It's no secret I love evolution.
But I usually feel like such an outsider when it comes both to how it's done professionally and in pop culture. I think it's my tendency to see proximate rather than ultimate causes and it's the ultimate causes that seduce and bedazzle. I've learned that if you question ultimate evolutionary narratives, you're a party pooper. I'm a party pooper.
Here I am
Typing to myself
I've got the outsider's blues
Let's start with some recent fish science. These guppies of the same species, born big and born little, have been very nicely shown to grow at the same pace. The big ones are born later and into a competitive food environment. Researchers offer that it's due to selection for context-dependent control over gestation length/birth timing. But why? What about a proximate view? Surely the mother's context and its impact on her biology and on her eggs and babies is important. There may be no need to imagine a fancy adaptation that switches birth timing so that babies are badass food competitors ... Like there is no need to imagine a fancy adaptation that switches birth timing so that human babies escape the birth canal in time.
And, also today, there's news of a conference paper on human inbreeding. Most everyone believes inbreeding is bad, especially evolutionary scientists, many of whom rely on it being bad to make sense of animal behavior through their own culturally-tinted, taboo-tainted goggles. It's also foundational to how many evolutionary scientists explain cooperation with non-kin and our taboos against inbreeding. The news report linked above describes an enormous study of parents, all over the world, who are cousins who produce children. There's a list of biological trends for the outcomes of inbreeding that are assumed to be less than ideal (e.g. these kids are 1 cm shorter than average and less than 1 kg lighter at birth) and it's explained by genetics, of combining genomes of close relatives. Included in these traits of interest is age at first sex (delayed in offspring of inbreeding), age at first birth (same), number of opposite-sex partners (fewer in the inbred), number of offspring (fewer begat by the inbred). Sooo, I trend with the inbred. Am I inbred? No. To me, these trends don't scream bad genes from naughty parents. These outcomes look like they'd be influenced pretty heavily by complex cultural conditions and socioeconomic status, which may be intimately linked with conditions that pair-up cousins in the first place. Did these factors enter into the analysis? We'll have to wait and see when the paper's published.
And another news item today has me kicking a can out here. What if, rather than it being due to a fancy adaptation to seasonal fluctuation in resources, shrews' skulls shrink over winter as they experience the pressure and temperature of hard, cold dirt?
For some reason today--and maybe it's because my life writ-large lacks much opportunity to hold these discussions with people in real life, and my life writ-small has me pulled hard away from learning and doing evolution, period--I'm feeling nostalgic. The guppies, the inbreeding, and the shrew skulls awoke some ghosts of my past...
What if perpetual evolution due to mutation* causes speciation, rather than natural selection?
There's no way that everything that differs between males and females is explained by sexual selection. So what if body size and strength differences are a bigger story than that?
In that vein, what if women are smart BECAUSE HUMANS ARE SMART, and not to outfox rapists?
What if man's big penis is due to man's big vagina and not so much due to survival of the biggest?
What if the same mutation in multiple individuals can be induced by a virus? That kind of head start would seem to make it much easier for a mutation to go to fixation whether due to drift or selection.
I'm more similar, genetically, than 50% to my mom, to you, and to every single person on this planet. So what are we actually supposed to learn from all these fancy evolutionary equations that insist I'm only 50% similar to my parents, and less and less similar to everyone else, including you, in the tree?
And, I realize this may sound silly and obvious, but animals don't know where babies come from. Given the words we use, reading about the evolution of animal behavior is so confusing, in this light.
To those who get it
To evolution's outsiders
Do you wanna form a band?
* (and, in the myriad species who have it, the coin-flip of extinction or inheritance for each part of the genome, known as recombination and segregation during the halving of the genome during sperm and egg production)
Tuesday, October 24, 2017
Sunday, October 15, 2017
Understanding Obesity? Fat Chance!
Obesity is one of our more widespread and serious health-threatening traits. Many large-scale mapping as well as extensive environmental/behavioral epidemiological studies of obesity have been done over recent decades. But if anything, the obesity epidemic seems to be getting worse.
There's deep meaning in that last sentence: the prevalence of obesity is changing rapidly. This is being documented globally, and happening rapidly before our eyes. Perhaps the most obvious implication is that this serious problem is not due to genetics! That is, it is not due to genotypes that in themselves make you obese. Although everyone's genotype is different, the changes are happening during lifetimes, so we can't attribute it to the different details of each generation's genotypes or their evolution over time. Instead, the trend is clearly due to lifestyle changes during lifetimes.
Of course, if you see everything through gene-colored lenses, you might argue (as people have) that sure, it's lifestyles, but only some key nutrient-responding genes are responsible for the surge in obesity. These are the 'druggable' targets that we ought to be finding, and it should be rather easy since the change is so rapid that the genes must be few, so that even if we can't rein in McD and KFC toxicity, or passive TV-addiction, we can at least medicate the result. That was always, at best, wishful thinking, and at worst, rationalization for funding Big Data studies. Such a simple explanation would be good for KFC, and an income flood for BigPharma, the GWAS industry, DNA sequencer makers, and more.....except not so good for those paying the medical price, and those who are trying to think about the problem in a disinterested scientific way. Unfortunately, even when it is entirely sincere, that convenient hope for a simple genetic cause is being shown to be false.
A serious parody?
Year by year, more factors are identified that, by statistical association at least and sometimes by experimental testing, contribute to obesity. A very fine review of this subject has appeared in the mid-October 201 Nature Reviews Genetics, by Ghosh and Bouchard, which takes seriously not just genetics but all the plausible causes of obesity, including behavior and environment, and their relationships as best we know them, and outlines the current state of knowledge.
Ghosh and Bouchard provide a well-caveated assessment of these various threads of evidence now in hand, and though they do end up with the pro forma plea for yet more funding to identify yet more details, they provide a clear picture that a serious reader can take seriously on its own merits. However, we think that the proper message is not the usual one. It is that we need to rethink what we've been investing so heavily on.
To their great credit, the authors melded behavioral, environmental, and genetic causation in their analysis. This is shown in this figure, from their summary; it is probably the best current causal map of obesity based on the studies the authors included in their analysis:
If this diagram were being discussed by John Cleese on Monty Python, we'd roar with laughter at what was an obvious parody of science. But nobody's laughing and this isn't a parody! And it is by no means of unusual shape and complexity. Diagrams like this (but with little if any environmental component) have been produced by analyzing gene expression patterns even just of the early development of the simple sea urchin. But we seem not to be laughing, which is understandable because they're serious diagrams. On the other hand, we don't seem to be reacting other than by saying we need more of the same. I think that is rather weird, for scientists, whose job it is to understand, not just list, the nature of Nature.
