The developmental origins of adult diseases

I weighed 7 pounds, 7 ounces when I was born on Saturday, 9 March 1957, at 7:07 in the morning. I know this because all the 7s were memorable, but mainly because this is what doctors and nurses do: they document everything.

You know this. Everytime we visit a doctor, they write down our weight, our height, our blood pressure, every parameter they can squeeze out of us. I can go online right now and read the doctor’s notes on every medical visit I’ve made in the last 20-some years — every prescription, every measurement, all of my complaints, every recommendation, every vaccination…it’s all there. Doctors are obsessive record keepers. There is so much medical data stored away that I sometimes wonder how anyone can extract useful information from it.

But they have! One attempt that has had significant influence was to correlate birth weight data in infants with their adult history of cardiovascular disease. Surprise, your weight on the day you were born is associated with your blood pressure, 60 years later (in a broad statistical sense, of course — this is a population-level correlation.) This led David Barker to make the specific hypothesis that “poor nutrition, health and development among girls and young women is the origin of high death rates from cardiovascular disease in the next generation.” This idea has since been broadened to form the developmental origin of adult disease hypothesis, that all kinds of medical phenomena have their origns in fetal development, and in the environmental effects that have influenced that development.

Credit where credit is due, the original exploration of the hypothesis was thanks to careful records kept by one midwife, Margaret Burnside, who assisted in the birth of over 15,000 babies in Hertfordshire between 1911 and 1930, and also the records of over 2000 births at Jessop Hospital in Sheffield between 1907 and 1924. They then compared birth records with death certificates in the 1950s-1990s to extract the first hints of associations.*

There’s a huge industry of papers being turned out now that look at correlations between birth weight and adult medical conditions. We’re also seeing more complex connections between disease and growth rate in the first year.

Some of them are very well established associations with low birth weight, like hypertension, coronary artery disease, non-insulin dependent diabetes, stroke, dislipidaemia, elevated clotting factors, and impaired neurodevelopment. Other ‘problems’ have been associated with low birth weight in a small number of studies — there really are amazing numbers of papers where researchers mine the medical data for connections, some of them possibly spurious. So small babies may be more likely to develop issues with chronic lung disease, depression, schizophrenia, and general behavioral problems. They may have reduced uterine and ovarian size and precocious pubarche. They might be more prone to breast and testicular cancer.

Surprisingly, they may also marry later, if at all, be left-handed, and have denser fingerprint whorls. You can find it all in the scientific literature.

If you are thinking that you were a plump, fat baby, so you have nothing to worry about, think again. There are correlations between large birth weight and breast cancer (everything seems to cause breast cancer,) prostate cancer, childhood leukemia, and polycystic ovary disease.

This week in my eco devo course, we talked about this hypothesis, and I also handed out a bunch of papers, a different one for each student (there are so many papers in this field!), and today we’re going to have the students assess the literature. It should be fun! The goal is to get a feel for how strong or how valid the various correlations actually are. We’ve also discussed the Dutch famine data. The Nazis starved much of Holland, including the major cities of Rotterdam, Amsterdam, and Leiden, for 7 months in 1945, until the country was liberated by the Allies.

Wasn’t that nice of Nazis to do a massive experiment on a whole nation of 9 million people for us? They let women in each trimester of their pregnancy subsist on 580 calories/day, and then went away and let us analyze the effects. Maternal malnutrition in the third trimester turns out to be bad for babies, who knew? Anyway, the subtext for this week, as it should be for every week, is that Nazis are bad***.

The bigger message is, of course, that development matters and has lifelong consequences, and good, responsible governments provide adequate nutrition to pregnant women and children.

*All these records were handwritten on pieces of paper! The effort to transcribe everything and extract the information in a computational form must have been daunting.**

**My daughter is currently involved in a research project to use natural language processing to synthesize information stored in modern medical records at UW Madison Department of Medicine. That’s useful for a lot of reasons, including drilling down through years of impenetrable treatment notes.

***I hope that overtly political message doesn’t get me in trouble with the university administration.

What are all these plastics doing to us?

In my eco devo course, we’ve been looking at increasingly subtle effects. We started out the semester examining obviously devastating agents in the environment — think thalidomide, stuff that outright kills embryos or causes gross distortions of developmental processes. Then we spent a few weeks looking at endocrine disruptors, agents that perturb developmental signaling and produce embryos with, for example, fertility problems or changes in sexual differentiation. There are a lot of ways chemistry can screw you up short of wrecking external morphology!

This past week we also looked at micro- and nanoplastics, which I personally find have the potential to be a colossal nightmare. The US is producing about 75 million tons of plastic waste each year, and that crap doesn’t go away. You can throw it in a landfill or dump it in the ocean, but it is just physically eroded down into smaller and smaller fragments, allowing it to infiltrate ever deeper into us and our world. Did you know that archaeologists are finding microplastics drifting down into soils 7 meters down, and that they’re finding them in thousand year old sites? We are filling the world with these novel stable polymers, and we have a poor idea of what they’re doing to us.

So we read a paper by Pederson et al. (2020) about the effect of nanoplastics on zebrafish embryos. Like every paper on this kind of topic, it has to tell us about the magnitude of the problem.

Plastic pollution is ubiquitous and an emerging concern in both freshwater and marine environments. Since mass production began in the 1940s, plastic manufacturing has increased rapidly, with 348 million tons produced globally in 2018. Large amounts end up in the oceans, which are now predicted to contain more than five trillion individual pieces of plastic materials (equaling 250,000 tons) in the first 20 m of the water column. Plastics have been identified virtually everywhere: from arctic sea ice to ocean sediments. In freshwater systems, plastics have been identified in large quantities in lakes, rivers, and basins, especially in areas near dense human populations. Their ubiquity has allowed for potential human exposure to plastics through the consumption of aquatic organisms and via drinking water, especially due to the inability of drinking water facilities to entirely remove anthropogenic particles sourced through freshwater environments. In 2019, the World Health Organization (WHO) called for a greater assessment of plastics in the environment after 90% of bottled water was found to contain small plastic particles (World Health Organization). In addition, anthropogenic particles, many of which are likely plastic fragments and fibers, have been detected in over 81% of tap water sources, allowing for an average of 5800 particles to be ingested annually per person.

This paper isn’t even talking about familiar microplastics — it’s all about nanoplastics, particles less than 1µm in diameter. Eventually, all plastics will be broken down to that degree, but we give these an additional boost by intentionally synthesizing these for use in toothpastes and cosmetics and cleansers, and we’ve added <1 parts per billion (ppb) to tens of thousands of ppb to freshwater and marine ecosystems. We don’t have a practical way to remove this stuff. Go ahead, take a swig of that water bottled in plastic, you’ll just absorb those exotic polymers, they’ll be circulating in your bloodstream and getting incorporated into your tissues. You’ll hardly notice.

Zebrafish embryos and larvae swimming in a solution of up to 10000 ppb nanoplastics didn’t seem to mind. There was no effect on mortality, no change in growth rate, no apparent deformities at all. Maybe we’ll all be OK after all.

Except…they do visibly accumulate the plastics in their tissues (they used plastics that fluoresce in the UV).

And then they looked at gene expression in various known pathways — metabolic genes, genes involved in nervous system function, the cardiovascular system — and whoa, they’re just shifted all over the place. It’s a sign of how robust development is that the organism was looking so normal to human eyes. We are all loaded with compensatory developmental mechanisms to make our construction more reliable, and it always impresses me how much damage and insult an embryo can take and still emerge fairly recognizable.

Heatmap indicating predicted upregulation or downregulation in subpathways based on z-scores. (Red is upregulated, blue is downregulated)

One disappointment in the paper is that the behavioral assays were fairly crude, but that’s not the investigators’ fault. They’re working with 5-day old larvae, which, while zebrafish are remarkable little sensory processing machines at that age, they’re still kind of stupid, with a limited behavioral repertoire. The authors looked at spontaneous motor activity, and the fish exhibited a dose-dependent increase in burst swimming. They’re twitchier. More hyperactive. Their brains are being randomly modified chemically, and we’re seeing changes that I’d expect to be more apparent with more sensitive assays.

