean-Baptiste Lamarck contributions to

evolutionary thought In early 1800s, Jean-Baptiste Lamarck

from France proposed that evolution occurred and proceeded in accordance to natural laws.

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Darwin & Natural Selection Charles Darwin first described his ideas

of evolution and natural history in 1842, but they were not widely circulated.

Charles Darwin and Alfred Russell Wallace independently described natural selection in 1858.

Darwin published On the Origin of Species in 1859 which describes how natural selection provides a mechanistic explanation of how species change over time and how new species evolve.

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Natural selection

Darwin articulated that species were not immutable and that through natural selection, selective retention of beneficial variation can be a mechanism for a species to change and evolve.

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Gregory Mendel & Inheritance In 1866, Gregory Mendel published his

article on the nature of inheritance in his experiments with plants.

Unfortunately, the importance of Mendels research was not appreciated until the early 1900s when it triggered the development of the field of genetics.

The understanding of inheritance and genetics aided the development of evolutionary science.

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Modern Synthesis Between 1936-1947, Ronald A. Fisher and other

scholars contributed to the integration of the fields of genetics, evolutionary biology, systematics, morphology, ecology, and quantitative statistics to create the Modern Synthesis.

Other contributors to this synthesis include Theodosius Dobzhansky, J.D.S. Haldane, Julian Huxley, and G. Ledyard Stebbins.

In 1942, Julian Huxley invented the term when he published his book, Evolution: The Modern Synthesis.

While this synthesis is well understood today in the biological sciences, its application to human biology and medicine is still emerging.

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Elucidation of DNA Structure In 1953, the elucidation of the

structure of DNA by Watson & Crick enabled evolutionary processes to be understood at a biochemical level.

This discovery aided the further development of molecular biology and evolutionary science.

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Human Genome mapped Completed in 2003 Human Genome Project publicly funded by

the US government (International Human Genome Sequencing Consortium, Nature 2001, 409 (6822): 860921)

Celera Genomics, private company headed by Craig Ventor, a US researcher (Science 291 (5507): 13041351.)

20,500 genes in Homo sapiens 29

Evolution in medical education

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Medical Education in 1870 in University College, London

Thomas Huxley was the most powerful voice in Britain in 1870 in medical education policy.

He did not include topics such as evolution and comparative anatomy in medical curricula.

He stated that there was simply too much information already required in medical school in the topics of human anatomy, physiology, pathology, and pharmacology.

Today, integration of evolutionary biology into medical education is still lacking.

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2009 was the 150th anniversary of the publication of On the Origin of Species

A joint committee of the Association of Medical Colleges and the Howard Hughes Medical Institute recommended that a core competency on scientific knowledge by future physicians includes an understanding of evolution by natural selection.

In April 2009, a meeting, Evolution in Health and Medicine sponsored by the National Academy of Sciences and the Institute of Medicine where a panel of deans and faculty from leading medical schools around the world endorsed incorporation of evolutionary principles in medical curricula.

Unfortunately, instruction on evolution in medical school education continues to be rare. 32

Education in medicine today Medical science has become dominated by

relatively reductionist approaches looking at levels of organization (gene, cell, tissue) individual organ systems, or different disciplines (physiology, biochemistry, or anatomy), without adequate attention on how these levels, systems, and disciplines interrelate with our ecological environment and evolutionary history.

Integration of evolutionary and ecological perspectives illuminates our understanding of the causes and mechanisms of health and disease both in individuals and populations.

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An evolutionary perspective broadens the way physicians and medical researchers think about

health and disease Enhances quality of diagnosis and

treatment of patients. Enhances our understanding of human

populations and contributes to design of appropriate public health interventions.

Helps identify important research questions to explore.

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Reasons evolution has not been included in medical education

Crowded medical curriculum. Bias against the relevance of evolution in

understanding health and disease. Lack of appropriately skilled faculty members

in medical schools available to teach evolutionary principles.

Up until recently, there has been a lack of appropriate, user friendly materials to teach the topic of evolutionary medicine.

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Books on evolutionary medicine Fortunately, in recent years, useful books and articles

on this topic have become more available. In 1994, Randolph Nesse and George Williams

published the groundbreaking book entitled Why We Get Sick: The New Science of Darwinian Medicine.