We said at the outset of this post that 'the obesity epidemic seems to be getting worse'. There's a deep message there, but one essentially missing even from this careful obesity paper: it is that many of the causal factors, including genetic variants, are changing before our eyes. The frequency of genetic variants changes from population to population and generation to generation, so that all samples will look different. And, mutations happen in every meiosis, adding new variants to a population every time a baby is born. The results of many studies, as reflected in the current summary by Ghosh and Bouchard, show the many gene regions that contribute to obesity, their total net contribution is still minor. It is possible, though perhaps very difficult to demonstrate, that an individual site might account more than minimally for some individual carriers in ways GWAS results can't really identify. And the authors do cite published opinions that claim a higher efficacy of GWAS relative to obesity than we think is seriously defensible; but even if we're wrong, causation is very complex as the figure shows.
The individual genomic variants will vary in their presence or absence or frequency or average effect among studies, not to mention populations. In addition, most contributing genetic variants are too rare or weak to be detected by the methods used in mapping studies, because of the constraints on statistical significance criteria, which is why so much of the trait's heritability in GWAS is typically unaccounted for by mapping. These aspects and their details will differ greatly among samples and studies.
Relevant risk factors will come or go or change in exposure levels in the future--but these cannot be predicted, not even in principle. Their interactions and contributions are also manifestly context-specific, as secular trends clearly show. Even with the set of known genetic variants and other contributing factors, there are essentially an unmanageable number of possible combinations, so that each person is genetically and environmentally unique, and the complex combinations of future individuals are not predictable.
Risk assessment is essentially based on replicability, which in a sense is why statistical testing can be used (on which these sorts of results heavily rely). However, because these risk factor combinations are each unique they're not replicable. At best, as some advocate, the individual effects are additive so that if we just measure each in some individual add up each factor's effect, and predict the person's obesity (if the effects are not additive, this won't work). We can probably predict, if perhaps not control, at least some of the major risk factors (people will still down pizzas or fried chicken while sitting in front of a TV). But even the known genetic factors in total only account for a small percentage of the trait's variance (the authors' Table 2), though the paper cites more optimistic authors.
The result of these indisputable facts is that as long as our eyes are focused, for research strategic reasons or lack of better ideas, on the litter of countless minor factors, even those we can identify, we have a fat chance of really addressing the problem this way.
If you pick any of the arrows (links) in this diagram, you can ask how strong or necessary that link is, how much it may vary among samples or depend on the European nature of the data used here, or to what extent even its identification could be a sampling or statistical artifact. Links like 'smoking' or 'medication', not to mention specific genes, even if they're wholly correct, surely have quantitative effects that vary among people even within the sample, and the effect sizes probably often have very large variance. Many exposures are notoriously inaccurately reported or measured, or change in unmeasured ways. Some are quite vague, like 'lifestyle', 'eating behavior', and many others--both hard to define and hard to assess with knowable precision, much less predictability. Whether their various many effects are additive or have more complex interaction is another issue, and the connectivity diagram may be tentative in many places. Maybe--probably?--in such traits simple behavioral changes would over-ride most of these behavioral factors, leaving those persons for whom obesity really is due to their genotype, which would then be amenable to gene-focused approaches.
If this is a friable diagram, that is, if the items, strengths, connections and so on are highly changeable, even if through no fault of the authors whatever, we can ask when and where and how this complex map is actually useful, no matter how carefully it was assembled. Indeed, even if this is a rigidly accurate diagram for the samples used, how applicable is it to other samples or to the future?Or how useful is it in predicting not just group patterns, but individual risk?
Our personal view is that the rather ritual plea for more and more and bigger and bigger statistical association studies is misplaced, and, in truth, a way of maintaining funding and the status quo, something we've written much about--the sociopolitical economics of science today. With obesity rising at a continuing rate and about a third of the US population recently reported as obese, we know that the future health care costs for the consequences will dwarf even the mega-scale genome mapping on which so much is currently being spent, if not largely wasted. We know how to prevent much or most obesity in behavioral terms, and we think it is entirely fair to ask why we still pour resources into genetic mapping of this particular problem.
There are many papers on other complex traits that might seem to be simple like stature and blood pressure, not to mention more mysterious ones like schizophrenia or intelligence, in which hundreds of genomewide sites are implicated, strewn across the genome. Different studies find different sites, and in most cases most of the heritability is not accounted for, meaning that many more sites are at work (and this doesn't include environmental effects). In many instances, even the trait's definition itself may be comparably vague, or may change over time. This is a landscape 'shape' in which every detail is different, within and between traits, but is found in common with complex traits. That in itself is a tipoff that there is something consistent about these landscapes but we've not yet really awakened to it or learned how to approach it.
Rather than being skeptical about these Ghosh and Bouchard's' careful analysis or their underlying findings, I think we should accept their general nature, even if the details in any given study or analysis may not individually be so rigid and replicable, and ask: OK, this is the landscape--what do we do now?
Is there a different way to think about biological causation? If not, what is the use or point of this kind of complexity enumeration, in which every person is different and the risks for the future may not be those estimated from past data to produce figures like the one above? The rapid change in prevalence shows how unreliable these factors must be, at prediction--they are retrospective of the particular patterns of the study subjects. Since we cannot predict the strengths or even presence of these or other new factors, what should we do? How can we rethink the problem?
These are the harder question, much harder than analyzing the data; but they are in our view the real scientific questions that need to be asked.
There's deep meaning in that last sentence: the prevalence of obesity is changing rapidly. This is being documented globally, and happening rapidly before our eyes. Perhaps the most obvious implication is that this serious problem is not due to genetics! That is, it is not due to genotypes that in themselves make you obese. Although everyone's genotype is different, the changes are happening during lifetimes, so we can't attribute it to the different details of each generation's genotypes or their evolution over time. Instead, the trend is clearly due to lifestyle changes during lifetimes.
