First of all, in the context of science, you should never speak of evolution as a “theory.” There is no theory about whether or not evolution happens. It is a fact.
Scientists have, however, developed tested theories about how evolution happens. Although several proposed and tested processes or mechanisms exist, the most prominent and most studied, talked about, and debated, is Charles Darwin’s idea that the choices of nature guide these changes. The fame and importance of his idea, natural selection, has eclipsed the very real existence of other ways that populations can change over time.
Evolution in the biological sense does not occur in individuals, and the kind of evolution we’re talking about here isn’t about life’s origins. Evolution must happen at least at the populationlevel. In other words, it takes place in a group of existing organisms, members of the same species, often in a defined geographical area.
We never speak of individuals evolving in the biological sense. The population, a group of individuals of the same species, is the smallest unit of life that evolves.
To get to the bottom of what happens when a population changes over time, we must examine what’s happening to the gene combinations of the individuals in that population. The most precise way to talk about evolution in the biological sense is to define it as “a change in the allele frequency of a population over time.” A gene, which contains the code for a protein, can occur in different forms, or alleles. These different versions can mean that the trait associated with that protein can differ among individuals. Thanks to mutations, a gene for a trait can exist in a population in these different forms. It’s like having slightly different recipes for making the same cake, each producing a different version of the cake, except in this case, the “cake” is a protein.
Natural selection: One way evolution happens
Charles Darwin, a smart, thoughtful, observant man. Via Wikimedia.
Charles Darwin, who didn’t know anything about alleles or even genes (so now you know more than he did on that score), understood from his work and observations that nature makes certain choices, and that often, what nature chooses in specific individuals turns up again in the individuals’ offspring. He realized that these characteristics that nature was choosing must pass to some offspring. This notion of heredity–that a feature encoded in the genes can be transmitted to your children–is inherent now in the theory of natural selection and a natural one for most people to accept. In science, an observable or measurable feature or characteristic is called a phenotype, and the genes that are the code for it are called its genotype. The color of my eyes (brown) is a phenotype, and the alleles of the eye color genes I have are the genotype.
What is nature selecting any individual in a population to do? In the theory of natural selection, nature chooses individuals that fit best into the current environment to pass along their “good-fit” genes, either through reproduction or indirectly through supporting the reproducer. Nature chooses organisms to survive and pass along those good-fit genes, so they have greater fitness.
Fitness is an evolutionary concept related to an organism’s reproductive success, either directly (as a parent) or indirectly (say, as an aunt or cousin). It is measured technically based on the proportion of an individual’s alleles that are represented in the next generation. When we talk about “fitness” and “the fittest,” remember that fittest does not mean strong. It relates more to a literal fit, like a square peg in a square hole, or a red dot against a red background. It doesn’t matter if the peg or dot is strong, just whether or not it fits its environment.
One final consideration before we move onto a synthesis of these ideas about differences, heredity, and reproduction: What would happen if the population were uniformly the same genetically for a trait? Well, when the environment changed, nature would have no choice to make. Without a choice, natural selection cannot happen–there is nothing to select. And the choice has to exist already; it does not typically happen in response to a need that the environment dictates. Usually, the ultimate origin for genetic variation–which underlies this choice–is mutation, or a change in a DNA coding sequence, the instructions for building a protein.
Don’t make the mistake of saying that an organism adapts by mutating in response to the environment. The mutations (the variation) must already be present for nature to make a choice based on the existing environment.
The Modern Synthesis
Darwin presented his ideas about nature’s choices in an environmental context, he did so in a book with a very long title that begins, On the Origin of Species by Means of Natural Selection.Darwinknew his audience and laid out his argument clearly and well, with one stumbling block: How did all that heredity stuff actually work?
We now know–thanks to a meticulous scientist named Gregor Mendel (who also was a monk), our understanding of reproductive cell division, and modern genetics–exactly how it all works. Our traits–whether winners or losers in the fitness Olympics–have genes that determine them. These genes exist in us in pairs, and these pairs separate during division of our reproductive cells so that our offspring receive one member or the other of the pair. When this gene meets its coding partner from the other parent’s cell at fertilization, a new gene pair arises. This pairing may produce a similar outcome to one of the parents or be a novel combination that yields some new version of a trait. But this separating and pairing is how nature keeps things mixed up, setting up choices for selection.
With a growing understanding in the twentieth century of genetics and its role in evolution by means of natural selection, a great evolutionary biologist named Ernst Mayr (1904–2005) guided a meshing of genetics and evolution (along with other brilliant scientists including Theodosius Dobzhansky, George Simpson, and R.A. Fisher) into what is called The Modern Synthesis. This work encapsulates (dare I say, “synthesizes?”) concisely and beautifully the tenets of natural selection in the context of basic genetic inheritance. As part of his work, Mayr distilled Darwin’s ideas into a series of facts and inferences.
Facts and Inferences
Mayr’s distillation consists of five facts and three inferences, or conclusions, to draw from those facts.
The first fact is that populations have the potential to increase exponentially. A quick look at any graph of human population growth illustrates that we, as a species, appear to be recognizing that potential. For a less successful example, consider the sea turtle. You may have seen the videos of the little turtle hatchlings valiantly flippering their way across the sand to the sea, cheered on by the conservation-minded humans who tended their nests. What the cameras usually don’t show is that the vast majority of these turtle offspring will not live to reproduce. The potential for exponential growth is there, based on number of offspring produced, but…it doesn’t happen.
The second fact is that not all offspring reproduce, and many populations are stable in size. See “sea turtles,” above.
The third fact is that resources are limited. And that leads us to our first conclusion, or inference: there is a struggle among organisms for nutrition, water, habitat, mates, parental attention…the various necessities of survival, depending on the species. The large number of offspring, most of which ultimately don’t survive to reproduce, must compete, or struggle, for the limited resources.
Fact four is that individuals differ from one another. Look around. Even bacteria of the same strain have their differences, with some more able than others to with stand an antibiotic onslaught. Look at a crowd of people. They’re all different in hundreds of ways.
Fact five is that much about us that is different lies in our genes–it is inheritable. Heredity undeniably exists and underlies a lot of our variation.
So we have five facts. Now for the three inferences:
First, there is that struggle for survival, thanks to so many offspring and limited resources. See “sea turtle,” again.
Second, different traits will be passed on differentially. Put another way: Winner traits are more likely to be passed on.
And that takes us to our final conclusion: if enough of these “winner” traits are passed to enough individuals in a population, they will accumulate in that population and change its makeup. In other words, the population will change over time. It will be adapted to its environment. It will evolve.
Darwin presented his idea of natural selection, he knew he had an audience to win over. He pointed out that people select features of organisms all the time and breed them to have those features. Darwin himself was fond of breeding pigeons with a great deal of pigeony variety. He noted that unless the pigeons already possessed traits for us to choose, we not would have that choice to make. But we do have choices. We make super-woolly sheep, dachshunds, and heirloom tomatoes simply by selecting from the variation nature provides and breeding those organisms to make more with those traits. We change the population over time.
Darwin called this process of human-directed evolution artificial selection. It made great sense for Darwinbecause it helped his reader get on board. If people could make these kinds of choices and wreak these kinds of changes, why not nature? In the process,
Darwin also described this second way evolution can happen: human-directed evolution. We’re awash in it today, from our accidental development of antibiotic-resistant bacteria to wheat that resists devastating rust.
Genetic drift: fixed or lost
What about traits that have no effect either way, that are just there? One possible example in us might be attached earlobes. Good? Bad? Ugly? Well…they don’t appear to have much to do with whether or not we reproduce. They’re just there.
When a trait leaves nature so apparently disinterested, the alleles underlying it don’t experience selection. Instead, they drift in one direction or another, to extinction or 100 percent frequency. When an allele drifts to disappearance, we say that it is lost from the population. When it drifts to 100 percent presence, we say that it has become fixed. This process of evolution by genetic drift reduces variation in a population. Eventually, everyone will have it, or no one will.
Gene flow: genes in, genes out
Another way for a population to change over time is for it to experience a new infusion of genes or to lose a lot of them. This process of gene flow into or out of the population occurs because of migration in or out. Either of these events can change the allele frequency in a population, and that means that gene flow is another was that evolution can happen.
If gene flow happens between two different species, as can occur more with plants, then not only has the population changed significantly, but the new hybrid that results could be a whole new species. How do you think we get those tangelos?
Horizontal gene transfer
One interesting mechanism of evolution is horizontal gene transfer. When we think of passing along genes, we usually envision a vertical transfer through generations, from parent to offspring. But what if you could just walk up to a person and hand over some of your genes to them, genes that they incorporate into their own genome in each of their cells?
Of course, we don’t really do that–at least, not much, not yet–but microbes do this kind of thing all the time. Viruses that hijack a cell’s genome to reproduce can accidentally leave behind a bit of gene and voila! It’s a gene change. Bacteria can reach out to other living bacteria and transfer genetic material to them, possibly altering the traits of the population.
Sometimes, events happen at a large scale that have huge and rapid effects on the overall makeup of a population. These big changes mark some of the turning points in the evolutionary history of many species.
The word bottleneck pretty much says it all. Something happens over time to reduce the population so much that only a relatively few individuals survive. A bottleneck of this sort reduces the variability of a population. These events can be natural–such as those resulting from natural disasters–or they can be human induced, such as species bottlenecks we’ve induced through overhunting or habitat reduction.
Founder effect: starting small
Sometimes, the genes flow out of a population. This flow occurs when individuals leave and migrate elsewhere. They take their genes with them (obviously), and the populations they found will initially carry only those genes. Whatever they had with them genetically when they founded the population can affect that population. If there’s a gene that gives everyone a deadly reaction to barbiturates, that population will have a higher-than-usual frequency of people with that response, thanks to this founder effect.
Gene flow leads to two key points to make about evolution: First, a population carries only the genes it inherits and generally acquires new versions through mutation or gene flow. Second, that gene for lethal susceptibility to a drug would be meaningless in a natural selection context as long as the environment didn’t include exposure to that drug. The take-home message is this: What’s OK for one environment may or may not be fit for another environment. The nature of Nature is change, and Nature offers no guarantees.
Hardy-Weinberg: when evolution is absent
With all of these possible mechanisms for evolution under their belts, scientists needed a way to measure whether or not the frequency of specific alleles was changing over time in a given population or staying in equilibrium. Not an easy job. They found–“they” being G. H. Hardy and Wilhelm Weinberg–that the best way to measure this was to predict what the outcome would be if there were no change in allele frequencies. In other words, to predict that from generation to generation, allele frequencies would simply stay in equilibrium. If measurements over time yielded changing frequencies, then the implication would be that evolution has happened.
Defining “Not Evolving”
So what does it mean to not evolve? There are some basic scenarios that must exist for a population not to be experiencing a change in allele frequency, i.e., no evolution. If there is a change, then one of the items in the list below must be false:
·Very large population (genetic drift can be a strong evolutionary mechanism in small populations)
·No migrations (in other words, no gene flow)
·No net mutations (no new variation introduced)
·Random mating (directed mating is one way nature selects organisms)
·No natural selection
In other words, a population that is not evolving is experiencing a complete absence of evolutionary processes. If any one of these is absent from a given population, then evolution is occurring and allele frequencies from generation to generation won’t be in equilibrium.
