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I think you're engaged in hindsight and rather glibly biting that bullet. Large swathes of sociology, medicine, nutrition, health research, governments (even wh
by gwern 9y ago
I think you're engaged in hindsight and rather glibly biting that bullet. Large swathes of sociology, medicine, nutrition, health research, governments (even where genetic influences are accepted) are premised on the assumption that one's environment and shared environment especially causally affect outcomes in ways that can be measured and quantified and used in research and provide paths towards understanding, control, and amelioration. Parenting, or air pollution, things of that ilk. It certainly is not obvious to most people that those are all minor effects of small importance compared to random developmental noise or other things.
Of course no one would be surprised to find non shared-environment variance components which were non-zero, but it's very surprising to find that they are so large: often larger than shared-environment effects, and sometimes as large or larger than heritability. This is one of the most interesting and counterintuitive findings of behavioral genetics, and experiments like OP put this in extremely stark relief. If clones in as exactly identical environments as researchers can create and perceive still wind up with such dramatic individual differences, how is science even possible on what causes the differences?
See:
- "Three Laws of Behavior Genetics and What They Mean" http://people.virginia.edu/~ent3c/papers2/three_laws.pdf http://people.virginia.edu/~ent3c/papers2/three_laws.pdf , Turkheimer 2000
- "Why Are Children in the Same Family So Different? Nonshared Environment a Decade Later" https://pdfs.semanticscholar.org/4091/dbfb736a4e793281e6b1aa4a0a0974874832.pdf https://pdfs.semanticscholar.org/4091/dbfb736a4e793281e6b1aa... , Plomin et al 2001
- "Epidemiology, genetics and the 'Gloomy Prospect': embracing randomness in population health research and practice" http://ije.oxfordjournals.org/content/40/3/537.full http://ije.oxfordjournals.org/content/40/3/537.full , Smith 2011
- "Top 10 Replicated Findings From Behavioral Genetics" https://www.gwern.net/docs/genetics/2016-plomin.pdf https://www.gwern.net/docs/genetics/2016-plomin.pdf , Plomin et al 2016
- choxi 9y agoI have a shaky understanding of "non-shared environment", I get the sense that it is based on the context of the study. e.g. If I do a study on genetically identical mice and control their sugar intake, "sugar intake" would be shared environment and something like "exposure to lead" would be non-shared. If I did the same study and controlled their exposure to lead, it would be "shared" in that case. Is that an accurate understanding? Is "non-shared environment" basically the "everything else" category after genetics and shared environment have been controlled for? Also, > If clones in as exactly identical environments as researchers can create and perceive still wind up with such dramatic individual differences, how is science even possible on what causes the differences? Another point in favor of simulation theory? :)
- jessriedel 9y ago> Is "non-shared environment" basically the "everything else" category after genetics and shared environment have been controlled for? Yes. For instance, in a study of childhood development, "shared environment" is the things that can plausibly be controlled since they are inflicted on all children in a family (e.g., household income, or frequency of family dinners), and "non-shared environment" is the "other" category that captures the infinite number of uncontrolled influences that different children within the family experience differently (e.g., having a scary fall down the stairs).
- deleted 9y ago[deleted]
- nabla9 9y agoMy guess is the evolutionary advantage of phenotypic heterogeneity. Phenotypic heterogeneity is linked to increased population-level fitness. Phenotypic heterogeneity exists in the context of cellular noise without any known environmental triggers [1]. Gene expression can have switches that turn genetically identical population into phenotypically different subpopulations. Evolution seems to push towards higher levels of expression noise in stress response genes, but genes that control basic functions are strongly shielded against expression noise[2]. Phenotypic heterogeneity can provide advantages when individuals are under stress. Predator can't predict behaviour as easily for example. Most of these studies relate only to small micro-organism, but I hypothesize that they may be factor in larger organisms as well. I would like to see followup study where that fish are divided in strong stress and low stress environment. If fish in strong stress environment show more behavioral differences from each other, than fish that grow in low stress environment, my hypothesis might have some merit. see: [1]: Nature, Nurture, or Chance: Stochastic Gene Expression and Its Consequences http://www.cell.com/abstract/S0092-8674(08)01243-9 http://www.cell.com/abstract/S0092-8674(08)01243-9 [2]: Single-cell proteomic analysis of S. cerevisiae reveals the architecture of biological noise http://www.nature.com/nature/journal/v441/n7095/full/nature04785.html http://www.nature.com/nature/journal/v441/n7095/full/nature0...
- thaumasiotes 9y ago> If clones in as exactly identical environments as researchers can create and perceive still wind up with such dramatic individual differences, how is science even possible on what causes the differences? Obviously science can't find the causes of differences that are uncaused. But science doesn't have much trouble dealing with identical objects behaving differently under identical circumstances; quantum physics and statistics are both pretty successful.