Of course, if you see everything through gene-colored lenses, you might argue (as people have) that sure, it's lifestyles, but only some key nutrient-responding genes are responsible for the surge in obesity. These are the 'druggable' targets that we ought to be finding, and it should be rather easy since the change is so rapid that the genes must be few, so that even if we can't rein in McD and KFC toxicity, or passive TV-addiction, we can at least medicate the result. That was always, at best, wishful thinking, and at worst, rationalization for funding Big Data studies. Such a simple explanation would be good for KFC, and an income flood for BigPharma, the GWAS industry, DNA sequencer makers, and more.....except not so good for those paying the medical price, and those who are trying to think about the problem in a disinterested scientific way. Unfortunately, even when it is entirely sincere, that convenient hope for a simple genetic cause is being shown to be false.
A serious parody?
Year by year, more factors are identified that, by statistical association at least and sometimes by experimental testing, contribute to obesity. A very fine review of this subject has appeared in the mid-October 201 Nature Reviews Genetics, by Ghosh and Bouchard, which takes seriously not just genetics but all the plausible causes of obesity, including behavior and environment, and their relationships as best we know them, and outlines the current state of knowledge.
Ghosh and Bouchard provide a well-caveated assessment of these various threads of evidence now in hand, and though they do end up with the pro forma plea for yet more funding to identify yet more details, they provide a clear picture that a serious reader can take seriously on its own merits. However, we think that the proper message is not the usual one. It is that we need to rethink what we've been investing so heavily on.
To their great credit, the authors melded behavioral, environmental, and genetic causation in their analysis. This is shown in this figure, from their summary; it is probably the best current causal map of obesity based on the studies the authors included in their analysis:
If this diagram were being discussed by John Cleese on Monty Python, we'd roar with laughter at what was an obvious parody of science. But nobody's laughing and this isn't a parody! And it is by no means of unusual shape and complexity. Diagrams like this (but with little if any environmental component) have been produced by analyzing gene expression patterns even just of the early development of the simple sea urchin. But we seem not to be laughing, which is understandable because they're serious diagrams. On the other hand, we don't seem to be reacting other than by saying we need more of the same. I think that is rather weird, for scientists, whose job it is to understand, not just list, the nature of Nature.
We said at the outset of this post that 'the obesity epidemic seems to be getting worse'. There's a deep message there, but one essentially missing even from this careful obesity paper: it is that many of the causal factors, including genetic variants, are changing before our eyes. The frequency of genetic variants changes from population to population and generation to generation, so that all samples will look different. And, mutations happen in every meiosis, adding new variants to a population every time a baby is born. The results of many studies, as reflected in the current summary by Ghosh and Bouchard, show the many gene regions that contribute to obesity, their total net contribution is still minor. It is possible, though perhaps very difficult to demonstrate, that an individual site might account more than minimally for some individual carriers in ways GWAS results can't really identify. And the authors do cite published opinions that claim a higher efficacy of GWAS relative to obesity than we think is seriously defensible; but even if we're wrong, causation is very complex as the figure shows.
The individual genomic variants will vary in their presence or absence or frequency or average effect among studies, not to mention populations. In addition, most contributing genetic variants are too rare or weak to be detected by the methods used in mapping studies, because of the constraints on statistical significance criteria, which is why so much of the trait's heritability in GWAS is typically unaccounted for by mapping. These aspects and their details will differ greatly among samples and studies.
Relevant risk factors will come or go or change in exposure levels in the future--but these cannot be predicted, not even in principle. Their interactions and contributions are also manifestly context-specific, as secular trends clearly show. Even with the set of known genetic variants and other contributing factors, there are essentially an unmanageable number of possible combinations, so that each person is genetically and environmentally unique, and the complex combinations of future individuals are not predictable.
Risk assessment is essentially based on replicability, which in a sense is why statistical testing can be used (on which these sorts of results heavily rely). However, because these risk factor combinations are each unique they're not replicable. At best, as some advocate, the individual effects are additive so that if we just measure each in some individual add up each factor's effect, and predict the person's obesity (if the effects are not additive, this won't work). We can probably predict, if perhaps not control, at least some of the major risk factors (people will still down pizzas or fried chicken while sitting in front of a TV). But even the known genetic factors in total only account for a small percentage of the trait's variance (the authors' Table 2), though the paper cites more optimistic authors.
The result of these indisputable facts is that as long as our eyes are focused, for research strategic reasons or lack of better ideas, on the litter of countless minor factors, even those we can identify, we have a fat chance of really addressing the problem this way.
If you pick any of the arrows (links) in this diagram, you can ask how strong or necessary that link is, how much it may vary among samples or depend on the European nature of the data used here, or to what extent even its identification could be a sampling or statistical artifact. Links like 'smoking' or 'medication', not to mention specific genes, even if they're wholly correct, surely have quantitative effects that vary among people even within the sample, and the effect sizes probably often have very large variance. Many exposures are notoriously inaccurately reported or measured, or change in unmeasured ways. Some are quite vague, like 'lifestyle', 'eating behavior', and many others--both hard to define and hard to assess with knowable precision, much less predictability. Whether their various many effects are additive or have more complex interaction is another issue, and the connectivity diagram may be tentative in many places. Maybe--probably?--in such traits simple behavioral changes would over-ride most of these behavioral factors, leaving those persons for whom obesity really is due to their genotype, which would then be amenable to gene-focused approaches.
If this is a friable diagram, that is, if the items, strengths, connections and so on are highly changeable, even if through no fault of the authors whatever, we can ask when and where and how this complex map is actually useful, no matter how carefully it was assembled. Indeed, even if this is a rigidly accurate diagram for the samples used, how applicable is it to other samples or to the future?Or how useful is it in predicting not just group patterns, but individual risk?
Our personal view is that the rather ritual plea for more and more and bigger and bigger statistical association studies is misplaced, and, in truth, a way of maintaining funding and the status quo, something we've written much about--the sociopolitical economics of science today. With obesity rising at a continuing rate and about a third of the US population recently reported as obese, we know that the future health care costs for the consequences will dwarf even the mega-scale genome mapping on which so much is currently being spent, if not largely wasted. We know how to prevent much or most obesity in behavioral terms, and we think it is entirely fair to ask why we still pour resources into genetic mapping of this particular problem.