Arguably the most famous of the egg-laying monotremes, the improbable- seeming platypus. License.
One of the best examples of the influences of environmental pressures is what happens in similar environments a world apart. Before the modern-day groupings of mammals arose, the continent of
Australiaseparated from the rest of the world’s land masses, taking the proto-mammals that lived there with it. Over the ensuing millennia, these proto-mammals in Australiaevolved into the native species we see today on that continent, all marsupialsor monotremes.
Among mammals, there’s a division among those that lay eggs (monotremes), those that do most gestating in a pouch rather than a uterus (marsupials), and eutherians, which use a uterus for gestation (placental mammals).
Elsewhere in the world, most mammals developed from a common eutherian ancestor and, where marsupials still persisted, probably outcompeted them. In spite of this lengthy separation and different ancestry, however, for many of the examples of placental mammals, Australiahas a similar marsupial match. There’s the marsupial rodent that is like the rat. The marsupial wolf that is like the placental wolf. There’s even a marsupial anteater to match the placental one.
How did that happen an ocean apart with no gene flow? The answer is natural selection. The environment that made an organism with anteater characteristics best fit in South America was similar to the environment that made those characteristics a good fit in
Australia. Ditto the rats, ditto the wolf.
When similar environments result in unrelated organisms having similar characteristics, we call that process convergent evolution. It’s natural selection in relatively unrelated species in parallel. In both regions, nature uses the same set of environmental features to mold organisms into the best fit.
Note: This explanation of evolution and how it happens is not intended to be comprehensive or detailed or to include all possible mechanisms of evolution. It is simply an overview. In addition, it does not address epigenetics, which will be the subject of a different explainer.
Children working in a London hosiery mill around the turn of the century. Did they have “Nature-Deficit Disorder (TM)”? Source.
Maybe you’ve heard of the scourge plaguing modern-day children, the one known as Nature Deficit Disorder (TM). You won’t find it in any of the standard diagnostic manuals used to identify true disorders, but the “disorder” arises, so the story goes, as a result of keeping children inside for fear of their safety and “stranger danger,” loss of natural surroundings in cities and neighborhoods, and increased attractions indoors that prevent spending time outdoors.
This “disorder” is supposed to be an effect of modern times, the combined effects of controlling and fearful parents along with the irresistible screen-based attractions indoors. As a result of this “disorder,” children can allegedly be susceptible to any number of ills, including less respect for and understanding of nature, depression, shorter life spans, and obesity.
Concerns like these, it seems, have arisen with the advent of each new technological advance. One wonders if the invention of the wheel raised alarms that children might move through their natural surroundings too quickly to take them in. At any rate, while the person who invented this disorder, Richard Louv, has actually trademarked the term, it doesn’t seem to have made a big splash in the scientific literature. Given that studies are lacking–i.e., completely absent–about “nature deficit disorder,” one thing we can do is take a look back at how children lived before the technological age to see if their indoor-outdoor lives and exposure to the natural world were substantially different.
Go far enough back in human history, and of course, we all spent a lot of time outside. But how did we spend our time with the rise of civilization? Children in agrarian societies then and now worked from dawn to dusk as part of the family to put food on the table. In such a position, they certainly had no lack of exposure to nature, although how much they appreciated that endless grind could be in question. That is, of course, if they didn’t die in infancy or early childhood, as a large percentage of them did in spite of all that fresh air and time outside.
But what happened with children and how they spent their time with the rise of towns and cities? In early times, many of those cities were walled compounds, not necessarily hives of scum and villainy, but generally stacks upon stacks of living quarters existing solely for functionality. Nature? Outside the walls, where danger–including the most extreme kind of “stranger danger”–lurked. Cities that lacked walls, as ancient Rome did for a long period, still were more focused on efficient crowding and function far more than on nature, with only the wealthy having gardens, the modern equivalent of today’s back yards. In general, there were people, there were buildings, and there were more people. Not wildly different from, say, Manhattan today–except for that whole natural jewel known as Central Park.
This piling on of people, brick, mortar, more people, and wood continued for children who didn’t live in agrarian societies. With the Industrial Revolution, what may have really been a nature deficit disorder for a child living, in, say, London, became a genuine threat to health. While they certainly didn’t have television to keep them indoors, they also didn’t have child labor laws. The result was that children who once might have been at work at age 4 in a field were now at work at age 3 or 4 in a factory, putting in 12 or so hours a day before stepping out into the coal-smoked, animal-dung-scented air of the city.
Child labor wasn’t something confined to Industrial Revolution Britain, and it continues today, both for agriculture and industry. I do wonder if the children harvesting oranges in Brazil feel any closer to nature than the children weaving carpets in Egypt. Likely, there are deficits more profound for them to worry about.
The trigger for this overview of whether or not things have really changed over recorded history in terms of children’s exposure to the natural world is this series of articles in the New York Times (NYT). In case you hit the paywall, it is the NYT’s “Room for Debate” series and includes four articles addressing whether or not nature shows and films connect people to the natural world or “contribute to ‘nature deficit disorder’” by keeping people glued to screens instead of being outside.
Louv, the coiner of “Nature deficit disorder TM”, is one of the four contributors to the debate. He argues that viewing nature documentaries can inspire us to go outside. He also thinks many of us grew up watching “Lassie” instead of the “Gilligan’s Island” my generation watched, but perhaps there’s not a huge difference between Timmy in the well and Gilligan in the lagoon and consequent outdoor inspiration. At any rate, Louv does argue in favor of viewing nature shows, although from a very first-world perspective (like the Romans and gardens, we don’t all have back yards, for example).
Perhaps the least-defensible perspective is the argument that Ming (Frances) Kuo, an associate professor of natural resources and environmental sciences, has to offer. She compares nature documentaries to “junk food” and offers the obvious: They’re no comparison for the real world. For some reason, she implies that someone has argued that when you have access to TV, you don’t need access to nature, saying, “Scientists have been discovering that even in societies where just about everyone has access to a TV, Internet, or both, having access to nature matters.” I honestly don’t think anyone’s ever argued against that.
Does “nature deficit disorder” exist and is indoor screen time with nature documentaries to blame? In addition to the historical observations I’ve made above suggesting that children from previous eras haven’t necessarily been wandering the glades and meadows like wayward pixies, all I have to offer is a bit of anecdata, and I’m curious about the experiences of others. Historical comparisons suggest that city-dwelling children are no more deficient nature-wise today than city-dwelling children of yesteryear. But do nature documentaries help… or hinder?
When I was young and watching too much “Sesame Street,” “Gilligan’s Island,” and “Star Trek,” the only nature show available to me was “Wild Kingdom” (Mutual of Omaha’s, natch). Other than that, we had nothing unless a periodic NOVA episode came on public television.
I was interested in science and nature, but acquiring knowledge outside of what I read in a book was difficult. As a resident of the great metropolis of Waco, Tex., yes, I had a natural world to explore, but let’s face it: The primates there weren’t that interesting, and bluebonnets get you only so far. I had no access to real-life live-motion visuals, auditory inputs, or information delivered in any form except what I could read in a book. Talk about sensory limitations.
These days, my children have a nature documentary library that extends to dozens and dozens of choices. And they have watched every single one, some of them repeatedly. That’s not to say that they don’t also have dozens of well-thumbed field guides and encyclopedias covering fossils, dinosaurs, plants, bugs, sharks, rocks–the usual obsessions of the young who are interested in nature. Our “movie nights” often kick off with a nature documentary, and our pick of choice will frequently be one involving narration from David Attenborough. My children want to be David Attenborough–so do I, for that matter–and I can’t recall ever really having that feeling about Marlin Perkins or Jim Fowler.
And the upshot of that access to an expanse of nature documentaries I never had is that their knowledge of nature is practically encyclopedic. I’m the biologist in the family–or at least the one who has the biology degree–but my children often know more than I do about a specific plant or animal or ecosystem or area of the world, all thanks to these documentaries they watch. And when we’re outside, they extrapolate what they’ve learned, generalizing it to all kinds of local natural situations.
Do children today just need to be moving around more, somewhere, somehow? Oh, yes. But watching nature shows hasn’t exacerbated some kind of “nature deficit” my children might have, Minecraft obsessed as they are. And these documentaries haven’t replaced “real” nature with televised nature. Instead, the shows have expanded on and given context to the nature my children encounter, wherever that is–city, country, farm, sky, ocean, parking lot, grocery store, or even inside their own home, which is currently the scene of a sci-fi-like moth infestation that has triggered much excitement. I’d hazard that far from causing a deficit, nature shows have given my children a nature literacy that was unknown in previous generations.
What is your take on nature deficits and nature documentaries?
Anyone who has ADHD—attention-deficit/hyperactivity disorder—can tell you the stories. Stories of getting into constant trouble, hearing “sit down, sit still, be quiet” repeatedly, endlessly, feeling the urge to move, touch, jump, talk, roll, do anything but sit quietly at a desk, working on math. And, as anyone who has ADHD can also tell you, these traits often don’t exactly help you get ahead in modern society. School requires stillness, attention, focus on pencil and paper work. Most jobs require focus, attention, sometimes an ability to tolerate the sheer boredom of four walls of a grey cubicle for eight hours each day. Most people would struggle with that, but with attention deficit, it’s more than a struggle.
A cubicle environment obviously is probably not the best place for someone with ADHD, although it may be beneficial in less boxy workplaces. And school can be a long, troubling, negative process, as well. People used to blame the parents of children with this disorder, laying the cause of ADHD at the feet of poor parenting–and some are still trying to lay that blame. Science has something else to say about it, having demonstrated that genes are actually the primary contributors to ADHD, specifically genes that encode proteins whose job is to “receive” messages from a brain chemical called dopamine.
Dopamine signaling underlies all kinds of behaviors, but primarily it is known for its involvement in reward pathways, novelty seeking, and addiction. Specific forms, or alleles, of dopamine receptor genes have been strongly associated with ADHD, and this disorder can be viewed in many cases as a constant search for reward and novelty, a search that can translate as inattentiveness or hyperactivity.
Given that this dopamine-based manifestation is rooted in genes, the question arises of why it has persisted in humans throughout our evolution. If we look around at modern society, it’s easy to see that ADHD behaviors generally are not conducive to being one of the “fittest” in many situations that take up most of our time. Yet, there has been enough associated advantage for these gene forms to persist and allow their carriers to reproduce and pass them along to offspring.
And that’s where we need to think in nature’s evolutionary terms. Modern society is just that—modern. This way of life has only been around for, at most, a few thousand years, which can be a blink of an eye for processes of natural selection. Dial back time about 10,000 years or 20,000 years, and you’ll be hard pressed to find any humans living in an environment anything remotely like a cubicle.
Natural selection results from the interaction of genes and environment, and the “selection” Nature’s making is for an individual’s genetic makeup to have some representation in future generations. To look at this process through Nature’s lens, take the gene forms associated with ADHD and place them in a different environment and ask the question: Do they help or hurt or make no difference at all?
This question is exactly what researchers addressed when they looked at the effects of an ADHD-related gene form on a group of nomadic people, the Ariaal, in
Kenya. Some members of this population had, in only the last few decades, made a transition to a sedentary, city-type lifestyle. Others continued to live the fast-moving, nomadic existence of their herding ancestors.
