The social brain: It’s all bottom-up priming
September 16, 2013 | James Kohl
Feature-based attention: it is all bottom-up priming [Subscription required]
Article excerpt: “…all behavioural and neuro-imaging studies suffer from the shortcoming that they cannot rule out an effect of priming, i.e. the notion that merely attending to a feature enhances the processing of that feature across the visual field, an effect that may occur in an automatic bottom-up way.”
In my model, the automatic effect of priming from the bottom-up perspective of ecological niche construction is consistently seen in the context of understanding social behavior. Panksepp, for example, said: “My feeling is that the social brain has many levels. If you don’t understand the foundational level, then you can do brain imaging until you’re blue in the face, but you still will not understand the process at a deep causal level.”
This is consistent with the biological facts about olfactory/pheromonal input and unconscious affects that we addressed in our 2001 award-winning review: Human pheromones: integrating neuroendocrinology and ethology, the year before Panksepp et al. won their award for publication of Comparative approaches in evolutionary psychology: molecular neuroscience meets the mind.
In these accurate portrayals from more than a decade ago, we can now see what neuroendocrinology, ethology, and evolutionary psychology have in common. The common thread is ecological and social niche construction. We also can see what these disciplines do not have in common, which is any theory about cause and effect that involves mutations. The integration by Kohl et al (2001) and by Panksepp et al (2002) clearly links molecular neuroscience and neuroendocrinology to an accurate representation of how brain-directed behavior develops in the context of niche construction. Evolutionary psychology and human ethology are largely based on theoretical misrepresentations of biological facts.
For example, as has always been the case, since Haldane helped to concoct the mutations theory that many evolutionary theorist simply accepted, no biological facts are consistent with mutation-driven evolution. In fact, that ridiculous theory was recently (i.e., finally) refuted via an experiment. An experimental test on the probability of extinction of new genetic variants.
Why was experimentation that might prove anything at all about mutations theory not attempted for more than 80 years? What kind of nonsensical approach to science is that. “We have a theory; that’s all we need” is nonsense, not science. So why not add more nonsense?
Theorists and fools are now claiming that data from the experiment does not refute mutation-driven evolution. Instead, they are attempting to define mutation in ways so that the definition can be extracted from the “muck” of evolutionary theory and natural selection. Little do they know that the muck is more like quick-sand than anything they’ve ever encountered. Thus, the more they struggle to obfuscate the facts about the requirement for fixation of new alleles, the faster they sink into the metaphorical abyss they have created because they refused to tether their hypothesis to any biologically-based scientific pursuits.
Earlier this year, I wrote in Kohl (2013): “The epigenetic effects of nutrients and pheromones extend across the life history of organisms, but from 1996 to 2012 the concept of molecular epigenetics and epigenetic effects on hormone-driven adaptive evolution of the human brain and behavior seems to have gone missing. Evolutionary psychologists and other social scientists, for example, refused to tether their hypotheses to a new discipline called ‘neuroevolutionary psychobiology’, to neurogenetics (Zoghbi & Warren, 2010), or to any biologically based discipline whatsoever (see for review Panksepp, Moskal, Panksepp, & Kroes, 2002). More than five decades of progress that directly links molecular epigenetics to behavior has been virtually ignored (Shapiro, 2012), but see Ledón-Rettig, Richards, and Martin (2012).
What we now see in the results of the experiment on fixation of new alleles is what might have been seen by Haldane, if he had merely looked first at what Darwin’s ‘conditions of life’ must be. Instead, he moved on to a theory of cause and effect with no consideration for the fact that ‘conditions of life’ are nutrient-dependent, which in my model means they are also pheromone-controlled. That’s why mutations theory has no explanatory power in the context of adaptive evolution. Mutations must be fixed in the organized genome of any species that has survived via nutrient acquisition and the metabolism of nutrients to species-specific chemicals that control reproduction. In the extremely rare cases where mutations are fixed, fixation is still nutrient-dependent and pheromone-controlled, and the fixed mutations are still associated with diseases and disordered genomes.