There are many papers on other complex traits that might seem to be simple like stature and blood pressure, not to mention more mysterious ones like schizophrenia or intelligence, in which hundreds of genomewide sites are implicated, strewn across the genome. Different studies find different sites, and in most cases most of the heritability is not accounted for, meaning that many more sites are at work (and this doesn't include environmental effects). In many instances, even the trait's definition itself may be comparably vague, or may change over time. This is a landscape 'shape' in which every detail is different, within and between traits, but is found in common with complex traits. That in itself is a tipoff that there is something consistent about these landscapes but we've not yet really awakened to it or learned how to approach it.
Rather than being skeptical about these Ghosh and Bouchard's' careful analysis or their underlying findings, I think we should accept their general nature, even if the details in any given study or analysis may not individually be so rigid and replicable, and ask: OK, this is the landscape--what do we do now?
These are the harder question, much harder than analyzing the data; but they are in our view the real scientific questions that need to be asked.
Tuesday, October 10, 2017
An article in Issues in Science and Technology
Regular MT readers will know that some of us here have a very skeptical view of the obsession with genomewide association mapping (GWAS) for every trait under the sun. We think that mapping served a purpose once upon a time, to show that complex apparently polygenic traits really were complex and polygenic. Identifying many contributing genome regions showed that, and that each individual has a unique genotype and that many or most relevant variants were too rare or their effects too weak to be detected (most heritability wasn't accounted for by the mapping). When tens, hundreds, or even thousands (yes!) of genome sites were claimed to contribute, it has seemed we're lost in never-never land when it comes to sensible explanations of causation.
But the funding keeps flowing for this mostly useless sort of Big Data (sorry, we can't salivate over that phrase the way so many do, because we're no longer out hunting for Big Grants). Our view, expressed many times and in many ways here, is that we need better ideas about the relationships between genes and health, and between genes and our traits and their evolution.
We've written about this in the past, but rather than do that again, I've written some of these issues in a somewhat different way in a new paper. That paper, in the new, Fall 2017, Issues in Science and Technology, "Is precision medicine possible?", lays out some thoughts about genetic causal complexity vis-à-vis 'precision' genomic medicine, and the challenges we face.
Rather than rehashing here what you can see in that article, if you're interested, just go to the article. It's in a journal related to policy, but the odds that any policymaker will read it carefully much less do anything constructive in response are between slim and none. Still, blogs are for stating a point of view!
The people whose truly genetic disorders are not being alleviated because we're dumping so much resource into stale ideas are being shortchanged. However, until we've made the alternative investment, in attack rather than 'mapping' disease, we'll not know how preventable or treatable they may be.
But the funding keeps flowing for this mostly useless sort of Big Data (sorry, we can't salivate over that phrase the way so many do, because we're no longer out hunting for Big Grants). Our view, expressed many times and in many ways here, is that we need better ideas about the relationships between genes and health, and between genes and our traits and their evolution.
We've written about this in the past, but rather than do that again, I've written some of these issues in a somewhat different way in a new paper. That paper, in the new, Fall 2017, Issues in Science and Technology, "Is precision medicine possible?", lays out some thoughts about genetic causal complexity vis-à-vis 'precision' genomic medicine, and the challenges we face.
Rather than rehashing here what you can see in that article, if you're interested, just go to the article. It's in a journal related to policy, but the odds that any policymaker will read it carefully much less do anything constructive in response are between slim and none. Still, blogs are for stating a point of view!
The people whose truly genetic disorders are not being alleviated because we're dumping so much resource into stale ideas are being shortchanged. However, until we've made the alternative investment, in attack rather than 'mapping' disease, we'll not know how preventable or treatable they may be.
Friday, August 18, 2017
This year's (2017) textbook-free Introduction to Human Origins and Evolution
This is a tradition now. You can search the archives for previous years' and for my philosophy behind this course. It's always evolving.
As usual there is no textbook. Students only need to get the much-loved book by Alice Roberts, The Incredible Unlikeliness of Being ("IUB"), and read it all along with many other articles as you'll see below.
This year I was happy to see a study supporting my own practice which I take to be common sense--that we should teach genetics before evolutionary theory for explaining how it works (e.g. its mechanisms): http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2002255
I haven't looked in a while, but teaching genetics before the mechanisms of evolution is not the approach of a single one of the textbooks for this course and that's one of the many reasons I stopped using them!
So, minus the in-class handouts and worksheets, here are the daily portfolio assignments for the newest incarnation of my big introductory, general education course on human evolution. As usual, I apologize for the formatting issues caused by pasting from a Word Document into this blog. It's all yours if you want it....
1. Observe and Explain - This view of life. Our place in nature
Big Questions: What is the anthropological perspective? What is the scientific approach to understanding human origins? What is a human? How do humans fit on the Tree of Life?
2. Explain and Predict - Explaining
the similarities and differences. How evolution works.
As usual there is no textbook. Students only need to get the much-loved book by Alice Roberts, The Incredible Unlikeliness of Being ("IUB"), and read it all along with many other articles as you'll see below.
This year I was happy to see a study supporting my own practice which I take to be common sense--that we should teach genetics before evolutionary theory for explaining how it works (e.g. its mechanisms): http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2002255
I haven't looked in a while, but teaching genetics before the mechanisms of evolution is not the approach of a single one of the textbooks for this course and that's one of the many reasons I stopped using them!
So, minus the in-class handouts and worksheets, here are the daily portfolio assignments for the newest incarnation of my big introductory, general education course on human evolution. As usual, I apologize for the formatting issues caused by pasting from a Word Document into this blog. It's all yours if you want it....
Fall 2017
APG 201: Human Origins and Evolution
3 credits
Dr. Holly Dunsworth
1. Observe and Explain - This view of life. Our place in nature
Big Questions: What is the anthropological perspective? What is the scientific approach to understanding human origins? What is a human? How do humans fit on the Tree of Life?
1.1 - Introduction to course
Assigned Reading/viewing
What is it like to be a biological
anthropologist? A Field Paleontologist's Point of View – Su (Nature Education)
Notes from the Field: A Primatologist's Point of
View – Morgan (Nature Education)
Expedition Rusinga (video; 8 min) https://www.youtube.com/watch?v=4y1puNyB9e8
The ape in the trees – Dunsworth (The Mermaid’s
Tale)
How Do We Know When Our Ancestors Lost Their
Tails? (video; 4 min)
Prompt: This is an
in-class prompt that you will be given in class.
