Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012

MZ vs. DZ twins.

1. 
   Criticism: even among MZ twins you have
   
   1. 
      Splitting before day 4 € two separate placentas (dichorionic) and two amniotic sacs
      
   2. 
      Splitting between day 4-7 € one placenta (monochorionic) but two amniotic sacs
      
   3. 
      Splitting after day 7 € one placenta and one amniotic sac
      
2. 
   Criticism: MZ twins are also treated more similarly than DZ twins
   

• 
  Adoption studies. Saying that traits more shared with closer relatives must be due to more shared genetics
  

because the environment is random and not shared.

1. 
   Cross-fostering in animals
   
2. 
   With MZ twins separated at birth
   
3. 
   Compare MZ and DZ twins separated at birth
   

   1. Criticism: adoptees are placed non-randomly

   2. Criticism: you're going to have pretty small sample size with these very unique cases

   3. Criticism: again, environment starts at conception, not at birth

• 
  Behavior in the absence of environmental influence
  

1. 
   Social smiling in congenitally blind babies and babbling in congenitally deaf babies
   
2. 
   Lab rats 100 generations away from ever seeing a cat are still averse to cat pheromones
   

What 3 important things happen in the pre-natal environment?

• Circulating hormones (from mother and from rat siblings strung up on the same circulatory chain)

  • Glucocorticoids and other stress hormones. High exposure to these brings, as an adult, smaller brain, lower capacity for learning, more tendency towards anxiety/hypertension/diabetes. Sheesh!

    • Leads to epigenetic effects of inability to shut down stress response thanks to smaller hippocampus

  • Maternal and sibling estrogen influences also influence subsequent development (earlier puberty, etc).

• Nutrition and metabolic programming

  • Prime example of epigenetics (non-mendelian inheritance of traits, even multi- generationally, that has nothing to do with genes - are not heritable traits).

  • We also see pelvic arch size evolutionary battles with Massai malnutrition

• Learning (mother's voice)

Some would say maternal and paternal genetic contributions are equal, and that mom also gives the prenatal environment.

How would you then explain any differences you saw in behavior as shared more with mom? Due to the influence of the prenatal environment. That's how we can control for it.
But what complicates that assertion? In what ways is mom more than just 50% genes + prenatal environment?

• Paternal uncertainty

• Mitochondrial DNA

• Imprinted genes

• TF inequality and Lamarkian inheritance

And say we do discover a strong genetic component for something like extroversion. What might the genes actually be influencing? 3 examples:

• 
  ^{Something indirectly related to extroversion, like attractiveness. These are indirect genetic effects.}
  
• 
  ^{Another example: high heritability for political affiliation may have to do with the genetics of ambiguity tolerance}
  
• 
  ^{Aggression in rats also seems highly heritable. Not actually genes for aggression! About pain tolerance} thresholds.
  

How do behavioral geneticists hone in on actual genes?

• 
  Find genetic differences, then look for differences in behavior.
  
• 
  To find genetic differences in order of awesomeness:
  

• 
  phenotypic marker linkage <
  
• 
  protein marker linkage/protein size <
  
• 
  RFLPs
• 
  QTLs

• 
  Drawback: it's about identifying covariants in the genes with the disease, so it's a statistical relationship
  

and often doesn't give 100% certainty.

• 
  Drawback: you do all this work in a family, but then in a different family they'll have different markers. So multiple genetic routes to a disease.
  
• 
  Drawback: even knowing the exact gene, it's usually not 100% deterministic
  

Or the reverse: find variations in genes and then study "where the light is" to figure out its effects. What three examples do we have?

• 
  Vasopressin receptor variants. Not just voles, also humans! The "monogamous" promoter version makes for more stable marriages and greater facial expression-reading ability in humans!
  

• Variants in BDNF in humans predict risk of anxiety and amygdalar metabolic rate (same with a neurotransmitter called NPY).

• 
  Variants in dopamine and serotonin receptors and risk-taking
  
• 
  Criticism: Looking where the light is. By looking where there is an expected effect, they’ve eliminated the chance
  

to find an unexpected effect.

• 
  Criticism: multiple genes affect the same outcome behaviors sometimes. Therefore one single gene variant probably has very small effects. You won't be illuminating complex human behavior.
  

What does heritability tell us?

• 
  Heritability DOES tell you the degree to which the variance of a trait is influenced by genes.
  
• 
  Heritability DOES NOT tell you the degree to which a trait (the average of the trait) is influenced by genes, or how much a trait "is genetic."
  
• 
  The fact that humans usually have 10 fingers reflects the fact that this trait is inherited. But cases where humans have fewer than 10 fingers involves 0% heritability.
  

How do we know if something is highly heritable?

• 
  Look at the variation in a trait and ask yourself did that variation result from differences in genes or differences in the environment? If it's differences in genes then it's highly heritable.
  
• 
  For traits that are highly heritable, then knowing the gene will give you huge predictive power over the variation displayed in your trait of interest.
  
• 
  For traits that are not highly heritable, knowing the environment or some other factor will give you more explanatory power over the variance in your trait of interest.
  

Which of the following show high heritability?

And for one more complication, what role does chance play in the development of an organism?

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