This is explained in two parts. I first wrote "Pecking Order I," April 5, 2001. Direct support was accumulating at the time so I posted it to various places on the internet as "Pecking Order." Direct Support of a Mechanism and Current Consequences." (This is "Pecking Order I" in this treatise.) The latest issue of Archives of General Psychiatry, volume 58, number 4, page 389-394, appeared soon after with some new data sufficiently important enough to rewrite this. The new material provides further support illustrating how pecking order directly affected human evolution, and continues to do so. This includes support of the involvement of testosterone in pecking order. (This will be explained in "Pecking Order II" in this treatise.) This effect of testosterone is linked to the mother. It is observable in living primates, Bonobos (Pan paniscus), and, I suggest, directs human evolution.

In 1985, I first developed my explanation of "pecking order" or the "fight or flight" mechanism. Basically, I suggested that the adrenal steroid hormone, dehydroepiandrosterone (DHEA), activates the brain during consciousness, so DHEA should be directly involved in activation of behavior. The more DHEA one has, the more active one is. (DHEA is the major steroid hormone of our bodies.) Also in 1985, I first suggested that the other major adrenal steroid hormone, cortisol, evolved to counteract DHEA. When the ratio of DHEA to cortisol is high, behavior is activated; when the ratio of DHEA to cortisol is low, behavior is repressed. Depending upon inheritance and experience, this ratio acts as a "set point," which affects most of our lives.

During fights, if DHEA is high, the individual pursues the fighting impulse. If cortisol exceeds a certain amount, the effectiveness of the DHEA is overcome and the individual alters behavior. This produces the advantage of allowing both individuals in a confrontation to avoid potential harm. This mechanism has survival advantage for both the dominant individual and the subordinate individual.

Individuals of low cortisol and high DHEA should be aggressive. That is, they should be less able to inhibit their behavior. In the past two years, both of these hypotheses have been directly supported. Girls who exhibit "conduct disorder" (CD) produce low levels of cortisol. "Morning plasma cortisol levels were significantly diminished in adolescent girls with CD. Decreased cortisol levels appear to be most strongly associated with antisocial girls who do not have other psychiatric disorders." (Archives of General Psychiatry 2001; 58: 297-302). In boys with CD, DHEA correlated with "disruptive behaviour" (Neuropsychobiology 2001; 43: 134-140). "Children with ODD [oppositional defiant disorder] had higher DHEAS levels than either the psychiatric control or normal control groups; DHEAS levels of the latter groups did not differ. Moreover, it was possible to classify children as having either ODD or ADHD on the basis of their DHEAS levels." (Journal of the American Academy of Child and Adolescent Psychiatry 2000; 39: 1446-51). "Low cortisol levels were associated with persistence and early onset of aggression, particularly when measures of cortisol concentrations were pooled. Boys with low cortisol concentrations at both time points exhibited triple the number of aggressive symptoms and were named as most aggressive by peers 3 times as often as boys who had higher cortisol concentrations at either sampling time." (Archives of General Psychiatry 2000; 57: 38-43). Individuals who produce a high DHEA to cortisol ratio characteristically exhibit aggressive behavior.

Pajer, et al., (Archives of General Psychiatry 2001; 58: 297-302), point out that "female adolescent antisocial behavior is increasing." Antisocial behavior is increasing in both sexes in our society. It occupies our newscasts almost nightly. There is an explanation for this increase. It is also my hypothesis that testosterone is increasing in our society. I suggest it is the basis of the "secular trend," which is the increase in weight and height along with earlier puberty in our children. It is real and robust in the U.S. (Arch Pediatr Adolesc Med. 2000; 154: 155-161). More specifically, I think individuals of higher testosterone are increasing more rapidly than those of lower testosterone. Testosterone is proven to be the hormone of sex drive in men and women (boys and girls), not estradiol in women. People who have greater sex drives will produce more children than those of lower sex drives. Given time, people of high testosterone will outnumber those of lower testosterone.

The secular trend has two basic components. One is the final increase of our children in size and earlier puberty. I think his is due to testosterone. The other part of the secular trend is an increase in the size of children which shows itself between ages two to five ("Normal Variations," Britannica CD, Version 99 3.00, 1994-1998, Encyclopædia Britannica, Inc.) and may "be relatively greater from age two to five than subsequently." This is a time when testosterone is not acting on children; it is a time when the only "androgenic" hormone acting on children is DHEA. At this time, measurable DHEA is very low, so this part of the secular trend from ages two to five depends on DHEA. DHEA is also increasing.

At the beginning of this treatise, I considered the impact of high DHEA on behavior. High DHEA increases the amplitude of behavior. High DHEA and high testosterone should combine to accelerate the increase in the percentage of people who are both high DHEA and high testosterone. People with a high sex drive and who are aggressive should reproduce faster than other people. High DHEA increases aggressive behavior prior to puberty. Attention-deficit hyperactivity (ADHD) is a form of aggressive behavior in children. The diagnosis of ADHD by medical doctors has increased "2.3-fold increase" from 1990 to 1995 (Clinical Pediatrics (Phila) 1999; 38: 209-17). (Remember, from above, that high DHEA is, essentially diagnostic, of ADHD. DHEA and testosterone should combine to increase violent behavior, especially in individuals who recently entered puberty. "Between 1985 and 1991, homicide rates among youths 15-19 years of age increased 154% and remain, today, at historically high levels." (American Journal of Preventive Medicine 1998; 14: 259-72). These combined effects of increasing levels of androgens are even beginning to affect the behavior of individuals at the low end of the scale of aggression and body size. We are beginning to witness an increase in aggressive, violent behavior, following puberty, in individuals who usually do not act on their impulses. I suggest the current increase in school shootings represents this increase in androgenic effects in individuals who are victims of bullying. Bullying is increasing and so are the responses to it. The percentage of individuals in our society whose "set points" are aggressive is increasing. The extreme measure of "boot camp" corrective institutions has had no greater, perhaps even less, effect on criminal recidivism than ongoing prisons. This is an endogenous change in individuals which is causing a population change with our society.

The new material which adds support to my explanation is in Archives of General Psychiatry 2001; 58: 389-394, D.S. Nagin and R.E. Tremblay, "Parental and Early Childhood Predictors of Persistent Physical Aggression in Boys from Kindergarten to High School." Nagin and Tremblay studied aggressive behavior in boys from ages 6 to fifteen years.

"Background: In a prior study, we identified 4 groups following distinct developmental courses, or trajectories, of physical aggression in 1037 boys from 6 to 15 years of age in a high-risk population sample from Montréal, Québec. Two were trajectories of high aggression, a persistently high group and a high but declining group. The other 2 trajectories were a low group and a moderate declining group. This study identified early predictors of physical aggression trajectories from ages 6 to 15 years."

While this does not include the first phase of the secular trend, i.e., from 2 to five years, it includes the results of the effects of first phase of the secular trend on aggression in boys in kindergarten. If one will remember from above, "Pecking Order I," if cortisol is low and dehydroepiandrosterone (DHEA) is high, children exhibit aggressive behavior. The first phase of the secular trend begins within ages 2 to five and is identified by Nagin and Tremblay at age six in the boys of their study. Nagin and Tremblay include the second phase of the secular trend, i.e., adolescence, which I suggested is affected more by testosterone. This is what I think Nagin and Tremblay support with their data, i.e., that aggressive individuals within and beyond adolescence are affected by effects of testosterone on the brain.

