Nature versus nurture: that is the question.

Well, it is a question, anyway, one that’s been asked for centuries. Do we look how we look and act how we act because of our genes?

Or because of our experiences? Am I this buff because my DNA wired me to be like this? Or because I ate all my spinach as a kid?

It’s a good question, it’s a very good question! My dad would probably tell you that it was the spinach. But, like with a lot of questions, the answer isn’t as straightforward as one or the other.

It’s a bit like asking “What makes a plate of nachos good? Is it the cheese or the chips?” When the answer is both! It’s only in the interaction between the chips and cheese that they truly become nachos.

And together, our genes and our environment shape our traits. From our height to our risk of disease… basically, you and I are a plate of nature and nurture nachos. Say that six times fast.

Hi, I’m Dr. Sammy, your friendly neighborhood entomologist, and this is Crash Course Biology. Nature nurture nachos, nature nurture nachos, nature nurture nachos, I-I’m getting lightheaded… we should cut to the theme music. [THEME MUSIC] Previously on Crash Course, we broke out our Punnett Squares to show how living things inherit versions of each gene, called alleles, that interact with each other.

Now sometimes, those interactions are as simple as dominant alleles talking over recessive ones, either partially or completely. That interaction can influence how features show up in the phenotype —an organism’s observable traits, like a cat’s fur color. But most human traits can’t be pinned down to a single gene or even a lone interaction between alleles.

They spring from a messy, complicated dialogue between your genes, your experiences, and the stuff that you’re exposed to, like radiation from the Sun. You’re like Play-Doh—shaped by the ingredients in your clay, but also by the toddler trying to smash you into a DVD player. For starters, most human traits are controlled by more than one gene, so we call them polygenic: “poly” meaning “many.” Multiple genes influence how other genes’ instructions get read and expressed.

And proteins made from those instructions can then interact with each other, further influencing how traits take shape. Turns out, there’s a lot of different perspectives in your genetic code —and it’s not always clear who’s in charge.  In fact, one gene can control another gene’s expression, or even stop it from expressing altogether. That’s called epistasis, which in Greek roughly means “standing upon,” because it’s like one gene is stepping on the other gene’s toes.

And this isn’t exclusive to humans either. Even if you’re like me and would rather keep a coconut crab as a pet rather than a dog (less 3 a.m. barking), you may have still noticed that Labrador Retrievers come in three basic colors: black, brown, or yellow. Labs have one pigment gene that expresses for either black or brown, and a second gene that controls that expression.

A dominant allele on that second gene can give the pigment gene the go-ahead, but two recessive alleles can stop the black or brown pigment from expressing at all, resulting in that third Labrador color: yellow. I mean…it’s fine if you’re into pedestrian colors like “yellow.” It’s no cerulean blue or radiant orchid but every creature can’t be as majestic as the coconut crab. Most human traits — including our skin, eye, and hair colors — are even more elaborate than that.

They’re not just the result of one-on-one chats between alleles, but more like Taco Tuesday with my family. Everybody has something to say and all at the same time. We call these complex traits, meaning that they’re influenced by multiple genes and heavily molded by the environment—nature and nurture.

You might also hear these called quantitative traits because they fall on a spectrum that can be measured continuously. In other words, these traits don’t exist on a binary scale. Like, humans don’t come in a distinct “tall” or “short mode,” the way some flowers are either purple or white.

We come in a wide range of heights, with people falling at both extremes and every single centimeter measurement in between. You know what, let’s take this conversation to the Thought Bubble… It’s 1914, and you’re an 18-year-old girl in the United States. Your favorite song is “Saint Louis Blues,” and your favorite cookie is the newfangled Oreo, and you’re a perfectly average height: 158 centimeters.

Jump forward a hundred years to 2014. And your great-granddaughter’s favorite song is “Chandelier.” And like you, she prefers Oreos. And she, too, is dead-center for her height range.

But wait: she’s taller than you? 163 centimeters? How did that happen if you’re both average height? Genetics can explain up to 80% of the differences in height within a population: tall parents tend to have tall kids, short parents tend to have short kids.

Over ten thousand different locations in the set of human DNA have been linked to height. Each one has only a small effect— like standing on a tiny, tiny platform. But together they can influence how tall someone eventually grows.

Still, genes alone don’t explain that upward trend across generations. That remaining 20% difference comes back to inputs from the environment— like better access to nutrition— that helped the whole population’s average height increase. Thanks, Thought Bubble!

Height is just one trait influenced by our genetics and our environment. That’s a good Oreo, that’s a really good Oreo. I see why these have been around for so long.

And there are plenty of others, and studying genetic trends in a population over time helps us better understand ourselves. And most of our traits are complex, so huge phenotypic variation can emerge from very little genetic variation. Consider this: you’ve got a whopping 99.9% of your genome in common with other humans.