The message I’m trying to get across to the students is that there is a wide range of phenomena that environmental factors are causing, and we don’t know most of them. It took us decades to get corporations to remove lead from our gasoline, despite the obvious ways it was perturbing our growth and behavior. Are plastics going to be the leaded gasoline of the 21st century?

There is a solution: make biodegradable plastics, ones that don’t reduce to dead stable particles, but instead are digestible by organisms and can be metabolized. Progress is being made in that direction!

An attractive solution to mitigate the environmental impact of microplastics is to develop plastics that do not generate persistent microplastics as part of their normal life cycle. Even plastics that are properly collected and recycled generate microplastics as part of the normal wear from everyday use or as a consequence of recycling or washing processes. Thus, to prevent the accumulation of microplastics, new plastic materials must be developed that are completely biodegradable so that any particles generated from these products will quickly degrade in the environment. Biodegradation is the process by which microbes break down polymers into simpler molecules that can be used as a source of carbon to produce biomass. This requires that the polymer contains chemical bonds, most notably in the polymer’s primary backbone structure, that are physically accessible to enzymes that naturally recognize these bonds as substrates, and that the underlying monomer molecules that are released through this enzymatic cleavage can be consumed by microorganisms. In natural environments, this process is typically performed by consortia of microbes, including bacteria and fungi, secreting hydrolytic enzymes, which sever the polymer to release a variety of monomers and oligomers that can then be utilized as a carbon nutrient source by the microbes. Catabolism of these polymer-derived oligomers and monomers leads to the generation of organismal biomass and CO2 via respiration.

Why would we want structural materials that inevitably break down? Well, maybe you don’t, but I think if we whisper “planned obsolescence” into the ears of corporate executives, maybe they’ll force us to accept them.

Pedersen AF, Meyer DN, Petriv A-MV, Soto AL, Shields JN, Akemann C, Baker BB, Tsou W-L,
Zhang Y, Baker TR (2020) Nanoplastics impact the zebrafish (Danio rerio) transcriptome: Associated developmental and neurobehavioral consequences. Environmental Pollution https://doi.org/10.1016/j.envpol.2020.115090.

Wilson’s Principles of Teratology

It’s another busy week of EcoDevo, and even though the campus was closed I still had to give a lecture on endocrine disruptors. I started by laying out Wilson’s Principles of Teratology…wait, what? You don’t know them? I guess I’d better explain them to the internet at large.

These principles are a bit like Koch’s Principles, only for teratology — you better know them if you want to figure out the causes of various problems at birth, and you do: about 3% of all human births express a defect serious enough for concern. Here’s the list:

  1. Susceptibility to teratogenesis depends on the genotype of the conceptus and the manner in which this interacts with adverse environmental factors.
  2. Susceptibility to teratogenesis varies with the developmental stage at the time of exposure to an adverse influence. There are critical periods of susceptibility to agents and organ systems affected by these agents.
  3. Teratogenic agents act in specific ways on developing cells and tissues to initiate sequences of abnormal developmental events.
  4. The access of adverse influences to developing tissues depends on the nature of the influence. Several factors affect the ability of a teratogen to contact a developing conceptus, such as the nature of the agent itself, route and degree of maternal exposure, rate of placental transfer and systemic absorption, and composition of the maternal and embryonic/fetal genotypes.
  5. There are four manifestations of deviant development (death, malformation, growth retardation and functional defect).
  6. Manifestations of deviant development increase in frequency and degree as dosage increases from the No Observable Adverse Effect Level (NOAEL) to a dose producing 100% lethality (LD100).

The first two tell you what is tricky about teratology. There are multiple variables that affect the response: genetic variability in the conceptus (and, I would suggest, maternal variations), and also timing is critical. A drug might do terrible things to an embryo at 4 weeks, but at 3 months the fetus shrugs it off.

Ultimately, though, the teratogen is having some specific effect (3) on a developing tissue. We just have to figure out what it is, while keeping in mind that that effect might be hiding in a maze of genetics (1) and time (2).

