The meandering of the Amazonian water lily from there to here

BBC Radio 4 is in the midst of a fascinating 25-part series, Plants: From Roots to Riches, on the history of botany from the perspective of the Royal Botanic Gardens at Kew.  Kew is of course Britain's botanical pride and joy, the world's largest collection of living plants.  The original gardens were established in the early 1700's, an unparalleled beneficiary of the expanding British empire as plants were collected around the world and sent to the Kew repository even before it was established as a national botanical garden in 1840.

As promised, the program sees botanical history through Kewian lenses -- the program on the rubber trade, for example, doesn't mention what Britain's successful transplantation of smuggled rubber trees from Brazil did to the Brazilian rubber trade and Brazil's economy, a bit of sanitized history as told by the victor.  Still, the program is fascinating, with the history of many individual plants, including the cycad (Encephalartos altensteinii) that arrived at the gardens in 1755, before Linnaeus devised his naming system, or notes from Charles Darwin on plants he brought to the garden.  Only at Kew could this long history be told.

And then there's the Amazonian water lily (now called Victoria amazonica, it was originally named Victoria regis after the queen).  In 1837 botanist Robert Schomburgk found this plant in the Berbice River as he was exploring British Guiana.  The plant is called "water maize" in its native habitat, where it grows abundantly.  The leaves can be up to 3m, or 9.8ft across, and sturdy enough to hold a small child.  The flowers are  huge, colorful and highly scented -- sometimes.  The plant produces 40 - 50 leaves in a single season.

Flowering Victoria amazonica,
Amsterdam Hortus Botanicus, Ellie Swindells; Wikipedia

Schomburgk sent seeds to Kew and to collectors elsewhere, starting a race among botanists to be the first to grow the plant and see it to flowering.  Schomburgk's seeds germinated the first year, but it was too late in the season for the plant to flower, so it died without going to seed.  Eventually seeds were sent from the Demerara River, and Kew was successful in getting them to flower in 1849 (The Royal Botanic Gardens, Kew; Bean et al., 1908).  The plant is a perennial in its native habitat but is treated as an annual in non-tropical climates; at Kew they have managed to grow it from seed every year since 1849.  It grows extraordinarily quickly, attaining its enormous size, from seed, every year.

Amazonian water lily at Kew Gardens; The Telegraph

As Bean et al. wrote in 1908: 

As one might infer from its enormous dimensions and extraordinarily quick growth, the Victoria regis is a gross feeder.  Every fresh plant has to be supplied with several cartloads of good loam, enriched by rotted manure.  The water is kept at first at a temperature of about 80 degrees F., deducted to 75 degrees as the plant becomes strong and established.  Perhaps the most important desideratum is abundant and unrestricted light.  With these needs supplied, the cultivation of this noblest of aquatics presents no difficulty, except that in late years a troublesome fungus has often disfigured the leaves.  

Flowers are a variety of pinks and whites, and the plant has an unusual mechanism of pollination.  The plant's first blossoms are large and white, and female.  The flowers open in the evening, and smell of pineapple, and actually heat up. The scent beckons to beetles, and when they sit on the flower, transferring pollen to the stigma, the flower closes around them.  The beetles are attracting mates, and then mating inside the flower, all easier at higher than ambient temperatures. The flower reopens the following night but it is pink, it has lost its smell and it is now male, its anthers mature and ready to shed pollen.  The beetle picks up the pollen and flies to the next white flower, still a female, waiting to be pollinated (source).



This is interesting in its own right.  Hermaphroditic flowers, with both male and female organs, aren't uncommon, but flowers that are one and then the other are less so. Here's an extremely successful plant in its native habitat, with a reproductive trick that it shares with few plants.

This could be, like any trait, an example of what Ken discussed in his final post on the mythology of natural selection about the meandering path from then to now.  Does this pollination mechanism have an adaptive advantage?  Is it due to natural selection, meaning that water lilies that are male or female, or hermaphrodites, with two sets of sex organs, reproduced less successfully than the V. amazonica in this plant's natural habitat long ago, allowing V. amazonica to overrun the habitat?

Or, alternatively, did some of these flowers, those with this dynamic gender ability, perhaps for locally specific reasons in a scenario we can only guess at, increase in frequency over eons just by chance?  Here a change and there, at some other time, another change until eventually the plant acquired this ability to change gender?  If or how much was aided by specific natural selection for the trait, and what kind of selection are unknown, and may not even be knowable.  Indeed, this may not be the most energy efficient way to reproduce, nor the only way the plant could reproduce.  It just happens to be the way that currently works.

Modified from Google Images images

It is tempting to view what we see today as examples of stages 'on the way' from ordinary two-sex plants to this kind of  ones, as if a kind of inevitability.  Rather, and here we repeat a figure from the last part of our recent series on natural selection, the evolution of what we see today could have had so many local reasons as to appear essentially random, relative to a straight development to today's system. The idea of an essentially straight path from there to here, so tempting, is in fact in many ways a teleological view of evolution that assumes, at the least, that the same kinds of selection, mutation, ecology and so forth are serially occurring everywhere there are these plants.  It's the sort of argument even Charles Darwin made in viewing various sorts of 'incomplete' hermaphrodism in barnacles.   One might argue that these extrapolations are true, that evolution will ineluctably drive these plants (and barnacles) to their end-points as we see them today (let's not quibble about why they'd be viewed as end-points). But plausibility then sneaks under the tent to be accepted as truth.

Such a good boy, Elroy

We lost a beloved friend yesterday. Our dog Elroy. He made many appearances on The Mermaid's Tale over the years, and he even visited a few classrooms, both in fur-person and via the lesson plan he helped create for Berkeley's Understanding Science website. But far beyond all he inspired, he was just pure goodness and we're grateful to have been loved by him and to have loved him in return. Such a delightful, clever, and utterly adorable friend will live with us forever.

