In this article I evaluate recent attempts to illuminate the human infant cry from an evolutionary perspective. Infants are born into an uncertain parenting environment, which can range from indulgent care of offspring to infanticide. Infant cries are in large part adaptations that maintain proximity to and elicit care from caregivers. Although there is not strong evidence for acoustically distinct cry types, infant cries may function as a graded signal. During pain-induced autonomic nervous system arousal, for example, neural input to the vocal cords increases cry pitch. Caregivers may use this acoustic information, together with other cues, to guide caregiving behavior. Serious pathology, on the other hand, results in chronically and severely abnormal cry acoustics. Such abnormal crying may be a proximate cause of adaptive infant maltreatment, in circumstances in which parents cut their losses and reduce or withdraw investment from infants with low survival chances. An increase in the amount of crying during the first few months of life is a human universal, and excessive crying, or colic, represents the upper end of this normal increase. Potential signal functions of excessive crying include manipulation of parents to acquire additional resources, honest signaling of need, and honest signaling of vigor. Current evidence does not strongly support any one of these hypotheses, but the evidence is most consistent with the hypothesis that excessive early infant crying is a signal of vigor that evolved to reduce the risk of a reduction or withdrawal of parental care.

An evolutionary model of crying requires consideration of nonhuman primate data. Chimpanzees do not have colic. Although they have a peak of fussiness at 6 weeks with a decline by 12 weeks whether raised by biological mothers or in a human nursery, their crying is always consolable. Colic may be a by-product of delayed rates of brain development; that is, neoteny.

I argue that in the first three months, crying is primarily a behavioral state rather than a signal and that its properties include prolonged and unsoothable crying bouts as part of normal development. However, these normal properties trigger Shaken Baby Syndrome, a form of child abuse that does not easily fit an adaptive infanticide analysis.

A proximal mechanism is proposed whereby early crying helps maintain ideal levels of brain activation during the first three postnatal months. The proposal is consonant with both animal and human infant literatures, and new data are presented in its support.

Unlike chimpanzees, human infants engage in persistent adult-directed (AD) crying, and human mothers produce a special form of infant-directed vocalization, known as motherese. These complementary behaviors are hypothesized to have evolved initially in our hominin ancestors in conjunction with the evolution of bipedalism, and to represent prelinguistic substrates that paved the way for the eventual emergence of protolanguage.

By synthesizing evolutionary, attachment, and acoustic perspectives, Soltis has provided an innovative model of infant cry acoustics and parental responsiveness. We question some of his hypotheses, however, because of the limited extant data on infant crying among hunter-gatherers. We also question Soltis' distinction between manipulative and honest signaling based upon recent contributions from attachment theory.

An evolutionary account of excessive crying in young infants – colic – has been elusive. A study of mothers with new infants suggests that more crying is associated with more negative emotions towards the infant, and perceptions of poorer infant health. These results undermine the hypothesis that excessive crying is an honest signal of vigor.

The crying curve across early infancy may reflect the developing interaction between circadian and homeostatic processes of sleep-wake regulation. Excessive crying may be interpreted as a misalignment of the two processes. On the basis of the proposed mechanism, excessive crying may be an honest signal of need, namely, to elicit parental resources to modulate the behavioral state.

Soltis' paper contains little data on the underlying neural substrate of the discussed signal function of early infant crying – probably because there is amazingly little known about it. We here discuss the interest of functional neuroimaging as an objective measurement of brain activity in (1) early infants during crying and (2) parents hearing their offspring cry.

The colic cry as a signal of undifferentiated vigour, and not a disease, is good news. This hypothesis also has neurobiological perspectives. Feeding increases the pain threshold of the infant and has an effect on its brain functions. These may contribute, by neurobiological mechanisms, to the gradual decline in the tendency for excessive crying during the first months of life.

We welcome Soltis' use of evolutionary signaling theory, but question his interpretations of colic as a signal of vigor and his explanation of abnormal high-pitched crying as a signal of poor infant quality. Instead, we suggest that these phenomena may be suboptimal by-products of a generally adaptive learning process by which infants adjust their crying levels in relation to parental responsiveness.

Colic may allow infants to obtain additional investment from their parents. The lack of clear fitness costs of colic and of differences in condition between colicky and non-colicky infants is inconsistent with the hypotheses that colic is an honest signal of need or vigor. These and other characteristics of colic, however, are consistent with the hypothesis that colic is a manipulative signal.

Our focus has been on the role of early cry as a commanding source of information about infant pain and distress that requires interpretation by an adult caregiver. Its inherent ambiguity may offer an adaptive advantage, as resolution requires adult presence and scrutiny of other behavioral, physical, and contextual factors.

The neural structures implicated in crying are reviewed, based on studies in animals. Brain regions involved include the anterior cingulate gyrus (a cortical structure), amygdala, thalamic tegmentum, periaqueductal gray of the midbrain, and the nucleus ambiguus of the caudal brainstem. It is hypothesized that the crying associated with colic may be a manifestation of differing developmental stages in the brain circuits involved.

Crying and laughter are innate, preverbal, species-typical vocalizations that have similarities and differences which are mutually illuminating.

This commentator has no argument with the explanations given by Soltis. Yet a different approach to the phenomenon of crying might be fruitful. Neonates elicit care. It is hypothesized that non-neonates evolved to mimic, when in need, the appearance of the neonate by crying and by shedding tears, thus inducing helping behavior by the spectator.

In addition to the infant cry being a signal for attention, it may also be a critical component of the early formation of attachments with caregivers. We consider the complex development of that attachment, which involves reciprocal interactive signaling and a host of evolutionarily conserved caregiver factors.

We find the idea that infant crying arises from thermoregulation more consistent with a coregulatory account of its evolutionary history than it is with the informational account advocated in the target article.

The signal functions of infant crying cannot be understood properly without due attention to their ontogenetic development. Based on our own research on the development of infant cries, we argue that the controversies in cry literature will not be solved by static models, but that progress will made only when considering ontogenetic changes in interpreting cry data.

Soltis' analysis of signal functions of young infants' cries stimulates testable questions regarding abuse, neglect, and infanticide. Nevertheless, his evolutionary perspective oversimplifies the cry event, and does little to promote developmental analysis of crying during infancy. Studies of the cry in its behavioral and developmental context are needed if we are to understand the proximate causes of optimal and suboptimal care.