Overall a sensible introduction. Turkheimer is very leftist by the field’s standards, you may want to try out some others for opposite political slant or no slant. Not all authors color their work so heavily as he does.
You make a mistake in your terminology. Epistasis is not the same as nonlinearnity. Linearity stands in contrast to nonlinearity, which is called dominance. This is when a subject’s phenotype does not change in a linear fashion from changing the alleles. So e.g., the change from TT to AT to AA does not have equal steps. This is common with severe genetic disorders, where having one copy usually does nothing. This is because a correct version of the protein (say) is still made half the time, and this is enough. Epistasis is gene-gene interactions between loci. In other words, there is no clean effect of changing from TT to AT because the effect depends on another locus where e.g. GG, or GC may be present.
There have been many papers looking for dominance and epistasis, but little has been found. EA4 tested across the genome for dominance and found nothing. Not due to low power. Epistasis generally causes MZ to be more than 2DZ, which is not commonly seen. Usually, the bias from assortative mating is stronger than any unmodelled epistasis or dominance.
There have been many papers looking for dominance and epistasis, but little has been found. EA4 tested across the genome for dominance and found nothing.
See §4.4.3 for my response.
Epistasis generally causes MZ to be more than 2DZ, which is not commonly seen.
See the collapsible box labeled “Box: Twin-study evidence of epistasis in adult personality, mental health, and behavior” in §4.4.2 for many apparent examples of precisely this. Do you disagree with that? Is there more evidence I’m missing?
Remember, I’m claiming that non-additive genetics are important in adult personality, mental health, and behavioral things like divorce, but that they’re NOT very important in height or blood pressure or (I think) IQ or EA.
You make a mistake in your terminology.
This is very possible!! It wouldn’t be the first time. I can still make changes. I found the use of terminology in the literature confusing … and I find your comment confusing too. :(
My background is physics not genetics, and thus I’m using the word “nonlinearity” in the linear algebra sense. I.e., if we take a SNP array that measures N SNPs, we can put the set of all possible genomes (as measured by this array) into an N-dimensional abstract vector space, I think. Then there’s a map from this N-dimensional space to, let’s say, extroversion. Both what you call dominance, and what you call epistasis, would make this map “nonlinear” (in the linear algebra sense). See what I mean?
If it’s true that people in genetics use the term “nonlinearity” to refer specifically to nonlinearity-at-a-single-locus, then I would want to edit my post somehow! (Is it true? I don’t want to just take your word for it.) I don’t want people to be confused. However, nonlinearity-in-the-linear-algebra-sense is a very useful notion in this context. I will feel handicapped if I’m forbidden from referring to that concept. Maybe I’ll put in a footnote or something? Or switch from “nonlinearity” to “non-additivity”? (Does “non-additivity” subsume both dominance and epistasis?)
Update: I replaced the word “epistasis” with “non-additive genetic effects” in a bunch of places throughout the post. Hopefully that makes things clearer??
Overall a sensible introduction. Turkheimer is very leftist by the field’s standards, you may want to try out some others for opposite political slant or no slant. Not all authors color their work so heavily as he does.
You make a mistake in your terminology. Epistasis is not the same as nonlinearnity. Linearity stands in contrast to nonlinearity, which is called dominance. This is when a subject’s phenotype does not change in a linear fashion from changing the alleles. So e.g., the change from TT to AT to AA does not have equal steps. This is common with severe genetic disorders, where having one copy usually does nothing. This is because a correct version of the protein (say) is still made half the time, and this is enough. Epistasis is gene-gene interactions between loci. In other words, there is no clean effect of changing from TT to AT because the effect depends on another locus where e.g. GG, or GC may be present.
There have been many papers looking for dominance and epistasis, but little has been found. EA4 tested across the genome for dominance and found nothing. Not due to low power. Epistasis generally causes MZ to be more than 2DZ, which is not commonly seen. Usually, the bias from assortative mating is stronger than any unmodelled epistasis or dominance.
Dominance is (a certain kind of) nonlinearity on a single locus, epistasis is nonlinearity across different loci.
See §4.4.3 for my response.
See the collapsible box labeled “Box: Twin-study evidence of epistasis in adult personality, mental health, and behavior” in §4.4.2 for many apparent examples of precisely this. Do you disagree with that? Is there more evidence I’m missing?
Remember, I’m claiming that non-additive genetics are important in adult personality, mental health, and behavioral things like divorce, but that they’re NOT very important in height or blood pressure or (I think) IQ or EA.
This is very possible!! It wouldn’t be the first time. I can still make changes. I found the use of terminology in the literature confusing … and I find your comment confusing too. :(
My background is physics not genetics, and thus I’m using the word “nonlinearity” in the linear algebra sense. I.e., if we take a SNP array that measures N SNPs, we can put the set of all possible genomes (as measured by this array) into an N-dimensional abstract vector space, I think. Then there’s a map from this N-dimensional space to, let’s say, extroversion. Both what you call dominance, and what you call epistasis, would make this map “nonlinear” (in the linear algebra sense). See what I mean?
If it’s true that people in genetics use the term “nonlinearity” to refer specifically to nonlinearity-at-a-single-locus, then I would want to edit my post somehow! (Is it true? I don’t want to just take your word for it.) I don’t want people to be confused. However, nonlinearity-in-the-linear-algebra-sense is a very useful notion in this context. I will feel handicapped if I’m forbidden from referring to that concept. Maybe I’ll put in a footnote or something? Or switch from “nonlinearity” to “non-additivity”? (Does “non-additivity” subsume both dominance and epistasis?)
Update: I replaced the word “epistasis” with “non-additive genetic effects” in a bunch of places throughout the post. Hopefully that makes things clearer??