Researchers looked at a version of a dopamine receptor called DRD4-7R, which also has been implicated in autism symptoms in people with ADHD. They found that city dwellers with this form of the gene didn’t fare as well in health as their sedentary cousins without it. But the Ariaal who continued their nomadic existence and carried the 7R form of the gene fared better than those nomadic tribesmen without it. To assess health, the researchers looked at body mass index and other factors. The results suggest that there might be some benefit to ADHD in the backdrop of a nomadic culture. although a more recent analysis of several studies together suggests a different form of this receptor may have an ADHD association (this kind of study, called a meta-analysis, doesn’t provide new data but synthesizes existing data).
Regardless of which gene forms are involved, you can imagine that in a nomadic culture, it might be useful to be always looking around, seeking novelty, thriving on the rewards of changing behaviors, defending food, and being always on the move. Someone with ADHD likely would be far better fit for this kind of lifestyle than would the best desk jockey in the world. This interesting study demonstrates that when it comes to some of the neurological developmental manifestations we call “disorders,” how negative or positive they are may be a matter of environment.
The four basic categories of molecules for building life are carbohydrates, lipids, proteins, and nucleic acids.
Carbohydrates serve many purposes, from energy to structure to chemical communication, as monomers or polymers.
Lipids, which are hydrophobic, also have different purposes, including energy storage, structure, and signaling.
Proteins, made of amino acids in up to four structural levels, are involved in just about every process of life.
The nucleic acids DNA and RNA consist of four nucleotide building blocks, and each has different purposes.
The longer version
Life is so diverse and unwieldy, it may surprise you to learn that we can break it down into four basic categories of molecules. Possibly even more implausible is the fact that two of these categories of large molecules themselves break down into a surprisingly small number of building blocks. The proteins that make up all of the living things on this planet and ensure their appropriate structure and smooth function consist of only 20 different kinds of building blocks. Nucleic acids, specifically DNA, are even more basic: only four different kinds of molecules provide the materials to build the countless different genetic codes that translate into all the different walking, swimming, crawling, oozing, and/or photosynthesizing organisms that populate the third rock from the Sun.
Big Molecules with Small Building Blocks
The functional groups, assembled into building blocks on backbones of carbon atoms, can be bonded together to yield large molecules that we classify into four basic categories. These molecules, in many different permutations, are the basis for the diversity that we see among living things. They can consist of thousands of atoms, but only a handful of different kinds of atoms form them. It’s like building apartment buildings using a small selection of different materials: bricks, mortar, iron, glass, and wood. Arranged in different ways, these few materials can yield a huge variety of structures.
We encountered functional groups and the SPHONC in Chapter 3. These components form the four categories of molecules of life. These Big Four biological molecules are carbohydrates, lipids, proteins, and nucleic acids. They can have many roles, from giving an organism structure to being involved in one of the millions of processes of living. Let’s meet each category individually and discover the basic roles of each in the structure and function of life.
You have met carbohydrates before, whether you know it or not. We refer to them casually as “sugars,” molecules made of carbon, hydrogen, and oxygen. A sugar molecule has a carbon backbone, usually five or six carbons in the ones we’ll discuss here, but it can be as few as three. Sugar molecules can link together in pairs or in chains or branching “trees,” either for structure or energy storage.
When you look on a nutrition label, you’ll see reference to “sugars.” That term includes carbohydrates that provide energy, which we get from breaking the chemical bonds in a sugar called glucose. The “sugars” on a nutrition label also include those that give structure to a plant, which we call fiber. Both are important nutrients for people.
Sugars serve many purposes. They give crunch to the cell walls of a plant or the exoskeleton of a beetle and chemical energy to the marathon runner. When attached to other molecules, like proteins or fats, they aid in communication between cells. But before we get any further into their uses, let’s talk structure.
The sugars we encounter most in basic biology have their five or six carbons linked together in a ring. There’s no need to dive deep into organic chemistry, but there are a couple of essential things to know to interpret the standard representations of these molecules.
Check out the sugars depicted in the figure. The top-left molecule, glucose, has six carbons, which have been numbered. The sugar to its right is the same glucose, with all but one “C” removed. The other five carbons are still there but are inferred using the conventions of organic chemistry: Anywhere there is a corner, there’s a carbon unless otherwise indicated. It might be a good exercise for you to add in a “C” over each corner so that you gain a good understanding of this convention. You should end up adding in five carbon symbols; the sixth is already given because that is conventionally included when it occurs outside of the ring.
On the left is a glucose with all of its carbons indicated. They’re also numbered, which is important to understand now for information that comes later. On the right is the same molecule, glucose, without the carbons indicated (except for the sixth one). Wherever there is a corner, there is a carbon, unless otherwise indicated (as with the oxygen). On the bottom left is ribose, the sugar found in RNA. The sugar on the bottom right is deoxyribose. Note that at carbon 2 (*), the ribose and deoxyribose differ by a single oxygen.
The lower left sugar in the figure is a ribose. In this depiction, the carbons, except the one outside of the ring, have not been drawn in, and they are not numbered. This is the standard way sugars are presented in texts. Can you tell how many carbons there are in this sugar? Count the corners and don’t forget the one that’s already indicated!
If you said “five,” you are right. Ribose is a pentose (pent = five) and happens to be the sugar present in ribonucleic acid, or RNA. Think to yourself what the sugar might be in deoxyribonucleic acid, or DNA. If you thought, deoxyribose, you’d be right.
The fourth sugar given in the figure is a deoxyribose. In organic chemistry, it’s not enough to know that corners indicate carbons. Each carbon also has a specific number, which becomes important in discussions of nucleic acids. Luckily, we get to keep our carbon counting pretty simple in basic biology. To count carbons, you start with the carbon to the right of the non-carbon corner of the molecule. The deoxyribose or ribose always looks to me like a little cupcake with a cherry on top. The “cherry” is an oxygen. To the right of that oxygen, we start counting carbons, so that corner to the right of the “cherry” is the first carbon. Now, keep counting. Here’s a little test: What is hanging down from carbon 2 of the deoxyribose?
If you said a hydrogen (H), you are right! Now, compare the deoxyribose to the ribose. Do you see the difference in what hangs off of the carbon 2 of each sugar? You’ll see that the carbon 2 of ribose has an –OH, rather than an H. The reason the deoxyribose is called that is because the O on the second carbon of the ribose has been removed, leaving a “deoxyed” ribose. This tiny distinction between the sugars used in DNA and RNA is significant enough in biology that we use it to distinguish the two nucleic acids.
In fact, these subtle differences in sugars mean big differences for many biological molecules. Below, you’ll find a couple of ways that apparently small changes in a sugar molecule can mean big changes in what it does. These little changes make the difference between a delicious sugar cookie and the crunchy exoskeleton of a dung beetle.
Sugar and Fuel
A marathon runner keeps fuel on hand in the form of “carbs,” or sugars. These fuels provide the marathoner’s straining body with the energy it needs to keep the muscles pumping. When we take in sugar like this, it often comes in the form of glucose molecules attached together in a polymer called starch. We are especially equipped to start breaking off individual glucose molecules the minute we start chewing on a starch.
Double X Extra: A monomer is a building block (mono = one) and a polymer is a chain of monomers. With a few dozen monomers or building blocks, we get millions of different polymers. That may sound nutty until you think of the infinity of values that can be built using only the numbers 0 through 9 as building blocks or the intricate programming that is done using only a binary code of zeros and ones in different combinations.
Our bodies then can rapidly take the single molecules, or monomers, into cells and crack open the chemical bonds to transform the energy for use. The bonds of a sugar are packed with chemical energy that we capture to build a different kind of energy-containing molecule that our muscles access easily. Most species rely on this process of capturing energy from sugars and transforming it for specific purposes.
Polysaccharides: Fuel and Form
Plants use the Sun’s energy to make their own glucose, and starch is actually a plant’s way of storing up that sugar. Potatoes, for example, are quite good at packing away tons of glucose molecules and are known to dieticians as a “starchy” vegetable. The glucose molecules in starch are packed fairly closely together. A string of sugar molecules bonded together through dehydration synthesis, as they are in starch, is a polymer called a polysaccharide (poly = many; saccharide = sugar). When the monomers of the polysaccharide are released, as when our bodies break them up, the reaction that releases them is called hydrolysis.
Double X Extra: The specific reaction that hooks one monomer to another in a covalent bond is called dehydration synthesis because in making the bond–synthesizing the larger molecule–a molecule of water is removed (dehydration). The reverse is hydrolysis (hydro = water; lysis = breaking), which breaks the covalent bond by the addition of a molecule of water.
Although plants make their own glucose and animals acquire it by eating the plants, animals can also package away the glucose they eat for later use. Animals, including humans, store glucose in a polysaccharide called glycogen, which is more branched than starch. In us, we build this energy reserve primarily in the liver and access it when our glucose levels drop.
Whether starch or glycogen, the glucose molecules that are stored are bonded together so that all of the molecules are oriented the same way. If you view the sixth carbon of the glucose to be a “carbon flag,” you’ll see in the figure that all of the glucose molecules in starch are oriented with their carbon flags on the upper left.
The orientation of monomers of glucose in polysaccharides can make a big difference in the use of the polymer. The glucoses in the molecule on the top are all oriented “up” and form starch. The glucoses in the molecule on the bottom alternate orientation to form cellulose, which is quite different in its function from starch.
Storing up sugars for fuel and using them as fuel isn’t the end of the uses of sugar. In fact, sugars serve as structural molecules in a huge variety of organisms, including fungi, bacteria, plants, and insects.
The primary structural role of a sugar is as a component of the cell wall, giving the organism support against gravity. In plants, the familiar old glucose molecule serves as one building block of the plant cell wall, but with a catch: The molecules are oriented in an alternating up-down fashion. The resulting structural sugar is called cellulose.
That simple difference in orientation means the difference between a polysaccharide as fuel for us and a polysaccharide as structure. Insects take it step further with the polysaccharide that makes up their exoskeleton, or outer shell. Once again, the building block is glucose, arranged as it is in cellulose, in an alternating conformation. But in insects, each glucose has a little extra added on, a chemical group called an N-acetyl group. This addition of a single functional group alters the use of cellulose and turns it into a structural molecule that gives bugs that special crunchy sound when you accidentally…ahem…step on them.
These variations on the simple theme of a basic carbon-ring-as-building-block occur again and again in biological systems. In addition to serving roles in structure and as fuel, sugars also play a role in function. The attachment of subtly different sugar molecules to a protein or a lipid is one way cells communicate chemically with one another in refined, regulated interactions. It’s as though the cells talk with each other using a specialized, sugar-based vocabulary. Typically, cells display these sugary messages to the outside world, making them available to other cells that can recognize the molecular language.
Lipids: The Fatty Trifecta
Starch makes for good, accessible fuel, something that we immediately attack chemically and break up for quick energy. But fats are energy that we are supposed to bank away for a good long time and break out in times of deprivation. Like sugars, fats serve several purposes, including as a dense source of energy and as a universal structural component of cell membranes everywhere.
Fats: the Good, the Bad, the Neutral
Turn again to a nutrition label, and you’ll see a few references to fats, also known as lipids. (Fats are slightly less confusing that sugars in that they have only two names.) The label may break down fats into categories, including trans fats, saturated fats, unsaturated fats, and cholesterol. You may have learned that trans fats are “bad” and that there is good cholesterol and bad cholesterol, but what does it all mean?