Since the publishing of this book, numerous other books and edited editions on the topic of evolutionary medicine have been published.

The 2009 publication or Principles of Evolutionary Medicine by Gluckman, Beedle, and Hanson is the first specifically designed textbook on evolutionary medicine.

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Evolutionary Medicine books in chronological order Nesse, Randolph; Williams, George Williams. (1994). Why We Get

Sick: The New Science of Darwinian Medicine. Stearns, Stephen C. (1999). Evolution in Health and Disease. New

York: Oxford University Press. Trevanthan, W.R., Smith, E. O., & McKenna, J. J. (1999). Evolutionary

Medicine. Oxford: Oxford University Press. Nabhan Gary Paul. (2004). Why Some Like it Hot: Food, Genes, and

Cultural Diversity, Island Press. Barnes, E. (2005). Diseases and Human Evolution. University of New

Mexico Press. pp 1-484. Trevanthan, W.R., Smith, E. O., & McKenna, J. J. (2008). Evolutionary

Medicine and Health: New Perspectives, Oxford University Press, Oxford, pp 1-532.

Stearns, S. C., and Koella, J. K. (2008). Evolution in Health and Disease, 2nd Edn. Oxford University Press, Oxford. pp. 1-374.

Gluckman, Peter; Alan Beedle; and Mark Hanson. (2009). Principles of Evolutionary Medicine, Oxford University Press. 37

Microevolution & Macroevolution (Futuyma 2009, Evolution)

Microevolution: usually refers to slight relatively short term changes within a species.

Macroevolution: usually meaning the evolution of substantial phenotype changes, typically great enough to place the changed lineage into a distinct new species or higher taxon.

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Trait Any detectable variation in a genetic character. A trait is a distinct variant of a phenotypic character of

an organism that may be inherited, environmentally determined, or be a combination of the two.

Traits typically result from the combined action of several genes, though some traits are expressed by a single gene (monogenic).

No trait is perfect. Every trait must be analyzed in terms of the benefits

and costs of the trade-offs inherent in a particular trait. Natural selection favors traits that improve the fitness

(reproductive success) of individuals and their kin. 39

Fitness Fitness = reproductive success. Selection operates to enhance fitness. Enhancement of fitness, does not necessarily

operate to enhance health or longevity Fitness involves trade-offs which enhance

reproductive success even if they incur other costs such as a shorter life.

Evolutionary biology considers how an organism trades-off one component of its biology against others to enhance fitness.

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Proximate versus ultimate causes of disease

Most medical training focuses on understanding the immediate mechanistic pathophysiologic pathways leading to the disease, the so-called proximate causes.

In this course we will explore the ultimate causes, the so called evolutionary factors which result in the emergence of pathways to health or disease.

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Ultimate causes of human disease and health

How has evolution led to a particular trait or set of traits persisting?

Is the trait helpful or not helpful under the present circumstances?

Have the limits of acclimatization been exceeded due to a mismatch of evolutionary history, ancestral environment, and present environment?

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Proximate causes The anatomical, physiological,

molecular, and pathophysiological mechanisms that lead to a biological phenomenon.

Insulin resistance leads to type 2 diabetes mellitus.

Mutation in hemoglobin gene leads to sickle cell anemia.

Exposure to tuberculosis may lead to pulmonary TB.

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Ultimate causes The ultimate cause is the evolutionary explanation

for why a person gets sick under certain circumstances.

To understand the ultimate cause, the following questions must be asked:

Why are some people prone to developing insulin resistance and type 2 diabetes mellitus?

Why do certain populations carry a mutation in hemoglobin gene which leads to sickle cell anemia?

Why do some people develop pulmonary tuberculosis as a result of being exposed to tuberculosis while other people do not?

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Normal versus abnormal Definitions of normality, abnormality,

and disease are not absolute and are influenced by the environmental context of the individual and the individual variation in phenotype.

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Normal vs abnormal Modern medical thinking has a tendency to

dichotomize into normal or healthy and abnormal or unhealthy/pathological.