Such a Good Boy, Elroy

He never stole a thing. Not from us, not from Murphy. We could leave a cheeseburger on our plate and leave the room and it’d be there when we returned.

Murphy was the sneaky one, the dog’s dog. Not Elroy. We thought he was so smart. To obey our rules while we were gone! Little did we realize until many years later that he just had a different dog’s strategy. Just take the food while we're looking, willing. Sometimes right out of our hands, sometimes right off our plates, sometimes right out of our mouths, even.

He never stole a thing, until today. Today he stole a whole day of living. He’d be dead already if Dr. Roy hadn’t taken today off.

Instead of dying, Elroy hung out with me. Mostly I lorded, and we quarreled some. He wanted to chew off his toes. I didn’t want him to chew off his toes. I refitted him with a tube sock each time he gently slid it off with his teeth. I’d get up to get a snack and by the time I was back, the sock would be off, blood would be spilled, I’d put on a new sock, and sit with my hand on his paw until he stopped nipping at the sock, panting, waiting.

Wearing just this one white sock, he’s suddenly naked.

And it’s like this, after hours of morning tube sock standoffs, that he and I are lounging this afternoon under the mulberry tree in the backyard. Not at all what we could have done if Dr. Roy hadn’t taken the day off to do whatever it is that he had to do today instead of be in his office to take our meek, phlegmy phone call this morning.

And this place? Back in the far corner near the compost pile and the bucket we use to collect dog turds? Yes. This place.

We're nestled down with five bare feet under the shade of this mulberry tree, pressed up against the grasses that grew purple irises in May, in this spot, in the berried dirt, that he chose, and he’s forgotten all about his tumor and his toes. 

We’re letting spiders crawl all over our skin and fur, and licking the blood that had splattered onto his good leg, and sniffing the blood that just squashed onto my fingers when I smashed a mosquito, and panting and drooling, and interpreting the crows perched in the tops of the pines, and humming with the lawnmower across the street, and smelling, through the snot that’s filled my face for days, the gentle gusts that rustle the tall grasses and the leaves and that push the mulberried branches and the puff clouds northwards up in the sky.

We spot our first hummingbird. We watch a bee chase a sparrow while Murphy herds the cars that travel the lane that circles our yard.

And I worry whether this fetus can tell that I’ve been crying so hard and for so long and whether doing this to him, on the heels of that electric Beck concert on Saturday night, is good parenting. He’ll never get to grab a chubby little handful of Elroy’s neck fur.

And I can’t get the needle to jump past, “These are the wo-oooords we use to say good-by-yyyyyyyye.”

And I’m reminded of another time I sat for hours with another kind of orange beast, fascinating her with the contents of my luggage, unpacked and repacked, over and over and over again.

And I wonder whether this vantage, under the mulberry tree, is where my lovely orange friend would like to be buried. And I start to cry again. So I stroke his cashmere ear some more.

And I think I’m sitting here for Elroy, but I know he’s sitting here for me.

Elroy Beefstu Stacey (2003-2014)

Common ground

By Eric Sannerud

Note:  We know Eric through our connection with a remarkable group of farmers, philosophers, economists, geneticists, innovators, writers, both academic and not, who share a concern for how we humans are mismanaging our place in the biosphere, and how we might make it better.  Eric describes himself as a farmer, thinker, and entrepreneur in Ham Lake, Minnesota. He is the Director of Sandbox Center for Regenerative Entrepreneurship and a member of the Minneapolis Hub of the Global Shapers. Connect with him on Twitter @ericsannerud.   Here are his thoughts:

As a 23 year-old American farmer who studies the US food system from the field I have a unique perspective on the serious challenges it faces. From drainage tiles that evacuate nutrient laden water to the nearest public water source, to obesity rates that cost untold lives, livelihoods, and money, the US food system is badly in need of regeneration.

Source: Wikipedia

Food and health policy in the United States.
In the United States food policy is a collection of local and national priorities that concern the supply of food. US food policy sets supports for certain crops that lead to a higher supply (and therefore lower price) of these crops in the market. Crops that are insured by the US government, against too much rain or too much drought, for example, such as corn, soy, and wheat, are more attractive to farmers than “non-insurable” crops, leading to greater production of insured crops.

United States Health policy is a collection of state and national regulations meant to minimize occupational and recreational dangers and to improve health. Seat belts, MyPlate.gov, the newest iteration of the government recommended diet, FDA regulations, and food labeling mandates are examples of health policy. The intended purpose of many of these regulations, as they relate to food, is to educate consumers to make informed decisions about what they eat. MyPlate identifies proper serving sizes for Americans (though it is not without criticism1). Food labels provide even, consistent criteria for comparing two different items (even if less than half2 of Americans read them).

The trouble is this...
On one hand we have food policies, such as government crop insurance, that encourage environmentally damaging fence row to fence row crop production, or government support for drain tile, drainage systems for fields that shuttle nutrient rich runoff to the nearest water body to be rushed downstream. On the other hand are well-meaning health policies. One can imagine that in the minds of the crafters of health policy each consumer carefully reads the food label on each product, compares the serving size of their meals against the MyPlate recommendations, and eats just the right amount of calories for their BMI each day. Real life food decisions are more complex and price is a big factor in purchasing. Price is where food policy gets involved. Government support makes certain crops cheap. These cheap crops can be used to create cheap food products (corn into chips and soda, for example). But chips and soda are shunned by health policy, and do not have healthy nutrition labels or a formal home on MyPlate.

Due to this disconnect between food policy and health policy the US food system is malfunctioning. A food system that creates historic rates of obesity3 while continuously exploiting the resources humans require for life, soil4 and water5, requires change. However, since the left hand doesn’t know what the right hand is doing, any efforts made, positive or negative, will be hindered by inefficiencies and ineffectiveness.