Let’s start with what we mean when we say saturated fat. The question is, saturated with what? There is a specific kind of dietary fat call the triglyceride. As its name implies, it has a structural motif in which something is repeated three times. That something is a chain of carbons and hydrogens, hanging off in triplicate from a head made of glycerol, as the figure shows. Those three carbon-hydrogen chains, or fatty acids, are the “tri” in a triglyceride. Chains like this can be many carbons long.
Double X Extra: We call a fatty acid a fatty acid because it’s got a carboxylic acid attached to a fatty tail. A triglyceride consists of three of these fatty acids attached to a molecule called glycerol. Our dietary fat primarily consists of these triglycerides.
Triglycerides come in several forms. You may recall that carbon can form several different kinds of bonds, including single bonds, as with hydrogen, and double bonds, as with itself. A chain of carbon and hydrogens can have every single available carbon bond taken by a hydrogen in single covalent bond. This scenario of hydrogen saturation yields a saturated fat. The fat is saturated to its fullest with every covalent bond taken by hydrogens single bonded to the carbons.
Saturated fats have predictable characteristics. They lie flat easily and stick to each other, meaning that at room temperature, they form a dense solid. You will realize this if you find a little bit of fat on you to pinch. Does it feel pretty solid? That’s because animal fat is saturated fat. The fat on a steak is also solid at room temperature, and in fact, it takes a pretty high heat to loosen it up enough to become liquid. Animals are not the only organisms that produce saturated fat–avocados and coconuts also are known for their saturated fat content.
The top graphic above depicts a triglyceride with the glycerol, acid, and three hydrocarbon tails. The tails of this saturated fat, with every possible hydrogen space occupied, lie comparatively flat on one another, and this kind of fat is solid at room temperature. The fat on the bottom, however, is unsaturated, with bends or kinks wherever two carbons have double bonded, booting a couple of hydrogens and making this fat unsaturated, or lacking some hydrogens. Because of the space between the bumps, this fat is probably not solid at room temperature, but liquid.
You can probably now guess what an unsaturated fat is–one that has one or more hydrogens missing. Instead of single bonding with hydrogens at every available space, two or more carbons in an unsaturated fat chain will form a double bond with carbon, leaving no space for a hydrogen. Because some carbons in the chain share two pairs of electrons, they physically draw closer to one another than they do in a single bond. This tighter bonding result in a “kink” in the fatty acid chain.
In a fat with these kinks, the three fatty acids don’t lie as densely packed with each other as they do in a saturated fat. The kinks leave spaces between them. Thus, unsaturated fats are less dense than saturated fats and often will be liquid at room temperature. A good example of a liquid unsaturated fat at room temperature is canola oil.
A few decades ago, food scientists discovered that unsaturated fats could be resaturated or hydrogenated to behave more like saturated fats and have a longer shelf life. The process of hydrogenation–adding in hydrogens–yields trans fat. This kind of processed fat is now frowned upon and is being removed from many foods because of its associations with adverse health effects. If you check a food label and it lists among the ingredients “partially hydrogenated” oils, that can mean that the food contains trans fat.
Double X Extra: A triglyceride can have up to three different fatty acids attached to it. Canola oil, for example, consists primarily of oleic acid, linoleic acid, and linolenic acid, all of which are unsaturated fatty acids with 18 carbons in their chains.
Why do we take in fat anyway? Fat is a necessary nutrient for everything from our nervous systems to our circulatory health. It also, under appropriate conditions, is an excellent way to store up densely packaged energy for the times when stores are running low. We really can’t live very well without it.
Phospholipids: An Abundant Fat
You may have heard that oil and water don’t mix, and indeed, it is something you can observe for yourself. Drop a pat of butter–pure saturated fat–into a bowl of water and watch it just sit there. Even if you try mixing it with a spoon, it will just sit there. Now, drop a spoon of salt into the water and stir it a bit. The salt seems to vanish. You’ve just illustrated the difference between a water-fearing (hydrophobic) and a water-loving (hydrophilic) substance.
Generally speaking, compounds that have an unequal sharing of electrons (like ions or anything with a covalent bond between oxygen and hydrogen or nitrogen and hydrogen) will be hydrophilic. The reason is that a charge or an unequal electron sharing gives the molecule polarity that allows it to interact with water through hydrogen bonds. A fat, however, consists largely of hydrogen and carbon in those long chains. Carbon and hydrogen have roughly equivalent electronegativities, and their electron-sharing relationship is relatively nonpolar. Fat, lacking in polarity, doesn’t interact with water. As the butter demonstrated, it just sits there.
There is one exception to that little maxim about fat and water, and that exception is the phospholipid. This lipid has a special structure that makes it just right for the job it does: forming the membranes of cells. A phospholipid consists of a polar phosphate head–P and O don’t share equally–and a couple of nonpolar hydrocarbon tails, as the figure shows. If you look at the figure, you’ll see that one of the two tails has a little kick in it, thanks to a double bond between the two carbons there.
Phospholipids form a double layer and are the major structural components of cell membranes. Their bend, or kick, in one of the hydrocarbon tails helps ensure fluidity of the cell membrane. The molecules are bipolar, with hydrophilic heads for interacting with the internal and external watery environments of the cell and hydrophobic tails that help cell membranes behave as general security guards.
The kick and the bipolar (hydrophobic and hydrophilic) nature of the phospholipid make it the perfect molecule for building a cell membrane. A cell needs a watery outside to survive. It also needs a watery inside to survive. Thus, it must face the inside and outside worlds with something that interacts well with water. But it also must protect itself against unwanted intruders, providing a barrier that keeps unwanted things out and keeps necessary molecules in.
Phospholipids achieve it all. They assemble into a double layer around a cell but orient to allow interaction with the watery external and internal environments. On the layer facing the inside of the cell, the phospholipids orient their polar, hydrophilic heads to the watery inner environment and their tails away from it. On the layer to the outside of the cell, they do the same.
As the figure shows, the result is a double layer of phospholipids with each layer facing a polar, hydrophilic head to the watery environments. The tails of each layer face one another. They form a hydrophobic, fatty moat around a cell that serves as a general gatekeeper, much in the way that your skin does for you. Charged particles cannot simply slip across this fatty moat because they can’t interact with it. And to keep the fat fluid, one tail of each phospholipid has that little kick, giving the cell membrane a fluid, liquidy flow and keeping it from being solid and unforgiving at temperatures in which cells thrive.
Steroids: Here to Pump You Up?
Our final molecule in the lipid fatty trifecta is cholesterol. As you may have heard, there are a few different kinds of cholesterol, some of which we consider to be “good” and some of which is “bad.” The good cholesterol, high-density lipoprotein, or HDL, in part helps us out because it removes the bad cholesterol, low-density lipoprotein or LDL, from our blood. The presence of LDL is associated with inflammation of the lining of the blood vessels, which can lead to a variety of health problems.
But cholesterol has some other reasons for existing. One of its roles is in the maintenance of cell membrane fluidity. Cholesterol is inserted throughout the lipid bilayer and serves as a block to the fatty tails that might otherwise stick together and become a bit too solid.
Cholesterol’s other starring role as a lipid is as the starting molecule for a class of hormones we called steroids or steroid hormones. With a few snips here and additions there, cholesterol can be changed into the steroid hormones progesterone, testosterone, or estrogen. These molecules look quite similar, but they play very different roles in organisms. Testosterone, for example, generally masculinizes vertebrates (animals with backbones), while progesterone and estrogen play a role in regulating the ovulatory cycle.
Double X Extra: A hormone is a blood-borne signaling molecule. It can be lipid based, like testosterone, or short protein, like insulin.
As you progress through learning biology, one thing will become more and more clear: Most cells function primarily as protein factories. It may surprise you to learn that proteins, which we often talk about in terms of food intake, are the fundamental molecule of many of life’s processes. Enzymes, for example, form a single broad category of proteins, but there are millions of them, each one governing a small step in the molecular pathways that are required for living.
Levels of Structure
Amino acids are the building blocks of proteins. A few amino acids strung together is called a peptide, while many many peptides linked together form a polypeptide. When many amino acids strung together interact with each other to form a properly folded molecule, we call that molecule a protein.
For a string of amino acids to ultimately fold up into an active protein, they must first be assembled in the correct order. The code for their assembly lies in the DNA, but once that code has been read and the amino acid chain built, we call that simple, unfolded chain the primary structure of the protein.
This chain can consist of hundreds of amino acids that interact all along the sequence. Some amino acids are hydrophobic and some are hydrophilic. In this context, like interacts best with like, so the hydrophobic amino acids will interact with one another, and the hydrophilic amino acids will interact together. As these contacts occur along the string of molecules, different conformations will arise in different parts of the chain. We call these different conformations along the amino acid chain the protein’s secondary structure.
Once those interactions have occurred, the protein can fold into its final, or tertiary structure and be ready to serve as an active participant in cellular processes. To achieve the tertiary structure, the amino acid chain’s secondary interactions must usually be ongoing, and the pH, temperature, and salt balance must be just right to facilitate the folding. This tertiary folding takes place through interactions of the secondary structures along the different parts of the amino acid chain.
The final product is a properly folded protein. If we could see it with the naked eye, it might look a lot like a wadded up string of pearls, but that “wadded up” look is misleading. Protein folding is a carefully regulated process that is determined at its core by the amino acids in the chain: their hydrophobicity and hydrophilicity and how they interact together.
In many instances, however, a complete protein consists of more than one amino acid chain, and the complete protein has two or more interacting strings of amino acids. A good example is hemoglobin in red blood cells. Its job is to grab oxygen and deliver it to the body’s tissues. A complete hemoglobin protein consists of four separate amino acid chains all properly folded into their tertiary structures and interacting as a single unit. In cases like this involving two or more interacting amino acid chains, we say that the final protein has a quaternary structure. Some proteins can consist of as many as a dozen interacting chains, behaving as a single protein unit.
A Plethora of Purposes
What does a protein do? Let us count the ways. Really, that’s almost impossible because proteins do just about everything. Some of them tag things. Some of them destroy things. Some of them protect. Some mark cells as “self.” Some serve as structural materials, while others are highways or motors. They aid in communication, they operate as signaling molecules, they transfer molecules and cut them up, they interact with each other in complex, interrelated pathways to build things up and break things down. They regulate genes and package DNA, and they regulate and package each other.
As described above, proteins are the final folded arrangement of a string of amino acids. One way we obtain these building blocks for the millions of proteins our bodies make is through our diet. You may hear about foods that are high in protein or people eating high-protein diets to build muscle. When we take in those proteins, we can break them apart and use the amino acids that make them up to build proteins of our own.
How does a cell know which proteins to make? It has a code for building them, one that is especially guarded in a cellular vault in our cells called the nucleus. This code is deoxyribonucleic acid, or DNA. The cell makes a copy of this code and send it out to specialized structures that read it and build proteins based on what they read. As with any code, a typo–a mutation–can result in a message that doesn’t make as much sense. When the code gets changed, sometimes, the protein that the cell builds using that code will be changed, too.
