"Such oxytocin-administration effects on activation of human social brain regions (brain areas that subserve the acquisition, processing and use of social informa- tion) have been best studied in the context of autism; thus, three recent studies have demonstrated strong oxytocin-induced increases in activation of speci c cortical social-brain areas (Gordon et al., 2013; Domes et al., 2014; Watanabe et al., 2014), especially in regions of the medial prefrontal cortex that regulate processes related to theory of mind (Amodio & Frith, 2006). In contrast to this increased activation of brain regions that underpin social cognition, oxytocin administration tends to dampen activation of the amygdala for negative emotions, thus reducing perception and processing of fear, stress and anger (e.g. Gamer, Zurowski & Büchel, 2010). Oxytocin administration also leads to increased functional connectivity between the amygdala and some social-brain regions such as the orbitofrontal cor- tex (Riem etal., 2012; Sripada etal., 2013), which may serve to foster the controlled mentalization that leads to enhanced, more-deliberative social decision-making; by direct contrast, testosterone reduces functional connectivity between these regions (Volman et al., 2011; Spielberg et al., 2014) and is thereby expected to reduce controlled mentalization, in contexts where aggressive behaviour is favoured over af liation or cooperation. Such opposite, ‘anticorrelated’ activation patterns have also been reported for the ventromedial prefrontal cortex (a key social-brain region that regulates social emotionality) in relation to the amygdala (e.g. Stanton et al., 2009), and more broadly for the ‘default network’ of the brain that subserves many social, mentalistic, and introspective cognitive systems, compared to the ‘task-positive’ network that is dedicated to mechanistic, non-social cognitive processing (Jack et al., 2012; Kubit & Jack, 2013). By this model, oxytocin thus represents, most simply, a hormone that promotes social cognition and mentalizing, in contexts that are both simple (such as positive af liation, emotion recognition, affective empathizing, or individual recognition) and more complex (such as theory of mind, complex social emo- tionality, or ingroup–outgroup balances of cooperation and competition), and may be transient or longer lasting. Dependency of prosocial oxytocin effects on social information is clearly exempli ed in a study by Declerck, Boone & Kiyonari (2010), who found that in two cooperative games, oxytocin administration led to increased cooperation when social information was present, but reduced cooperation when it was not."
From this we could suggest that oxytocin and testosterone affects organic and mechanistic encoding.
"One of the clearest examples of this pattern is the effect of testosterone administration in reducing connectivity of the orbitofrontal cortex (OFC) with the amygdala, connectivity that would enhance social-brain input into emotionally driven behaviour. As noted above, oxytocin exhibits the opposite effect, increasing OFC – amygdala connectivity. Comparable diametric effects are seen for actual performance in mentalistic, empathic tasks: for example, oxytocin administration, or high-oxytocin genotypes for single nucleotide polymorphisms in the oxytocin receptor gene, are associated with better per- formance on reading emotions from the eye region of faces (Domes et al., 2007); by contrast, testosterone administration is associated with reduced performance on the same task, with even stronger effects when an indicator of higher prenatal testosterone is also taken into account (van Honk et al., 2011). Testosterone administration also leads to reduced trust (Bos, Terburg & van Honk, 2010; Boksem et al., 2013), in direct oppo- sition to the effects of oxytocin that enhance it (Kosfeld et al., 2005).
Such opposite effects, and emerging evidence for physiological mechanisms whereby these two hormone systems interact, are of considerable interest because they appear to de ne a pivotal axis of human neuroen- docrine architecture that modulates degrees and forms of sociality."
So testosterone leads to decreased connectivity (plausibly) in social cognition and therefore less Organic encoding in NJT. Due to the anti-correlation of Organic and Mechanistic a decrease of Organic encoding would create ideal circumstances for an increase in Mechanistic encoding. But it doesn't neccesarily mean that a increase in testosterone increase Mechanistic encoding, it just probably decreases Organic encoding.