[TRANSCRIBE YOUR ANSWER TO THE IN-CLASS PROMPT
HERE.]
1.2 - Do animals know where babies come from?
Assigned Reading/viewing
“Do animals know where babies come from?” by H.
Dunsworth (Scientific American)- Located
on Sakai, and linked here:
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
[WRITE YOUR ANSWER HERE, AND SO ON AND SO FORTH
FOR ALL BELOW…]
1.3 - Scientific process
Assigned Reading/viewing
IUB, Chapter 1: Beginnings - Roberts
How Science Works (video; 10 min):
Understanding science: How Science Works, pages
1-21; starts here:
Carl Sagan’s Rules for Critical Thinking and
Nonsense Detection
10 Scientific Ideas That Scientists Wish You
Would Stop Misusing
Prompt 1: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t. What do you expect to
learn from the rest of the book?
Prompt 2: This has two
parts, A and B. First, choose one
of the following well-known and established observations. Indicate your choice
by highlighting it.
- Children from low income homes show evidence of malnutrition.
- In most humans, the right humerus (upper arm bone) is larger than the left one.
- Pregnant mothers who smoke tend to have smaller babies than mothers who do not smoke.
- Chimpanzees living in zoos tend to be overweight compared to their relatives living in the wild.
A. Without using anything but your own mind, come up with
two different hypotheses to explain that one observation.
B. Briefly describe how you would test these hypotheses
you have offered. Include discussion of the methods and variables for
obtaining evidence and the kinds of evidence that you would need
to find to both refute and to support each hypothesis.
1.4 - Linnaeus
and the Order Primates
Assigned Reading/viewing
Characteristics of Crown Primates – Kirk (Nature
Education)
Prompt: Answer the following questions (complete sentences are
not necessary) by sticking to the reading above and these excellent resources:
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/
1.
My primate is a(n) [will be assigned to you in class]
2.
What is the species?
3.
Here is a link to a video of this species:
4.
Where does it live on Earth?
5.
What is the range of its habitat? Describe the nature of the
habitat.
6.
Is your primate nocturnal, diurnal, or crepuscular?
7.
What does it eat?
8.
How does it move about?
9.
How does it socialize? (i.e. solitary? groups?...)
10.
How does it raise offspring? (i.e. solitary? groups?...)
11.
Body size (both kg/g and lb/oz)? Are male and female
different?
12.
Coloration?
13.
What are its predators?
14.
Is it protected or endangered?
15.
Anything else fascinating about it?
16.
At what point in the past (millions of years ago) did it share
a most recent (aka “last”) common ancestor with humans? (go to www.timetree.org to find out)
1.5 - Overview
of Primate taxonomy
Assigned Reading/viewing
Many primate video clips –Posted on Sakai
Additional resources
Old World monkeys – Lawrence and Cords (Nature
Education)
Prompt: In 200 words or more, write about your primate video
viewing experience, for example, you might write about what you saw, at face
value, or you might want to write about what defied your expectations or what
surprised you, or what you would like to learn more about.
Prompt: Without looking at any resources except for these
films, come up with some categories for the different types of primate
locomotion, give those categories names and definitions, and list which species
in the films fall into which categories you’ve created.
1.6 -
Assigned Reading/viewing
IUB, Chapter 2:
Heads and brains – Roberts
Additional resources
Primate locomotion – Gebo (Nature Education)
Our Fishy Brain (video; 2.5 mins) http://video.pbs.org/video/2365207797/
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
[Prompt for practice: Label all the
bones that you can on the human skeleton. No need to demonstrate it here. Print
out an image and draw on it, but no need
to scan into your portfolio (let’s keep this low tech, I trust you!). If you
cannot name them all using only your memory, use a quality on-line resource
(like https://askabiologist.asu.edu/bone-anatomy) to help you. (Do not concern
yourself with the location of the individual carpals and tarsals but point out
where the carpals and tarsals are.) ]
[Prompt for practice: Go to http://www.eskeletons.org/ and based on what you see, draw the os coxa (half of the
pelvis) of a chimpanzee and a human. (Same as before, do on your own, no need
to include here… let’s keep it low tech.)]
Prompt: Describe the similarities and differences in anatomy between
chimp and human pelves/pelvises (do not worry about applying technical jargon).
What kinds of behavioral differences might correlate with the anatomical
differences in the pelvis and why?
[Prompt for practice: Go to http://www.eskeletons.org/ and based on what you see, draw the skull (including teeth) of a
chimpanzee and a human(Same as before, do on your own, no need to include here…
let’s keep it low tech.).]
Prompt: Describe the similarities and differences in anatomy between
chimp and human skulls and teeth (do not worry about applying technical jargon.
What kinds of behavioral differences might correlate with the anatomical
differences in skulls and teeth and why?
1.7 - continued
Assigned Reading/viewing
IUB, Chapter 3:
Skulls and senses – Roberts
Additional resources
Finding the Origins of Human Color Vision
(video; 5 mins) http://video.pbs.org/video/2365207765/
We Hear with the Bones that Reptiles Eat With
(video; 4 mins) http://video.pbs.org/video/2365207244/
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
1.8 - Primate encephalization, tool use and communication
Assigned Reading/viewing
IUB, Chapter 4:
Speech and gills - Roberts
Additional resources
Primate Communication – Zuberbuhler (Nature Ed)
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
1.9 - Primate sociality
Assigned Reading/viewing
The Human Spark 2: So Human So Chimp – PBS,
hosted by Alan Alda (video; 55 mins IF
LINK IS BROKEN JUST SEARCH FOR IT)
Additional resources
What Influences the Size of Groups in Which
Primates Choose to Live? – Chapman & Teichroeb (Nature Ed)
Primate Sociality and Social Systems – Swedell
(Nature Ed)
Primates in communities – Lambert (Nature Ed)
Prompt: In 200 words or more, react to The Human Spark 2,
highlighting something you already knew and also something you learned that was
brand new to you. What is the human spark?
