This 2015 US/Canadian human study of people ages 6 to 22 years found:
“Testosterone-specific associations between amygdala volume and key prefrontal areas involved in emotional regulation and impulse control:
- Testosterone-specific modulation of the covariance between the amygdala and medial prefrontal cortex (mPFC);
- A significant relationship between amygdala-mPFC covariance and levels of aggression; and
- Mediation effects of amygdala-mPFC covariance on the relationship between testosterone and aggression.
These effects were independent of sex, age, pubertal stage, estradiol levels and anxious-depressed symptoms.
For the great majority of individuals in this sample, higher thickness of the mPFC was associated with lower aggression levels at a given amygdala volume..this effect diminished greatly and disappeared at more extreme amygdala values.”
The study provided noncausal associations among the effects (behavioral, hormonal, and brain measurements).
From the Limitations section:
“No umbilical cord or amniotic measurements were available in this study and we therefore cannot control for testosterone levels in utero, a period during which significant testosterone-related changes in brain structure are thought to occur.”
There’s evidence that too much testosterone for a female fetus and too little testosterone for a male fetus both have lifelong adverse effects. The researchers dismissed this etiologic line of inquiry with a “supporting the notion” referral to noncausal studies.
The researchers were keen to establish:
“A very specific, aggression-related structural brain phenotype.”
This putative phenotype hinged on:
- Older subjects’ behavioral self-reports, and
- Parental assessments of younger subjects’ behavior
exhibited during the previous six months, and within six months of their fMRI scan.
These self-reports and interested-party observations were the entire bases for the “aggressive behavior” and “anxious–depressed” associations. The researchers provided multiple references and models for the reliability of these assessments.
Experimental behavioral measurements – such as those done to measure performance in decision studies – may have been more accurate and informative than what the older subjects chose to self-report about their own behavior over the previous six months.
People of all ages have an imperative to NOT be completely honest about their own behavior. One motivation for this condition is that some of our historical realities are too painful to enter our conscious awareness and inform us about our own behavior. As a result, our feelings, thoughts, and behavior are sometimes driven by our histories without us being aware of it.
For example, would a teenager/young adult subject self-report an impulsive act, even if they didn’t fully understand why they acted that way? Maybe they would if the act could be viewed as prosocial, but what if it was antisocial?
What are the chances that the lives of these teenager/young adult subjects were NOT filled with impulsive actions during the six months before their fMRI scans? Could complete and accurate self-reports of such behaviors be expected?
Experimental behavioral measurements may have also been more accurate and informative than second-hand, interested-party observations of the younger subjects. Could a parent who provided half of the genes and who was responsible for many of their child’s epigenetic changes make anything other than subjective observations of their handiwork’s behavior?
Epigenetic studies have shown that adaptations to environments are among the long-lasting causes for effects that include behavior, hormones, and brain measurements. Why, in 2015, did researchers spend public funds developing what they knew or should have known would be noncausal associations, while not investigating possible causes for these effects?
Why weren’t the researchers interested enough to gather and assess etiologic genetic and epigenetic evidence? Was it that difficult to get blood samples at the same time the subjects gave saliva samples, and perform selected genetic and DNA methylation analyses?
What did the study contribute towards advancing science? Who did the study really help?
http://www.psyneuen-journal.com/article/S0306-4530%2815%2900924-5/fulltext “A testosterone-related structural brain phenotype predicts aggressive behavior from childhood to adulthood”