However, such assessments are contextual: an adaptation (e.g., sickle cell) may prevent a certain disease (i.e., malaria) in a heterozygous carrier and thus make a person healthy, while this same adaptation puts a homozygous individual at risk for another disease (sickle cell crisis) and thus makes the individual unhealthy.

We will explore these trade-offs in this course.

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Determinants of an individuals biological health status

Environment: physical, biological, and social world they lives in.

Development: which stage of development they are in.

Behavior: how they live in world. Physiology/anatomy: how they function in

world. Transgenerational ancestral influences

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Relevant histories in systematic evolutionary framework

#1: Medical history of the complaint/illness. #2: Developmental history of the individual since

conception. #3: Evolutionary history of the individuals lineage. Hx of probands (persons) population (including

genetics, drift, isolation, & migration) Hx of hominid clade (including consideration of how

our environment has changed) Assessment of all these histories is essential for a

comprehensive understanding of how an individual responds to their environment.

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Evolutionary Pathways to Disease and/or Health

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Evolutionary Pathways to Disease and/or Health An evolutionary matched environment. An evolutionary mismatched or novel environment. Outcomes of demographic history. Outcomes of cultural history. Outcome of evolutionary constraints. Sexual selection and sexual competition and their

consequences. Life-history and/or developmental associated factors. Antagonistic pleiotropy. A harmful allele when homozygous is maintained by heterozygote

advantage. Effects of deleterious allele does not become apparent until after

reproductive age. Spontaneous mutations for a deleterious gene defect replace

alleles eliminated by selection. Exaptation. Excessive and uncontrolled defense mechanisms. Fighting the evolutionary arms race with microbes.

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An evolutionary mismatched or novel

environment

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An evolutionary mismatched or novel environment

The biological processes that determine our present structure and function may have evolved in very different environments compared to those we now live in.

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Evolutionary change of our biological structure and function is slow while our physical, nutritional, and social environments may be changing relatively quickly.

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Many humans now live in environments that are very different from those in which our ancestors lived and evolved.

These environmental mismatches can challenge our health.

Constraints on evolutionary processes (the speed, substrate, or direction of selection, or in scope of plasticity) in the presence of environmental novelty can lead to ill health.

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Many populations of people are living in the same geographical area where their ancestors emerged, however, the ecological, nutritional, and/or physical activity environment has changed compared to the environment of their ancestors.

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The ancestral Homo sapiens diet and level of exercise was very different than the contemporary sedentery lifestyle with diet of highly processed foods.

The mismatch between the ancestral and contemporary diet and exercise regimes has resulted in dramatic increase in rates of obesity, insulin resistance, type 2 diabetes mellitus, and cardiovascular disease.

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Demographic history of migration can result in an evolutionary mismatched environment.

Some populations of people have a demographic history of migration which has resulted in a contemporary population living in a novel (and potentially mismatched) environment compared to their ancestors.

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Outcomes of demographic history

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Outcomes of demographic history A persons evolutionary history includes the

adaptations of his or her ancestral lineage to their ecosystems/environments.

A person may now live in a different ecosystem/environment where the ancestral lineage adaptations may be maladaptive.

For example if a person with a evolutionary history of ancestors from a far northern latitude (e.g., Norway) migrates close to the equator, their level of skin melanin will be maladaptive to the high levels of UV radiation at these latitudes.

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Outcomes of demographic history

Homo sapiens migrated out of Africa about 60,000 years ago.

Depending on where they migrated to, humans may have passed through population bottlenecks which generated founder effects.

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Outcomes of cultural history

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Outcomes of cultural history Social behaviors characteristic of a

persons cultural group which can influence health and disease.

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Outcomes of cultural history

A persons family, peers, and/or broader culture may have very specific practices of what kind of food they eat which can influence health and disease; a persons choice of how they eat is influenced by their culture.

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Outcomes of cultural history A womans family, peers, and/or

broader culture may have strong opinions on how a female should approach labor and delivery e.g., whether she plans to get an epidural for labor or a scheduled C-section for delivery; this can influence a womans choice on how she approaches birth options.