1.10 - Evolution (shared ancestry over deep time) and Darwin's evidence for it
Assigned Reading/viewing
Two chapters from The Autobiography of Charles Darwin: "Voyage…" (p. 71-81
) and "An account of how several books arose" (p. 116- 135) http://darwin-online.org.uk/content/frameset?viewtype=text&itemID=F1497&pageseq=1
Additional resources
Amazing Places, Amazing Fossils: Tiktaalik
(video; 5 mins) https://www.youtube.com/watch?v=T2vKlEUX7DI
The Ancient History of the Human Hand (video; 4
mins) https://www.youtube.com/watch?v=RUL8hKDdY84
Prompt: In 200 words or more, according to your impression of
Darwin’s writings, reflect on the circumstances or experiences that influenced
Darwin's thinking.
1.11 - Phylogeny
Assigned Reading/viewing
Reading a phylogenetic tree – Baum (Nature Ed)
Trait Evolution on a Phylogenetic Tree – Baum
(Nature Ed)
Prompt: How could someone falsify the accepted fact of
evolution? Remember, for something to exist within the realm of that which is
knowable via science, there must be a hypothetical way to falsify it.
**
2. Explain and Predict - Explaining
the similarities and differences. How evolution works.
Big Questions: Why are we like our parents but not exactly? Why are we like other species but not exactly? How did human traits and human variation evolve? How do we know what the last common ancestor (LCA) was like?
2.1 - How eggs and sperm get made and how they make you
Assigned Reading/viewing
IUB, Chapter 5:
Spine and segments – Roberts
Additional resources
Gregor Mendel and the Principles of Inheritance
– Miko (Nature Ed)
Mendelian Genetics: Patterns of Inheritance and
Single-Gene Disorders – Chial (Nature Ed)
Developing the Chromosome Theory – O’Connor
(Nature Ed)
Genetic Recombination – Clancy (Nature Ed)
What is a Gene? Colinearity and Transcription
Units – Pray (Nature Ed)
RNA functions – Clancy (Nature Ed)
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
2.2 - continued
Assigned Reading/viewing
Things Genes Can’t Do – Weiss and Buchanan
(Aeon)
Additional resources
Phenotypic Range of Gene Expression:
Environmental Influence – Lobo & Shaw (Nature Ed)
Genetic Dominance: Genotype-Phenotype
Relationships – Miko (Nature Ed)
Pleiotropy: One Gene Can Affect Multiple Traits
– Lobo (Nature Ed)
Polygenic Inheritance and Gene Mapping – Chial
(Nature Ed)
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t. Why is it important to
consider what genes can and cannot do?
2.3 - Inheritance, gene expression, Mendel's simplicity and reality’s
complexity
Reading/viewing
IUB, Chapter 6: Ribs, lungs and hearts– Roberts
Additional resources
Hox Genes in Development: The Hox Code – Myers
(Nature Ed)
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
2.4 - Mutation and gene flow
Assigned reading/viewing
Evolution is the only natural explanation –
Dunsworth (The Mermaid’s Tale)
The F-words of Evolution – Dunsworth (The Mermaid’s Tale)
Another F-word of evolution – Dunsworth (The Mermaid’s Tale)
Additional resources
Evolution Is Change in the Inherited Traits of a
Population through Successive Generations – Forbes and Krimmel (Nature Ed)
Mutations Are the Raw Materials of Evolution –
Carlin (Nature Ed)
Mutation not natural selection drives evolution
– Tarlach (about Nei; Discover Magazine)
Prompt: Reflect back on your answer to “what is evolution”
from Day 1.1 of class. What did you get right? What did you get wrong? What did
you omit? How do the three assigned readings shape your view of evolution? What
are you still left wondering about evolution?
2.5 - Natural selection
Assigned Reading/viewing
none
Additional Resources
Natural selection, genetic drift and gene flow
do not act in isolation in natural populations – Andrews (Nature Ed)
Sexual selection – Brennan (Nature Ed)
Prompt: Write an answer for each of the
questions below. In other words, come up with a hypothesis to explain the
evolution of each of the four phenomena. These are evolutionary scenarios that
you are writing. This is brainstorming,
so have no fear, but you should still write with clarity.
1.
How did the mandrill get that colorful face? What about the
rear?
2.
How did the colobus monkey get a long, specialized gut?
3.
How did silverback gorillas become twice as big as females?
4.
How did humans become “naked”? (i.e. how
did we cease to be as furry as the other primates)?
2.6 - Genetic drift
Assigned Reading/viewing
The Evolution of Your Teeth (video; 3 mins) https://www.youtube.com/watch?v=ohq3CoOKEoo
Additional Resources
Neutral Theory: The null hypothesis of molecular
evolution – Duret (Nature Ed)
Negative selection – Loewe (Nature Ed)
On the mythology of natural selection. Part I:
Introduction – Weiss (The Mermaid’s Tale)
On the mythology of natural selection. Part II:
Classical Darwinism– Weiss (The Mermaid’s Tale)
Secrets of Charles Darwin’s Breakthrough - Bauer (Salon)
Prompt:
Read on and answer questions when asked (A and B):
Remember…
•
Most
of us were taught incorrectly or led, wrongly, to believe that ‘evolution’ =
‘natural selection’ and that all evolution occurs through natural selection.
This leads us to see every evolutionary scenario, all the way from fairy tale
ones to the most scientifically legitimate ones, as natural selection. This is,
of course, not a correct understanding of evolution.
•
Natural
selection can result in new adaptations or in the elimination of bad traits.
The former is “positive” selection, the latter is “negative” and is always
occurring no matter what. Positive selection does happen but is not easy to
test, since natural selection occurs via differential reproductive success, but
“survival of the luckiest” alleles via genetic drift can look exactly the same
by increasing and decreasing allele frequencies just by chance. The difference
between the two is that, in a selection scenario, the trait that’s evolving is causing the differential
reproduction (whether enhancing or inhibiting, even if ever so slightly
affecting it slowly over time), but in a genetic drift scenario the trait is
randomly “drifting” to lower or higher frequencies merely due to chance
(unlinked to the trait in question) effects on differential reproduction and
chance passing of one allele or the other to offspring. Like selection, drift
can completely fix or completely eliminate traits. Genetic drift is always
occurring, and so is negative selection to some degree (filtering out mutations
that prevent survival and reproduction) and positive selection to some degree
(increasing the prevalence of mutations, new or old, that enhance survival and
reproduction).