Another complication is that in us mammals the embryo is sheltered deep inside the mother, who has defense mechanisms. The agent has to somehow get in (4). A complication within a complication: sometimes the teratogenic agent is harmless until Mom chemically modifies it as part of her defense, and instead creates a more potent poison.

#5 is just listing the terrible outcomes of screwing with development.

#6 I do not trust. It’s saying the effect is going to follow a common sense increase with increasing dosage, but even that isn’t always true. There is a phenomenon called the inverted-U response where the effect increases with dosage, then plateaus, and then drops off at high concentrations. We’re dealing with complex regulatory phenomena with multiple molecular actors that may have unpredictable interactions. There are teratogens that do terrible things to embryos at low concentrations, but do nothing at ridiculously high concentrations — as if the high dose triggers effective defense mechanisms that the low dose sidesteps.

I had to review these principles in class yesterday, because although I’d also discussed them earlier in the semester, we are currently dealing with teratogens of monstrous subtlety, these compounds that mimic our own normal developmental signals, the same signals our bodies use to assemble critical organ systems. It’s as if some joker were placing inappropriate traffic signals along a busy highway — most would do no harm, but some may totally confuse travelers who then end up detouring up into the kidneys rather than down the genitals, as they preferred, or they end up crashing into the thyroid.

Unfortunately, in this case the responsible jokers are mainly gigantic megacorporations who are spewing these dangerous signals all over the countryside…and then we get to wait until the people swimming in them try to have children, and then the teratologists get to say “death, malformation, growth retardation and functional defect”.

In case you were wondering, Wilson didn’t come up with his list first — a 19th century scientist named Gabriel Madeleine Camille Dareste did it first. No, not first. Lots of people have been documenting these developmental problems as long as there’s been writing, like on this Chaldean tablet:

When a woman gives birth to an infant:
With the ears of a lion There will be a powerful king
That wants the right ear The days of the king will be prolonged
That wants both ears There will be mourning in the country
Whose ears are both deformed The country will perish and the enemy rejoice
That has no mouth The mistress of the house will die
Whose nostrils are absent The country will be in affliction and the house of the man will be ruined
That has no tongue The house of the man will be ruined
That has no right hand The country will be convulsed by an earthquake
That has no fingers The town will have no births
That has the heart open with no skin The country will suffer from calamities
That has no penis The master of the house shall be enriched by the harvest of his field
Whose anus is closed The country shall suffer from want of nourishment
Whose right foot is absent His house will be ruined and there will be abundance in that of the neighbor
That has no feet The canals of the country will be cut and the house ruined
If a queen gives birth to:
An infant with teeth already cut The days of the king will be prolonged
A son and a daughter at the same time The land will be enlarged
An infant with the face of a lion The king will not have a rival
An infant with 6 toes on both feet The king shall rule the enemies’ country

Nowadays we’re more interested in causes than imagined consequences, I hope.

You know, alcohol is not good for children and other growing things

A few weeks ago, I had an absolutely delicious stout at a brew pub in Alexandria. I’m going to have to remember it, because it may have been the last time I let alcohol pass these lips. Why? Because I’m slowly turning into one of those snooty teetotalers who tut-tut over every tiny sin. It started with vegetarianism, now it’s giving up alcohol, where will it end? Refusing caffeine, turning down the enticements of naked women, refusing to dance? The bluenose in me is emerging as I get older. I shall become a withered, juiceless old Puritan with no joy left in me.

It didn’t help that last week I was lecturing on alcohol teratogenesis in my eco devo course, and it was reminding me of what a pernicious, sneaky molecule it is. I’ve known a lot of this stuff for years, but there’s a kind of blindness brought on by familiarity that led me to dismiss many of the problems. You know the phenomenon: “it won’t affect me, I only drink in moderation” and other excuses. Yeah, no. There are known mechanisms for how alcohol affects you, besides the obvious ones of inebriation.

  1. It induces cell death.
  2. It affects neural crest cell migration.
  3. It downregulates sonic hedgehog, essential for midline differentiation.
  4. It downregulates Sox5 and Ngn1, genes responsible for neuron growth and maturation.
  5. It weakens L1-modulated cell adhesion.

