This investigation evaluates hypotheses that seek to explain temporal
retardation or prolongation of human ontogeny. Current hypotheses that
address this issue are poorly defined and conflate several distinct t
heoretical positions. A model that predicts homogeneity in the extensi
on of human growth periods is evaluated. This model is contrasted with
two alternatives. The first alternative predicts heterogeneity in the
extension of human growth periods. The second anticipates that human
growth prolongation is the result of the uniquely derived ''insertion'
' of a human childhood period into an ancestral ontogenetic trajectory
. Allometric analyses of body mass growth data from 21 species of anth
ropoid primates suggest that human female and male ontogenies often de
part from patterns established by other primates, but these departures
are not uniformly exceptional. Comparisons imply that derived changes
in human growth are heterogeneous. Relative to interspecific expectat
ions, early growth periods are much prolonged, but later growth period
s are actually reduced. Moreover the attributes of early growth period
s, including growth rates, timing of growth events, and size-for-age,
are highly variable across primates. Low correlations among growth per
iods suggest independence among growth phases. These analyses highligh
t minimal distinctions between competing models (heterogeneous extensi
on and insertion hypotheses) that attempt to explain human growth prol
ongation. More important, the present study facilitates refinements of
causal models that have been proposed to explain human growth prolong
ation. Specifically, human growth prolongation may be related to deriv
ed changes in patterns of brain development. Alternatively, metabolic
factors may have exerted influences on human ontogeny However, models
that predict long growth periods as a byproduct of metabolic factors d
o not adequately explain temporal retardation of human ontogeny. (C) 1
998 Wiley Liss, Inc.