The objective of this report is to critically review past reports and present new data on the psychobiology of self-injurious behavior (SIB) and/or "risky" or "impulsive" behavior in primates (human and nonhuman). One aim was to reexamine how early social deprivation and neurobiological changes caused by deprivation might contribute to SIB in monkeys, and how the causes of SIB in monkeys might inform us about the psychobiology of suicide in humans. A second aim was to examine the evidence that social deprivation in monkeys produces reductions in brain 5-HT system function that are causal or coincident factors associated with self-injurious or impulsive behavior. Prior studies and new data indicate that the environmental causes of SIB and unusual aggression in rhesus monkeys do not produce reductions in brain 5-HT system activity and that experimental production of low levels of brain 5-HT system activity does not reliably promote either SIB or unusual other-directed aggression in monkeys. A third and final aim was to suggest that in severe cases of environmentally induced SIB and/or aggression in monkeys, having relatively high or low levels of 5-HT system activity may not be related to ongoing behavior because the 5-HT system may not interact with other neurotransmitter systems in the usual way. Overall, the contention is that primates exhibiting SIB and unusual aggression may have altered 5-HT system function, but this may be but one aspect of a more profound disorganization of brain function involving many neurohormonal and transmitter systems. Contemporary theorizing and experimentation tends to be restricted to the idea that altered function in one key system might be the cause of a specific form of psychopathology. In the future, research examining the probable change interactions of neurotransmitter and neuroendocrine systems as underlying causes of behavioral disorders should have a high priority.