Read this blurb from a
website below about a very common perception of human evolution:
_______________________________________________________________________________
Wisdom teeth might be lost as people continue to evolve
Why the modern diet may make wisdom teeth unnecessary
About
25 to 35 per cent of people will never get their wisdom teeth
By: Astrid Lange Toronto
Star Library, Published on Tue Jun 25 2013
Wisdom
teeth are the third and final set of molars that most people get in their late
teens or early 20s. But not everyone does — the American Dental Association
estimates that about 25 to 35 per cent of people will never get their wisdom
teeth. Another 30 per cent will only get 1 to 3 of them. Anthropologists
believe wisdom teeth evolved due to our ancestors’ diet of coarse, rough food —
leaves, roots, nuts and meat — which required more chewing power and resulted
in excessive wear of the teeth. Since people are no longer ripping apart meat
with their teeth and the modern diet is made of softer foods, wisdom teeth have
become less useful. In fact, some experts believe we are on an evolutionary
track to losing them altogether.
_____________________________________________________________________________________
A. Briefly explain the evolutionary
mechanism behind the evolutionary scenario for future wisdom tooth loss that
the author of the blurb alludes to. In other words, think about what the writer
is really hypothesizing for future human evolution and rephrase his
explanation, but scientifically, in terms of all or just some of the four main
mechanisms of evolution that we discussed in class which are mutation, gene
flow, genetic drift, and selection. Important!
Banned words for your scenario include: Need(s/ed/ing), want(s/ed/ing),
try(s/ed/ing), best, most and fittest.
B. Write out an alternative scenario
where natural selection is responsible for the loss of wisdom teeth in our
future selves. If it’s not obvious, this will be a significantly different
scenario from what the writer has imagined in the blurb and from what you wrote
in response to ‘a.’ Important! Banned
words for your scenario include: Need(s/ed/ing), want(s/ed/ing), try(s/ed/ing),
best, most, and fittest.
2.7 - Malaria resistance and lactase persistence
Assigned Reading/viewing
None
Additional resources
Natural Selection: Uncovering Mechanisms of
Evolutionary Adaptation to Infectious Disease – Sabeti (Nature Ed)
Prompt: Answer the following questions:
A.
What
are the components of natural selection scenarios?
B.
What
are the potential benefits to losing grasping abilities in our feet? In what
environmental context?
C. Write an evolutionary scenario, using
natural selection, to explain how humans lost grasping ability in our feet.
D. Write an evolutionary scenario, without
using any form of selection, to explain how humans lost grasping ability in our
feet.
E.
Give
a plausible explanation, in Darwinian terms (i.e. using the components of
natural selection, or if you want, sexual selection), for how humans lost our
body fur and are now what’s often called ‘the naked ape.’ There are many ways
to answer this for full credit as long as you incorporate all the components of
selection properly
F.
Explain
body fur loss without selection, using drift:
2.8 - Building evolutionary scenarios
Assigned Reading/viewing
none
Prompt: Look back at 2.5, for each of
your evolutionary scenarios (i.e. your answers to the four questions), describe
which evolutionary mechanisms (discussed in class) that you hypothesized were
at work.
1. “How did
the mandrill get that colorful face? What about the rear?” Mechanisms you
used (even if you didn’t use the official terms):
2. “How did
the colobus monkey get a long, specialized gut?” Mechanisms you used (even
if you didn’t use the official terms):
3. “How did
silverback gorillas become twice as big as females?”Mechanisms you used
(even if you didn’t use the official terms):
4. “How did
humans become ‘naked’?” (i.e. how did we cease to be as furry as the other
primates)? Mechanisms you used (even if you didn’t use the official terms):
Prompt: Rewrite each of the four explanations you wrote for
2.5 to make them more scientifically accurate, using only the four main
mechanisms of evolution that we discussed in class and those terms: mutation,
gene flow, genetic drift, and natural selection. You may need to just change a
few words or you may need to completely revise the entire answer, it depends on
what you originally wrote. Important!
Banned words for your scenarios include: Need(s/ed/ing), want(s/ed/ing),
try(s/ed/ing), best, most, and
of course fittest.
1.
How did the mandrill get that colorful face? What about the
rear?
2.
How did the colobus monkey get a long, specialized gut?
3.
How did silverback gorillas become twice as big as females?
4.
How did humans become “naked”? (i.e.
how did we cease to be as furry as the other primates)?
2.9 – Species and speciation
Assigned Reading/viewing
Planet without apes? – Stanford (Huffington
Post)
Additional resources
Primate Speciation: A Case Study of African Apes
– Mitchell & Gonder (Nature Ed)
http://www.nature.com/scitable/knowledge/library/primate-speciation-a-case-study-of-african-96682434
Why should we care about species? – Hey (Nature
Ed)
Speciation: The origin of new species – Safran
(Nature Ed)
The maintenance of species diversity – Levine
(Nature Ed)
Macroevolution: Examples from the Primate World
– Clee & Gonder (Nature Ed)
Prompt: In 200 words or more, reflect on the reading
assignment and explain why apes are in danger of extinction (thoughtful guesses
are welcome).
2.10 - Genomics,
molecular clocks, and the LCA
Assigned Reading/viewing
Lice and Human Evolution (video; 11 mins) http://video.pbs.org/video/1790635347/
Additional resources
The Onion Test – Gregory (Genomicron)
The Molecular Clock and Estimating Species
Divergence – Ho (Nature Ed)
http://www.nature.com/scitable/topicpage/the-molecular-clock-and-estimating-species-divergence-41971
Prompt: What are molecular clocks for and how do they work? What do
the molecular clocks of lice tell us about human evolution?
**
3. Test and Observe - Evolving humans, past and present. Ancient evidence for our extinct relatives. Human variation.
Big Questions: 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 - The earliest hominins
Assigned Reading/viewing
IUB, Chapter 7:
Guts and yolk sacs – Roberts
Desktop Diaries: Tim White (video; 7 mins)
Ancient Human Ancestors: Walking in the woods
(video; 4 mins)
Additional
resources
How to Become a Primate Fossil – Dunsworth
(Nature Ed)
Dating Rocks and Fossils Using Geologic Methods
– Peppe (Nature Ed)
Overview of hominin evolution – Pontzer (Nature
Ed)
The Earliest Hominins: Sahelanthropus, Orrorin, and Ardipithecus - Su (Nature Ed):
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
3.2 - Australopithecus and Paranthropus
Assigned Reading/viewing
Ardi-Ardipithecus
ramidus and human evolution ((video; 3:33 mins) https://www.youtube.com/watch?v=S5c5syi0124
Lucy (video; 5 mins) https://www.youtube.com/watch?v=m8Lkk6u-wQM
Trowelblazers (blog): http://trowelblazers.com/
An Unsuitable Job for a Woman (blog): http://www.ellencurrano.me/blog/
Additional
resources
Lucy: A marvelous specimen – Schrein (Nature Ed)
The "Robust" Australopiths –
Constantino (Nature Ed)
Prompt: Find a woman from the ‘Trowelblazers’ blog and briefly
(in less than 100 words) describe why she is there. Do the same for ‘An
Unsuitable Job for a Woman’.
