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Estimated reading time: 7 minutes

Rob Mank Features
James J. McKenna, Ph.D, IN, USA
Photo: Rob Mank

A conceptual model of the biological origins of sudden infant death syndrome (SIDS) and colic: is the human infant’s susceptibility to either SIDS or colic due to our species’ unique breathing control system that is necessary for speech?

Part 1 


Christina Simantiri

It’s a frustrating and helpless experience for any parent to experience a child’s suffering from inconsolable crying or “colic.” At its worst, it can lead some parents to lose control and forcefully shake and injure their infants, causing serious brain damage and death (shaken baby syndrome). Even without a loss of control, parental despair is acute, as there is no agreement on what causes colic. Is it a digestive problem? An allergic reaction? Intestinal pains? It may sometimes even seem as if the infant is purposefully refusing to stop crying, regardless of the relentless efforts by the parents to be responsive and sympathetic.

But what if, in regard to this seemingly inconsolable crying, the infant is as much, if not more, a victim than are its parents? What if the infant has no control whatsoever over stopping its crying, nor the involuntary breathing that sustains it, with voice and breath being temporarily locked together, not permitting the infant to disassociate one from the other? And sensing this inability to stop crying, the infant, in fear, does more of what it is attempting to reverse, by crying all the more, seemingly caught in a cruel, positive loop.

And what if the much worse tragedy of SIDS, a syndrome not found to occur in other species, is related, like colic, to this process, where a missing or insufficient signal fails to stimulate a transition back to involuntary or “vegetative” (brain stem-based) breathing after an active sleep bout? During active sleep—a stage of sleep called Rapid Eye Movement (REM), in contrast to Non-REM or quiet sleep—the lower brain stem is in charge of sustaining breathing, and the infant must rely on its own purposeful, voluntary (higher brain-based or cortical controlled) breathing to terminate apneas or breathing pauses by reinitiating a breath: a type of breathing necessary for humankind’s most impressive adaptation, language. 

This is essentially what my colleagues Wendy Middlemiss and Mary Tarsha and I propose in a new paper published earlier this year (McKenna, Middlemiss and Tarshay, 2016). It integrates evolutionary, neuro-physiological, and developmental lines of research to help understand what is unique, if risky, about the human respiratory system and its development. Using epidemiological and neuro-developmental data, we propose that when the neuro-pathways and structures that control both voluntary and involuntary breathing are becoming integrated at around one to seven months of age, learning when and how to communicate with each other, the human infant can be vulnerable either to inconsolable crying while awake or to SIDS while asleep.

Over the first seven months of life, the regulation of numerous life-sustaining systems (including breathing) by the brain stem gradually gives way to an integrated, dual system, by which control of both voice and breath comes to be shared with the cortex or higher brain, i.e. the intellectual, thinking center. During this period, in which infants are most susceptible to SIDS and colic (especially between about two to four months of age), the cortex increasingly receives connecting neuronal projections tying the two parts of the brain and other breathing-related neural pathways together, moving from a single respiratory system, housed in the brain stem at birth, to a dual-control system. Gradually the infant becomes able to purposefully manipulate air pressure behind the throat, and calibrate the amount and speed of air release during exhalation through the voice box, making intentional and well-timed specific vocalizations possible. Through practice and hearing others and ourselves speak, we humans learn how to control and integrate voice with breath.

In fact, the infant learns to “speech breathe” by getting better and better at controlling the pitch, volume, and tempo of its cry in relation to its breathing. The manipulation of air flow out of the mouth, of residual pressure of air left in the lungs, and of the speed of the released air, in the form of short inspirations and prolonged expirations, is necessary for fully fledged language.

Over time, these developing neurological connections between higher and lower neural structures get better at communicating with each other, learning who is in charge, so to speak, at any given moment. But for a short developmental time period this integration can be less complete and, thus, less reliable. We propose that during this period of instability one of these two breathing glitches could arise, with one, SIDS, being far more serious than the other, inconsolable crying.