There is no one elegant solution to reducing the negative effects of such disconnected policies. Anyone claiming to have a trump card is lying: GMOs will not solve all of our problems, neither will organic production nor sin taxes on fizzy drinks and new government serving size suggestions. When dealing with interconnected systems solutions require a full deck of answers.

Three cards to add to the deck

1. Regenerating Health
US consumers shop with their wallets while health policy targets their minds. Health policy that acts on this fact will be moving in the right direction. The question for the discerning health policy strategist then is how to make healthy food price competitive?

One argument that I find persuasive as a low-paid, full-time change maker is the prudence of home cooking. Too often on the run I need food that is grab and go. Frozen burritos at the store cost me $2.00 each, I can make similar quality, though I must say, far tastier, burritos at home for just $.75.

A more aggressive strategy than home cooking promotion is artificially adding cost to unhealthy food. The reasoning goes that if that 76oz soda costs $5.00 instead of $1.00 less people will imbibe. Unfortunately, according to a recent US Supreme Court ruling all Americans have the right to drink cheap soda.6

One inventive way that communities across the United States are improving the cost competitiveness of healthy food is by offering “bonus bucks” to Electronic Benefits Transfer (EBT), government food support, purchases. Spend $20 of EBT at a participating farmers market and get $5 additional “market bucks” good for any fresh produce at the market.

2. Regenerating Land
More healthy food in the market will make healthy food cheaper and more accessible. A benefit of coordinated food and health policy is an increase in the overall supply of healthy food.

Farm fields: Wikipedia

For starters, imagine if US food policy aligned what farmers were incentivized to grow with what health policy encourages Americans to consume. The landscapes of rural America, and the tables of all Americans, could change drastically. This map7, by Emily Cassidy at the University of Minnesota’s Institute on the Environment, shows the caloric efficiency of crop production across the world. Caloric efficiency is the ratio of calories produced on a landscape to the number of produced calories consumed directly by humans. Developed countries producing commodities show horrendous caloric efficiency. Globally just 41% of calories produced are consumed by humans. According to Cassidy, maximizing caloric efficiency could feed an additional 4 billion people. In the US, food policy structures that support big commodity production could be amended to support crops, meat, and production methods of higher caloric efficiency including growing more crops for direct human consumption and more caloric efficient animal proteins such as chicken and fish.

Photo by Eric Sannerud

Private actors have their own part to play in addressing this disconnect. Non-governmental actors can work to aggregate and add scale to local food systems: decreasing prices of the freshest produce by harvesting efficiencies of scale.

Photo by Eric Sannerud

Two up and coming projects, Urban Oasis in St.Paul, Minnesota and New Moran in Burlington, Vermont, are examples of private sector innovation. By serving as aggregation, processing, and distribution hubs for local farmers these projects can increase the scale of healthy local food systems.

3. Regenerating Governance
Solutions also exist in state and local governments that can induce dialogue between government food and health policy makers.

At the state level food policy councils are popping up across the nation. These food policy councils are often created with the express purpose of increasing dialogue between state departments of agriculture, natural resources, and health. The Iowa Food Systems Council is one of the most longstanding and studied State food councils.

City level food councils are also developing. Similar to the state level councils these organizations are made up of a diverse group of stakeholders from across the food system including farmers, nutritionists, academics, and entrepreneurs. In Minneapolis, Minnesota “Minneapolis Homegrown” is a food policy council made up of appointed community members who serve an advisory role to the elected city council on food and health policies.

Hand, eye coordination

Food and health policies in which the left hand doesn’t know what the right is doing are only effective at continuing the failing status quo. At their best, food policy attempts to tackle resource issues in food production while health policy encourages healthy grocery store purchases. Discontinuity contributes to the symptomatic nature of present day solutions and thinking. A focus on symptomatic solutions leaves the underlying disease untouched. In order to cure the cause the US needs a new coordination between food and health policy. Thankfully, there are many luminaries across public, private, and government sectors who understand the underlying problem and are generating bold ideas to address it. 

1 The Nutrition Source. (2014): Healthy Eating Plate vs. USDA’s MyPlate. Harvard School of Public Health [online]. -URL: http://www.hsph.harvard.edu/nutritionsource/healthy-eating-plate-vs-usda-myplate/

2 The NPD Group. (2014, Feb 27): U.S. Consumers’ Interest in Reading Nutrition Facts Labels Wanes as Time Goes On, Reports NPD. NPD Group [online]. -URL: https://www.npd.com/wps/portal/npd/us/news/press-releases/u-s-consumers-interest-in-reading-nutrition-facts-labels-wanes-as-time-goes-on-reports-npd/

3 Centers for Disease Control and Prevention. (2012): Overweight and Obesity, Centers for Disease Control and Prevention [online]. - URL: http://www.cdc.gov/obesity/data/adult.html

4 Lang, S. (2006, Mar 20): ‘Slow, insidious’ soil erosion threatens human health and welfare as well as the environment, Cornell study asserts, by Cornell University [online]. - URL: http://www.news.cornell.edu/stories/2006/03/slow-insidious-soil-erosion-threatens-human-health-and-welfare

5 Bielle, D. (2008, Mar 14): Fertilizer Runoff Overwhelms Streams and Rivers, in Scientific American [online]. - URL: http://www.scientificamerican.com/article/fertilizer-runoff-overwhelms-streams/

6 Klepper, D. (2014, Jun 26): Drink Up NYC: Ban on Big Sodas Canned, in ABC News [online]. -URL: http://abcnews.go.com/Health/wireStory/court-reinstate-york-citys-big-soda-ban-24314227

7 Cassidy, E. (2013): Hotspots of inefficiency Mapping the difference between crop production and food calorie delivery. Institute on the Environment [online]. -URL: http://gli.environment.umn.edu/wp-content/uploads/2013/04/EmilyCassidy_AGU_small.pdf

Two-eyed cyclops -- the plasticity of the brain

The brain is a remarkable thing.  Part of what's so remarkable about it is how it responds to and molds itself around experience.  Alfred Wallace exempted humans from the march of evolution because we are able to do so many things that can't be attributed to natural selection: calculus, the invention of televisions and robots, smell tar and Twinkies, none of which are abilities that we specifically can thank natural selection for since they are all recent.  We can do them because of our brain's adaptability, its ability to make sense of input it clearly isn't hardwired to understand.