Biohazard!The names associated with nucleic acids can be confusing because they all start with nucle-. It may seem obvious or easy now, but a brain freeze on a test could mix you up. You need to fix in your mind that the shorter term (10 letters, four syllables), nucleotide, refers to the smaller molecule, the three-part building block. The longer term (12 characters, including the space, and five syllables), nucleic acid, which is inherent in the names DNA and RNA, designates the big, long molecule.
DNA vs. RNA: A Matter of Structure
DNA and its nucleic acid cousin, ribonucleic acid, or RNA, are both made of the same kinds of building blocks. These building blocks are called nucleotides. Each nucleotide consists of three parts: a sugar (ribose for RNA and deoxyribose for DNA), a phosphate, and a nitrogenous base. In DNA, every nucleotide has identical sugars and phosphates, and in RNA, the sugar and phosphate are also the same for every nucleotide.
So what’s different? The nitrogenous bases. DNA has a set of four to use as its coding alphabet. These are the purines, adenine and guanine, and the pyrimidines, thymine and cytosine. The nucleotides are abbreviated by their initial letters as A, G, T, and C. From variations in the arrangement and number of these four molecules, all of the diversity of life arises. Just four different types of the nucleotide building blocks, and we have you, bacteria, wombats, and blue whales.
RNA is also basic at its core, consisting of only four different nucleotides. In fact, it uses three of the same nitrogenous bases as DNA–A, G, and C–but it substitutes a base called uracil (U) where DNA uses thymine. Uracil is a pyrimidine.
DNA vs. RNA: Function Wars
An interesting thing about the nitrogenous bases of the nucleotides is that they pair with each other, using hydrogen bonds, in a predictable way. An adenine will almost always bond with a thymine in DNA or a uracil in RNA, and cytosine and guanine will almost always bond with each other. This pairing capacity allows the cell to use a sequence of DNA and build either a new DNA sequence, using the old one as a template, or build an RNA sequence to make a copy of the DNA.
These two different uses of A-T/U and C-G base pairing serve two different purposes. DNA is copied into DNA usually when a cell is preparing to divide and needs two complete sets of DNA for the new cells. DNA is copied into RNA when the cell needs to send the code out of the vault so proteins can be built. The DNA stays safely where it belongs.
RNA is really a nucleic acid jack-of-all-trades. It not only serves as the copy of the DNA but also is the main component of the two types of cellular workers that read that copy and build proteins from it. At one point in this process, the three types of RNA come together in protein assembly to make sure the job is done right.
According to Leslie Brunetta, she now has much more hair than she had last July.
We became aware of Leslie Brunetta because of her book, Spider Silk: Evolution and 400 Million Years of Spinning, Waiting, Snagging, and Mating, co-authored with Catherine L. Craig. Thanks to a piece Leslie wrote for the Concord Monitor (and excerpted here), we also learned that she is a breast cancer survivor. Leslie agreed to an interview about her experience, and in her emailed responses, she candidly talks about her diagnosis, treatment, and follow-up for her cancers, plural: She was diagnosed simultaneously with two types of breast cancer.
DXS: In your Concord Monitor piece, you describe the link between an understanding of the way evolution happens and some of the advances in modern medicine. What led you to grasp the link between the two?
LB: I think, because I’m not a scientist (I’m an English major), a lot of things that scientists think are obvious strike me as revelations. I somehow had never realized that the search for what would turn out to be DNA began with trying to explain how, in line with the theory of evolution by natural selection, variation arises and traits are passed from generation to generation. As I was figuring out what each chapter in Spider Silk would be about, I tried to think about the questions non-biologists like me would still have about evolution when they got to that point in the book. By the time we got past dragline silk, I realized that we had so far fleshed out the ways that silk proteins could and have evolved at the genetic level. But that explanation probably wouldn’t answer readers’ questions about how, for example, abdominal spinnerets—which are unique to spiders—might have evolved: the evolution of silk is easier to untangle than the evolution of body parts, which is why we focused on it in the first place.
I decided I wanted to write a chapter on “evo-devo,” evolutionary developmental biology, partly because there was a cool genetic study on the development of spinnerets that showed they’ve evolved from limbs. Fortunately, my co-author, Cay Craig, and editor at Yale, Jean Thomson Black, okayed the idea, because that chapter wasn’t in the original proposal. Writing that chapter, I learned why it took so long—nearly a century—to get from Darwin and Mendel to Watson and Crick and then so long again to get to where we are today. If we non-scientists understand something scientific, it’s often how it works, not how a whole string of people over the course of decades building on each other’s work discovered how it works. I knew evolution was the accumulation of gene changes, but, until I wrote that chapter, it hadn’t occurred to me that people began to look for genes because they wanted to understand evolution.
So that was all in the spider part of my life. Then, a few months into the cancer part of my life, I was offered a test called Oncotype DX, which would look at genetic markers in my tumor cells to develop a risk profile that could help me decide whether I should have chemotherapy plus tamoxifen or just tamoxifen. The results turned out to be moot in my case because I had a number of positive lymph nodes, although it was reassuring to find out that the cancer was considered low risk for recurrence. But still—the idea that a genetic test could let some women avoid chemo without taking on extra risk, that’s huge. No one would want to go through chemo if it wasn’t necessary. So by then I was thinking, “Thank you, Darwin!”
And then, coincidentally, the presidential primary season was heating up, and there were a number of serious candidates (well, serious in the sense that they had enough backing to get into the debates) who proudly declared that they had no time for the theory of evolution. And year after year these stupid anti-evolution bills are introduced in various state legislatures. While I was lying on the couch hanging out in the days after chemo sessions, I started thinking, “So, given that you don’t give any credence to Darwin and his ideas, would you refuse on principle to take the Oncotype test or gene-based therapies like Gleevec or Herceptin if you had cancer or if someone in your family had cancer? Somehow I don’t think so.” That argument is not going to convince hard-core denialists (nothing will), but maybe the cognitive dissonance in connection with something as concrete as cancer will make some people who waver want to find out more.
DXS: You mention having been diagnosed with two different forms of cancer, one in each breast. Can you say what each kind was and, if possible, how they differed?
LB: Yes, I unfortunately turned out to be an “interesting” case. This is one arena where, if you possibly can, you want to avoid being interesting. At first it seemed that I had a tiny lesion that was an invasive ductal carcinoma (IDC) and that I would “just” need a lumpectomy and radiation. Luckily for me, the doctor reading my mammogram is known as an eagle eye, and she saw a few things that—given the positive finding from the biopsy—concerned her. She recommended an MRI. In fact, even though I switched to another hospital for my surgery, she sent emails there saying I should have an MRI. That turned up “concerning” spots in both breasts, which led to more biopsies, which revealed multiple tiny cancerous lesions. The only reasonable option was then a double mastectomy.
The lesions in the right breast were IDCs. About 70% of breast cancers are diagnosed as IDCs. Those cancers start with the cells lining the milk ducts. The ones in the left breast were invasive lobular carcinomas (ILCs), which start in the lobules at the end of the milk ducts. Only about 10% of breast cancers are ILCs.
Oncologists hate lobular cancer. Unlike ductal cancers, which form as clumps of cells, lobular cancers form as single-file ribbons of cells. The tissue around ductal cancer cells reacts to those cells, which is why someone may feel a lump—she’s (or he’s) not feeling the cancer itself but the inflammation of the tissue around it. And because the cells clump, they show up more readily on mammograms. Not so lobular cancers. They mostly don’t give rise to lumps and they’re hard to spot on mammograms. They snake their way through tissue for quite a while without bothering anything.
In my case, this explains why last spring felt like an unremitting downhill slide. Every time someone looked deeper, they found something worse. It turned out that on my left side, the lobular side, I had multiple positive lymph nodes, which was why I needed not just chemo but also radiation (which usually isn’t given after a mastectomy). That was the side that didn’t even show up much on the mammogram. On the right side, the ductal side, which provoked the initial suspicions, my nodes were clear. I want to write about this soon, because I want to find out more about it. I’ve only recently gotten to the place emotionally where I think I can deal with reading the research papers as opposed to more general information. By the way, the resource that most helped us better understand what my doctors were talking about was Dr. Susan Love’s Breast Book. It was invaluable as we made our way through this process, although it turned out that I had very few decisions to make because there was usually only one good option.
DXS: As part of your treatment, you had a double mastectomy. One of our goals with this interview is to tell women what some of these experiences with treatment are like. If you’re comfortable doing so, could you tell us a little bit about what a double mastectomy entails and what you do after one in practical terms?
LB: A mastectomy is a strange operation. In a way, it’s more of an emotional and psychological experience than a physical experience. My surgeon, who was fantastic, is a man, and when we discussed the need for the mastectomies he said that I would be surprised at how little pain would be involved and how quick the healing would be. Even though I trusted him a lot by then, my reaction was pretty much, “Like you would know, right?” But he did know. When you think about it, it’s fairly non-invasive surgery. Unless the cancer has spread to the surrounding area, which doesn’t happen very often now due to early detection, no muscle or bone is removed. (Until relatively recently, surgeons removed the major muscle in the chest wall, and sometimes even bone, because they believed it would cut the risk of recurrence. That meant that many women lost function in their arm and also experienced back problems.) None of your organs are touched. They don’t go into your abdominal cavity. Also, until recently, they removed a whole clump of underarm lymph nodes when they did lumpectomies or mastectomies. Now they usually remove just a “sentinel node,” because they know that it will give them a fairly reliable indicator of whether the cancer has spread to the other nodes. That also makes the surgery less traumatic than it used to be.
I opted not to have reconstruction. Reconstruction is a good choice for many women, but I didn’t see many benefits for me and I didn’t like the idea of a more complicated surgery. My surgery was only about two hours. I don’t remember any pain at all afterwards, and my husband says I never complained of any. I was in the hospital for just one night. By the next day, I was on ibuprofen only. The bandages came off two days after the surgery.
That’s shocking, to see your breasts gone and replaced by thin red lines, no matter how well you’ve prepared yourself. It made the cancer seem much more real in some way than it had seemed before. In comparison, the physical recovery from the surgery was fairly minor because I had no infections or complications. There were drains in place for about 10 days to collect serum, which would otherwise collect under the skin, and my husband dealt with emptying them twice a day and measuring the amount. I had to sleep on my back, propped up, because of where the drains were placed, high up on my sides, and I never really got used to that. It was a real relief to have the drains removed.
My surgeon told me to start doing stretching exercises with my arms right away, and that’s really important. I got my full range of motion back within a couple of months. But even though I had my surgery last March, I’ve noticed lately that if I don’t stretch fully, like in yoga, things tighten up. That may be because of the radiation, though, because it’s only on my left side. Things are never quite the same as they were before the surgery, though. Because I did have to have the axillary nodes out on my left side, my lymph system is disrupted. I haven’t had any real problems with lymphedema yet, and I may never, but in the early months I noticed that my hands would swell if I’d been walking around a lot, and I’d have to elevate them to get them to drain back. That rarely happens now. But I’ve been told I need to wear a compression sleeve if I fly because the change in air pressure can cause lymph to collect. Also, I’m supposed to protect my hands and arms from cuts as much as possible. It seems to me that small nicks on my fingers take longer to heal than they used to. So even though most of the time it seems like it’s all over, I guess in those purely mechanical ways it’s never over. It’s not just that you no longer have breasts, it’s also that nerves and lymph channels and bits of tissue are also missing or moved around.