I already knew all about those first four — I’ve done experiments in zebrafish like these done in mice.

Take a normal, healthy embryo like the one in A, expose it to alcohol, and stain the brain for cell death with any of a number of indicator dyes, like Nile Blue sulfate in this example B (I’ve used acridine orange, it works the same way). That brain is speckled with dead cells, killed by alcohol. If you do it just right, you can also see selective cell death in neural crest cell populations, so you’re specifically killing cells involved in the formation of the face and the neurons that innervate it. In C, you can see the rescuing effects of superoxide dismutase, a free radical scavenger, and that tells you that one of the mechanisms behind the cell death is the cell-killing consequences of free radicals. I could get a similar reduction in the effects with megadoses of vitamin C, but that doesn’t mean a big glass of orange juice will save you from your whisky bender.

I was routinely generating one-eyed jawless fish, a consequence of the double-whammy of knocking out sonic hedgehog and cell death in the cells that make branchial arches.

You can wave away these results by pointing out those huge concentrations of alcohol we use to get those observable effects, but we only do that because we don’t have the proper sensitivity to detect subtle variations in the faces of mice or fish. So we crank up the dosage to get a big, undeniable effect.

I only just learned about the L1 effects, and that’s a case where we have a sensitive assay for alcohol’s effects. L1 is a cell surface adhesion molecule — it helps appropriate populations of cells stick together in the nervous system. It also facilitates neurite growth. It’s good for happy growing brains.

It also makes for a relatively easy and quantitative assay. Put neuronal progenitors that express L1 in a dish, and they clump together, as they should in normal development. Add a little alcohol to the medium, and they become less sticky, and the clumps disperse.

What’s troubling about this is the dosage. Adhesion is significantly reduced at concentration of 7mM, which is what the human blood alcohol level reaches after a single drink. The fetal brain may not be forming as robustly when Mom does a little social drinking that doesn’t leave her impaired at all, not even a slight buzz.

Maybe you console yourself by telling yourself a little bit does no harm, your liver soaks up most of the damage (and livers are self-repairing!), that it’s only binge drinkers who have to worry about fetal alcohol syndrome, etc., etc., etc. We have lots of excuses handy. Humans are actually surprisingly sensitive to environmental insults, we have mechanisms to compensate, but there’s no denying that we’re modifying our biochemistry and physiology in subtle ways by exposure to simple molecules.

Now maybe you also tell yourself that you’re a grown-up, I’m talking about fetal tissues, and you also don’t intend to get pregnant in the near future or ever. I’m also a great big fully adult person who is definitely not ever going to get pregnant, but development is a life-long process, and we’re all fragile creatures who nonetheless soak up all kinds of interesting and dangerous chemicals during our existence. We know alcohol will kill adult brain cells, but what else does it do? Do you want to be a guinea pig? I think that, as I age, I am becoming increasingly aware of all the bad stuff I did to myself in my heedless youth, and am starting to think that maybe I need to be a little more careful, belatedly.

Oh, you want some reassuring information? Next week we’re discussing endocrine disruptors in my class — DDT, DES, BPA, PCB, etc. — all these wonderful products of plastics and petrochemical technology. You’re soaking in them right now. They never go away. How’s your sperm count looking? Any weird glandular dysplasias? Ethanol looks pretty good compared to chlorinated and brominated biphenyls.

It’s symbiosis week!

Yesterday’s lecture began with a dilemma. The topic this week is all about symbiosis, so of course I had to talk about Lynn Margulis, a very complicated person. I have a lot of respect for her contributions to the field, but also had to mention some of her wrong ideas, like that 9/11 was a false flag operation, and that AIDS was caused by a spirochete. It was also a dilemma back in 2007, when Margulis was a guest on this blog and also on our IRC channel. Whew, that was awkward. There might be a few old timers here who remember that.

Also awkward: most of the students had never heard of Margulis until now (they also had no idea what IRC was). At least I got to expose them to a little significant scientific history, which is my job, even when Margulis expressed the opinion that “I believe at all zoologists are intrinsically poorly educated in biology and that medical people are misinformed.” Ouch. There’s a grain of truth there, but mainly my students got to learn that some famous scientists can be colossal dicks. I did tell my students that if she were alive today she’d be a popular guest on Joe Rogan’s awful show.