Toy tin robot in the show. Boston MA United States. Picture taken by Jonathan McIntosh, 2003; Wikimedia

I remember lying in bed when I was a child, before I was even in kindergarten, closing one eye and then the other and noticing that I could clearly see the books on the bookshelf across the room with one eye but the same books were a blurry mass with the other.  This was just a fact of life, of idle interest to my 4-year old self but nothing more, and I don't think I ever thought to mention it to anyone. I was fine; I could read up close, I could see in the distance, just not with both eyes at once, so it didn't occur to me that anything was weird or wrong about that.  A routine eye exam at school found me out and I finally got glasses to correct this thing that wasn't really a problem.

As I've gotten older, my vision has gotten worse, each eye in its own way.  My eyes are equidistant from 20:20 in opposite directions, one myopic, the other hyperopic; I can still see without glasses, though not perfectly. And still, without my glasses, it's one eye working at a time.

Vision pathway; Weiss and Buchanan, The Mermaid's Tale, 2009

But think about what that means.  Without my glasses, light is pouring into both eyes, hitting my retina at essentially the focally right place in one eye, but all wrong in the other.  The curious thing, to me, is that my brain long ago learned not to pay attention to the blurry input, to only interpret the light waves hitting my retina in the 'right' place. How did it know which was right?

And at some point, in managing input anywhere along the continuum from my eyes to the furthest point I can see, my brain switches from paying attention to my right eye to paying attention to my left.  All the light waves are getting passed along in the same way to both eyes and on to my visual cortex -- I know this because if I close the 'good' eye, of course I'm seeing something, it's just blurry -- but at the very final step in the vision pathway, when my visual cortex is coordinating all the input into a single image, my brain dumps the blurry images and retains the clear.

But it's even more impressive, I think -- with my glasses on, my brain allows input from both eyes to make its way to the final image.  It's switching from monocular to binocular vision all the time.  Again, how does it know to do that?

My eyes as a metaphor for life
The plasticity of the brain isn't confined to the vision pathway, of course.  Plasticity defines the brain -- it's why we can meet new people, learn things, have new experiences, create memories, and then make sense of it all as we go.  Not only are we constantly making new synapses between neurons, we are still making new neurons well into old age, which is what makes our brains able to successfully make sense of all the information with which we're bombarded all the time.  Adaptability, or facultativeness, is so fundamental to evolutionary success that we think of it as a basic principle of life (see chapter 3, The Mermaid's Tale).

And yes, there's a larger point here.  The idea that some of us evolved 'for' sprinting, ping-pong, money-lending, economic prowess, or the ability to do well in 20th century school systems is based on, we think, a superficial understanding of evolution, and the way the brain works.  But it's an appealing one, one that too many scientists and journalists still believe.

Ideology assumes, science asks.

Environmental risk factors - can we ever know when we're done?

Complexity, confounding, heterogeneity: these are just a few of the issues that can and do play havoc with biomedical research where we attempt to infer causation from observational data. A paper just published in Cancer Research ("Circadian and Melatonin Disruption by Exposure to Light at Night Drives Intrinsic Resistance to Tamoxifen Therapy in Breast Cancer," Dauchy et al.) is a good example of some of the issues.  Reported all over the web, including here by the BBC, the study suggests that low levels of light might inhibit the effectiveness of breast cancer drugs.

Many breast tumor cells have receptors for estrogen on their cell membranes; the hormone binds to the receptors and activates cell growth and proliferation, the signal characteristics of cancer cells.  To inhibit that growth, many women with estrogen-positive breast cancers are treated with an estrogen agonist or antiestrogen such as tamoxifen, the metabolites of which bind to the receptor and slow or halt further growth of the tumor.  However, 30 - 50% of tumors become resistant to tamoxifen over time.

Antiestrogens: National Cancer Institute

Dauchy et al. write:

Resistance to endocrine therapy is a major impediment to successful treatment of breast cancer. Preclinical and clinical evidence links resistance to antiestrogen drugs in breast cancer cells with the overexpression and/or activation of various pro-oncogenic tyrosine kinases. Disruption of circadian rhythms by night shift work or disturbed sleep-wake cycles may lead to an increased risk of breast cancer and other diseases. Moreover, light exposure at night (LEN) suppresses the nocturnal production of melatonin that inhibits breast cancer growth.

Many previous studies have shown a relationship between sleep disturbance and cancer risk, and more specifically, between melatonin and cancer risk, so Dauchy et al. focused their research on the role of melatonin as a mediator between tamoxifen and cancer cell growth.  Human breast tumor xenografts (cross species tissue transplants) were implanted into rats and the animals then spent 12 hours in light and 12 hours in dim light or in total darkness every day, and the progression of the tumors followed. The animals exposed to dim light had lower melatonin levels, and their tumors were larger than the rats in total darkness.  Once the tumor reached a specific size, the animals were treated with tamoxifen, and progression or regression of the tumor was then documented.  Further, supplementing the mice in dim light with melatonin lead to smaller tumors and lower tamoxifen-resistance.  The equivalent of the dim light the rats were exposed to would be, according to the authors, the light entering a room under a door.  They suggest that exposure to light from electronic devices before sleep may also lower melatonin levels.