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Outcomes of cultural history A womans family, peers, and/or broader

culture may have strong opinions on whether a female should choose to feed her infant breast milk or formula; this can influence a womans choice on how she approaches infant feeding which influences the health of the infant.

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Results of evolutionary constraints

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Result of evolutionary constraints

Bipedal walking results in constraints on size of pelvic inlet/outlet in females which can make some newborn deliveries difficult.

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Results of evolutionary constraints

The change in shape and position of larynx necessary for human speech has resulted in increased likelihood of sleep apnea.

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Life-history and/or developmental

associated factors

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Life-history and/or developmental associated factors

The human life-course strategy is one of deployment of resources in the period up to peak reproductive performance, but trading-off that investment against the associated loss of reparative function in the post-reproductive period when a direct fitness advantage is not possible.

Thus the primary investment in maintenance and repair is prior to peak reproductive age and declines in post-reproductive years.

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Tradeoffs emerge when stress in early life cues an individual to go into puberty early to increase the likelihood of reproduction, however, earlier puberty has its inherent risks/costs.

The adaptive strategy of advancing puberty can result in a mismatch between biological and psychosocial maturation.

Individuals who go into puberty earlier have a higher likelihood of risk-taking behavior, depression, and even suicide. 71


Early-life events with late life consequences e.g., infants with early nutritional stress are at greater risk for developing obesity, Type 2 diabetes, hypertension, and coronary artery disease as adults, especially if they grow up in a sedentary environment with abundant access to calories.

These early life events can trigger epigenetic changes

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dreammareSticky NoteThe body performs maintenance and repair before the time when reproduction peaks. However, after that, the body's maintenance and repair function wane.

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dreammareTypewriterConsequencesof early healthproblems canmanifest inadulthood

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Antagonistic pleiotropy

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Traits that have been selected to have benefits in early life but then have detrimental effects later in life.

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Antagonistic pleiotropy Antagonistic pleiotropy is related to life

history and describes traits which have been selected for because they are advantageous in early life in promoting reproductive fitness, but these same traits may have costs later in life.

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Antagonistic pleiotropy An example is the presence of stem

cells in tissues which are adaptive during growth and reproduction to promote tissue maintenance and repair, but the persistence of certain stem cells can increase the risk of neoplasia (cancer) later in life.

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Antagonistic pleiotropy, IGF-1 Nutritional factors acting at multiple levels

regulate the secretion of insulin-like growth factor-1 (IGF-1) and IGF-1 promotes fetal growth and muscle and skeletal growth during childhood and adolescence and fitness in early reproductive life.

However, in later life, high IGF-1 levels are associated with and increased risk of certain cancers.

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Antagonistic pleiotropy testosterone

An example of this is the hormone testosterone, which is essential for enhancing fitness in males in early life and in young and middle adult years, however, in later life, testosterone can increase risk of prostate cancer and heart disease.

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dreammareSticky NoteEarly advantages: Allow fetal growth, muscular growth, skeletal growth, and fitness for childhood and adolescence

Late disadvantage: increased risk of certain cancer.

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dreammareSticky Noteeither by acting directly on older animals, or y causing latent damage in younger animals that will manifest in older animals

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Antagonistic pleiotropy Given the higher rates in extrinsic

mortality and shorter lifespans in humans until recent centuries, the negative effects in later life of such antagonistic pleiotropic selection would have been largely hidden, further favoring selection for the beneficial early-life effects.

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Antagonistic pleiotropy (Fig. 5.8) Mutations that may improve early-life

reproductive fitness may have deleterious effects in older age, either by acting directly on older animals or by causing latent damage in younger animals which is unmasked in older animals.

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Sexual selection

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Sexual selection (Futuyma 2009, Evolution)

Differential reproduction as a result of variation in the ability to obtain mates.

Variation in the number of offspring produced as a consequence of a competition for mates.

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Mate choice and ratio of testes/body size

Humans also have a relatively small testes weight/body size compared to some other primates e.g., chimpanzees.

Relatively small testes as in humans is associated with relatively monogamous mating systems.