The bigger question is how one deals with now lacking breasts. I’ve decided not to wear prostheses. I can get away with it because I was small breasted, I dress in relatively loose clothes anyway, and I’ve gained confidence over time that no one notices or cares and I care less now if they do notice. But getting that self-confidence took quite a while. Obviously, it has an effect on my sex life, but we have a strong bond and it’s just become a piece of that bond. The biggest thing is that it’s always a bit of a shock when I catch sight of myself naked in a mirror because it’s a reminder that I’ve had cancer and there’s no getting around the fact that that sucks.
DXS: My mother-in-law completed radiation and chemo for breast cancer last year, and if I remember correctly, she had to go frequently for a period of weeks for radiation. Was that you experience? Can you describe for our readers what the time investment was like and what the process was like?
LB: I went for radiation 5 days a week for about 7 weeks. Three days a week, I’d usually be in and out of the hospital within 45 minutes. One day a week, I met with the radiology oncologist and a nurse to debrief, which was also a form of emotional therapy for me. And one day a week, they laid on a chair massage, and the nurse/massage therapist who gave the massage was great to talk to, so that was more therapy. Radiation was easy compared to chemo. Some people experience skin burning and fatigue, but I was lucky that I didn’t experience either. Because I’m a freelancer, the time investment wasn’t a burden for me. I’m also lucky living where I live, because I could walk to the hospital. It was a pleasant 3-mile round-trip walk, and I think the walking helped me a lot physically and mentally.
DXS: And now to the chemo. My interest in interviewing you about your experience began with a reference you made on Twitter to “chemo brain,” and of course, after reading your evolution-medical advances piece. Can you tell us a little about what the process of receiving chemotherapy is like? How long does it take? How frequently (I know this varies, but your experience)?
LB: Because of my age (I was considered young, which was always nice to hear) and state of general good health, my oncologist put me on a dose-dense AC-T schedule. This meant going for treatment every two weeks over the course of 16 weeks—8 treatment sessions. At the first 4 sessions, I was given Adriamycin and Cytoxan(AC), and the last 4 sessions I was given Taxol (T). The idea behind giving multiple drugs and giving them frequently is that they all attack cancer cells in different ways and—it goes back to evolution—by attacking them frequently and hard on different fronts, you’re trying to avoid selecting for a population that’s resistant to one or more of the drugs. They can give the drugs every two weeks to a lot of patients now because they’ve got drugs to boost the production of white blood cells, which the cancer drugs suppress. After most chemo sessions, I went back the next day for a shot of one of these drugs, Neulasta.
The chemo clinic was, bizarrely, a very relaxing place. The nurses who work there were fantastic, and the nurse assigned to me, Kathy, was always interesting to talk with. She had a great sense of humor, and she was also interested in the science behind everything we were doing, so if I ever had questions she didn’t have ready answers for, she’d find out for me. A lot of patients were there at the same time, but we each had a private space. You’d sit in a big reclining chair. They had TVs and DVDs, but I usually used it as an opportunity to read. My husband sat through the first session with me, and a close friend who had chemo for breast cancer 15 years ago sat through a few other sessions, but once I got used to it, I was comfortable being there alone. Because of the nurses, it never felt lonely.
I’d arrive and settle in. Kathy would take blood for testing red and white blood counts and, I think, liver function and some other things, and she’d insert a needle and start a saline drip while we waited for the results. I’ve always had large veins, so I opted to have the drugs administered through my arm rather than having a port implanted in my chest. Over the course of three to four hours, she’d change the IV bags. Some of the bags were drugs to protect against nausea, so I’d start to feel kind of fuzzy—I don’t think I retained a whole lot of what I read there! The Adriamycin was bright orange; they call it the Red Devil, because it can chew up your veins—sometimes it felt like it was burning but Kathy could stop that by slowing the drip. Otherwise, it was fairly uneventful. I’d have snacks and usually ate lunch while still hooked up.
I was lucky I never had any reactions to any of the drugs, so actually getting the chemo was a surprisingly pleasant experience just because of the atmosphere. On the one hand, you’re aware of all these people around you struggling with cancer and you know things aren’t going well for some of them, so it’s heartbreaking, and also makes you consider, sometimes fearfully, your own future no matter how well you’re trying to brace yourself up. But at the same time, the people working there are so positive, but not in a Pollyannaish-false way, that they helped me as I tried to stay positive. The social worker stopped in with each patient every session, and she was fantastic—I could talk out any problems or fears I had with her, and that helped a huge amount.
DXS: Would you be able to run us through a timeline of the physical effects of chemotherapy after an infusion? How long does it take before it hits hardest? My mother-in-law told me that her biggest craving, when she could eat, was for carb-heavy foods like mashed potatoes and for soups, like vegetable soup. What was your experience with that?
LB: My biggest fear when I first learned I would need chemo was nausea. My oncologist told us that they had nausea so well controlled that over the past few years, she had only had one or two patients who had experienced it. As with the surgeon’s prediction about mastectomy pain, this turned out to be true: I never had even a single moment of nausea.
But there were all sorts of other effects. For the first few days after a session, the most salient effects were actually from the mix of drugs I took to stave off nausea. I generally felt pretty fuzzy, but not necessarily sleepy—part of the mix was steroids, so you’re a little hyped. There’s no way I’d feel safe driving on those days, for example. I’d sleep well the first three nights because I took Ativan, which has an anti-nausea effect. But except for those days, my sleep was really disrupted. Partly that’s because, I’m guessing, the chemo hits certain cells in your brain and partly it’s because you get thrown into chemical menopause, so there were a lot of night hot flashes. Even though I’d already started into menopause, this chemo menopause was a lot more intense and included all the symptoms regularly associated with menopause.
By the end of the first session, I was feeling pretty joyful because it was much less bad than I had thought it would be. By the second week in the two-week cycle, I felt relatively normal. But even though it never got awful, the effects started to accumulate. My hair started to fall out the morning I was going to an award ceremony for Spider Silk. It was ok at the ceremony, but we shaved it off that night. I decided not to wear a wig. First, it was the summer, and it would have been hot. Second, I usually have close to a buzz cut, and I can’t imagine anyone would make a wig that would look anything like my hair. My kids’ attitude was that everyone would know something was wrong anyway, so I should just be bald, and that helped a lot. But it’s hard to see in people’s eyes multiple times a day their realization that you’re in a pretty bad place. Also, it’s not just your head hair that goes. So do your eyebrows, your eyelashes, your pubic hair, and most of the tiny hairs all over your skin. And as your skin cells are affected by the chemo (the chemo hits all fast-reproducing cells), your skin itself gets more sensitive and then is not protected by those tiny hairs. I remember a lot of itching. And strange things like my head sticking to my yoga mat and my reading glasses sticking to the side of my head instead of sliding over my ears.
I never lost my appetite, but I did have food cravings during the AC cycles. I wanted sushi and seaweed salad, of all things. And steak. My sense of taste went dull, so I also wanted things that tasted strong and had crunch. I stopped drinking coffee and alcohol, partly because of the sleep issues but partly because it didn’t taste very good anyway. I drank loads of water on the advice of the oncologist, the nurses, and my acupuncturist, and I think that helped a lot.
During the second cycle, I developed a fever. That was scary. I was warned that if I ever developed a fever, I should call the oncologist immediately, no matter the time of day or day of week. The problem is that your immune response is knocked down by the chemo, so what would normally be a small bacterial infection has the potential to rage out of control. I was lucky. We figured out that the source of infection was a hemorrhoid—the Adriamycin was beginning to chew into my digestive tract, a well-known side effect. (Having to pay constant attention to yet another usually private part of the body just seemed totally unfair by this point.) Oral antibiotics took care of it, which was great because I avoided having to go into the hospital and all the risks entailed with getting heavy-duty IV antibiotic treatment. And we were also able to keep on schedule with the chemo regimen, which is what you hope for.
After that, I became even more careful about avoiding infection, so I avoided public places even more than I had been. I’m very close to a couple of toddlers, and I couldn’t see them for weeks because they were in one of those toddler constant-viral stages, and I really missed them.
The Taxol seems to be much less harsh than the AC regimen, so a lot of these side effects started to ease off a bit by the second 8 weeks, which was certainly a relief.
I was lucky that I didn’t really have mouth sores or some of the other side effects. Some of this is, I think, just because besides the cancer I don’t have any other health issues. Some of it is because my husband took over everything and I don’t have a regular job, so I had the luxury of concentrating on doing what my body needed. I tried to walk every day, and I slept when I needed to, ate when and what I needed to, and went to yoga class when my immune system was ok. I also went to acupuncture every week. I know the science is iffy on that, but I think it helped me with the side effects, even if it was the placebo effect at work (I’m a big fan of the placebo effect). We also both had extraordinary emotional support from many friends and knew we could call lots of people if we needed anything. That’s huge when you’re in this kind of situation.
Currently, I’m still dealing with some minor joint pains, mostly in my wrists and feet. I wasn’t expecting this problem, but my oncologist says it’s not uncommon: they think it’s because your immune system has to re-find its proper level of function, and it can go into overdrive and set up inflammation in the joints. That’s gradually easing off, though.
Most people don’t have it as easy as I did in terms of the medical, financial, and emotional resources I had to draw on. I’m very mindful of that and very grateful.
DXS: You say that you had “few terrible side effects” and a “very cushy home situation.” I’m sure any woman would like to at least be able to experience the latter while dealing with a full-body chemical attack. What were some factors that made it “cushy” that women might be able to talk to their families or caregivers about replicating for them?
LB: As I’ve said, some of it is just circumstance. For example, my kids were old enough to be pretty self-sufficient and old enough to understand what was going on, which meant both that they needed very little from me in terms of care and also that they were less scared than they might have been if they were younger. My husband happens to be both very competent (more competent than I am) around the house and very giving. I live in Cambridge, MA, where I could actually make choices about where I wanted to be treated at each phase and know I’d get excellent, humane care and where none of the facilities I went to was more than about 20 minutes away.
Some things that women might have some control over and that their families might help nudge them toward:
Find doctors you trust. Ask a lot of questions and make sure you understand the answers. But don’t get hung up on survival or recurrence statistics. There’s no way to know for sure what your individual outcome will be. Go for the treatment that you and your doctors believe will give you the best chance, and then assume as much as possible that your outcome will be good.
Make sure you talk regularly with a social worker or other therapist who specializes in dealing with breast cancer patients. If you have fears or worries that you don’t want to talk to your partner or family about, here’s where you’ll get lots of help.
Find compatible friends who have also had cancer to talk to. I had friends who showed me their mastectomy scars, who showed me their reconstructions, who told me about their experiences with chemo and radiation, who told me about what life after treatment was like (is still like decades later…). And none of them told me, “You should…” They all just told me what was hard for them and what worked for them and let me figure out what worked for me. Brilliant.
Try to get some exercise even if you don’t feel like it. It was often when I felt least like moving around that a short walk made me feel remarkably better. But I would forget that, so my husband would remind me. Ask someone to walk with you if you’re feeling weak. Getting your circulation going seems to help the body process the chemo drugs and the waste products they create. For the same reason, drink lots of water.
Watch funny movies together. Laughter makes a huge difference.
Pamper yourself as much as possible. Let people take care of you and help as much as they’re willing. But don’t be afraid to say no to anything that you don’t want or that’s too much.