Senior author Steven Hill was quoted in The Telegraph as saying that because resistance to tamoxifen is an increasing problem, this study could be significant.

“Our data, although they were generated in rats, have potential implications for the large number of patients with breast cancer who are being treated with tamoxifen, because they suggest that night-time exposure to light, even dim light, could cause their tumours to become resistant to the drug by suppressing melatonin production.

How melatonin encourages tamoxifen to inhibit breast cancer growth is not understood, although melatonin may play multiple roles in inhibiting cancer cell growth.  The result, if it is replicable, is important however, and because this is not just an association study but an experiment based on a prior hypothesis it is at least that much more persuasive.  But we know from legions of work on inbred mice that mimicking a human effect in one strain doesn't seal the deal, because the results widely differ among strains when investigators are conscientious enough to test multiple strains -- and sometimes some strains show essentially no effect. Presumably this is for genetic reasons, which could mean that the current rat-based study may apply to some, but not to all women.  That would not make it a bad study nor a dismissible result, but it would temper that result.  

The rats in this study were exposed to complete darkness or dim light consistently, 12 hours every day, so it's impossible to know whether variation in light exposure by phase of the moon, say, or other  kinds of varying light sources would make a significant difference in the amount of melatonin a woman makes, nor in how much melatonin is required for tamoxifen to maintain its effectiveness.  
Often, one doesn't know when study results are important or convincing enough to warrant complex changes in drugs, treatment, or behavior.  In this case, it seems rather benign to ask women in treatment to avoid light at bedtime. But even here, should they be compulsive about it?  Shut the curtains in a full-moon?  Nothing to light their way to the bathroom?  And, the authors caution that women shouldn't begin taking melatonin as a result of this study.  

But this work is interesting in its own right, and clearly worth paying attention to.  It also is a reminder of why it's so hard to study environmental risk factors for disease.  As far as we know, when the benefits of tamoxifen were first shown, there was no a priori reason to suspect that it would lose its effectiveness, at least in part, because of exposure to light at night, or interruption in melatonin cycles.  This is a sobering but important reminder that there is always the potential for unidentified and unexpected interactions between unknown and unexpected risk factors (confounders).

We now know at least that there seems to be an interaction between melatonin and tamoxifen in rats, at least in regard to implanted human tumor cells, but we don't know how much of the tamoxifen resistance in human breast cancers this particular interaction might explain (if any, since these were rats, not humans).  But complexity is a hallmark of diseases like cancers, and there's not going to be a single, simple explanation.

On the mythology of natural selection. Part X: Finally: Traveling evolution's geodesics

Science recognizes Charles Darwin's contributions to knowledge because he was a deep thinker who largely transformed a whole area of human knowledge in ways that seem likely to be permanent.   One often refers to such inspirational figures by coining terms to acknowledge their views.  'Darwinism' is one.  To name a concept after him is entirely deserved (even his co-recognizer of the salient facts of life as an evolving history, Alfred Wallace, in 1889 referred to the idea with the very title of a book summarizing the field: Darwinism: An Exposition of the Theory of Natural Selection, with Some of Its Applications).

By greatly honoring his name, science and history recognize his contributions.  But his work is not to be read exegetically as a source of The Word.  He's respected, but not sanctified.  No scientist we know of  checks what Darwin said as a means of testing whether something is true or not. This is science; exegesis is for historians.

Charles Darwin would not want a halo!

Darwin would want it that way ("And get that halo off me, please!").  He was a brilliant, doggedly thorough and persistent gentleman scholar.  His works are a wonder to read, because he was a keen and incredibly patient observer and a master synthesizer of reams of data from various fields.  But he was human and lived in the times in which he lived and with the knowledge and technologies then available.  Even he, the developer of the selectionist 'law' of nature, mainly offered hand-waving assertion and circumstantial evidence, but definitely did not in the Origin of Species by Means of Natural Selection show that the origin of species was by means of natural selection.  If you doubt this, read the Origin yourself, especially Chapter IV.  But that's a topic for another day.

Nonetheless, we think that Darwin's view of natural selection as a universal determinative law to account for the evolution of the traits of organisms has become widely and without deep thought adopted as a given rather than a matter of science to be examined in the real world.  This is in many ways taken almost directly from Darwin's personal view, though most who use the term have done little if any actual reading of Darwin's voluminous works.  Such a worldview becomes dogma, or the assumption of a belief system, an ideology, rather than science, as we have tried to show in this series. That is the sense in which we discuss its mythology--the tales told and assumptions made about it that don't reflect what we actually know, and don't know.

The public and professional literature are awash in 'gene for' or 'evolved for' assertions that go largely unquestioned (thoughtful, pointed reviews of this season's recent pulp eugenics book excepted).  Such stories about genomic causation or reconstructions of evolutionary history are often expressed as if they explain traits in question, but by equating plausibility with truth in fact verge on tautology, and serve preconceptions rather than testing how the living world actually works.  The pervasive explanatory 'ether' that is invoked, is natural selection.  Most biologists probably don't quite realize how close they come to explanations that would be the same if God's will were used instead.  That universal acid or Darwin's 'dangerous idea', as one philosopher referred to it, is indeed dangerous both to human society and to science.

In this series, we have discussed various ways in which purely historical processes of proliferation and divergence from common ancestry can potentially account for aspects of the origin of complex traits within organisms, and by extension among organisms, that are not due, or not just due, to natural selection.