Large testes like in chimpanzees are associated with promiscuous mating systems where both females and males have multiple partners (Fig 7.2); because there are multiple male partners, releasing more sperm per ejaculation enhances sperm competition for egg. 84

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Testes are larger in males in species where there is a multi-male mating system and

sperm competition would be predicted to be a factor in fitness (Fig. 7.2)

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Mate choice & sexual diphorphism Sexual dimorphism in body size is associated with

polygynous mating systems, e.g., with gorillas. Human males are on average taller and heavier than

females. Human males have a higher % of body mass as muscle

compared to females. However, humans have a relatively small degree of

sexual dimorphism in body size and hence monogamous pair bonding rather than extreme polygyny has been and continues to be most typical for humans.

Some evolutionary biologists suggest that a mild partial-harem mating system may have been the norm in human evolution.

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Parental investment

The cost of reproduction is much higher for the female than the male.

The female needs to gestate the fetus and breast feed the infant.

Both parents can potentially provide considerable effort to provide resources, protections, and education to their offspring.

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Evolutionary pathways that enable alleles that cause

monogenic disease to not be eliminated from the

population

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Evolutionary pathways that enable alleles that cause monogenic disease to

not be eliminated from the population Heterozygote advantage (e.g., sickle cell

disease, cystic fibrosis, Tay-Sachs). Effects of the deleterious allele may not

become apparent until after peak reproductive age (e.g., Huntingtons chorea).

Recurrent mutation may retain a deleterious allele in the population (e.g., some forms of hemophilia).

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A harmful allele when homozygous

is maintained by heterozygote advantage

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Reason why alleles that cause monogenic disease persist in population:

heterozygote advantage

The deleterious effects of the disease-promoting allele are confined to or expressed most strongly in homozygotes, but heterozygotes for the allele have some selective advantage over homozygotes and this causes the frequency of the allele to be maintained in the population.

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heterozygote advantage provides protection in the following ways

Sickle cell allele protects against malaria Cystic fibrosis allele protects against diarrhea and

tuberculosis Tay-Sachs allele protects against tuberculosis Phenyketonuria allele: pregnant mothers who are

carriers of this allele have lower spontaneous abortion rates and their fetuses are less likely to get cross-placental infection by the potentially fatal mycotoxin, ocratoxin A (see Woolf, Am J Hum Genetics, 1986, 38(5):773-5)

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Effects of deleterious allele does not become

apparent until after reproductive age

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effects manifest after peak reproductive age

The effects of the deleterious allele may not become apparent until after reproductive age, so the parent may pass on the allele to a child before negative selection has had a chance to operate.

An example of this is Huntingtons chorea/disease which has symptoms that typically do not emerge until middle age adult years.

Familial transmission accounts for more than 95% of new cases of Huntington chorea/disease.

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Spontaneous mutations for a deleterious gene defect replace alleles

eliminated by selection

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Spontaneous mutations for a deleterious gene defect replace alleles eliminated by selection.

A deleterious allele is maintained in the population by recurrent mutation.

Even if copies of the deleterious allele are lost from the population because individuals carrying them die before reproducing, the allele is created anew at some finite rate by spontaneous mutation within the population.

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recurrent spontaneous mutations Examples of this includes some forms of

hemophilia as well as some aneuploid conditions e.g., Trisomy 13, and Trisomy 18.

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Reason why alleles that cause monogenic disease persist in population: recurrent spontaneous mutations

Hemophilia: recessive sex-linked X chromosome disorder

Hemophilia A (clotting factor VIII deficiency) and Hemophilia B (clotting factor IX deficiency) are the two most common forms of hemophilia and both are maintained by new spontaneous mutations that replace the alleles eliminated by negative selection.

Both are recessive sex-linked X chromosome disorders. Since males have only one X chromosome, all males with

the allele have hemophilia. Females need to be homozygous with allele on both X

chromosomes to have hemophilia; for this reason, it is rare in females.

