What We Know and What We Don't
This first part is all about introductions.
Behavior Genetics is a field that is defined by a common set of questions and methods, rather than being focused on any particular topic of study. This week we discuss some of the commonalities, or themes, that recur throughout research across topics, in terms of the questions we ask, what we know, and what we don’t (and maybe can’t) know.
This week we will:
- Introduce common terminology and themes in behavior genetics.
- Become comfortable with the typical weekly course structure.
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Evaluate and share what knowledge you come to this course with and what you hope to learn.
- If you haven’t taken (or don’t remember) biology, you can review the following Crash Course: Biology videos that cover concepts that will be relevant to material throughout the semester.
- #9 Heredity (10:17)
- #10 DNA Structure & Replication (12:58)
- #11 DNA Transcription & Translation (14:07)
- #13 Meiosis (11:42)
- #14 Natural Selection (12:44)
What is Behavior Genetics?
Behavior genetics is a field that is defined by a common set of methods that broadly attempt to answer two questions:
- Why do individuals differ from one another? and
- What causes someone to be who they are?
These questions are related but can require very different approaches to address, and we will spend the semester discussing the approaches and limitations of our attempts to understand the answers to both of them.
Like any field, behavior genetics commonly uses a unique set of terms that is quite inscrutable to outsiders. Some that will come up CONSTANTLY throughout the semester:
- Phenotype: This is any outcome that we are interested in. It can be a behavior, a physical characteristic, a low-level biological function, literally (almost) anything - except for the genotype itself.
- Genotype: The sequence of As, Cs, Gs, and Ts that make (or rather, represent) the rungs on the ladder of everyone’s DNA (humans and non-humans alike).
- Environment: Everything that is not the genotype. This can be what we usually think of when we hear the word environment (family, culture), it can be your experiences, personal traits, it can even be biological environments, like hormones and what you’ve had to eat today, or ever. (Note: the difference between a “phenotype” and an “environment” is in the eye of the beholder - phenotypes can be environments and vice versa.)
Why do we use jargon? Well, it makes us sound fancy and, as with all language, it provides shortcuts to understanding that save time once you’re familiar with it. But in behavior genetics, we have another layer of communication to contend with: historical context. Behavior genetics, as a field, is inextricably linked with eugenics (the “father” of behavior genetics, Francis Galton, coined the term eugenics and most of the prominent early scientists in the field were avid advocates). Jargon makes our papers hard to read, and when they are hard to read, fewer people will read them, and we (the scientists) spend less time having to publicly contend with that historical (and, honestly, present) context. We’ll talk more about eugenics and the real-world applications of behavior genetics (both good and evil - but, on balance, mostly evil) in the coming weeks.
So, we have a whole field of defensive scientists writing dense papers, either on purpose or (for the same reason MOST academic writing is dense and boring) because we’re not trained to write well. That’s fine if there’s nothing terribly interesting or practically important in those papers. But the reality is this information, and how we arrive at it, is becoming critically more important all the time as technology advances and the potential applications expand.
In the past few years, we’ve seen a rapid decline in the cost of genotyping, combined with an incredible explosion in the development of new technologies. Genetic information is used in reproductive decision-making (from pre-conception genetic counseling to embryo selection to prenatal and neonatal screening), diagnosis and prediction of disease and non-disease phenotypes (in medical and non-medical settings, including direct-to-consumer genotyping services), and criminal proceedings (identification of individuals and, occasionally, determining responsibility). I keep seeing a sponsored tweet advertising a service to tell me what I should eat based on my DNA.
I have one goal for this course: Scientific Literacy. In life, and soon if not already, you are going to be asked to make decisions and buy services based on the research we talk about in this class. I want you to be an educated consumer.
There are no course prerequisites for Psyc 408, but there is a personal one: you need to be interested in the journey we are about to embark on. This material is not easy, but motivation will take you as far as you need to go. If you’ve made it this far, and you’ve browsed the course website, and you are still thinking “This sounds interesting!”: you are ready to go.
Twenty Themes in Behavior Genetics
Although there is essentially an infinite number of phenotypes that a person might be interested in, as a field organized around a common set of methods we’ve noticed over the years that, regardless of the phenotype, some consistencies tend to emerge, in both basic findings and new questions/theories that emerge. In this course, we will refer to these as Themes in Behavior Genetics, and we will use these Themes to organize the many topics (and many, MANY readings and other source materials) that we will cover.
We will refer to these extensively throughout the semester, so keep this list handy.
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Everything is at least a little bit heritable (that is, more closely genetically related individuals are more similar phenotypically).
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Nothing is 100% heritable (even identical twins are a little different from one another on anything we can measure).
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Heritability is caused by many genes of small effect (there is no “gene for” in psychology, human behavior, or indeed ANY trait that commonly varies between people).
- Correlations between phenotypes are partly due to correlated genetic/heritable influences.
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Heritability increases through development (at least through middle adulthood).
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Trait stability or consistency across time within an individual is due to stable genetic influences.
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Even things we think of as “the environment” show non-zero heritability (example: divorce).
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Correlations between phenotypes and environments are partly due to correlated genetic/heritable influences.
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Most environments are not shared between people, even siblings or twins raised together.
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Abnormal is normal (influences on extremes that we label as “disorders” versus normal-range traits are not different in kind, just amount).
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Interpretation of results means understanding the strengths and weaknesses of choices made in the design of a study (for example: how to measure a phenotype, how participants were selected or excluded).
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Phenotypes (means, variances, and presentations) change over development - we cannot use the same measures or interpretations without knowing the developmental context.
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The development of an individual is not necessarily the same as the average developmental course.
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Gene-environment interaction (GxE) potentially explains why people exposed to the same environments respond differently.
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Most behavior genetic research necessarily assumes (because of data limitations) that genetic and environmental influences are independent (that is, uncorrelated).
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Gene-environment correlation (rGE; the tendency of individuals to be selected or select into environments partly on the basis of their heritable characteristics) exists and, if not accounted for, causes biases in our estimation of heritability and genetic effects.
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Mating is non-random (although random mating is an assumption of many of our models, again because of data limitations).
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Population structure, or genetic ancestry, is a major confound in models because individuals are systematically exposed to different environments as a result of their perceived ancestry.
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Correlation is not sufficient to demonstrate either causation or mechanism.
- No influences exist in a vacuum: simultaneous gene-environment interplay (rGE & GxE) is almost certainly happening all the time, to all of us, in parallel, in sequence, reciprocally. The True Model (if such a thing exists) is almost certainly more complex than we could ever gather data for and test.
It is not my expectation that you memorize or understand these this first week. The goal now is awareness - these themes will pop up over and over again, throughout the course, across topics both in class and in your paper. Keep them handy as a reference, and know that you’re going to learn so much about all of them by the end of the semester.
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