Our objective has not been to denigrate the idea of natural selection, but to show that there are other entirely natural processes that can lead to the evolution of complex traits.  Evolution and genomics are not just one-trick ponies.  As we have noted, how and when (or even whether) these processes are at work is a matter that can be studied by clever designs or choice of material--they are testable ideas.  In fact one of them suggests that natural evolutionary historical processes could generate complex traits without any involvement of force-like natural selection at all.  However, if one clings to a selectionist ideology, selection as an axiom rather than a scientific assertion, then of course one will never even ask the questions as to whether such ideas might be correct, much less test them.

We can, however, ask a far more fundamental question, which is how selection works when it does occur.  For this, and as elsewhere in this series, we suspend skepticism for the moment and take universal, Newtonian force-like natural selection as a given.  To try to make our point, an analogy to astrophysics might be instructive.

The 'spacetime geodesics' of evolution by natural selection
In cosmology--the real thing--travel in the universe is governed by relativistic spacetime.  An object at any time moves in a way that is determined by its motion at the time and the gravitation field--one might say the gravitational 'ecology' due to the physical objects in the area.  The bigger or closer another object, the more spacetime is curved.  But the net curvature is the total of these effects in this location in spacetime.  We use the term because on the cosmic scale, space and time are inseparably part of the nature of existence.  We can say that the past has existed and, from our vantage point, we can get a glimpse of it from the distribution of matter and energy at the present time.  In real cosmology, we can also 'see' the future to the extent that we can know and (in principle, at least) predict the state and location of the objects towards which our object is moving.  Any object in motion essentially integrates all of the forces acting upon it, and moves through spacetime accordingly.  Unless driven by some separate impulsive force, the path it follows is determined by these local spacetime properties, and is known as a geodesic, which one can think of as the shortest path between points spacetime.

SpaceTime trajectory real and imaginary (modified from GoogleImages)

If the object of our interest is affected by several small local objects in the area, it meanders geodesically past them.  If or when there is a large nearby object, it follows a more greatly affected curvature around it (blue inset).  At the end of a period of interest (which we call now), and if we knew the location of the point at our chosen starting time (then), and we're oblivious to what happened between then and now, we can always assert that what happened was that the object of our desire was shot by a specific force directly along that path (shown as dotted arrow).  

But that assertion is a fiction, and science is supposed to be about fact.  That fact is that our object got to now through a path that essentially had nothing to do with now--it was not aiming toward now, its movement at any time was locally determined, sometimes by major (one might say clear-cut) factors, often by a host of minor even seemingly trivially small ones, collectively setting up the position at the next major influence.  Note that in our cosmic analogy all of our object's meanderings are considered to be totally determined by the shape of gravitational spacetime--we assumed that no probabilities were involved.

This should be enough about spacetime geodesics in astrophysics.  The point of the analogy should hopefully be clear.   Even if the implicit complete determinism of Darwinian assumptions were true, the complex dynamic nature of earthly ecologies means that an evolutionary geodesic need not follow a retrospectively reconstructable path from then to now.  A species or trait need not have evolved 'for' its current use, not even in stages aimed in a particular direction, not with its various components evolving synchronously or even sympatrically.  Indeed, if and where ecologies are complex and dynamic, the meanderings of our object--a trait or species--may be essentially indistinguishable from random movement relative to any long-term 'purpose'.  

An organism is a collection of traits, often correlated by shared genomic mechanisms, that are continually being pulled every which-way by selection of various intensities for various reasons (the nearby gravitational objects).  These pulls are based on the local context, and that context (the 'stars' etc. in the area) change over time and space--over evolutionary 'spacetime'.  The position in the future may not be predictable from its local conditions at any given time: evolution has no 'momentum' by which the past actively propels species through the present--or if it does, we need a much-revised theory of its causal dynamics.

The shape of the head (something I've worked on with collaborators for years) is measurable in its many dimensions, and we can look at fossils and comparative species, some of whose evolutionary past history we shared through common ancestry.  But the head is not a unitary trait, perhaps not a very meaningful trait to ask about its evolutionary trajectory in selectionist terms. The length of the face, say, need not have evolved 'for' language, or reduced smell, or balance in upright posture, or change in diet, or forward-looking stereo vision, or.....  

These factors and their importance for 'fitness' need only be synchronized if they share genomic pathways, and otherwise need not be synchronous in time or space, and the 'same' trait can serve multiple or even changing functions.

As one zooms one's lens closer and closer, the picture dissolves into every more graininess. No two individuals have the identical trait or genotype. We don't see 'spandrels' or other states that set the stage for the trait as we see it today. We don't see a ladder of discrete improvements towards today. No punctuated equilibrium, saltations, and the like except as we choose to impose them on our observations. To the extent the picture given here is apt, each local point in evolutionary spacetime is so local, so dependent on its context at that instant in time, that it need not suggest the kind of longterm arrow from then to now that is so commonly explicit or explicit in our texts, papers, and so much of the rhetoric even in professional biology.

Realizing in this way how things are--or at least might be--under deterministic assumptions, it is now time to re-introduce the other complications discussed in this series, including chance in its many manifestations, at the scales of change that are relevant.  The 'geodesic' path of evolution meanders in no one direction, by no one cause.  Even if it is 'driven' by selection at every instant, it is a path whose determinants are problematic to identify in practice. Whatever is the truth, selection is not obviously simple in a force-like way. 

And here's something to think about:   Scientists often say that the simplest--the most 'parsimonious' explanation is the preferred one most likely to be true.   In the case of our cosmological analogy, I think it's right to say that the straight-arrow path from then to now is not the simplest explanation of the change!   In fact, it may be among the least simple explanations.  That's because the geodesic path is actually the simplest: it only involves the explanation that the path follows spacetime curvature (e.g., gravity). In that sense, that is the 'straight' path.  Given the complexity of space, you'd need a host of ad hoc reasons to try to account for the usual notion of a 'straight' path (like our dashed arrow).  