Family members and caregivers should also take care of themselves by making some time for themselves and talking to social workers or therapists if they feel the need. It’s a big, awful string of events for everyone involved, not just the patient.
DXS: In the midst of all of this, you seem to have written a fascinating book about spiders and their webs. Were you able to work while undergoing your treatments? Were there times that were better than others for attending to work? Could work be a sort of occupational therapy, when it was possible for you to do it, to keep you engaged?
LB: The book had been published about 6 months before my diagnosis. The whole cancer thing really interfered not with the writing, but with my efforts to publicize it. I had started to build toward a series of readings and had to abandon that effort. I had also started a proposal for a new book and had to put that aside. I had one radio interview in the middle of chemo, which was kind of daunting but I knew I couldn’t pass up the opportunity, and when I listen to it now, I can hear my voice sounds kind of shaky. It went well, but I was exhausted afterwards. Also invigorated, though—it made me feel like I hadn’t disappeared into the cancer. I had two streams of writing going on, both of which were therapeutic. I sent email updates about the cancer treatment to a group of friends—that was definitely psychological therapy. I also tried to keep the Spider Silk blog up to date by summarizing related research papers and other spider silk news—that was intellectual therapy. I just worked on them when I felt I wanted to. The second week of every cycle my head was usually reasonably clear.
I don’t really know whether I have chemo brain. I notice a lot of names-and-other-proper-nouns drop. But whether that’s from the chemo per se, or from the hormone changes associated with the chemically induced menopause, or just from emotional overload and intellectual distraction, I don’t know. I find that I’m thinking more clearly week by week.
DXS: What is the plan for your continued follow-up? How long will it last, what is the frequency of visits, sorts of tests, etc.?
LB: I’m on tamoxifen and I’ll be on that for probably two years and then either stay on that or go onto an aromatase inhibitor [Ed. note: these drugs block production of estrogen and are used for estrogen-sensitive cancers.] for another three years. I’ll see one of the cancer doctors every three months for at least a year, I think. They’ll ask me questions and do a physical exam and take blood samples to test for tumor markers. At some point the visits go to every six months.
For self-care, I’m exercising more, trying to lose some weight, and eating even better than I was before.
DXS: Last…if you’re comfortable detailing it…what led to your diagnosis in the first place?
LB: My breast cancer was uncovered by my annual mammogram. I’ve worried about cancer, as I suppose most people do. But I never really worried about breast cancer. My mother has 10 sisters and neither she nor any of them ever had breast cancer. I have about 20 older female cousins—I was 50 when I was diagnosed last year–and as far as I know none of them have had breast cancer. I took birth control pills for less than a year decades ago. Never smoked. Light drinker. Not overweight. Light exerciser. I breastfed both kids, although not for a full year. Never took replacement hormones. Never worked in a dangerous environment. Never had suspicious mammograms before. So on paper, I was at very low risk as far as I can figure out. After I finished intensive treatment, I was tested for BRCA1 and BRCA2 (because mutations there are associated with cancer in both breasts) and no mutations were found. Unless or until some new genetic markers are found and one of them applies to me, I think we’ll never know why I got breast cancer, other than the fact that I’ve lived long enough to get cancer. There was no lump. Even between the suspicious mammogram and ultrasound and the biopsy, none of the doctors examining me could feel a lump or anything irregular. It was a year ago this week that I got the news that the first biopsy was positive. In some ways, because I feel really good now, it’s hard to believe that this year ever happened. But in other ways, the shock of it is still with me and with the whole family. Things are good for now, though, and although I feel very unlucky that this happened in the first place, I feel extremely lucky with the medical care I received and the support I got from family and friends and especially my husband.
Leslie Brunetta’s articles and essays have appeared in the New York Times,Technology Review, and the Sewanee Review as well as on NPR and elsewhere. She is co-author, with Catherine L. Craig, of Spider Silk: Evolution and 400 Million Years of Spinning, Waiting, Snagging, and Mating (Yale University Press).
On the second Sunday in May in the United States, mothers reign supreme, receiving tributes of breakfast in bed, hand-made cards, flowers, and obligatory long-distance phone calls. Meanwhile, for the rest of the animal kingdom, it’s just another day: eat, hunt, mate, birth, nest, migrate, defend, and rest.
Some go it alone, but others—like spotted hyenas and bison—live in groups with complex social structures, and moms are at the top, year-round. In a matriarchy, females hold central roles of leadership and power. This might sound like a nice change of pace for some of us, but most anthropologists now agree that there have likely been no true matriarchal human societies (in spite of popular books like The Chalice and the Blade). Instead, matriarchies are more likely to be found in the rest of the animal kingdom, from meerkats to mammoths. Here are a few examples:
The Queen, surrounded by her supportive workers.
Honey bees: Bee colonies are giant matriarchal societies ruled by a single queen—quite literally the “queen mum.” Her offspring (as many as 25,000 at a time) make up the entire clan of female workers and male drones. The queen spends her life tended to by her worker daughters. These workers have underdeveloped reproductive systems, so the queen is the only female in the hive who gets to mate. The females do the work of the hive and tend to the queen while the male drones laze about until it’s time to mate with the queen. This setup might sound appealing at first, but it comes with a couple of important caveats. The Queen only mates once in her lifetime with a select handful of drones who were bred for that sole purpose (assuming they weren’t pushed out or killed by their worker sisters during tough times, when freeloading is less tolerated). During a series of nuptial flights, the queen gets all the sperm she’ll ever need for an entire lifetime—as many as five million individuals. She uses this sperm for to around 2500 eggs a day, which are tended to by her sterile daughters while she dines on royal jelly. The males get no reward for their service, but instead perish shortly after depositing their sperm, the unfortunate victims of an acute case of exploded abdomen.
Meerkats: Meerkat societies are highly structured, with a complex ranking system based on dominance. If you want to get ahead in the meerkat world, perfect the art of chin swiping and hip checking, practiced on those lower down the totem pole while someone more powerful than you is looking the other way. Being on top has its rewards; alpha female meerkats are the only ones who get to mate in meerkat town. A matriarch chooses her partner, who becomes the dominant (and only mating) male. Males initiate copulation by ritually grooming the female until she submits. If the matriarch tires of her partner, he’s quickly deposed by beta males who are more than eager to earn a chance at mating. Alpha females make all the decisions in the group: where to sleep, where to burrow, when to go outside, when to forage. Like bees, meerkat females are typically mother to all the pups in the group (females typically kill pups born of unsanctioned unions). In addition to being free to engage in mating, being a matriarchal meerkat comes with free baby-sitting and nursemaid service from the subordinate females (who also will lactate to feed her pups). The downside is that all the other females want your job; as they get older, the young females start hip-checking, stealing food, and even picking fights. Often, the alpha kicks young competitors out of the group before they get old enough to pose a threat.
Positives: Your clan, your rules; mate selection; ritual grooming; cooperative breeding. Negatives: High risk.
Cooperative and matriarchical.
Killer whales (orcas): Killer whales have some of the most complex social structures known in nature and are found in large resident groups (mostly fish eaters), smaller transient groups (seal hunters), or offshore groups (of which relatively little is known). Killer whale societies are entirely structured around the maternal line, in a hierarchy of groups. The smallest of these is the matriline, which contains the oldest female and her direct descendents—as many as four generations in one (great grand-whale, grand-whales, mama whales, and baby whales). Several matrilines together make a pod, and groups of pods with the same dialect and shared maternal lineage form a clan. For killer whales in resident groups, the young live with their mothers for the their entire lives, while in the smaller, transient groups, females tend to depart once they become mothers of their own. Meanwhile, male killer whales are mama’s boys, maintaining a strong relationship with their mothers for life. Even siblings remain close after their mother dies. Unlike bees or meerkats, all females can mate as they wish, although almost always only with males from other pods. These close-knit groups are important for successful hunting, as well as for rearing young that require a lot of parental investment (like humans do!). A killer whale’s female relatives assist her during labor, and even help guide her 400 lb calf to the surface to take its first breath. This cooperative behavior is a key part of teaching calves important life skills like the complex group hunting strategies similar to those that wolf packs use.
Positives: Strong family structure, cooperative breeding, matrilineal. Negatives: The kids never leave home.
Don’t let the tusks fool you: It’s a she, and she’s the boss.
Elephants: Female elephants live together in small family groups, typically consisting of a matriarch and her young or closest relatives. The oldest female elephant in each family group gets the job, and the position is passed down to her oldest daughter when she dies. Matriarchs have a lot of social power but are also the source of important lore in the herd, like where the water is, how to avoid predators, and even how to use various tools like makeshift fly-swatters. Meanwhile, males live bachelor lifestyles, fending for themselves alone or in small groups after getting kicked out at puberty. Male and female elephants occasionally come together to socialize or mate, but otherwise live separately. Unlike bees, meerkats, and killer whales, female elephants have a lot less control in the mating process. Fertile females are followed around by aggressive bulls who rumble, produce a musky scent that they disperse by flapping their ears, and fight off other interested parties. For young female elephants, this mating behavior can be a bit intimidating, and so her female relatives will often stay by her side to provide moral support. After a two-year pregnancy, a female will give birth to a calf, which quickly becomes the center of herd life, as female relatives caress and welcome the newborn. The perks of elephant motherhood include free babysitting and protection from predators; females will circle the young when they sense danger. In some Asian elephant populations, multiple families have even been observed coming together to form specialized groups for nursing or juvenile care, like a cooperative preschool.
Positives: Strong family ties, cooperative parenting. Negatives: Lack of mate control, two-year pregnancy (!).
Many different kinds of matriarchy exist in the animal kingdom, as do many kinds of moms. Whether you’re a queen or a worker, an alpha or a beta, a subdominant or a matriarch, Happy Mother’s Day to moms everywhere.
The Living Elephants: Evolutionary Ecology, Behavior, and Conservation, Raman Sukumar. Oxford University Press, Oxford, UK. Kalahari Meerkat Project, Cambridge University
Killer Whales: The Natural History and Genealogy of Orcinus Orca in British Columbia and Washington, Kenneth C. Ford, Graeme M. Ellis, & Kenneth C. Balcomb. University of British Comumbia Press, Vancouver.
WebBeePop, Carl Hayden Bee Research Center, USDA Agricultural Research Service
[Photo credits: all photos are from Wikipedia with Creative Commons with Attribution liceneses except for #3, which is Public Domain: (1) A queen bee surrounded by her worker daughters. Photo by Waugsberg. (2) A meerkat in the Kalahari. Photo by Muriel Gottrop. (3) A mother-calf killer whale pair. Photo by Robert Pitman. (4) A matriarchal elephant and her family. Photo by Amoghavarsha.]Continue reading →
Leah Gerber is an Associate Professor of ecology at Arizona State University. Her research is motivated by a desire to connect academic pursuits in conservation science to decision tools and effective conservation solutions. This approach includes a solid grounding in natural history and primary data collection, quantitative methods and an appreciation for the interactions between humans and the environment. She is keenly aware of the need for the communication of scientific results to the public and to government and non-governmental agencies. This communication is essential for the translation of scientific results into tenable conservation solutions.
DXS: First, can you give me a quick overview of what your scientific background is and your current connection to science?