Nagin and Tremblay observed four "trajectories" of behavior from ages 6 to fifteen: "4 distinctive developmental trajectories of physical aggression from ages 6 to 15 years: a chronic physical aggression trajectory (4%) composed of boys displaying persistently high levels of physical aggression; a high level declining trajectory (28%) composed of boys who displayed a high level of physical aggression in kindergarten but whose aggression thereafter declined; a moderate level declining trajectory (52%) composed of boys who displayed modest physical aggression in kindergarten but whose aggression thereafter declined to virtual cessation; and a low trajectory (17%) composed of boys who rarely displayed physical aggression." I have already explained, in "Pecking Order I," the connection of DHEA to cortisol ratios and "conduct disorder" and "oppositional defiant disorder." Nagin and Tremblay study conduct disorder (CD) in their subjects, including behavior labeled "opposition." They report data which, I suggest, identifies aggressive behavior controlled by a high DHEA to cortisol ratio: "A host of risk factors were identified that distinguish the 2 low physical aggression trajectories from the 2 high trajectories. Concerning these risk factors, 2 findings stand out. The most powerful predictors of membership in a high aggression trajectory groups were high levels of hyperactivity and opposition assessed in kindergarten. Individually, these risk factors increased the odds of membership in a high physical aggression trajectory by a factor of 3. In combination, the increase is more than 9-fold. Individually, these risks are comparable in magnitude to the impact of high serum cholesterol levels on risk of coronary hear disease. In combination, they far exceed it." I suggest these are due to the first phase of the secular trend and are identified in kindergarten in this study. (See "Pecking Order I" to read the research concerning these behaviors and levels of DHEA and cortisol.)

Nagin and Tremblay identify four trajectories of behavior, three of which decline in adolescence. Some of the trajectories begin as high levels of aggression, but do not continue. These are probably due to increased DHEA to cortisol levels of childhood. In "Pecking Order I," I suggested that DHEA activates the brain. Subordinate to that, and a major part of my explanation of human evolution, is that testosterone evolved to direct use of DHEA by testosterone-target-tissues. That is, testosterone exerts its effects by directing use of DHEA. This is how I explain the decline in the group, "high level declining trajectory," and "moderate level declining trajectory" of Nagin and Tremblay. That is, in both of the foregoing trajectories, I think DHEA is high. As testosterone is produced at puberty, the testosterone directs use of DHEA for testosterone-target-tissues. This reduces the overall availability of DHEA. This effect would reduce the available DHEA for brain activity. The individual would begin will excessive DHEA, which would increase aggression prior to puberty, and the testosterone of puberty would redirect excessive DHEA, thus reducing aggression. Yes, in this group, testosterone would actually reduce aggression at puberty. "Moderate level declining trajectory" would represent a milder form of this change.

Nagin and Tremblay’s "chronic physical aggression trajectory" is explained by testosterone, also, but it involves effects of testosterone at puberty and before. They reported the following findings (edited):

"Results: The teenage mother, low maternal education, household not intact, low IQ, high hyperactivity, high opposition, high inattention, and high prosociality variables significantly distinguished group membership.

However, neither mother’s nor father’s low SES [socioeconomic status] was significant, nor were the early parenthood or low education factors for the father significant. Thus, in toto, the fathers’ characteristics did not distinguish trajectory group membership. In addition, child high anxiety was no significant predictor.

Maternal risk factors of low education and teenage motherhood increased the odds of a high aggression trajectory by 77% and 57% respectively. The largest impacts were for the behavioral and cognitive risk factors of the child himself. Low verbal IQ was associated with a nearly 2-fold increase in the odds of a high aggression trajectory, while high hyperactivity and high opposition increased the odds by nearly 3-fold. In contrast, prosociality decreased the odds of high aggression by more than half. In combination, the 2 largest risk factors, high hyperactivity and high opposition, increased the odds of high aggression by a factor of 8.0. Only the high inattention risk factor was statistically insignificant in this multivariate model.

A second prominent finding concerned the predictive power of parental characteristics: only characteristics of the mother have predictive power. Whereas teen onset of parenthood and low educational attainment for mothers were significant predictors of their son’s high aggression, these characteristics in the father had no predictive power.

The prominent predictive power of maternal characteristics again revealed itself in the analysis of factors that distinguished between the 2 high physical aggression groups, the high declining and the chronic trajectories. Here, we were concerned with identifying characteristics that distinguish the modestly large fraction (28%) of boys who start off displaying high levels of physical aggression but subsequently desist, from the small but prominent group (4%) of boys who continue their physical aggression unabated. Only 2 such characteristics were identified, mother’s low educational attainment and teenage onset of childbearing. The odds of male offspring of poorly educated teenage mothers not desisting from a high level of physical aggression at age 6 years are 9.3 times greater than those of their counterparts without such mothers.