The same can be said of evolution.  The straightest path is that which follows the dynamic local 'pulls' of selection; to avoid following that path, as if somehow 'insisting' on a direct rather than geodesic path from then to now, it would have to resist the myriad local conditions to keep on that path--and that then becomes teleological!  Is that a suitable 'simpler' explanation?

As we navigate our search for truth, if we are not careful in our thinking we, like Odysseus, face the twin threats of Scylla and Charybdis:  the mesmerizing sirens of examples of strong recent or artificial selection that can lead us onto rocks of extrapolation to events on a slow, long time-scale, and there is a danger of being sucked into a whirlpool of complacency by taking criteria like DNA sequence conservation too casually.

Between Scylla and Charybdis; Wikimedia

Darwin's magnificent legacy

Darwin's realization that life today is the legacy of processes of descent with modification and differential proliferation, was profound and correct as far as anything we know.  (Somewhat separate from, but related to the effectiveness of selection, is that branching from common ancestry into distinct entities such as species that are isolated from each other was also part of the theory in Darwin's view, as it is of ours today.)  But none of this implies there is only one manner of differential proliferation nor that we cannot find and flesh out the basic concepts--even if there are no fundamentally different phenomena yet to be discovered.  For example, with organismal selection, genetic variation and its effects can be sorted out by the organisms in their various local areas, with no competitive differential reproduction required, and in that sense no nasty competition to the death, necessary.

There has been nothing spooky in our use of the analogy of an imaginary odyssey through evolutionary 'spacetime'.  We are not invoking heresies, that Darwin himself would not recognize. Indeed, what we have said may be imperfectly stated but is perfectly consistent with the long-standing insistence that evolution is locally contingent and not teleological.   But that in fact is inconsistent with the ubiquitous simplistic 'evolved for' and 'gene for' tales in the public as well as professional literature.

Just to be clear, with all of its nuances, including chance effects, evolution can be accounted for by historical, material processes; there is nothing that we know that requires any external force (as in religious arguments) to guide evolution. 

Just because a story is plausible does not make it either probable nor true.  Think of it this way:  The dashed arrow in our geodesic figure is the direct then-to-now path.  We can note that by comparing a fossil to its descendants we can always construct the usual simple, direct here's-how adaptation story. But not only is plausibility not the same as truth, but considering what we've tried to say in this series, perhaps such stories are least likely to be the truth!  Perhaps it's very naive to think, much less to assert, that such simplicity is what we should expect in our evolutionary tales.  Indeed, Darwin himself tacitly was led by temptation to make some similar assumptions, basically if implicitly and unintentionally teleological ones, in his books describing barnacle evolution.

What is important to us is the difference between a nuanced view, and the way people act and speak in practice (despite perhaps their being clever enough to include briefly-stated caveats).  One can always defend business-as-usual, the direct then-to-now Just-So story, by asserting that, "Yes, yes, all the details you mention are true, but they don't really matter in my example." But one should ask whether that's sincere rather than a dismissive acknowledgement-in-passing, a lazy excuse for clinging to a comfortable ideology--especially, but not only, when it comes to explaining human variation.  If so, the invocation of 'natural selection' is an exercise in mythology, in ideology.

Ideology assumes, science asks.

On the mythology of natural selection. Part IX: What would it mean if selection really were deterministic?

Today's post will have to do with the question, "What is cause?". This will be a bit abstract, but I hope it will be at least somewhat understandable.

We have been writing about the subject of genetic determinism and its twin, deterministic natural selection.  Pure determinism means that when I know an organism's genotype I can perfectly predict its traits and that given different organisms' genotypes I can perfectly predict their relative fitness (reproductive success).  It's one thing to consider skylarks and oak trees in this regard, because nobody really cares; but now we know that humans are part of Nature rather than separate creations, we naturally want to apply the same principles to ourselves as we do to plants and other animals.  And though issues about determinism apply to all of Nature and its evolution, it's the way they hit home that makes it important for the human sciences, above all, to realize the implications of how we view ourselves in light of our ideas about evolution.

Some people object to suggestions that natural selection might not be genetically deterministic--that there might be other aspects to the organisms' traits, such as environment which in the case of humans includes their culture.  An unstated or perhaps even not even fully aware objection to any challenge to genetic determinism is that if you open the door, even a tiny crack, to the uncertainties of probabilism or environmental, or in the case of humans to cultural effects, you'll venture off into 'softer' non-scientific views of Nature.   That point of view suggests that we can peer into genomes to see individuals' or groups' inherent worth, as one can fancy that Nature in the form of selection sees and has seen it.

To use humans further to illustrate the point, the fact that we wear coats in winter and domesticate our food sources would seem to be manifestly obvious examples of niche construction.  To push this further, can any sane scientist argue that, say, Doric architectural columns were built because of specific genotypic differences between their architects and the architects who built Ionic columns?  If not, and if it's not cultural (environmental), what is the 'cause' of the style differences?  An honest assessment raises the question how far can assertions of genetic determinism go, and if the door is opened to cultural/environmental causation, where do you stop, if you can't read individuals' traits off their genomes?

Doric Order of the Parthenon (Wikimedia)

Ionic Order (Wikimedia)

But let's think a bit deeper than this superficial bit of sociocultural generalizing.

If evolutionary fitness were truly determined
In this series on natural selection we've often accepted, temporarily for the sake of argument, a proposition that genetic causation, and hence selection really are perfectly deterministic.  That means selection reads two organisms' genotypes, say, and determines everything about them, including who will win the evolutionary race, in the same law-like way that gravity pulls objects towards each other as a deterministic force.  Let's again take this as true for the purposes of argument, and see its consequences.