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Recessive sex-linked X chromosome inheritance Dominant allele X (normal clotting)

Recessive allele x (abnormal clotting) Y is male sex chromosome

Mom is carrier and Dad is unaffected

Sex chromosomes X x

X XX Unaffected

Xx Carrier

Y YX Unaffected

Yx Affected with hemophilia

Reason why alleles that cause monogenic disease persist in population: recurrent spontaneous mutations

Hemophilia: recessive sex-linked X chromosome disorder

Mother and father has two daughters and two sons Mother is carrier of hemophilia allele Father is unaffected One son is unaffected One daughter is unaffected One daughter is carrier of hemophilia allele One son is affected with hemophilia

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Recessive sex-linked X chromosome inheritance

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Excessive & uncontrolled defense mechanisms

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Excessive and uncontrolled defense mechanisms

Diseases of autoimmunity e.g., eczema, rheumatoid arthritis, and inflammatory bowel disease can be considered as situations where the normal evolved processes of defense are inappropriately and excessively activated causing persons own antibodies to attack their own tissues.

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Fighting the evolutionary arms race

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Fighting the evolutionary arms race

Humans are in a co-evolutionary relationship with viruses, bacteria, fungi, and parasitic diseases.

The short generation times of microorganisms compared to the long generation times of humans enables the microbes to evolve much more rapidly to attempt to out-compete human defense systems.

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Fighting the evolutionary arms-race: Hypotheses on life history strategies of

viruses, bacteria and other microbial pathogens

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Evaluation of biological phenomena through

Niko Tinbergens 4 questions

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Niko Tinbergens 4 questions applicable to biological phenomena

#1: What is the mechanism underlying the phenomenon of interest?

#2: How does the phenomenon develop during the lifetime of the individual? That is, what is its ontogeny? (Ontogeny = the origin and development of an individual organism from embryo to adult)

#3: What is the function of the phenomenon? How does it serve the organisms interests?

#4: How did the phenomenon evolve? What is its evolutionary history? Are there analogous phenomena in other species, and what is their evolutionary relationship to humans? What is the evidence for a selected origin?

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#1: What is the mechanism underlying the phenomenon of interest?

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#2: How does the phenomenon develop during the lifetime of the individual? That is, what is its ontogeny? (ontogeny = the origin and development of an individual organism from embryo to adult)

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#3: What is the function of the phenomenon? How does it serve the organisms interests?

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#4: How did the phenomenon evolve? What is its evolutionary history? Are there analogous phenomena in

other species, and what is their evolutionary relationship to humans?

What is the evidence for a selected origin?

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Answers to Tinbergens 4 questions on how and why we sweat when frightened

Question #1: what is the mechanism underlying the phenomenon of interest?

Question #1 answer: the proximate mechanism is activation of the sympathetic nervous system fight/flight response which stimulates sweat glands to sweat.

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Question #2: How does the phenomenon develop during the lifetime of the individual? That is, what is its ontogeny? (Ontogeny = the origin & development of an individual organism from embryo to adult)

Question #2 answer: Sweat gland innervation is not completely mature until an infant is a few months of age. Also, the infant must be old enough to have the ability to perceive a threat that frightens and triggers the activation of the sympathetic nervous system fight or flight response.

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dreammareTypewriterCase: sweat when frightened

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Developmental plasticity of sweat glands continued answer to question #2: Sweat glands are innervated in the

early weeks after birth and the density of innervation and thus the capacity to sweat and tolerate extreme heat is influenced by whether or not an infant is brought up in a cold or hot environment.

This influences how an adult is able to sweat and tolerate heat.

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Question #3: What is the function of the phenomenon? How does it serve the organisms interests?

Question #3 answer: Sympathetic fight/flight activation generates increased heat in the body and the sweating helps dissipate this excess heat and maintain normal body temperature.

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Question #4: How did the phenomenon evolve? What is its evolutionary history? Are there analogous phenomena in other species, and what is their evolutionary relationship to humans? What is the evidence for a selected origin?

Question #4: answer: The evolution of the fear, fight, or flight response is beneficial to

any species who faces the risk of predation. Since a successful fight/flight response will require the capacity

to lose the excess heat to maintain normal body temperature, homeothermic species may thermoregulate and lose heat by sweating and/or panting.

Humans have evolved to sweat to thermoregulate. Thus sweating may have evolved as a thermoregulatory system

but has been integrated into the fear response because of the need to dissipate heat during the fight or flight response.

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Date post:	21-Nov-2015
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169 Topic 1, Intro-Overview '15

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