Although ours is the first analysis to document that these 2 maternal characteristics distinguish persistence in from desistence of chronic physical aggression, there is a large body of evidence linking teen onset of childbearing with a litany of unfavorable behaviors and outcomes for the offspring. These include CD and other problem behaviors in childhood, delinquency and school dropout in adolescence, and criminality as an adult.

This study does not explain why teen onset of motherhood and low maternal education are risk factors for chronic physical aggression in a mother’s offspring."

These "results" may be interpreted to demonstrate that testosterone and excessive DHEA to cortisol are involved in the early phase of the "chronic physical aggression trajectory," and continuation from kindergarten to puberty. Low socioeconomic status (SES) was not important for either parent; this effect could occur at any socioeconomic level and the father’s characteristics were not directly involved. "Thus, in toto, the fathers’ characteristics did not distinguish trajectory group membership."

As it turns out the effects produced by the mother are directly involved in chronic physical aggression. As I stated above, I think the secular trend represents an increase in the percentage of individuals of higher testosterone. They arrive at puberty earlier and, therefore, are more likely to produce children earlier. Nagin and Tremblay found a direct relationship between chronic aggression and early age of maternal parenthood. "The odds of male offspring of poorly educated teenage mothers not desisting from a high level of physical aggression at age 6 years are 9.3 times greater than those of their counterparts without such mothers." A subordinate hypothesis of my explanation of the secular trend is that the earlier puberty of the trend adversely affects final development of the advanced forebrain. That is, the structures of the brain that develop prior to the prefrontal areas are more affected by testosterone so they develop faster. These structures control puberty. The advanced forebrain is the seat of abilities utilized in learning. This adversely affects the level of education the individual may attain. A significant connection of the mother and chronic physical aggression is underachievement in education. Thus, early puberty accounts for the characteristics of the mother that are connected with chronic physical aggression in offspring.

It is known that treatment with testosterone will increase aggression in some males, but not in others. I suggest the explanation is exposure to testosterone in utero. I am not referring to exposure to testosterone produced by the male fetus that establishes development of genitalia. Because of Nagin and Tremblay’s findings, I suggest exposure to maternal testosterone affects the development of receptors for testosterone. That is, I think exposure to the mother’s testosterone increases testosterone receptors that are activated later in life, specifically puberty, as are receptors produced by the fetus’s testosterone. These "maternally produced" receptors in the brain would be available for activation by the testosterone of puberty. Individuals who exhibit these additional receptors would be more activated by testosterone. This could explain why some individuals exhibit increased aggression to treatment with testosterone while others are not. More importantly, this could explain why boys who are already overly aggressive due to a heightened DHEA to cortisol ratio continue on their trajectory of increased aggression when the testosterone of puberty arrives. Mothers of high testosterone increase the receptors, and therefore, the effects of testosterone of puberty in their offspring.

It is my suggestion that individuals who exhibit chronic physical aggression have an advantage in reproduction in free-living primates. They succeed because of pecking order. Both males and females of this type should increase their numbers because of increased access and earlier puberty. I think the hominid line developed because of this behavior. This exact situation has been identified in free-living Bonobos.

"Intracommunity relationships, dispersal pattern and paternity success in a wild living community of Bonobos (Pan paniscus) determined from DNA analysis of faecal samples"

"Differences in social relationships among community members are often explained by differences in genetic relationships. The current techniques of DNA analysis allow explicit testing of such a hypothesis. Here, we have analyzed the genetic relationships for a community of wild Bonobos (Pan paniscus) using nuclear and mitochondrial DNA markers extracted from faecal samples. Bonobos show an opportunistic and promiscuous mating behaviour, even with mates from outside the community. Nonetheless, we find that most infants were sired by resident males and that two dominant males together attained the highest paternity success. Intriguingly, the latter males are the sons of high-ranking females, suggesting an important influence of mothers on the paternity success of their sons." (Proc R Soc Lond B Biol Sci 1999; 266: 1189-95)

This also occurs in humans. It produces children who are more aggressive. It produces the secular trend.