Anyway, duty done, I lectured on mycorrhizae and gut microbiomes and a lot on Wolbachia. The paper of the week that the students will be telling me all about on Friday is “Eco-Evo-Devo: developmental symbiosis and developmental plasticity as evolutionary agents” by Gilbert, Bosch, and Ledón-Rettig, which you can read if you want to catch up on the course.

Self-assessment time!

We’ve finished the third week of classes, I need to pause and think about my eco-devo class. You know, teachers do this: a class isn’t a set of railroad tracks taking us to a destination, and sometimes it’s worthwhile to reassess.

My goals with the course are clear. We’re studying a fairly new interdisciplinary science, we’ve got a good solid textbook, I’ve got a dozen smart students, let’s explore. I explicitly want to avoid turning it into a lecture course, where I just stand up and tell them what they need to know, so I constrained myself with some serious guardrails. I only lecture once a week, on Monday, and I don’t just tell them the answers, but give them a lot of questions that they have to answer as a group on Wednesday. I also give them a primary research paper to take apart on Friday.

Does it all work? Yes, mostly.

It wrecks my weekend, though. My Monday lectures have to cover some complex material while focusing the students on relevant questions. I can’t sink comfortably into a flurry of detail, as would be easy to do, I have to bring out the broader issues while simultaneously fleshing out examples with an appropriate amount of detail. This week we’re discussing developmental plasticity, for instance, and while the textbook sings a siren song of numerous examples that I could just recite, I have to provide context and ideas and questions that will motivate discussion on Wednesdays. I think this part of the class is going OK.

I think the students are doing the actual learning part of the course on Wednesdays. This is the day I do things like put them into groups, put stuff on the whiteboards, show that they are actually engaging with the material they’re being exposed to. It’s all on the students, and these are all smart students, so I’d really have to be bad at my job to screw this part up. I prime them with a few ideas that they get at the start of the week, and then let them go.

Fridays…I’ve got to work on my Friday class. I’ve got two problems here. One is that I appoint two students to lead the discussion of a research paper, which is fine, except that these danged ambitious students charge in to do all the work. I tell them to split it up, delegate, and put the rest of the class to work figuring out what is going on in the paper, but no, they try to do it all, and then the whole class sits quietly listening along. I may have to change how I organize those days.

The second problem is me. For instance, last week the theme was about the importance of integrating multiple perspectives to answer complex question, going beyond reductionism. And then I picked what I thought was a good paper that did exactly that, trying to identify the ecological factors behind snake evolution. It was too much. It started with a phylogenetic analysis, then applied a principal component analysis to skull morphology (uh-oh, bio students don’t get much experience with PCA here), added a bit of development/heterochrony work, and then tied all of those approaches together in a nice bit of synthesis. Cool, but too much for some undergrads to handle all at once. I am challenging them, at least, but I think I’d better take next week’s paper down a notch. While my goal was to make them read primary research, maybe I’ll have to ease them in with some review papers for a while, and give their brains a chance to release some pressure.

When I say it all mostly works, that’s entirely from my perspective. Maybe the students hate it, but because they’re all polite Midwestern people, they’re too nice to say it. I’m going to have to put together some kind of student evaluation form to hand out next week so I can find out if I’ve gone off the rails.

This is where I’m at on a Saturday morning at the end of the third week of classes, and now it’s time to immerse myself in background reading and lecture prep. One source I’m finding extremely useful for this course is Mary Jane West-Eberhard’s Developmental Plasticity and Evolution, which is a wonderfully rich source of ideas…but also would have undergraduate brains melting out their ears if I tried making this their textbook. One of my aspirations for this course is that they should be able to emerge from it at the end of the semester and be prepared to read West-Eberhard’s book without having a nervous breakdown.

That would be a fun graduate-level class to teach. Also about ten times more work than this one.

Oh no! It’s Monday!

It happened again. Monday rolled around. When will Science master the ability to predict these cataclysmic disasters? Surely there is some cause that we can treat. Vaccinations, maybe? Monday shelters, buried deep underground? Is there a pesticide that will selectively kill off all Mondays?