The sum total of our genetic differences comes down to a measly one-tenth of one percent. And a fraction of that fraction, combined with how much sun we get and how our skin reacts to it, forms the basis for the WHOLE spectrum of human skin color. I mean seriously people have been fighting and enslaving people over generations for something that’s barely a blip on the genetic radar!

Health problems like heart disease, diabetes, and cancer are complex traits too. And they can develop in different people for different reasons. Like, one person might suffer from emphysema, a lung condition that causes breathing problems, because of smoking cigarettes.

While another develops it due to a mutation in their genes that heightens their risk. Being genetically predisposed to a disease doesn’t guarantee that someone develops it. But it does increase their chances.

That makes it all the more important to understand how both genes and the environment influence complex traits. One way that’s happening is through the rapidly developing field of epigenetics. Things we experience in our lifetimes can turn  small portions of our genetic  instructions on or off, without actually editing our DNA.

That can change how genes express not just within one’s lifetime, but across generations. Let’s take a peek in the Theater of Life. Maybe you’ve heard the phrase “you are what you eat.” But are you also what your parents ate?

Or your grandparents? That’s a question that Dr. Folami Ideraabdullah has been pondering for years.

Her research examined how a mom’s health can influence her kids’ health or even her grandkids’ health. Take vitamin

D: our brains, bones, and bodies need it in order to grow strong. But as much as half of the world’s population doesn’t get enough of it, putting them at risk of rickets, osteoporosis, or broken bones. Dr. Ideraabdullah wanted to know if that deficiency can also pass effects onto offspring.

So she tracked several generations of genetically similar lab mice. When a pregnant mouse didn’t get enough vitamin D, it had lower levels of chemicals called methyl groups on its DNA. These methyl groups would typically block genes from being read.

Since the DNA had fewer methyl groups, Vitamin D deficiency essentially turned genes on, which could put the mice at risk for genetic conditions they might not have otherwise. This small change, called methylation,  didn’t end with those first  vitamin D-deprived mice. It passed on to their babies and grandbabies.

The implications of those changes aren’t fully clear, and more research is needed, but ongoing epigenetic research challenges the notion that things that happen to us end with us. And Dr. Ideraabdullah is still working to understand if similar effects happen in people —which could help us understand and treat  deficiencies before they  impact multiple generations.

While those studies are ongoing in mice, other researchers are studying the connection between DNA methylation and social inequality in humans. We’ll have more on that in a later episode.  Another area of genetic research you might come across is heritability. Scientists study heritability to figure out how much the differences between individuals within a population can be explained by their genes.

While the study of heritability is a legitimate scientific pursuit, it has at times been misused to justify social inequality. There have been arguments made on the basis of “heritability” that genetics is a deciding factor for things like intelligence, success, or wealth. But, those arguments fail to account for the ways that the environments and societies we live in affect us all.

Scientific research actually shows that genes  contribute very little to  these kinds of social traits. Complex traits are determined by the interactions between multiple genes and the environment, and that includes,  at least for us humans, the  societies that we live in. Access to proper nutrition, healthcare, education, and more are tied together with our genes to determine a spectrum of phenotypes.   On top of that, many individual organisms’ phenotypes change within their own lifetime: a thing called phenotypic plasticity.

Take, for example, female honey bees. When they’re babies, the bees all start out eating the same milky, gooey food, called “royal jelly.” But only the ones who continue on the royal jelly diet will become queens: large and in charge, and the only lady in the whole hive able to propagate the next generation of worker bees. It’s likely that the royal jelly shields her reproductive organs from plant toxins while providing the full complement of nutrition needed to make them grow and function, so she develops into a fertile adult.

The rest of the babies get weaned onto fermented pollen, or “beebread,” rich in chemical compounds called flavonoids. Flavonoids boost the babies’ immunity while also shrinking their ovaries, s o they grow up to be big and strong but sterile worker bees. You might say queens have to “avoid the ‘noid” —a deep cut for all of you ‘80s pizza mascot fans…all four of you.

Anyway, the point is, different diets nudge female bees to express different phenotypes, and take two wildly different life paths. Why would we expect humans to be any different? Life consists of a dizzying array of diversity.

So, it makes sense that the factors determining our traits are complex. Most traits can’t be linked to any single gene, much less to genes alone. There is no nature versus nature, only nature and nurture.

Chips and cheese in these  nachos that we call life. Hey! That’s not your cheese, that is nach-o’s.

And in our next episode, we’re gonna take a closer look at how these nachos get made: I’m talking about DNA. Peace! This series was produced in collaboration with HHMI BioInteractive.

If you’re an educator, visit BioInteractive.org/CrashCourse for classroom resources and professional development related to the topics covered in this course. Thanks for watching this episode of Crash Course Biology which was filmed at our studio in Indianapolis, Indiana, and was made with the help of all these nice people. If you want to help keep Crash Course free for everyone, forever, you can join our community on Patreon.