LG: I learned about ecology and environmental conservation as an undergraduate and quickly became motivated to do science that impacted the real world of conservation. Learning about the impacts of humans on nature was a wake-up call for me, and inspired me to channel my feeling of concern for the demise of nature in a positive way.
From there, I have walked the tightrope between science and policy. After getting my undergraduate degree in environmental biology, I wanted to do more than just the science. So I enrolled in a masters program at the University of Washington – an interdisciplinary program called Marine Affairs. It was a great experience, but I wanted to have more substance to my science background – I wanted to know how to do the science in addition to how to apply the science.
This compelled me to enter a PhD at the University of Washington, which was largely funded by NOAA. My thesis involved trying to figure out how to make decisions about endangered species – how to determine which were endangered and which were threatened. This was a perfect project given my interest in developing tools to solve problems. After finishing my PhD, I did a postdoc at the National Center for Ecological Analysis and Synthesis (NCEAS) and developed approaches for marine reserve design and endangered species recovery. I was at NCEAS for three years before starting on the tenure track at Arizona State University. I’ve been at ASU for about 10 years now.
A major theme in my work has remained constant – that is, how to use the information we are generating in the natural and social sciences to better manage our natural world. Pre-tenure I focused a lot more on doing the science, publishing in good journals, and hoping that it made its way into good policy. Now that I am midcareer, meaning that I have a good amount of papers and tenure, I am enjoying the opportunity to work with practitioners outside of academia. For instance, I just got off the phone with someone from National Geographic regarding my recent publicationon seafood health and sustainability. In that study, we performed an analysis regarding seafood in the context of health and sustainability, to answer simple questions like, what to order when out to sushi? How do we educate about health benefits and risks? We will be organizing a workshop to help restaurant chains, grocery stores, as well as environmental NGOs identify a path forward in informing consumers about healthy and sustainable seafood choices. As a tenured professor, I feel fortunate to have the opportunity to work at the science-policy interface and to give society some science that is truly applicable.
DXS: It is too bad that you have to wait until you are more established and have tenure to go out and engage with the public, because this type of thing is just so important!
LG: Yes, I agree. There isn’t a clear path in academia when it comes to public engagement. But in recent years I have felt optimistic – the landscape within academia is starting to change, and at ASU this change is noticeable. We have a fabulous president, Michael Crow, who has really transformed ASU from just another state institution to a leader in sustainability. Part of this is the establishment of the Global Institute for Sustainability, and one of Michael Crow’s mantras is “community embeddedness.” He is really on board with this type of thing and I have seen evidence of his commitment trickle down throughout the University. For instance, when I first arrived, I had to justify and explain why I was serving on these federal recovery teams for endangered species. Now I feel that there is no justification needed. Developing solutions is not only so important for society, but should also be a key aspect of what we do at Universities.
DXS: We were introduced by another fantastic science communicator, Liz Neeley, who you met at a communications workshop. Why is it important to take part in this type of training?
LG: I met the Fantastic and Fashionable Liz through the Leopold Leadership Program, offered through the Woods Institute for the Environment at Stanford University. The Leopold Leadership training was the best professional development experience of my career, and has made me a better translator and communicator of science to policy. Pre-Leopold, I had little training in communications, and there I was, in a teaching position where I taught hundreds students. I thought to myself, well, how do I do this? The Leopold experience has solidified my commitment to teaching students about communication and engaging in policy.
One development emerging from this training is a science communication symposium at the AAAS meeting. Elena Bennett and I are giving a talk on overcoming institutional barriers for community engagement, and we will address the issues head on. We put out a survey asking others if they faced institutional barriers, and how they might work to engage more.
DXS: What ways do you express yourself creatively that may not have a single thing to do with science?
LG: I have 2 young kids, a 3yo and a 7yo. Being a mom helps me keep it real - I love that I get to enjoy the awe of discovering the world with my girls. We just got a puppy this weekend and we are having fun dressing her up and painting her nails (only partly joking). Other things that I do that are creative – truthfully, I am uninteresting – I don’t bake bread or go to the opera. I just work and take care of my kids. I practice yoga for my own sanity and also love to work in the garden. Doing these things gives me a reason to pause and step off the treadmill of keeping up with everything.
DXS: Do you find that your scientific background informs the creativity you have with your kids or your yoga practice, even though what you do may not specifically be scientific?
LG: I think there is synergy with my science and my kids and my yoga practice in helping me to accept things and be mindful – but not in any conscious way. For instance, when doing my science, the type A person that I am, I have an inclination to keep pushing, pushing, pushing. My kids and my yoga help me to shift gears and accept that things are going to happen when they happen. I try to let the kids be kids, including the associated chaos, and accept that this is a snapshot in time that they will be little. Now I find joy in that chaos. Having kids and yoga gives me a little more perspective, and the knowledge that things aren’t lined up and neatly placed in a box. It rounds me out.
DXS: Are your kids are major influencers in your career?
LG: My first child, Gabriella, was born just after I submitted my application for tenure – so it was good timing. And I was able to slow down. I quickly realized that I wasn’t able to work a 60+hour week. Before kids, I lived to work. Now, I work to live. I absolutely love my job and I feel so lucky that I have a career that I believe in and that I am actually paid to do it – it’s not just a hobby. But having kids made me chill out a little. If I get a paper rejected, I can let it go instead of lamenting about it for weeks. It has made me healthier. I don’t necessarily know if it has had positive impact on my career – time will tell. While my publication rate may be slightly smaller, I think my work now has different dimensions, and greater depth.
I am still pretty passionate about my work, and my kids know what I do and are proud of it. They share it with their classmates, and take every opportunity to wax poetic about how their mom saves animals in the ocean. They also have a built in conservation effort – my 7YO gets irritated when she can’t find a compost bin, and her new thing is to only fill her cup half way because she will only drink a little bit of water.
DXS: When you decided to have children, did your colleagues view you differently? Did they consider that you were sending your career down the tubes or was it a supportive environment?
LG: I honestly had a really positive experience. I can’t think of any negative sentiments from my colleagues, and they were actually really supportive. For instance, when I was pregnant with my first daughter, ASU did not have a maternity leave policy. Before that, you would have to take sick leave. So my colleague worked within the parameters of the unit to give me maternity leave. And then with my second daughter, our new president had established a maternity policy.
The support of my colleagues at ASU has made me feel loyal to my institution. Normally, I am loyal to people and not institutions, but overall, the support has been fabulous. Of course, with having the kids in each case, I did decline a lot of invitations – some pretty significant ones – but I did not have a desire to drag a newborn to give a talk, especially when I was nursing. And it was hard for me to do this at times, especially given my career driven nature, and I had to learn to accept that there would be other opportunities.
I had to shift it down a notch and realize that the world wasn’t going to freeze over, and that I could shift it back to high gear later. With “mommy brain”, I knew I wasn’t going to be at the top of my game at that point in my life. But I have incredible role models. Most notable is Jane Lubchenco, currently the Director of the National Oceanic and Atmospheric Administration. During the first part of her career, she shared a position with her husband – each did 50% – and they did that on purpose so they’d be able to enjoy having children and effectively take care of them. Now, she is in the National Academy, is having major scientific impacts, and she did it all despite having kids. If she can do it, why cant the rest of us?
DXS: Given your experiences as a researcher, as a mother, and now as a major science communicator, do you feel that your ability to talk to people has evolved?
LG: Absolutely. I think that the Leopold Training Program, which selects 20 academics from North America to participate in retreats to learn how to be better communicate and lead, has re-inspired all who attended. It has recharged our batteries and allowed us to make realizations that doing good science and putting it out there via scientific publication is just not enough. We also have to push it out there and make it available to a broader, more diverse population. As part of the training, we also learned about different thinking styles – super analytical or super emotional – and after I returned, I had my lab group participate in this type of exercise. And now I feel like I can better assess a persons thinking style and adjust the way I communicate accordingly.
DXS: Did you always have the ability to talk to the general public or does having kids help you to better understand some of the nuances associated with science communication?
LG: I think so. In fact, I am thinking back to when I had a paper in Sciencecome out around the time that I had my first child. It got a lot of news coverage and was featured in Time magazine. I thought it was so cool at the time, but looking back on it I realized that have come a long way. I said something to a journalist, who then asked me to translate it into “plain English.” It was a little bit of a jab.
Now, with kids, I can tell you a lot more about my research and can better see the broader impact. Talking to them helps me to do that. Here is a conversation about my research with my daughter:
L: Mama is working on figuring out how to help the whales that people like to eat. It’s a big problem because some people like to eat whales and some like to see them swimming in the ocean.
G: What we have to do is let the people eat the whales in the ocean, and buy some whales from the pet store to put back in the ocean. How much do whales cost?
L: Good idea. But you can’t buy whales at the store. They are too big. And if we take them all out of the ocean there will be none left.
G: Well instead we should ask the people to eat bad things like sharks.
L: Another good idea. But if we take sharks out there will be no predators to eat the big fish. And the whole ecosystem would collapse.=
G: Well then the people should eat other things like fish instead of whales. They should buy a fishing pole and catch a fish and eat those instead of whales.
L: What about chicken, shouldn’t people just eat chicken?
G: Mama, we can’t kill chickens. Chickens are nicer than fish, so that’s why we have to eat fish.
L: What about just eating vegetables?
G: Oh mama, some people are meat-eaters. And there are no more dinosaurs. They all got extinct. They should have saved some of the dinosaur meat in the freezer for the meat-eaters. When the dinosaurs come back, there will be enough meat to eat and people won’t want to eat whales.
The simplicity of taking myself out of my research bubble and engaging with a creative (and nonlinear?) 7YO has taught me how to be a better communicator – with the media, with my students, and with the general population.
DXS: Do you think these efforts in science communication are helping to shift other peoples perspectives about who a scientist actually is? For instance, are we changing the old crazy haired white guy stereotype?
LG: Well, I hope so. A couple of examples – again, as a mom, one of my daughters a Girl Scout and I get to help with the troop. One of the themes was to teach about environmental and conservations awareness. We did this Crayola molding experiment where we put our fingers into cold water. We then did the same thing except we put modeling clay over our fingers before putting them into the cold water and to learn about adaptations to extreme environments. Also, we play games where they simulate fishing – what if there is plastic? What happens to you if you eat that? My hope is that this shows these young girls that science is both interesting and fun.
Another thing that just happened today is that I was contacted by Martha Stewart’s office, and it seems that some of my research results will be featured in the October issue of Martha Stewart Living. The message here is that I happen to care about the ocean, but I also love sushi. I also I care about health. I am not just a nerd in a lab coat. I am a mom, I do yoga, I have wonderful friends, and here is the kind of science that I do. It seems to me that it is better to connect with others when I can give them something that is relevant to their lives instead of a more abstract ecological theory.
DXS: If you had something you could say to the younger you about getting on your chosen career path, what would you say?
LG: I feel like I have been very effective at figuring out how to get from point A to point B, but less successful at savoring the process. I think that I’d tell myself to make time to celebrate the small victories. I have also learned to identify what kind of research is most exciting, and I would tell myself to say “no” to everything that is only moderately interesting. I tell my grad students that if you don’t dive in head first, you won’t ever know. So why just not give it a try! And if it doesn’t work, move on. Also, if something isn’t making you happy, change! Academia isn’t for everyone, and there is a lot more to life than science.