3.3 - Technological
and ecological hypotheses for encephalization
Assigned Reading/viewing
IUB, Chapter 8: Gonads, genitals and gestation –
Roberts
Ancient Hands, Ancient Tools (video; 5 mins) https://www.youtube.com/watch?v=5_ew9J8lpwo
Additional resources
A Primer on Paleolithic Technology – Ferraro
(Nature Ed)
Evidence for Meat-Eating by Early Humans –
Pobiner (Nature Ed)
Archaeologists officially declare collective
sigh over “Paleo Diet”
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
3.4 - Homo erectus
Reading/viewing
IUB, Chapter 9:
On the nature of limbs – Roberts
Additional
resources
Homo erectus - A Bigger, Smarter, Faster Hominin Lineage –
Van Arsdale (Nature Ed)
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
3.5 - Neanderthals
Reading/viewing
IUB, Chapter 10: Hip to Toe – Roberts
Portfolio Assignment
In a half-page or more: Reflect on Roberts’ chapters and be sure to
include what it’s got to do with human evolution.
Additional resources
Archaic Homo
sapiens – Bae (Nature Ed)
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
3.6 - Homo sapiens
Assigned reading/viewing
What happened to the Neanderthals? – Harvati
(Nature Ed)
The Neanderthal Inside Us (video; 4 mins)
Additional resources
The Transition to Modern Behavior – Wurz (Nature
Ed)
Neanderthal Behavior – Monnier (Nature Ed)
Prompt: In 200 words or more, offer an explanation for what
happened to the Neanderthals. Where did they go and why?
3.7 - Social hypothesis for encephalization
Assigned reading/viewing
IUB, Chapter 11: Shoulders and Thumbs – Roberts
Prompt: In 200 words or more, react to the assigned reading.
Include one thing you knew and one thing you didn’t.
IMPORTANT: For the remaining days, students will also be completing the
workbook for the skin color lesson provided by the Smithsonian’s Human Origins
team. (http://humanorigins.si.edu/education/teaching-evolution-through-human-examples
) We’ll be accomplishing it bit-by-bit in class and with assignments to carry
on outside of class. The complete workbook is due on the last day of class, in
class. I find that having something due then increases attendance for
evaluations and increases the audience
for my final, profound thoughts.
3.8 - The evolution of Homo sapiens diversity; Evolution, race,
racism, sex, and sexism
Assigned reading/viewing
Testing models of modern human origins with
archaeology and anatomy – Tryon & Bailey (Nature Ed)
Additional resources
Anthropological genetics: Inferring the history
of our species through the analysis of DNA – Hodgson & Disotell (Evolution:
Education and Outreach)
Human Evolutionary Tree – Adams (Nature Ed)
Paternity Testing: Blood Types and DNA – Adams
(Nature Ed)
Prompt: In 200 words or more, react to the assigned reading.
Include a description of one question that is important and how these authors
are going about helping to answer it here.
3.9 - continued
Assigned reading/viewing
Understanding Race: http://www.understandingrace.org/
Additional Resources
Human Skin Color Variation (NMNH): http://humanorigins.si.edu/evidence/genetics/skin-color
Prompt: Peruse the whole site ‘Understanding
Race’ then take the Human Variation Quiz, there, and record all of the correct
answers here. (No, you’re not being asked to share how you did on the quiz
because many will feel embarrassed.)
3.10 - continued
Assigned reading/viewing
There's no such
thing as a 'pure' European—or anyone else – Gibbons (Science)
A lot of Southern
whites are a little bit black – Ingraham (Washington Post)
Prompt: In 200 words or
more, react to the assigned readings. Be sure to include your take on whether
Gibbons is being literal or rhetorical when she writes “untainted by mixing
with immigrants.”
3.11 - continued
Assigned Reading/viewing
From the Belgian Congo to the Bronx Zoo (NPR)
A True and Faithful Account of Mr. Ota Benga the
Pygmy, Written by M. Berman, Zookeeper – Mansbach
In the Name of Darwin – Kevles (PBS) http://www.pbs.org/wgbh/evolution/darwin/nameof/
Are humans hard-wired for racial prejudice? - Sapolsky (LA Times)
Prompt: In 200 words or
more, react to the assigned readings. What’s the link between racism and
evolutionary theory? Is Ota Benga’s treatment justified by evolution? Is
equality and peace possible, given our evolutionary history?
3.12 - continued
Assigned Reading/viewing
How Donald Trump Got Human Evolution Wrong –
Dunsworth (Washington Post)
https://www.washingtonpost.com/news/speaking-of-science/wp/2017/07/13/human-evolutions-biggest-problems/
https://www.washingtonpost.com/news/speaking-of-science/wp/2017/07/13/human-evolutions-biggest-problems/
Peace Among Primates – Sapolsky (The Greater
Good)
Prompt: In 200 words or
more, react to the assigned readings. From your point of view, how prevalent is
Trump’s take on human evolution in pop culture?
Do you believe it’s harmful? Why or why not?
3.13- continued
Assigned reading/viewing
Humans never stopped
evolving – Hawks (The Scientist)
We are not the boss of natural selection –
Dunsworth (io9)
Prompt: In 200 words or
more, argue whether or not we’re still evolving. Why is this a question?
3.14 - Conclusions
Assigned reading/viewing
IUB, Chapter 12: The Making of Us - Roberts
Evolution reduces the meaning of life to
survival and reproduction... Is that bad? – Dunsworth (The Mermaid’s Tale)
Prompt: In 200 words or
more, briefly describe what you learned this semester and what, if anything, it
means to you. Also, be sure to reflect on what you're still left wondering and
describe how you could find the answers to your remaining questions.
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