Once again, I’ve done it to myself: I set up all the material for my classes for the students on Monday, which effectively means my weekends are shot. This week we’re finishing up The Triple Helix with a conversation about the limitations of reductionism, Wednesday we discuss strategies for answering thorny research problems, and Friday we’re reading a paper about snake ecology, development, and evolution that takes a multidisciplinary approach. I’ve got it all queued up, almost as if I have a plan and know what I’m doing. I’m also tired, bleary-eyed, and I have a headache.

It is all my fault. The easy thing to have done would be to trundle through a series of lectures in which the students sit back with glazed eyes and absorb my wisdom, but instead I’m setting up frameworks and making the students do most of the work, at least two out of three classes. It turns out that’s far more work than just telling them what they need to know, so Mondays are going to be my days of pain.

The rest of the week, though, is cake. Mostly. Then this weekend I have to prep for next week, when we dive into the first chapter of our eco-devo textbook. Plasticity. Plasticity, plasticity, plasticity. That’ll keep us busy for a while.

Also, every day is grading day, and Tuesdays and Friday mornings are my spider days. I’ll recover tomorrow.

First round of Survivor: Morris cleared

Class went fairly well this afternoon, mainly because I’ve got a good, engaged bunch of students. The omens bode well for a good semester.

Me, lecturing

One catch: I haven’t spoken in over a month. Little bits of conversation, sure, but I haven’t used my voice in a sustained discussion in all that time, and I think it’s atrophied a bit. I made it through an hour, but at the end, it was all rough and gravelly and actually starting to hurt a bit. I’ve got to practice more.

I was also feeling a bit dehydrated. I’m going to start bringing a water bottle to work and take regular swigs throughout the day. Minnesota winters don’t help much, either: humidity bottoms out when it’s this cold, as my spiders will attest.

Evolution is the control of development by ecology

Today is my actual first day of classes. We had MLK Day off, and I have no classes on Tuesday, and today I get to meet the 12 students in my Ecological Developmental Biology course. It should be fun. I plan to present that famous aphorism by Van Valen, “Evolution is the control of development by ecology,” and then I’m done for the entire semester — once they’ve grasped that, there is nothing else left to teach, so we can just coast through February, March, April, and May.

OK, so maybe we should also think about the details. We’re going to spend the first two weeks diving into Lewontin’s The Triple Helix: Gene, Organism, and Environment. It’s short but clears the stage beautifully of any vestige of genetic determinism and primes us with an introduction to some fundamental concepts. Everyone ought to read it!

The rest of the semester we’ll work through Gilbert and Epel’s Ecological Developmental Biology. We’re going to talk about plasticity, epigenetics, symbiosis, developmental physiology, and the book has lots of material on teratogenesis, cancer, and aging (those are all developmental concerns, you know — we’re doing all the interesting and important stuff).

We’re also going to dig into the primary literature. This week, we’re reading a review by Sultan, “Development in context: the timely
emergence of eco-devo” to get everyone filled in with the background, but subsequent weeks will be mainly about primary research papers. There’s going to be a fair amount of reading in this class!

I’ve also made the radical decision to abolish all exams: about 60% of the grade is derived from just showing up, alert and ready to contribute. We’ll see how well that flies.

I’ll let you know. I’m thinking I’ll try to post a weekly wrap-up here, so that if I fail it’ll be visible.

Should I take attendance in my classes?

I’m working on my class policy for next semester. Last semester was rough — I had bent over backwards to provide maximum flexibility, with an online option and no mandatory attendance, and it was fairly typical to have only half, or less, of the class show up. I considered changing the policy mid-semester, but it was written into the syllabus, so I had to stick with it. There will be changes next term, I tell you what.

This little video illustrates my problem.

I really like the prisoner’s dilemma twist in the middle — if only one student shows up, they pass the course and everyone else fails. There was one day fall term where that could have been invoked.

To answer the question in the title: yes, I’m going to take attendance, and it’s going to count. My big class this spring is going to be heavily interactive, and I’ll need people to show up.