The video explores the intricacies of the age-old debate of nature versus nurture, emphasizing the complex interplay between genetics and environmental factors in shaping human traits. Dr. Sammy, an entomologist, guides viewers through the concept using engaging analogies like comparing our genetic and environmental aspects to nachos made from chips and cheese. This approach not only makes the subject accessible but also highlights how both nature and nurture contribute to our physical and behavioral characteristics.

The discussion extends to the genetic concept of polygenic traits, explaining how multiple genes, alongside environmental influences, determine human characteristics such as height and skin color. Emphasizing examples such as Labrador retrievers' coat colors and the varying heights across generations due to improved nutrition, the video demonstrates how genetic and environmental variations culminate in the diverse phenotypes observed in humans.

Main takeaways from the video:

Please remember to turn on the CC button to view the subtitles.

Key Vocabularies and Common Phrases:

1. epistasis [ˌɛpɪˈsteɪsɪs] - (noun) - The interaction between genes where one gene can interfere with or suppress the expression of another. - Synonyms: (gene suppression, interaction, inhibition)

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.

2. polygenic [ˌpɒlɪˈdʒɛnɪk] - (adjective) - Describing a trait that is influenced by multiple genes. - Synonyms: (multigenic, complex, multifactorial)

Most human traits are controlled by more than one gene, so we call them polygenic.

3. phenotype [ˈfiːnəˌtaɪp] - (noun) - The observable characteristics or traits of an organism. - Synonyms: (characteristics, traits, appearance)

That interaction can influence how features show up in the phenotype

4. methylation [ˌmeθɪˈleɪʃən] - (noun) - A biochemical process that influences gene expression by adding methyl groups to DNA. - Synonyms: (DNA modification, gene regulation, alteration)

This small change, called methylation, didn't end with those first vitamin D deprived mice.

5. complex traits [ˈkɒmplɛks treɪts] - (noun phrase) - Traits influenced by multiple genetic and environmental factors. - Synonyms: (multifaceted traits, intricate traits, mixed traits)

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.

6. phenotypic plasticity [fiːnəˈtɪpɪk plæˈstɪsɪti] - (noun) - The ability of an organism to change its phenotype in response to environmental influences. - Synonyms: (adaptive change, flexibility, variableness)

On top of that, many individual organisms, Phenotypes change within their own lifetime, A thing called phenotypic plasticity

7. heritability [ˌhɛrɪtəˈbɪlɪti] - (noun) - The proportion of variability in a trait within a population that can be attributed to genetic differences. - Synonyms: (genetic transmission, inheritance, genetic passing)

Scientists study heritability to figure out how much the differences between individuals within a population can be explained by their genes.

8. quantitative traits [ˈkwɒntɪˌteɪtɪv treɪts] - (noun phrase) - Traits that can be measured on a continuous scale. - Synonyms: (measurable traits, gradational traits, scalable traits)

You might also hear these called quantitative traits because they fall on a spectrum that can be measured continuously.

9. epigenetics [ˌɛpɪdʒɪˈnɛtɪks] - (noun) - The study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself. - Synonyms: (gene regulation, epigenome study, chromatin research)

One way that's happening is through the rapidly developing field of epigenetics.

10. predisposed [ˌpriːdɪˈspəʊzd] - (adjective) - Inclined to or susceptible to beforehand. - Synonyms: (inclined, prone, susceptible)

Being genetically predisposed to a disease doesn't guarantee that someone develops it, but it does increase their chances.

Genetic Traits - Nature? Nurture? Not That Simple - Crash Course Biology #32

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 of 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 the 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. Nature, nurture. Ooh, I'm getting light headed. We should cut to the 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 influenc 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 3am Barking. You may have still noticed the Labrador retrievers come in three basic 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 that 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 the St. Louis Blues and your favorite cookie is the new fangled Oreo. And your perfectly average height, 158cm. Jump forward 100 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. And over 10,000 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 help 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 1/10 of 1%. 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. Fulomi Adirabdulla has been pondering for years. Her research examined how a mom's health can influence her kid's 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. Adhir Abdullah wanted To know if that deficiency can also pass effects on to 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 that 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. Adirabdulla 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 that 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 environment 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 honeybees. 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 bee bread rich in chemical compounds called flavonoids. Flavonoids boost the baby's immunity while also shrinking their ovaries so they grow up to be big and strong.

But sterile worker bees, you might say. Queens have to avoid the noid deep cut for all of you 80s pizza mascot fans out there, 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, much less to genes alone. There's no nature versus nurture, only nature and nurture. Chips and cheese in these nachos that we call life.

Hey, that's nacho cheese. That is nachos. And in our next episode, we're gonna take a closer look at how these nachos get made. Talking about DNA. Peace.

BIOLOGY, GENETICS, INNOVATION, EPIGENETICS, COMPLEX TRAITS, EPISTASIS, CRASHCOURSE