Nature | News
Social-priming research needs “daisy chain” of replication. Ed Yong
Excerpt: “Kahneman, a psychologist at Princeton University in New Jersey, addressed his open e-mail to researchers who work on social priming, the study of how subtle cues can unconsciously influence our thoughts or behaviour.”
My comment: From behavioral epigenetics it is now clearer that an environmental drive evolved from that of nutrient chemical ingestion in unicellular organisms to that of socialization in insects. The honeybee model organism exemplifies that fact. What the queen eats determines her pheromone production and everything else about the interactions in the colony. It is also clear that, in mammals, food odors and pheromones cause changes in hormones that have developmental affects on behavior in nutrient-dependent reproductively fit individuals.
Social scientists may want to include knowledge of the basic principles of biology and levels of biological organization in their studies of social priming. In all vertebrates, for example, the effects of social odors on hormones cause unconscious affects on the development of behavior. A sensory stimulus-> effect-> hormone-> affect approach could incorporate what is known about the requirement for gene, cell, tissue, organ, organ system reciprocity in adaptive evolution, and help to ensure that no missing steps in this critical path lead to results that cannot be replicated because the requirements for adaptive evolution of behavior via ecological, social, neurogenic, and socio-cognitive niche construction were not considered.
For example, social priming doesn’t begin with a visual stimulus or a hormone like oxytocin in mammals. It begins with gene activation by a sensory stimulus that epigenetically effects intracellular signaling and stochastic gene expression. It’s gene expression in gonadotropin releasing hormone neurosecretory cells of brain tissue that links sensory stimuli directly to changes in nutrient chemical-dependent species-specific social priming and behaviors — via downstream effects on other hormones in all vertebrates. Starting with something that affects behavior in individuals or groups from one species and expecting to find reproducible results at different developmental stages in another species virtually ensures missing the involvement of genetic predispositions and experience-dependent epigenetic effects.
Replication attempts are doomed to fail if only for the fact that each individual of each group tested has slightly different genetic predispositions and experiences that epigenetically effect hormones that affect behavior during development. No matter what measure of behavior is used, if a model for behavioral development is not used there’s likely to be a problem with replication.