Colic may well be an example of a developmental mismatch between these two systems. Inadequate or missing neuronal signals prevent the infant from stopping its cry (its breath) , which itself has been initiated by immature voluntary and involuntary neural structures firing simultaneously in the form of a hyper arousal while the infant is awake. Rather than colic reflecting digestive pain, as has often been assumed, we propose that it could be fear. After the infant realizes it cannot stop crying, it does more of what it is trying to reverse—more crying, becoming a victim of its own immature neural structures, with voice and breathing being locked together, out of the infant’s control. There is some evidence that points to the possibility that a particular group of cells in the mammalian cry circuit, (a structure called the anterior cingulate gyrus, that functions during the vulnerable period with the help of a relatively small number of oval-shaped spindle cells called von Economo neurons (VENs)), begin to proliferate after infants pass both through the peak age for SIDS and colic. This set of structures also functions in relationship to an adjacent neural structure called the insula, a part of the brain that, among other things, keeps tabs on how well the body itself is meeting all its physiological and/or metabolic, life-sustaining requirements. The relatively small number of VENs, during this vulnerable period, may, for some infants, drop below some minimum requirement needed to terminate crying; after this narrow window of vulnerability the number of these cells increases significantly, thus ending, as we propose, the infant’s susceptibility to inconsolable crying.

Rather than colic reflecting digestive pain, as has often been assumed, we propose that it could be fear.

Newborn baby in a basket

Athena courtesy Lena Ostroff

With SIDS, which occurs during sleep, another kind of insufficient neuronal signaling glitch could occur, but this time while the infant is either moving in or out of the voluntary breathing that accompanies active sleep (REM), often when the infant is dreaming. After a month of life, human infants lose the gasping reflex which until this age automatically, by way of the brain stem, reinitiates breathing, without the infant’s purposeful effort. After a month, in order to terminate an apnea, an infant must be alerted to awaken and by way of the cortex voluntarily take a breath. But if the neural pathways (voluntary and involuntary) are not maturing at the same rate, which is possible, the infant could experience either an apnea or breathing pause in which the necessary cortical signal alerting the baby to arouse and take a breath does not occur, leading to a deadly desaturation of the infant’s oxygen supply. Or, it could be that simply the signal to move from one control system to the other, as sleep stages change, is simply insufficient, causing the baby similarly to cease breathing altogether, leading to death.

All of this process represents unique adaptations of our species that are a prerequisite for humankind’s most defining adaptation, language, and more specifically, speech breathing, which is mastered by infants before speech itself, over the first five to seven months of life. Unlike other mammals, human infants learn to vary their cries to reflect more precisely what is making them cry, and the degree to which they want to express hunger, loneliness, discomfort, boredom or pain. These neurologic and pulmonary manipulations are exactly the same ones used and required for human speech production and are, in fact, practice for it.

We realize that this is a model that makes several big interdisciplinary conceptual bridges and is in wait of testing. Testing would be done using magnetic resonance imaging that will first focus on whether during sleep and/or inconsolable crying episodes there is any evidence of neuronal firing in the predicted neural structures and/or networks. Pediatric studies are not yet planned for my sleep laboratory, which lacks the appropriate equipment; but the ideas have generated enough interest that we hope that they will be tested elsewhere, at least preliminarily.

Of course, we must always remember that “science has a nasty habit of ruining beautiful ideas,” but even so, we do hope that wherever we may be wrong or incomplete, these ideas will refresh and stimulate an entirely new direction of research into what makes us humans susceptible to these seemingly very different phenomena, SIDS and colic, two areas where new testable ideas are especially needed.


Kathy Grossman

McKenna, J., Middlehaus, W., Tarsha, M. Potential evolutionary, neuro-physiological and developmental origins of the sudden infant death syndrome (SIDS) and inconsolable crying (colic): Is it about controlling breath? Family Relations: International Journal of Applied Family Studies. (2016); 65 (1): 239-258 (refereed). 

In part 2 Dr. McKenna will explain what “breastsleeping” is and how theoretically it can function to help protect infants as they transition out of (as he argues here) susceptibility to either SIDS and/or colic.

Sids-and-colicJames McKennaB.A., University of California, Berkeley; M.A., San Diego State University; Ph.D., University of Oregon) Rev. