A first run at a textbook-free 'Introduction to Biological Anthropology'

This post has been updated since it was first published.

None of the textbooks share my curricular vision or path. And I believe that the path I take with students is instrumental to their learning evolution and to overcoming the gripping misconceptions. So I'm all done with textbooks for "Introduction to Biological Anthropology" and I've posted my thoughts on this before:

• A new curriculum for Introduction to Biological Anthropology
• Open access, peer-reviewed Human Evolution resources
• A textbook-free [Introduction to Biological Anthropology] curriculum

As promised in the last link, here's a serious draft of what I'll be implementing in Spring 2015 when I'm back to the classroom after having a baby.

It's for APG 201: Human Origins, a fundamental major requirement and a course that fulfills 3 general education credits in the natural sciences for anyone wishing to graduate from URI. I teach to a small auditorium of 120 students both Fall and Spring semesters every year, 50 minutes each meeting, three times a week per semester. Sometimes I have TAs, sometimes I don't. (We don't have a graduate program.)

Notice how I have the students make observations first (mostly on primates) before we explain them with evolution. And at first, evolution is only about common ancestry and change over time (i.e. even though we bring in Darwin at this point, we do not talk about  natural selection or adaptation). Then evolution's about inherited continuity with recombination and mutation, then it's about trait complexity, and then, and only then, it's about processes like drift and selection.

I've decided that even though it's a lot of fun, and even though I do introduce sexual selection, there's just no room in this introductory course for primate sex and reproductive strategies, the evolution of ours, and reconstructing these things in our ancestry.  I'll be relegating all that content to my "Sex and Reproduction in Our Species" (aka The Baby Makers) course, instead.

I've been increasing homework assignments, in frequency and intensity, over the past few years but this will be, by far, the most I've had them do for this course. I like to have them struggle through things on their own before we tackle them in class, which is why so may assignments are due on the day we're slated to cover the same topic. This means, I don't grade for complete accuracy. What's more, students clearly aren't reading and writing enough (in general, in life) to meet my standards for thinking and thought expression in my courses, so this journal approach is how I'm addressing that problem. Because it would be nearly impossible to deal with in such a large course, I won't collect their daily assignments. Instead, I'll have them add assignments to their journals which I will spontaneously check only a few times. I've issued many of these assignments in the past, so I'm already aware of what the students will write and have built the course in such a way that anticipates and addresses the obstacles they face as it goes along. "Lecture resources" are not assigned readings but are highly recommended study resources, especially for students who were not satisfied with our discussion of the content for a particular day (either because they didn't understand or they want to learn more) or for students who missed class that day.

Here's the course (minus the worksheets and my in-class materials, including handouts with content that's not covered fully by the readings/resources). Sakai, for anyone unfamiliar, is like Blackboard and other on-line aids for courses. Sorry for not making the links neater but this is how I've formatted the syllabus for maximum clarity. The syllabus looks great, yet transferring it here looks awful. I hope you can forgive me and also get something out of this! Day 1.1 might look unconventional but it will light them up before we go over the course properly, and I'm always looking for excuses to bring one of my wonderful dogs to class with me.

APG 201: Human Origins

A textbook-free curriculum
Assignments are due on the day they're listed
Books you'll need for this course:

1. Your Inner Fish - Neil Shubin

2. Paleofantasy - Marlene Zuk

Unit 1.

This view of life. Our place in nature.

What is the anthropological perspective? What is the scientific approach to understanding human origins? What is a human? What are human traits? How do humans fit on the Tree of Life?

1.1 – Dog origins

Lecture Resources

·        The Woof at the Door - Shipman (American Scientist)

http://www.americanscientist.org/issues/pub/2009/4/the-woof-at-the-door

·        How to Build a Dog - Ratliff (National Geographic)

http://ngm.nationalgeographic.com/2012/02/build-a-dog/ratliff-text

·        Genetics of Dog Breeding - Adams (Nature Education)

http://www.nature.com/scitable/topicpage/genetics-of-dog-breeding-434

Journal Assignment
• With at least one word, term, or phrase from today’s class, start a glossary. Whenever a word, term, or phrase is used in class that you think is important, jot it down, and define it. Whenever something's said in class that you’re unfamiliar with, jot it down and then go look it up (or ask a peer or me about it), and define it. 

1.2 – Overview of course

Journal Assignment

·        In a page or more: Without looking anything up or discussing with anyone else, writing just from your own mind at present... What is evolution?

1.3 – Doing biological anthropology

Assigned reading/viewing

·        What is it like to be a biological anthropologist? A Field Paleontologist's Point of View – Su (Nature Education) http://www.nature.com/scitable/knowledge/library/what-is-it-like-to-be-a-59719064

·        Notes from the Field: A Primatologist's Point of View – Morgan (Nature Education) http://www.nature.com/scitable/knowledge/library/notes-from-the-field-a-primatologist-s-54334509

·        Expedition Rusinga (video; 8 mins)  http://vimeo.com/50614968

·        YIF: How Do We Know When Our Ancestors Lost Their Tails? (video; 4 min) http://video.pbs.org/video/2365211775/

Journal Assignment

·        In a page or more: Why do biological anthropology?

Lecture Resources

·        The ape in the trees – Dunsworth (The Mermaid’s Tale)

http://ecodevoevo.blogspot.com/2014/02/the-ape-in-trees.html

·        Metabolic hypothesis for human altriciality – Dunsworth et al. (PNAS) http://www.pnas.org/content/109/38/15212.short

·        Challenges to human uniqueness: bipedalism, birth and brains - Roberts and Thorpe (J Zool) - Posted on Sakai

1.4 – The scientific process

Assigned reading/viewing

·        Understanding science: How Science Works, pages 1-21; starts here: http://undsci.berkeley.edu/article/0_0_0/howscienceworks_01

Journal Assignment

·        Scientific Process worksheet - Located at end of syllabus

1.5 – Linnaeus and the Order Primates

Assigned reading/viewing

·        Arkive: http://www.arkive.org/

·        Animal Diversity Web: http://animaldiversity.ummz.umich.edu/

·        Primate Factsheets: http://pin.primate.wisc.edu/factsheets

·        Encyclopedia of Life: http://eol.org/

·        Time Tree: http://www.timetree.org/

Journal Assignment

·        Primate Expert worksheet - Located at end of syllabus

Lecture Resources

·        Characteristics of Crown Primates – Kirk (Nature Education) http://www.nature.com/scitable/knowledge/library/characteristics-of-crown-primates-105284416

1.6 – Overview of primates

Assigned reading/viewing

·        Many primate video clips –Posted on Sakai

Journal Assignment

·        In a page or more: Write about your viewing experience, for example, you might write about being surprised that some of these creatures are primates or how some behaviors are surprisingly human.

Lecture Resources

·        Old World monkeys – Lawrence and Cords (Nature Education)

http://www.nature.com/scitable/knowledge/library/old-world-monkeys-83033815

1.7 – Primates: Encephalization and locomotion

Assigned reading/viewing

·        Many primate locomotion video clips –Posted on Sakai

Journal Assignment

·        In a page or more: Without looking at the lecture resource, come up with some categories for the different types of primate locomotion, give those categories names and list which species fall into them.

Lecture Resources

·        Primate locomotion – Gebo (Nature Education)

http://www.nature.com/scitable/knowledge/library/primate-locomotion-105284696

1.8 – Primates: Diet, tool use, and communication

Assigned reading/viewing

·        ·        http://www.eskeletons.org/
·        http://www.efossils.org/
The Human Spark 2 (video; 55 mins) https://www.youtube.com/watch?v=roqTXf5UNyc&feature=kp

Journal Assignment

·        Anatomy worksheet - Located at end of syllabus

·        In a page or more: Summarize the film, highlighting something you already knew and also something you learned that was brand new to you. What is the human spark?

Lecture Resources

·        Chimps with everything: Jane Goodall's 50 years in the jungle – McKie (The Guardian) http://www.theguardian.com/science/2010/jun/27/jane-goodall-chimps-africa-interview

1.9 – Primates: Sociality

Assigned reading/viewing

·       Peace Among Primates – Sapolsky (The Greater Good) http://greatergood.berkeley.edu/article/item/peace_among_primates

Journal Assignment

·        In a page or more: Reflect meaningfully on the reading, relating it to your life is fine but not required.

Lecture Resources

·        What Influences the Size of Groups in Which Primates Choose to Live? – Chapman and Teichroeb (Nature Ed)

http://www.nature.com/scitable/knowledge/library/what-influences-the-size-of-groups-in-58068275

·        Primate Communication – Zuberbuhler (Nature Ed)

http://www.nature.com/scitable/knowledge/library/primate-communication-67560503

·        Primate Sociality and Social Systems – Swedell (Nature Ed)

http://www.nature.com/scitable/knowledge/library/primate-sociality-and-social-systems-58068905

·        Primates in communities – Lambert (Nature Ed)

http://www.nature.com/scitable/knowledge/library/primates-in-communities-the-ecology-of-competitive-59119961

1.10 – Evolution and Darwin’s evidence

Assigned reading/viewing

·        Three parts from The Autobiography of Charles Darwin:

o   "Voyage of the 'Beagle'" (p. 71-81 ) and "An account of how several books arose" (p. 116- 135) and "An estimation of my mental powers" (p. 136-145)

http://darwin-online.org.uk/content/frameset?viewtype=text&itemID=F1497&pageseq=1

Journal Assignment

·        In a page or more: What circumstances or experiences influenced Darwin's thinking?

Lecture Resources

·        Evolution Is Change in the Inherited Traits of a Population through Successive Generations – Forbes and Krimmel (Nature Ed)

http://www.nature.com/scitable/knowledge/library/evolution-is-change-in-the-inherited-traits-15164254

·        Charles Darwin spotlight (1809-1892) http://www.nature.com/scitable/spotlight/charles-darwin-7567158

1.11 – The evidence that Darwin wishes he had

Assigned reading/viewing

·        Your Inner Fish, Chapter 1: Finding Your Inner Fish - Shubin

·        YIF: Amazing Places, Amazing Fossils: Tiktaalik (video; 5 mins) https://www.youtube.com/watch?v=T2vKlEUX7DI

·        Your Inner Fish, Chapter 2: Getting a Grip - Shubin

·        YIF: The Ancient History of the Human Hand (video; 4 mins) https://www.youtube.com/watch?v=RUL8hKDdY84

Journal Assignment

·        In a page or more: What does Shubin mean by "your inner fish"? What's the connection between a fish’s fin and your hand?

1.12 - Phylogeny

Journal Assignment

·        Phylogeny worksheet - Located at end of syllabus

Lecture Resources

·        Reading a phylogenetic tree – Baum (Nature Ed)

 http://www.nature.com/scitable/topicpage/reading-a-phylogenetic-tree-the-meaning-of-41956

·        Trait Evolution on a Phylogenetic Tree – Baum (Nature Ed)

http://www.nature.com/scitable/topicpage/trait-evolution-on-a-phylogenetic-tree-relatedness-41936

1.13 – The human primate (encephalization, locomotion, diet, tool use, communication, sociality)

Lecture Resources

·        Overview of hominin evolution – Pontzer (Nature Ed)

http://www.nature.com/scitable/knowledge/library/overview-of-hominin-evolution-89010983

Unit 2.

Explaining the similarities and differences. How evolution works.

Why are we like our parents but not exactly? Same for other species: why are we like them but not exactly? How did human traits evolve? What is our "inner fish" etc.? What was the last common ancestor (LCA) between humans and chimps like? How do we know when and where it lived?

2.1 – Inheritance: Chromosomes

Assigned reading/viewing

·        Your Inner Fish, Chapter 3: Handy Genes - Shubin

·        Your Inner Fish, Chapter 4: Teeth Everywhere - Shubin

·        YIF: The Evolution of Your Teeth (video; 3 mins) https://www.youtube.com/watch?v=ohq3CoOKEoo

·        Your Inner Fish, Chapter 5: Getting ahead - Shubin

·        YIF: Our Fishy Brain (video; 2.5 mins) http://video.pbs.org/video/2365207797/

Journal Assignment

·        In a page or more: What did you learn about how to do paleontology from the reading? What does he mean by your "inner shark"?

Lecture Resources

·        Developing the Chromosome Theory – O’Connor (Nature Ed)

http://www.nature.com/scitable/topicpage/developing-the-chromosome-theory-164

·        Genetic Recombination – Clancy (Nature Ed)

http://www.nature.com/scitable/topicpage/genetic-recombination-514

2.2 – Inheritance and gene expression: DNA, RNA, proteins

Assigned reading/viewing

·        Your Inner Fish, Chapter 6: The Best-Laid (Body) Plans - Shubin

·        Your Inner Fish, Chapter 7: Adventures in Bodybuilding - Shubin

Journal Assignment

·        In a page or more: What are  Hox genes and what do they have to do with linking a fruit fly to you? What is one benefit of being a sponge?

Lecture Resources

·        What is a Gene? Colinearity and Transcription Units – Pray (Nature Ed)

http://www.nature.com/scitable/topicpage/what-is-a-gene-colinearity-and-transcription-430

·        RNA functions – Clancy (Nature Ed)

http://www.nature.com/scitable/topicpage/rna-functions-352

·        Hox Genes in Development: The Hox Code – Myers (Nature Ed)

http://www.nature.com/scitable/topicpage/hox-genes-in-development-the-hox-code-41402

2.3 – Inheritance and gene expression: Mendelian genetics

Assigned reading/viewing

·        Your Inner Fish, Chapter 8: Making Scents - Shubin

·        Your Inner Fish, Chapter 9: Vision - Shubin

·        YIF: Finding the Origins of Human Color Vision (video; 5 mins) http://video.pbs.org/video/2365207765/

·        Your Inner Fish, Chapter 10: Ears - Shubin

·        YIF: We Hear with the Bones that Reptiles Eat With (video; 4 mins) http://video.pbs.org/video/2365207244/

Journal Assignment

·        In a page or more: Is it fair to say that when you smell something, that something is touching your brain? Why is it called the eyeless gene if you can have it and still have eyes? How does hearing work? What does your ear do besides hear, and how? What does drinking lots of alcohol do to your ears?

Lecture Resources

·        Gregor Mendel and the Principles of Inheritance – Miko (Nature Ed)

http://www.nature.com/scitable/topicpage/gregor-mendel-and-the-principles-of-inheritance-593

·        Mendelian Genetics: Patterns of Inheritance and Single-Gene Disorders – Chial (Nature Ed)

http://www.nature.com/scitable/topicpage/mendelian-genetics-patterns-of-inheritance-and-single-966

2.4 - The reality of inherited traits = Complexity; Hox genes and development

Assigned reading/viewing

·        Things Genes Can’t Do – Weiss and Buchanan (Aeon)

http://aeon.co/magazine/nature-and-cosmos/kenneth-weiss-anne-buchanan-genetics/

·        Insanity: genes 'versus' environment as causes – Weiss (The Mermaid’s Tale)

http://ecodevoevo.blogspot.com/2014/06/insanity-genes-versus-environment-as.html

·        Developmental Plasticity and the “Hard-Wired” Problem – Clarkin (kevishere)

http://kevishere.wordpress.com/2014/06/10/developmental-plasticity-and-the-hard-wired-problem/

Journal Assignment

·        In a page or more: Reflect meaningfully on these articles and highlight something that you already knew, but also the things that you learned that are brand new to you.

Lecture Resources

·        Phenotypic Range of Gene Expression: Environmental Influence – Lobo and Shaw (Nature Ed)

http://www.nature.com/scitable/topicpage/phenotypic-range-of-gene-expression-environmental-influence-581

·        Genetic Dominance: Genotype-Phenotype Relationships – Miko (Nature Ed)

http://www.nature.com/scitable/topicpage/genetic-dominance-genotype-phenotype-relationships-489

·        Pleiotropy: One Gene Can Affect Multiple Traits – Lobo (Nature Ed)

http://www.nature.com/scitable/topicpage/pleiotropy-one-gene-can-affect-multiple-traits-569

·        Polygenic Inheritance and Gene Mapping – Chial (Nature Ed)

http://www.nature.com/scitable/topicpage/polygenic-inheritance-and-gene-mapping-915

·        What Works Works. But What Works?: Genomes as works in progress – Weiss (Evol Anth) – Posted on Sakai

2.5 - Population genetics and evolution

Assigned reading/viewing

·        Paleofantasy , Intro - Zuk

·        Paleofantasy,  Chapter 1: Cavemen in Condos - Zuk

Journal Assignment

·        Scenario worksheet, 1 - Located at end of syllabus

·        In a page or more: What's the point of Zuk’s book? How familiar are you with "paleo" diet and other kinds of lifestyle choices that fall under that umbrella?

Lecture Resources

·        Mutations Are the Raw Materials of Evolution – Carlin (Nature Ed)

http://www.nature.com/scitable/knowledge/library/mutations-are-the-raw-materials-of-evolution-17395346

·        Natural selection, genetic drift and gene flow do not act in isolation in natural populations – Andrews (Nature Ed)

http://www.nature.com/scitable/knowledge/library/natural-selection-genetic-drift-and-gene-flow-15186648

·        Neutral Theory: The null hypothesis of molecular evolution – Duret (Nature Ed)

http://www.nature.com/scitable/topicpage/neutral-theory-the-null-hypothesis-of-molecular-839

2.6 - Natural selection

Assigned reading/viewing

·        Paleofantasy,  Chapter 2: Are We Stuck? - Zuk

Journal Assignment

·        In a page or more: What does Zuk mean by, "are we stuck?" and what's the answer?

Lecture Resources

·        Negative selection – Loewe (Nature Ed)

 http://www.nature.com/scitable/topicpage/negative-selection-1136

2.7 - Sexual selection, Modern Synthesis, and more on epigenetics

Assigned reading/viewing

·        Paleofantasy,  Chapter 3: Crickets, sparrows, and Darwins- or, evolution before our eyes - Zuk

Journal Assignment

·        Scenario worksheet, 2 - Located at end of syllabus

·        In a page or more: How can natural selection explain the silent crickets?

Lecture Resources

·        Sexual selection – Brennan (Nature Ed)

http://www.nature.com/scitable/knowledge/library/sexual-selection-13255240

2.8 - Recent human evolution: Malaria resistance and lactase persistence

Assigned reading/viewing

·        Paleofantasy,  Chapter 4: The perfect paleofantasy diet: Milk - Zuk

Journal Assignment

·        Wisdom Teeth worksheet - Located at end of syllabus

·        In a page or more: How can natural selection explain lactase persistence?

Lecture Resources

·        Natural Selection: Uncovering Mechanisms of Evolutionary Adaptation to Infectious Disease – Sabeti (Nature Ed)

http://www.nature.com/scitable/topicpage/natural-selection-uncovering-mechanisms-of-evolutionary-adaptation-34539

2.9 - Understanding evolutionary mechanisms; Building evolutionary scenarios

Assigned reading/viewing

·        Evolution is the only natural explanation – Dunsworth (The Mermaid’s Tale)

http://ecodevoevo.blogspot.com/2013/06/evolution-is-only-natural-explanation.html

·        The F-words of Evolution  – Dunsworth (The Mermaid’s Tale)

http://ecodevoevo.blogspot.com/2011/05/f-words-of-evolution.html

·        Another F-word of evolution  – Dunsworth (The Mermaid’s Tale)

http://ecodevoevo.blogspot.com/2011/05/another-f-word-of-evolution.html

·        Mutation not natural selection drives evolution –  Tarlach (about Nei; Discover Mag)

http://discovermagazine.com/2014/march/12-mutation-not-natural-selection-drives-evolution

Journal Assignment

·        Drift vs. Selection worksheet - Located at end of syllabus

·        In a page or more: Reflect on what you already knew and, more importantly, what you learned from each of the readings that's new.

2.10 - Species and speciation

Assigned reading/viewing

·        Primate Speciation: A Case Study of African Apes – Mitchell and Gonder (Nature Ed)

http://www.nature.com/scitable/knowledge/library/primate-speciation-a-case-study-of-african-96682434

Journal Assignment

·        In a page or more: What are some hypotheses for how or why the African apes, including humans, diverged? Why might gene trees and species trees not agree with one another?

Lecture Resources

·        Why should we care about species? – Hey (Nature Ed)

http://www.nature.com/scitable/topicpage/why-should-we-care-about-species-4277923

·        Speciation: The origin of new species – Safran (Nature Ed)

http://www.nature.com/scitable/knowledge/library/speciation-the-origin-of-new-species-26230527

·        The maintenance of species diversity – Levine (Nature Ed)

http://www.nature.com/scitable/knowledge/library/the-maintenance-of-species-diversity-13240565

·        Macroevolution: Examples from the Primate World – Clee and Gonder (Nature Ed)

http://www.nature.com/scitable/knowledge/library/macroevolution-examples-from-the-primate-world-96679683

2.11 - Genomics, fused chromosomes, molecular clocks, and the LCA

Assigned reading/viewing

·        Lice and Human Evolution (video; 11 mins) http://video.pbs.org/video/1790635347/

·        Time Tree: http://www.timetree.org/

Journal Assignment

·        Speciation and molecular clocks worksheet - Located at end of syllabus

Lecture Resources

·        The Onion Test – Gregory (Genomicron) http://www.genomicron.evolverzone.com/2007/04/onion-test/

·        The Molecular Clock and Estimating Species Divergence – Ho (Nature Ed)

http://www.nature.com/scitable/topicpage/the-molecular-clock-and-estimating-species-divergence-41971

Unit 3.

Evolving humans, past and present. Our extinct hominin ancestors and relatives. Modern human origins and variation. The cultural controversy over evolution.

How did human traits evolve? How and why do humans vary? Should we look to our ancestors as a lifestyle guide? Are we still evolving? Why is human evolution misunderstood and why is it controversial?

3.1 - Fossils, geology, dating methods; Extinction

Assigned reading/viewing

·        Planet without apes? – Stanford (Huffington Post)

http://www.huffingtonpost.com/craig-stanford/planet-without-apes_b_1933073.html

Journal Assignment

·        In a page or more: What could lead to a future on Earth without apes? What kinds of evidence would such a process leave behind for future humans to use to explain why apes went extinct?

Lecture Resources

·        Dating Rocks and Fossils Using Geologic Methods – Peppe (Nature Ed)

http://www.nature.com/scitable/knowledge/library/dating-rocks-and-fossils-using-geologic-methods-107924044
How to Become a Primate Fossil – Dunsworth (Nature Ed; in press) – Posted on Sakai

3.2 - Primate fossil record; Origins and evolution of bipedalism

Assigned reading/viewing

·        Dating Rocks and Fossils Using Geologic Methods – Peppe (Nature Ed)

http://www.nature.com/scitable/knowledge/library/dating-rocks-and-fossils-using-geologic-methods-107924044

Journal Assignment

·        Geology worksheet - Located at end of syllabus

Lecture Resources

·        Milankovitch Cycles, Paleoclimatic Change, and Hominin Evolution – Campisano (Nature Ed)

http://www.nature.com/scitable/knowledge/library/milankovitch-cycles-paleoclimatic-change-and-hominin-evolution-68244581

·        Studying function and behavior in the fossil record – Benton (PLOS Biology)

http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1000321

3.3 - Bipedalism, diet: Sahelanthropus, Orrorin, Ardipithecus, Australopithecus, Paranthropus

Assigned reading/viewing

·        Lucy – Dunsworth (Icons of Evolution) – Posted on Sakai

·        Desktop Diaries: Tim White (video; 7 mins)

http://www.sciencefriday.com/video/08/09/2013/desktop-diaries-tim-white.html

·        YIF: Ancient Human Ancestors: Walking in the woods (video; 4 mins) http://video.pbs.org/video/2365207936/

·        YIF: Lucy (video; 5 mins) https://www.youtube.com/watch?v=m8Lkk6u-wQM

·        Trowelblazers: http://trowelblazers.tumblr.com/

·        An Unsuitable Job for a Woman: http://www.ellencurrano.me/blog/

Journal Assignment

·        In a page or more: Describe something monumental (either for paleoanthropology or for you personally) to be learned or realized thanks to Lucy. Then summarize each of the films. For the two websites/blogs, choose one featured woman from each, and briefly describe at least one of her contributions to humankind.

Lecture Resources

·        The Earliest Hominins: Sahelanthropus, Orrorin, and Ardipithecus - Su (Nature Ed)

http://www.nature.com/scitable/knowledge/library/the-earliest-hominins-sahelanthropus-orrorin-and-ardipithecus-67648286

·        The "Robust" Australopiths – Constantino (Nature Ed)

http://www.nature.com/scitable/knowledge/library/the-robust-australopiths-84076648

·        Paleoecology and Paleoenvironment: a Case Study of Plio-Pleistocene Mammals from Laetoli – Kovarovic (Nature Ed)

http://www.nature.com/scitable/knowledge/library/paleoecology-and-paleoenvironment-a-case-study-of-68245441

3.4 – Technology and encephalization: Homo habilis

Assigned reading/viewing

·        Paleofantasy,  Chapter 5: The perfect paleofantasy diet: Meat - Zuk

·        YIF: Ancient Hands, Ancient Tools (video; 5 mins) https://www.youtube.com/watch?v=5_ew9J8lpwo

Journal Assignment

·        In a page or more:  Can you name something at the grocery store that could count as "paleo"? Why did I ask this question?

Lecture Resources

·        A Primer on Paleolithic Technology – Ferraro (Nature Ed)

http://www.nature.com/scitable/knowledge/library/a-primer-on-paleolithic-technology-83034489

·        Evidence for Meat-Eating by Early Humans – Pobiner (Nature Ed)

http://www.nature.com/scitable/knowledge/library/evidence-for-meat-eating-by-early-humans-103874273

3.5 – Ecology and encephalization: Homo erectus

Assigned reading/viewing

·        Paleofantasy,  Chapter 6: Exercising the paleofantasy - Zuk

Journal Assignment

·        In a page or more: Is exercising in a "paleo" way good, bad, both, or neither?

Lecture Resources

·        Homo erectus - A Bigger, Smarter, Faster Hominin Lineage – Van Arsdale (Nature Ed)

http://www.nature.com/scitable/knowledge/library/homo-erectus-a-bigger-smarter-97879043

3.6 – Sociality and encephalization: Neanderthals

Assigned reading/viewing

·        What Happened to the Neanderthals? – Harvati (Nature Ed)

http://www.nature.com/scitable/knowledge/library/what-happened-to-the-neanderthals-68245020

Journal Assignment

·        In a page or more: What happened to the Neanderthals?

Lecture Resources

·        Archaic Homo sapiens – Bae (Nature Ed)

http://www.nature.com/scitable/knowledge/library/archaic-homo-sapiens-103852137

·        Neanderthal Behavior – Monnier (Nature Ed)

http://www.nature.com/scitable/knowledge/library/neanderthal-behavior-59267999

3.7 - Sociality and encephalization: Modern Homo sapiens 

·        Research Projects due today

Lecture Resources

·        The Transition to Modern Behavior – Wurz (Nature Ed)

 http://www.nature.com/scitable/knowledge/library/the-transition-to-modern-behavior-86614339

3.8 - Origins and evolution of speech and language

Assigned reading/viewing

·        The Human Spark 1 (video; 55 mins) https://www.youtube.com/watch?v=2HgVl27j4Mk

Journal Assignment

·        In a page or more: Summarize the film, highlighting something you already knew and also something you learned that was brand new to you. What is the human spark?

Lecture Resources

·        Tracking the Evolution of Language and Speech: Comparing Vocal Tracts to Identify Speech Capabilities – Lieberman and McCarthy (www.museum.upenn.edu/expedition)

http://www.cog.brown.edu/people/lieberman/pdfFiles/Lieberman,%20P.%20&%20McCarthy,%20R.%202007.%20Tracking%20the%20evolution%20of.pdf

3.9 - Models of human origins and geographic dispersal; Ancestry genetics

Assigned reading/viewing

·        From the Belgian Congo to the Bronx Zoo (NPR)

·        http://www.npr.org/templates/story/story.php?storyId=5787947

·        A True and Faithful Account of Mr. Ota Benga the Pygmy, Written by M. Berman, Zookeeper – Mansbach

http://adammansbach.com/other/otabenga.html

·        Human Races May Have Biological Meaning, But Races Mean Nothing About Humanity – Khan (Discover blogs)

http://blogs.discovermagazine.com/crux/2012/05/02/human-races-may-have-biological-meaning-but-races-mean-nothing-about-humanity/#.U5XBl_ldWSo

Journal Assignment

·        In a page or more: (Regarding Ota Benga: The first is a short article and audio news piece and the second is fiction based in fact.) Why was Ota Benga brought to the U.S.? Why was Ota Benga brought to the Bronx Zoo? Regarding issues that Ota Benga’s story raised, what do religious and evolutionary perspectives have in common? Why doesn’t a story like Ota Benga’s take place in 2014? Do you agree or disagree with Khan about races having biological meaning? Do you agree or disagree with Khan about races meaning nothing about humanity? Why or why not (for both)? What would you like to learn more about as a result of reading Khan's piece? Describe how you would go about doing that.

Lecture Resources

·        Anthropological genetics: Inferring the history of our species through the analysis of DNA – Hodgson and Disotell (Evolution: Education and Outreach)

http://link.springer.com/article/10.1007%2Fs12052-010-0262-9#page-1

·        Testing models of modern human origins with archaeology and anatomy – Tryon and Bailey (Nature Ed)

http://www.nature.com/scitable/knowledge/library/testing-models-of-modern-human-origins-with-96639156

·        Human Evolutionary Tree – Adams (Nature Ed)

http://www.nature.com/scitable/topicpage/human-evolutionary-tree-417

·        Paternity Testing: Blood Types and DNA – Adams (Nature Ed)

http://www.nature.com/scitable/topicpage/paternity-testing-blood-types-and-dna-374

·        The Neanderthal Inside Us (video; 4 mins)

http://www.nytimes.com/video/science/100000002887069/science-profile-svante-paabo.html?playlistId=100000002891080

3.10 - Race and evolution's P.R. problem

Assigned reading/viewing

·        Understanding Race: http://www.understandingrace.org/

·        In the Name of Darwin – Kevles (PBS) http://www.pbs.org/wgbh/evolution/darwin/nameof/

·        The visible colors: and the falseness of human races as natural categories – Weiss (The Mermaid’s Tale)

http://ecodevoevo.blogspot.com/2014/06/the-visible-colors-and-falseness-of.html

Journal Assignment

·        Peruse the whole site then take the quiz at Understanding Race and prove that you completed it by listing the correct answers (just letters is fine)

·        In a page or more: What is eugenics and what’s it got to do with Darwin? Genes contribute to performance on IQ tests (and others like SAT), but what else contributes to performance on those tests? Does social Darwinism contribute to the cultural controversy over accepting and teaching evolution in the U.S.A.? Why doesn't the color metaphor work for categorizing humans?

3.11 - Race and the evolution of human skin color variation; Future evolution

Assigned reading/viewing

·        Paleofantasy,  Chapter 10: Are we still evolving? - Zuk

·        We are not the boss of natural selection – Dunsworth (io9)

http://io9.com/we-are-not-the-boss-of-natural-selection-it-is-unpwnab-1325126849

Journal Assignment

·        In a page or more: Are we still evolving?

Lecture Resources

·        Human Skin Color Variation (NMNH): http://humanorigins.si.edu/evidence/genetics/skin-color

3.12 - The cultural controversy over evolution; Overcoming misconceptions

Assigned reading/viewing

·        Your Inner Fish, Chapter 11: The Meaning of It All - Shubin

·        Evolution reduces the meaning of life to survival and reproduction... Is that bad? – Dunsworth (The Mermaid’s Tale)

http://ecodevoevo.blogspot.com/2012/06/evolution-reduces-meaning-of-life-to.html

Journal Assignment

·        In a page or more: After re-reading your very first journal entry on "what is evolution?" compose a letter to yourself highlighting what you were right about and what you were wrong about or what was incomplete in your answer based on what you learned this semester. Also reflect on what you're still left wondering and how you could find the answers to your remaining questions.

Lecture Resources

·        Kitzmiller v. Dover Area School District

http://ncse.com/files/pub/legal/kitzmiller/highlights/2005-12-20_Kitzmiller_decision.pdf

You'd have to be science illiterate to think "believe in evolution" measures science literacy –Kahan (The Cultural Cognition Project)

http://www.culturalcognition.net/blog/2014/5/24/weekend-update-youd-have-to-be-science-illiterate-to-think-b.html

Genes vs environment: more on the misunderstood subtleties

Yesterday we tried to explain why the idea of a trait being due to genes versus environment was a false distinction.  We proposed two basic theorems of life, that everything is due to genes, and everything is due to environment, just to make the point that arguments about whether one or the other is 'the' cause of a trait of interest are often in never-never land.  Also, even saying 'both' are true, or that they 'interact' is so vague as often to be rather meaningless or unhelpful.  Do we mean pairwise interactions between factor A and factor B?  Is it just multiplicative (A x B yields trait)?  Or, say, A x B-squared?  Or Pi times A divided by B?

And, by the way, how many factors interact?  If it's very many, it's essentially impossible for observational data to resolve the causal process, even if just in pairs.  And are the effects just linear?  We are after all 4-dimensional (space and time) organisms, and action of some factor or factors need not be linear.  Maybe their 'interaction' is like this:

             T=G1 + E1^(E5*E5)+ (G2*G3*E2*E1^1/2)/(π*G4+G5)

This equation is imaginary, but one might ask why on earth would pi or these variables raised to strange-seeming powers ever be relevant?  Because, for example, genes are expressed in quantities like copies of the protein, but they act in 3-dimensional cells with 2-dimensional surfaces interacting with environments, changing over time, that may themselves be linear doses (like amounts of, say, sugar) but may work through other dimensions, like pressure on cell surfaces....)

All this raises another, deeper question that is often if not typically quite misperceived, usually innocently, in the argument.  It is that there are deep semantic issues even in stating the propositions, so naturally there is disagreement about the answers.

More on the semantics of the problem

Part of the problem is the use of the terms themselves.  When we say that 'genes cause X' do we mean that genes (however you may wish to define them) are involved in the mechanism that leads to or maintains trait X?  This is the meaning sometimes used, such as in developmental biology when speaking of how retinal cells end up expressing opsin (light-sensing) genes.  Some regulatory region is bound by a protein and that transcribes the green-opsin in retinal cells, etc. 

But the genes vs environment argument often means something quite different.  If the first meaning of 'genetic' is about mechanism, a second meaning is about variation.  When we say that genes 'cause' something what we really mean is that genetic variation (among individual organisms) is causally responsible, through mechanistic means, for variation in the trait among those organisms.  So, variation in the coding sequence of opsin genes is associated with variation in color perception.  Likewise for variation in height, obesity, intelligence.  Even if what we choose to measure is a cultural choice and our definitions of traits culturally determined, what we choose to consider causation is in this case about inter-individual genetic variation, not the mechanism that's responsible.

The same, of course, goes for environment.  Smoking mechanistically causes heart disease by (say) raising blood pressure.  But epidemiologically, the amount of smoking is associated with the risk of heart attack.  This again is about causal variation.

And it is fair to ask just what one means, and how secure one's assertions are when a 'cause' of some trait--like hypertension or many others, raises your absolute risk by only a few percent (or less) and only by the time you are 50 or 60 years old?  When is that 'causation' in a seriously reliable sense?

The mechanism vs variation distinction is not always clear even when geneticists are speaking about genetics.  Much less for others who don’t really understand the subjects in much depth (e.g., many news reporters, even many outspoken scientists or people pushing some ideology about causation).

If we have to infer causation by relating variation in environmental conditions to genomic variation, we have a different kind of problem from working out mechanisms:  We have to decide how to quantify or measure our putative factors and their variation and to relate them to each other.   In both cases we may need either experimental or observational data.  If we do our science right, which is often far from the case, we should relate these to some theoretical framework that is more than trivial or self-confirming. Naturally, especially given the array of vested interests, perspectives, methodological preferences and approaches, along with the sociopolitical aspects of science and its funding, it is no surprise that the genes-vs-environment imbroglio is so persistent. Cultural inertia and our human fallibilities account for a lot of Einstein's observation about insanity being doing the same thing over and over and expecting different results.  

But even this is not the whole story.

There is a third 'genetic'

The word 'genetic' has an additional meaning, which has to do with the changes that occur in genes among cells within each person during his/her lifetime.  These 'somatic' mutations are inherited by our cells during our lifetime but are not inherited from parent to offspring.  We all harbor genes whose variation among our tissues or within segments of our tissues, affecting their mechanism of action, yield biological effects including disease.  Epigenetic changes in gene usage also occur in local tissues during life, but unless they are in the sperm or egg cells they are (usually) not inherited by the next generation, even if they may be inherited by your body cells when they divide.  There are various clear demonstrations of the importance of somatic genetic changes, and they are not controversial (but usually ignored by scientists, acting like ostriches, because somatic changes are devilish hard to document).

None of these things are secret!  But they show how difficult it is to understand biological causation of complex traits, even for someone not committed to some simplified worldview being defended against all comers.  A lot of confusion, hot air, wasted resources, and unnecessary competition results from failure to understand these things clearly.  Thinking about them seriously can give you a nasty headache, because the realities of Nature are not divided into neat categories, and our means of peeking into Nature's truth are limited, or even at present so deeply flawed that some better ways of thinking or even some better ways of identifying the important questions are called for. 

Thinking about these issues should also raise the difficult but obvious problem that what we choose to call important--be it environment or genes or how we define our trait in the first place--is a subjective decision, often not that clear among peers and often changeable over time (e.g., the definition of blood pressure and how to measure it, the definition of 'hypertension' or 'intelligence', or even a 'thumb').

What is the trait (if it's a trait)?

A philosophical point about genomic and evolutionary causation

One can argue, in principle, that if Nature and natural selection generated life, it would favor less rather than more finely tuned genomic programming.  Given the inevitably probabilistic aspect of survival, finding mates and food and so on, in environmental circumstances that are usually complex and changeable, fine-tuning might seem rather implausible  The default assumption should instead be a lack of rigid programming and a stress on ability to respond to unpredicted circumstances. Adaptability would seem to be obviously more robust than genetic hard-wiring.  Yet too much theory, even by evolutionary biologists and manifestly by those in other fields (including much of biomedicine and anthropology) looks for the hard-wired--it's easier to think about and design projects to find.

Instead, perhaps the burden of proof should be on anyone claiming that their trait, be it disease or adaptation or behavior etc., is hard-wired.  One should have to falsify the more likely assumption that what passes through the sieve of Natural selection is that which can find the holes in the sieve, wherever they may be.  In that sense, causation is 'designed' to be complex and elusive.

Insanity: genes 'versus' environment as causes

There are two statements about humans, or other organisms for that matter, that may seem inconsistent but that are both as solid as the Rock of Gibraltar, as fundamental and central as atoms to chemistry. Because of their deep importance, we feel that we must go beyond just stating these bedrock findings, and give rigorous proof of their truth.

Theorem 1. Genes cause every human trait!
Proof:  Without genes cells could not function, embryos could not develop, and there would be no humans to have any traits.

Theorem 2. Environment causes every human trait!
Proof:  Without their surroundings, differential gene expression would not occur, tissues would not differentiate, and there would be no humans to have any traits.

Given these incontrovertible proofs, it should seem rather trivially obvious that the search for the causation of any trait, should never be couched in one term or the other (genes or environment).  It is always genes and environment.  The legitimate interest in any search for biological causation should be clarified, first of all in the investigator's mind.  But this seems often, or even usually, not what happens when studies are designed, funding requested, or results reported.

Rock of Gibraltar; Wikimedia

As a result, there is a lot of needless contention and, sometimes, even abusive dismissal of points of view, in discussions of both the evolution and presence of human traits--be they normal or disease traits.

Unfortunately, it is not easy--even in principle--to separate these issues neatly.  For example, those who cling to genetic essentialism dismiss environmental causation as largely incidental or beside the point. Even 'epigenetics' is too close to environmental causation to be acceptable.  True enough, like many things in today's world of science (indeed, probably always typical of human affairs), we have fads and current epigenetic studies are in part just that--a way to get grants, get papers in the 'name' journals and get news attention.

However, epigenetics refers to the means by which gene expression is regulated.  Cells are always sensing their environment in various ways that lead to modification of their chromosomes that controls which genes are used and which are shut down.  In that very fundamental sense, every trait is an epigenetic trait.  Indeed, a given gene's 'environment' includes what's going on in the rest of the genome in that same cell.  The nontrivial scientific questions concern when, where, and how epigenetic mechanisms are at work in some context of interest--how the environment affects gene usage and its results.

Pure environmentalism is, however, also a fantasy.  Cells are genetically programmed to respond to their environments in various ways, ignoring some signals from the outside world, but responding to others, depending on its developmental stage and context.  Likewise intracellular conditions.  Genetic variation simply must be related to and circumscribes these responses.  It's this kind of sensing of environment-specific signals that causes one cell to become a stomach cell and another a brain cell, or for cells to divide or not, or produce particular proteins. Multicellular organisms wouldn't exist without differential cellular responses to environmental signals.

In this context, genomic causation and the evolution of genomic causation are similar.  Evolution only affects genotypes and environments that exist at any given time and place.  That variation changes in terms of its proliferation in its immediately local ecological context, which for convenience and perhaps having no better ideas, we usually consider as a phenomenon of relative frequency in some specified population. But these are abstractions of convenience whose relevance should be (but often rarely is) tested.  In any case, biomedical causation--like the genomic basis of autism or any trait you want to consider--similarly refers to some specific local context.

When incidence of a disease changes very rapidly, even if the trait has a genomic underpinning--and as we said above, every trait does--the change in incidence is very unlikely to be due to major changes in the local gene pool.  In that sense, it would be properly said to be 'environmental'.  Traits like autism, obesity, asthma, the success of Chinese ping-pong players, and many others are in this category.  Such attributions get under the collar of those whose careers and worldview are centered around genomes as the sole important determinants of life.  The response to rapid change may be acknowledged to be environmental, but in what seems to be a rather trivializing sense (yes, they might agree, China has manufactured millions of ping-pong tables which didn't before exist, but the champions are champions because of their Chinese genes).

A defense of the largesse of medical genomic research is that increased prevalence of disease is due to specific genotypes responding to the environmental change.  That is, environmental variation is leading to an epidemic of obesity because McFood triggers responses from some tractably few variants in the population that, before McFood, did not lead to disease.  Thus, the justification for expecting genomic 'causation' even when environment is the real 'cause'.

In fact, genomic variation changes just as fast as environments.  In a population (however you choose to specify it), alleles are coming and going.  A trait may in large part be the result of action of many different, individually rare, elements in the genome acting in their particular environment.  This coming and going means that the genes are as fluid in many ways as is the environment (however you may specify that).

The same applies to evolution
The same applies to much of the selectionist arguments for traits we see today.  Environmental change is of course the 'cause' of natural selection, and in a new environment selection will favor those few genes that confer major advantage (and will remove the alternative variants that, in the new environment, don't function well any longer).  So, our traits today should reflect selection history in a tractable way and we can see what is 'good' and not so good based on Nature's past decisions.

You can see the tangle of interests and rhetoric in contending views that are prevalent these days and soak up a lot of resources that might be devoted to things that are overwhelmingly 'genetic' (like cystic fibrosis) or 'environmental' (like the effects of exposure to CT scans).  But even this is a bit of false reasoning in defense of vested interests, because even most such traits are not so genetic rather than environmental or vice versa.

"What?  You don't think even a broken gene, that doesn't even work at all, doesn't lead to consequences that are purely genetic?  You don't think even smoking is an environmental cause of disease?"  The answer is: that's right.  For example, most of us are walking around with many 'broken' genes that have been identified as causes of disease, yet we don't have the disease.  We do a gene knockout in lab mice and they may get the same disease as found with the same mutation in humans---but it may have little, different, or even no effect in other strains of mice.  And, of course, most smokers don't get lung cancer.

If the arguments for simple genomic selective or biomedical expectations were accurate, then mapping would identify those few genes that responded to selection pressures or that respond to environments and make us sick.  Instead, what we typically find is that traits like obesity and autism and many others (we fancy that Chinese ping-pong ability would be similar) are not arising in those with particular alleles in a few genes.  Instead, variation in tens or hundreds of genome regions contribute to the trait, in the current environment.

It is in this sense that one can make the argument that a trait like autism or obesity is mainly an environmental trait.  Even if the responses of many genes lead to the manifestation of the trait in those individuals, the genotype is different in each, and what is in common is some aspect(s) of the environment.   Similarly, environmental 'causes' may be as individual, and diverse.  So the chase for explanations makes no sense if one insists on denying one or the other category or type of causation.

Not so simple
How one relates Theorem 1 to Theorem 2 in a real-world problem is not at all easy, even to think about clearly.  It is not enough to say we'll do regression on all genomic and environmental variables (G1, G2,...Gn, E1, E2,...En), assuming such enumeration and identification could actually be done, and then add some product (non-linear) 'interaction' terms:  G1 x E1, G1 x E2,.....   This quickly leads to essentially infinitely many things to test, even with just the product assumption.  And then there is how to measure the factors.  If one gene is part of another gene's environment (in some types of cell, under some conditions) then genes can be both genes and environments.

Saying these factors 'interact' may mean there is some complex sort of network of factors that, acting in some ways as a unit, affects some other network in each individual, each uniquely, to generate some output--like a disease--and then you have to decide what the right measure is.  Are 'blood pressure', 'IQ', 'average ping-pong victory differential', or 'stature' reasonable measures of a 'trait' for which you wish to understand the causal basis? Maybe, say, the square of blood pressure or the 2/3 power, more accurately reflect what is going on.

So how genetic variants  and environmental exposures 'cause' outcomes deeply depends on definitions and what one chooses to study.  It is far from clear what to do even once you've made decisions about that.   In this light, scientists' confident assertions and grandiose study design claims are very far from actually even acknowledging much less reflecting the depth of the problem we want to solve.  So we can just say "it's genes and environment" or "only genes really matter", and try to buffalo our way through.

The question may be scientific, but the problem is sociocultural
The problem, as we often note, is the polarized view of contending parties in the face of what is so obvious.  And the explanation has to do with human society and psychology and resources.  The explanations are choices in that sense, and that makes them sociopolitical.  Each of us somehow formulates a view about what is important, what we mean by 'genes' and 'environment' and how they relate to each other.  We have to judge what is most important, what risk effects matter, where to put research resources.  Nature herself doesn't provide a guide.  Facing up to complex, uncertain causal situations is more difficult than carrying on with what one knows and has been doing....and an keep one's lab running and churning out papers.  But the ability to face up is also something a culture itself may affect.  Often, we do what we learned or what has fed us, avoiding the risk of acknowledging that there may be something better or very different to do.

Albert Einstein famously quipped that the definition of insanity is doing the same thing over and over again and expecting different results.  Maybe he was wrong.  Maybe that's the definition of human nature.

Autism -- back to blaming the mother?

Two recent reports of the cause of autism reach different conclusions, though they are alike in that neither implicates genetics, at least not directly.  The first, published in the International Journal of Epidemiology ("Maternal lifestyle and environmental risk factors for autism spectrum disorders," Lyall et al.), reviews the evidence for environmental risk factors and finds that diet can influence risk, and that folic acid supplements taken around conception are associated with reduced risk.  Further,

Although many investigations have suggested no impact of maternal smoking and alcohol use on ASD [autism spectrum disorder], more rigorous exposure assessment is needed. A number of studies have demonstrated significant increases in ASD risk with estimated exposure to air pollution during the prenatal period, particularly for heavy metals and particulate matter. Little research has assessed other persistent and non-persistent organic pollutants in association with ASD specifically.

Lyall et al. call for larger epidemiological studies of maternal exposure to vitamins, fats and other nutrients, as well as pesticides and endocrine-disrupting chemicals, even though environmental epidemiological studies of autism have been done for decades.

The second paper, in  Molecular Psychiatry ("Elevated fetal steroidogenic activity in autism," Baron-Cohen et al.), reports the results of looking at hormone levels in amniotic fluid samples collected at between 15 and 16 weeks gestation from a sample taken from a registry of nearly 20,000 male infants in Denmark, born between 1993 and 1999.  The final sample was fairly small, including 128 male infants with autism and 217 controls; the 24 females in the registry who were later diagnosed with autism were excluded from the study because they were atypical for a variety of reasons.  Prevalence of autism is generally higher in males.

We find that amniotic fluid steroid hormones are elevated in those who later received diagnoses on the autism spectrum. Rather than the abnormality being restricted to a specific steroid hormone, a latent steroidogenic factor is elevated, which includes all hormones in the Δ4 pathway, as well as cortisol.

The effect on the developing brain, Baron-Cohen et al. suggest, may be epigenetic.  That is, steroids modify DNA in ways that affect gene expression without changing coding sequence.

Steroids and their receptors act as epigenetic fetal programming influences on early brain development. Through their nuclear hormone receptors, steroids can alter gene expression via direct or indirect influence on multiple epigenetic processes such as histone acetylation, DNA methylation and have transcriptional and post-transcriptional effects on noncoding mRNAs such as microRNAs. Furthermore, during early sensitive periods of brain development, there are sex differences in DNA methylation, methyl-binding proteins, chromatin modifications and microRNA expression, and these effects are mediated in part by early steroid hormone effects.

What is the source of the excess steroid?  "The fetus, the mother, the placenta or other external factors" -- that is to say, it could be anything and this study couldn't answer that question.  Indeed, it is also impossible to know, if the excess hormone really is involved, whether it's the cause of the disorder or the result.  Perhaps maternal stress is the source, the authors suggest, and perhaps, the authors note, steroids such as testosterone and cortisol are also elevated in other disorders with a skewed sex ratio.  In any case, they write, "Each of these sources require further investigation to determine how such influences might affect fetal development in autism."

Cortisol molecule

A story on the BBC website about this work quotes an autism "expert" saying that this is "an important first step" on the path to discovering what causes autism.  First step!? This is a curious way to describe things, since probably billions of dollars have been spent in the last 30 or 40 years on efforts to identify the cause of this disorder, much of it on genetic studies, with no robust results.  Given this track record, what criteria should we use to decide whether this study is worth paying any attention to?

As with many complex diseases and disorders, many genes with small effect have been identified, but none of these explains the high rates of autism now reported around the world.  It is interesting to see these two reports of possible environmental risk factors after a sea of genetic studies, though.  Decades ago autism was believed to be the result of "refrigerator mothering," but then blame swung toward genes and away from environment, and now it seems autism is epigenetic. The gene switch never could have been exactly right given the dramatic, rapid increase in prevalence of autism, and other than because genes are techy and faddish, why would one ever expect genes to be a main cause in the first place, other than as a rationale to do genetics (which we knew how to do) and a paucity of other ideas?  Or, environmental causes being difficult to replicate and confirm.

But many epidemiological studies looking for environmental causes have been done.  A 2010 paper in Current Opinion in Pediatrics reports, with respect to environmental risk factors, e.g.:

...the most powerful proof-of-concept evidence derives from studies specifically linking autism to exposures in early pregnancy – thalidomide, misoprostol, and valproic acid; maternal rubella infection; and the organophosphate insecticide, chlorpyrifos. There is no credible evidence that vaccines cause autism.

Older mothers and fathers have been associated with autism, birth order, toxic chemicals, vaccines and thimerosol, and so forth, though none reliably so.  And of those factors that have been replicated, they can't explain all cases.

Autism is a difficult trait to study.  The trait itself is hard to define, varies enormously, there are no biomarkers with which to make a definitive diagnosis, diagnostic criteria have changed over the years, and so forth.  But many traits are similarly complex -- asthma, schizophrenia, heart disease, etc. -- and similarly resistant to current methods for determining cause.  So it seems fair to assert that many attempts to determine causes of complex traits are fad-following approaches to understanding complexity with reductionist science.

What is scientific knowledge and how hard is it to come by?

Two stories we're looking at reflect issues that we care about, and that we think everyone who thinks about how we know what we know should care about.  They have to do with the fragility of knowledge in at least some areas of science, including biomedical and genetic knowledge.  There are some lessons here, and they are perhaps surprisingly indirect.

What's in a name?  A rose by any other name (except Rosenkrantz) would be as sweet
The tweetosphere is resounding with comments on the study that looked at whether hurricane names affect the damage they do.  This is not some group of mystics studying Karma, but real scientists (perhaps with nothing else to do, since the subject would seem rather remote from what people on a payroll ought to be spending their time at).  

Hurricane Katrina; Wikimedia

As reported in this PNAS paper, ("Female hurricanes are deadlier than male hurricanes," Jung et al.),  more people die in hurricanes with women's names than hurricanes with male names.  This sounds wholly silly since the names are chosen before any hurricanes arise, and, anyway, were selected in different ways over the years.  But according to this paper, hurricanes with female names give people the impression that they are kinder and gentler than those with male names; the Rose that smells sweet.  At least, the authors' interpretation of their result is that when a female-named hurricane is barreling toward you, you may be tempted to stay home rather than evacuate, given that the storm is just a girl.  Or, if you expect that male-named hurricanes are more deadly, the treacherous Rosenkrantz to be suspected and feared, you either evacuate or you stay home, in the basement, with a helmet on, under a cover so you can pretend the monster isn't at your very door trying to huff and puff and blow your house down.

This paper is not being treated with much respect, and at least some critiques of the findings are over at Ed Yong's post about this story, and there are important issues about science communication and the respect that prominent scientific journals deserve, or not.  And, methodological issues as well.  These raise serious doubts about the validity, or at least the interpretability of the study, and about the journal's acceptance criteria (if the study's methods or conclusions were only marginally solid, it perhaps belonged in a supposedly lesser journal).  

However, our point here is different, and has to do with the many subtle ways in which exposures to all sorts of things epidemiologists or geneticists might never think of, much less be able to measure, could have major effects on our behavioral and physical traits.

What if this study is not poorly done and its reports have identified a real effect, and at least a handful of University of Illinois undergrads associate gender with relative danger--or power, or aggressivity, or some other trait that they associate with a hurricane's force?  Fear-by-name would be a cultural trait, and it might be very different in other age groups, or states, or other cultures--in matriarchal cultures, for example, the effect might be reversed.  This would be an instance of what is an undeniably real problem with many epidemiological studies--the problem of confounders, unmeasured variables that influence the outcome but whose effect is unseen because it's unconsidered, but that are actually causal. The identified cause could be so indirect in a multiplicity of ways, that it may be 'true' but basically uninterpretable in terms of what one might hope to find as the actual primary causes, or to determine whether there was or was not a causal link between the correlated risk factors.

Whether one accepts or questions the validity of this particular correlation study, how many other such kinds of subtle causation actually do affect our lives?  How many studies' interpretations such problems they undermine?  How can the outcomes be predicted in a sea of causes?

What's up, Doc?
The second story, old but good, is a commentary by a physician who's been around the block a few times, observing that older physicians are more likely to admit that neither they, nor anyone, understands biomedical causation as well as they like to claim.

Even as a med student, I was struck by the discrepancy between how much the junior doctors (particularly the interns and second-year residents) seemed to know, and how much the more experienced doctors knew: with few exceptions, the junior doctors seemed to know a lot more.

Students and young physicians have explanations for everything, and seem very confident about the extent and precision of knowledge about cause and treatment and so on.

In contrast, the expert physicians – the doctors who had spent decades of their lives treating particular types of patients, and studying a specific disease – tended to be far less definitive, and much more likely to say, “to tell you the truth, we really don’t know.”

One would expect, if science and experience in seeing purportedly causal symptoms and the effect of treatment are so fundamental, that senior physicians would be spot-on much more of the time than their greenhorn juniors.  They have had the experience by which to put two and two together, after all. Instead, at least the thoughtful and candid seniors have far less confidence than their younger upstarts. Why is this?

Holly Dunsworth reminded us the other day that there's a name for this phenomenon.  It's the Dunning-Kruger effect and Wikipedia describes it this way: "Unskilled individuals suffer from illusory superiority, mistakenly rating their ability much higher than is accurate. This bias is attributed to a metacognitive inability of the unskilled to recognize their ineptitude," citing a NYTimes piece about a bank robber who painted his face with lemon juice, under the misapprehension that it would make him invisible to surveillance cameras.  As David Dunning (he of the effect) read about this bank robber, who had been immediately caught from video tape pictures, he thought, if the guy "was too stupid to be a bank robber, perhaps he was also too stupid to know that he was too stupid to be a bank robber — that is, his stupidity protected him from an awareness of his own stupidity."

So, medical students don't know yet how much they don't know.  Further, young people are have just been taught courses by professors who don't get paid to teach what isn't known, but instead (especially, perhaps, in medical school) teach the truth--the symptoms and their causal results and the miracles of physicians' interventions.  They have a vade mecum drummed into their heads: a code book of diagnosis and treatment.  Indeed, the growth of HMO and computing power has to a great extent led to a hegemony that leads them to be trained not to use their individual judgment.

The young are also starting their careers, and they have the excited belief that they'll be implementing this crisp knowledge they've been taught.  Even if they go into academic research, careers are made by declaring what we know and don't know in confidently specific terms.  Give me a big grant and I'll answer this big question.  They are committed to the idea that questions, as they're often posed, actually have answers.  Doubt doesn't sell so there's no incentive to doubt a simple line.  Indeed, even some skilled individuals are trained to have the belief, if not illusion, of their superiority as experts, with degrees and salaries to match, and journalists hanging on their every word.

Both phenomena--the indirect effects of hurricane names and the over-confidence of those who don't take (or care not to take) what science tells us seriously enough, lead to expensive over-confidence in science and scientists, and not nearly enough humility in the face of the complexity that Nature throws at us.

Plant sociality and solidarity

Plants aren’t nearly as passive as their stationary state might lead one to think.  They have similar immune system needs to animals, because they are routinely attacked by hungry microbes and larger creatures intending to munch their way around a leaf.  And, like animals, they have ways of battling the ever-evolving attackers, that allow them to adapt to changing assailants.

We've blogged recently about how plants communicate through their roots and in other ways (here) and about how they may even be altruistic (here).  Here’s another interesting paper, in PNAS, about sophisticated responses and sociality among plants ("Intake and transformation to a glycoside of (Z)-3-hexenol from infested neighbors reveals a mode of plant odor reception and defense," Sugimoto et al.).  The authors report that tomato plants affected by cutworms produce a volatile chemical called Hex Vic ((Z)-3-Hexenylvicianoside) that diffuses through the air to neighboring plants.  When the neighbors detect this, they then express genes that produce a substance that makes them resistant to cutworm attack, as well as weakens the worm.

In response to herbivory, plants emit specific blends of volatiles. When undamaged plants are exposed to volatiles from neighboring herbivore-infested plants, they begin to defend against the impending infestation of herbivores. This so-called “plant–plant signaling” has been reported in several plant species. For example, a study on the expression profiles of defense-related genes when Arabidopsis was exposed toseveral volatiles, including green leaf volatiles and a monoterpene, showed that the manner of induction varied with the gene monitored or the volatile used, suggesting that the plant responses were specific to the individual volatile compound.

Unlike defenses against microbial infection, this is a mechanism related to a mega-scale predator, an animal that is too big for the plant easily to defend itself, unless it evolves some form of toxin to kill the worms.  

Here, one might speculate about why plants under attack would help other plants, rather than just do their best to beset the cutworms on their own. Normally, one would say they ‘should’ (from a Darwinian perspective) raise their defenses as best they can, but not tip-off their neighbors, and hence competitors of the danger.  Let them fend for themselves, and if they fail, the plant with the best defenses wins an evolutionary skirmish.

Micro Toms;  Wiki source

Of course if the neighbors are clones from the same artificial domestic strain, as these appear to be (the authors say they are Micro-Toms, a hybrid strain), the evolutionary issues are moot, since whatever led to the plants' behavior didn't occur in a field of clones.  So one wouldn't be able to say this evolved so they could help their close-kin neighbors in the usual sense.  But if natural tomato seed dispersal isn't distant, then nearby plants would be close relatives, and the kinship argument might work, that the attacked plant may be harmed or even doomed, but by warning its neighbors it’s warning its kin.

But, if natural tomato seed dispersal is distant, spread in the droppings of birds that ate the fruits, e.g., than the explanation must be something different.  And indeed, if the volatile emissions are detected by non-kin, plants of other species, as Sagimoto et al. seem to suggest, below, then the kinship explanation doesn't work at all.

Because (Z)-3-hexenol is a common volatile compound emitted by most herbivore-damaged plants, andbecause we found that a wide range of plant species could accumulate (Z)-3-hexenyl glycosides after exposure to volatiles, absorption and glycosylation of exogenous airborne (Z)-3-hexenol might be a general response in plants.

In any case, here we have yet another example of a more complex living world than traditional understanding of botany has generally allowed.  It's a reminder that we should curtail our hubris when it comes to assuming we higher animals do everything best.  

The visible colors: and the falseness of human races as natural categories

There is a constant tension between the tendencies to view the world in continuous vs discrete terms.  Even in science, this can be a problem, because a continuous view can lead to different interpretations than a discrete view.  Disputes about reality can arise, perhaps, over the distinction.  Is something a particle, or is it a wave?  Are the categories of a discrete view natural realities, or are they being imposed on Nature for some human reason?

The argument currently afoot has to do with how culpable it is to use genomic variation data to claim that there are a small number (usually stated as 5) major or primary human races, that blur at the intersections between them.  And, as commonly used software has it, those 'blurred' individuals are considered to be admixed between parents from the 'pure' races.

This is very misleading scientifically and, worse, unnecessarily so.  No analogy is perfect, but we can see the major issues using the example of color, which is often cited as comparable and showing the validity of the 'race' assertion (here, e.g.).  Color is the word we use for our sensory perceptions, the qualia, or psychological experience, by which we perceive light.  In physical terms, a given color is produced by light photons with a given energy level, with particular wavelengths or frequency (since light has a fixed speed, higher frequency means more waves pass by per second, and hence are shorter so they add up to the distance traveled in a second). From that point of view, here is the range of the colors to which the 'standard' human eye (that is, genotype) can respond, that is, a graphic portrayal of the wavelengths we detect:

The spectrum of visible light (wavelength in nanometers).  Wikimedia commons

The word 'color' refers to the qualia of perception, but we assign names to particular wavelengths, a cultural phenomenon based on our particular detection system. In those terms, visible light is a continuum of detectable wavelengths.  But traditionally, given that we are trichromat beings (with three distinct opsin genes, that is, whose three coded proteins each responds most efficiently to a different wavelength--see diagram below) we name three what we term 'primary' colors.  Each retinal 'cone' cell normally produces one of these opsin pigment proteins.  Each color of light that enters the eye triggers an appropriately weighted mix of red, green, and blue signals.  So for example pure
blue' frequency light basically only triggers a response from retinal cone cells that express the blue opsin gene product.

Basically, our ability to perceive any wavelength across the visible range is due to our brain's ability to mix the signal strength received from the retinal cells reporting its respective color activations. We often think of colors as being a mix of these primary colors, but there is nothing physically primary about them. They are artificial mark-points chosen by us because of our particular opsin repertoire.  One could choose other mark-points, and there need not be three (some species have fewer or more), and still perceive light in the entire visible (or even broader) wavelength range.  Various activities such as printing and the like have used different 'primary' colors (e.g., Google primary colors).   When we receive a mix of frequencies, our brain can sort out that mix and identify it.

What 'typical' human cone cells respond to.  Source: http://www.unm.edu/~toolson/human_cone_response.htm

In a sense, so long as you realize what is being done, there is no problem.  But if you think of the light-world as being inherently made of truly primary color categories, and of other colors as blurs in the edge of these categorical realities, then you are seriously misunderstanding the physical reality. First, the color spectrum reflects the color, as we perceive it, of single-wavelength radiation.  No individual wavelength is 'primary'.  Second, other colors are a mix of wavelengths that a trigger response by red, green, and blue opsins, and are synthesized (such as to be interpreted as 'pink') by the brain.

This is also a stereotype for two other reasons.  First, there is considerable variation among humans in the response characteristics of our opsins--the figure shows a typical response pattern for a reference blue, green, and red rhodopsin protein.  And of course a substantial fraction of people can't see some colors because they are missing one or more normally functioning opsin gene.  Secondly, the qualia, or what makes a given wavelength be experienced as 'blue,' is beyond current understanding, nor do we know that what you see as blue is the same as what I see as blue--even if we both have learned to call it 'blue'.  At present this is in the realm of philosophers, and causes a discussion--but no harm is done.

But that is not always the case.  Sometimes when falsely dividing a phenomenon into categories assumed to be true units rather than arbitrary reference points, with some rather unimportant blurs at the boundaries between the categories, the results of the error can be, literally, lethal.  This has been one consequence of the mis-use of theoretical misrepresentation of quantities as categories in human affairs.

Races are not like primary colors
We are writing this because there has been a recent resurrection of science that knowingly misrepresents the global distribution of human biological variation.  People are not photons, and we do not exist in 'primary' groups with blurred boundaries between them--any more than blue, red, and green are sacred and special points in the color spectrum.

We hear a lot of innocent-sounding talk about how one can argue for the existence of human 'races' as genetic, not just sociocultural, entities--but not be a 'racist'.  Yes, the argument goes, there is blurring at the edges, but the categories are real and they exist.

Human populations have long lived on different continents and some of our recent evolution as a species has taken place across great spans of distance, with geographic effects on the rates of gene flow over distance. Time and local geography, climate, culture, food sources, prey and predators and the like vary over space as well, and have in various ways led to adaptive differences among people, differently in different places.  Both cultural and genomic variation has accumulated around the globe.  But with few exceptions, such as truly isolated islands, genomic differences are correlated with geographic distance. 

Europe and Africa are not wholly discrete parts of the world.  The Americas may have been close to that, but only for about 10,000 or so years.  To assert that Europeans are genomically different from Africans, you must define what you mean by these categories.  Do you mean Italians are different from Egyptians?  Or do you mean Bantu speakers from South Africa are not the same as Norwegians?  This is important because with the same statistical methods of analysis, the same sorts of variation, if proportionately less in quantity, occur within these areas.  And had the analysis been done 1000 years ago, the major population of the world might be considered to be the Middle East, not Europe, because the decision of what are the major races, and what the admixed blurs would have been made by Islamic scholars, perhaps with some complaints by the high culture in India.   Choosing other populations as reference points ('parental' populations, or actual 'races')--Tahitians, Mongolians and South Indians, say, rather than the usual Africans, Europeans and Native Americans--would yield very different admixture statistics, because admixture programs are based on assumptions about history, not some inherent 'truth'.

So even those who want to stress differences, for whatever reasons, and who want to make assertions based on the several 'continents', themselves somewhat arbitrarily defined, have to be clear about what they are asserting--what they define as 'race', in particular.  This, of course, is made far more complicated by the 'admixture' that has occurred throughout known history of mass migration. Indeed, even the concept of 'admixture' itself requires specifying who is mixing with who--which in turn determines the outcome of admixture studies.

This sort of analysis has another aspect that is not properly understood.  The user chooses which and/or how many populations are considered parentals, of which other sampled individuals are admixed product.  These are statistical rather than history-based assumptions, using various sorts of significance criteria (which are subjective choices).  And, importantly, this type of analysis is based on alleles that were chosen for study because they are global--that is, the same variants are shared by the different  'races', just in different frequencies. Truly local variation is just that, local, so groups can't be compared in the same way.  Any sample you might choose to take will have lots of rare variants, found nowhere else.  So races in much if not most of the modern discussion, are groups defined in part because their frequencies of the same variants differ.  The genotypes in one 'race' can appear in others as well, but with lower probability.  If you want group-specific variants, you will usually find that they depend essentially on how you define the groups, and very rarely will everyone in a group that is more than very local have the purportedly characteristic variant.  A given genotype may be more likely in one pre-defined sample or group, but these are quantitative rather than qualitative differences largely based on local proximity.  Locally restricted variants can be important in adaptive traits, depending on the dynamics of history, and they can be exceedingly important, but they are generally far from characterizing everyone in a group or in defining groups.  People come into this world as discrete entities, but this is not how populations are generally constructed or evolve.

If we were talking about turtles or ostriches or oaks, nobody would care about these distinctions, even if there is absolutely no need to use such categories.  There are ways to represent human biological variation over space in more continuous terms, avoiding the obviously manifest problems with false, vague, or leaky categories of people, or making excuses for the 'blurring' at the edges, as if those blurred individuals were just no-accounts staggering around polluting the purity of our species!  Asserting the supposed reality of 'race', that is, of true categories on the ground rather than just in the mind, leads to all sorts of scientific problems and, of course, historically to the worst of human problems.

Does it make sense to ask whether members of 'the' European' race are taller than those in the African 'race'?  What part of Europe, and what part of Africa do you mean?  Ethiopia?  Nigeria?  Botswana?  Norway?  Greece? And does the person have to be living there now, or just have had all his/her ancestry from there?  And what about that 'his/her'?  Do we have to consider only living 'Africans' and 'Europeans', or can we use, say, skeletons from these 'races' from any time in the past (should be OK, if the trait is really 'genetic' since gene pools change slowly).  Or can we use Kazakhs or Saamis or Mbutis in our 'race' comparison?  Clearly we have to start refining our statements, and when that is the case even for societally rather neutral traits like stature, how much more careful need we be when we raise topics--as those who like to assert the reality of 'race' can't resist focusing on--with sociocultural or policy relevance (criminality, intelligence, addictability, reckless behavior, genes for ping-pong skill or running speed or being a violinist)?  Why do we need the categories, unless it really is a subterranean desire to focus on such traits to make a political point....or to affect policy?

At the same time, when scientists who think carefully and avoid this sort of categorical thinking, or even deny the reality of categories, or denigrate the idea that the categories are 'just' social constructs, they (the scientists) are denying what is an even greater reality.  That is that, for many people, 'race' is an entirely real category, one they experience on a daily basis.  If in the US you are 'black' or 'white' or 'Hispanic' or 'Asian' you are treated in a group-based way culturally.  If you have any phenotypically discernible African ancestry, for example, you may very well be treated as, and feel as if you were  'black', regardless of your ancestry fraction.  You may have some legal rights if you have at least 1/8 Native American ancestry, and for that and other reasons, you may know very well that 'race' does exist as a reality in your life.  This is inherently a sociocultural construct, and hence a reality.  In that very correct sense, the existence of 'race' is a scientific fact.

Scientists who acknowledge this but then continue to assert the genomic reality of race, essentially  because it is a convenient shorthand and because the bulk of data come from widely dispersed people, play into the hands of the ugliest aspects of human history, and given that history, which they know very well, they do so willingly.  Some even do it with great glee, knowing how it angers 'liberals'. One can speak of genetic (and cultural) variation having a geographic-historic origin that is (except for recent long-distance admixture) proportional to distance, and can think about local adaptations,  without using categorical race concepts.  Some may argue with what is genomic, what is the result of natural selection, and what is basically cultural. But there is no need to wallow in categories, and then  no need to try to define the 'fuzzy boundaries' between them.

Evolutionary genetic models as they are conventionally constructed contribute to the problem, because they are based on the frequency of genetic variants, and frequency is inherently a sample statistic. That is, frequencies are based on a population of inference, specified by the user.  A population is defined as if it had specific boundaries.  Natural selection is also modeled as if 'environments' were packaged in population-delimited ways.  For many reasons, it would be better if we developed less boxed-in evolutionary concepts and analysis, but that's not convenient if it takes time or means your book or grant can't just be dashed off without considering serious underlying issues like these, or if the hurried press likes to take whatever you say and make hay with it.

The use of 'primary' color category concepts is arbitrary relative to the actual color spectrum, but at least is based on our retinal genes, which in a natural way provide a convenient set of what are otherwise arbitrary physical reference points.  Nobody is disadvantaged by the use of those categories in human affairs.  But human populations are not in natural categories, categories are not needed, and they are not neutral relative to human affairs.

Like the light spectrum, there are not, and never have been 'primary' colors of humans.  What is true, however, is that when it comes to that topic, a lot of people cannot see the light.