First, such determinism if true would mean that everything--everything--about every organism is perfectly predictable.  And if what happens is perfectly determined and predictable, then we can follow what's here today, using the force-like laws that make it predictable, back as well as forward in time, so that in fact everything--everything--is just following those laws and hence was already predictably inevitable from the instant of the Big Bang.  Of course, to actually predict everything you'd have to have all the information, perfectly understood, which in turn requires that you be above or out of the system whose properties you want to know: in a sense you need to know more than everything there is to know.  Arguing that position is logically no different from just saying "God willed it to be that way." It's not science, and it doesn't explain anything.

Even total genotypic predictability, however, should give no solace to genetic and darwinian determinism. That's because if everything were pre-determined, then there is no 'natural selection': there's no random mutation screened competitively by the environment, because winners and losers and their genotypes were always already in the works waiting to happen.  In that case, 'evolution' really holds only its original sense of the world: an 'unrolling' of what's already there.  Even before its conception, the future rabbit was doomed to be caught by this particular future fox, in the same sense that we would not say the apple 'evolved' onto Newton's head, but that it just followed the law of gravity.  If so, everything including the misleading (under our working assumption of determinism) evidence of chance (genetic drift, mutation) is simply predetermined!  Unfortunately, perfect determinism cannot be tested or proved, so we're not any further along in our understanding.

The role of 'chance'
The point of science is to understand causation and that is essentially the same as making predictions of the future from observations in the present.  However, even if perfect determinism were the case, things are not predictable in the usual informal sense of deterministic world-views: since we can't have perfect information, only the artifacts of measurement and sampling make a perfectly deterministic world seem non-determined.  We have to make assumptions about when, where, how, and how much our measurements were off--about the distribution and probabilities of what would only appear to be chance.  And those probabilities are themselves determined in some way, if you think about it.

We know from such things as chaos theory among others, that even tiny measurement errors can lead predictions to be completely wrong in a way that's largely unpredictable and untestable (this is often referred to as the 'butterfly effect').  From A to Z we face measurement errors and make assumptions about phenomena that lead us to treat them as driven by chance even if they were entirely pre-determined.

We thus seem to face an inevitable degree of unpredictability even if we're in a wholly deterministic cosmos.  And many physicists argue that the cosmos in fact is at its most fundamental level irreducibly probabilistic (this, for example, in quantum mechanics).  In turn, this means that things cannot be predicted more precisely than by probability--and the conditions under which we can actually know what that probability is, or how it limits the accuracy to which we can aspire, are very limited.

And what if life and its working-out really do have a fundamentally probabilistic component--that is, selection, mutation, mate choice, and genetic interactions with environments?  In that case, at present we generally have scant knowledge of what such probabilities actually are or even how to identify them.  In other words, whether life is or is not wholly deterministic, it at least inescapably appears to be probabilistic. And that means that individuals' natures cannot just be read off a DNA sequencer.

Either, neither, both!

There is some strangeness here.  Think about this:

Natural selection can in principle be
either deterministic, because it moves traits in some direction over time
or probabilistic, because its direction inherently wavers over time
or both deterministic and probabilistic, because a trait can change in a given ‘direction’ over time yet
    not in a straight projection,
or neither deterministic and probabilistic, because a trait doesn’t change in a straight line nor does it just
    change purely randomly.  

As we'll discuss in the next po, one can always see after-the-fact then-to-now evolutionary change and argue that it was somehow determined and inevitable, in a force-like way.  Alternatively, one can argue that it's at least largely luck where things have got to where they are today.  Or, one can say it was deterministic at any given time but that the driving context changed over time.

The very same either-or-both-neither characteristics apply to the causal relationships between an organism's genotype and its traits.  Not all bearers of a given genotype have the same trait value, and a given environment doesn't seem always to have the same effect. Most genetic variants empirically, at as current studies are designed, have small or unstable effects relative to each other; the exceptions are often lethal.  That in turn means that natural selection cannot be a deterministic screen--it can't 'see' each individual's genotype.

We as yet have nothing close to a precise general theory for how deterministic these factors could be, or if not deterministic what causes them to be probabilistic, or if probabilistic what the determines the probability values.  Even in the latter case, we're usually stuck with very limited sampling and observation, not strong theory.

One deep but simple truth might be that DNA is basically an inert molecule that has no function until it interacts with (a physicist might say is 'measured by') its environmental context, however that itself is determined.  Genes and environment are not as simply separable as their separate names indicate.

We should take what we know about what we don't know seriously and make more of an effort to understand it.  Ignorance the the proper driver of science, but only if we acknowledge it.

In the end
Dogma is not helpful here.  Even to acknowledge that natural selection is a mix of determinism and probabilism is a rather empty tautology.  What sort of 'mix'?  Are there general laws that can tell us?  Causation, determinism, probability, uncertainty: are in themselves elusive concepts.

Most scientists acknowledge these facts when they’re pointed out, even if grudgingly when a vested point of view is threatened by that acknowledgment. While the facts we know may require that we gain a deeper insight into what determinism and probabilism actually may mean here, declarations of what is the primary mover are simply not very helpful.

All of this should temper the fervor with which stances are taken on this subject. Opening the door of complexity threatens ideological stances, in science and more acutely when applied to human life and society, but it's the only way to try to gain a deeper understanding, even if once the door is open you can't control the uncertainties that come pouring in.

The drug that reinforces staunch positions are those clear-cut conditions that we do know of, and this goes back to Mendel himself.  But even strongly causal individual alleles, even purportedly lethal alleles, demonstrably vary in their effects and sometimes have essentially no effects.  This is very clear from lots of data, including in humans where it is not just a politically-correct dream-world.  Neither environmentalists nor genomic determinists should shut the door on the nature of biological and evolutionary causation, including the important role of unpredictable chance.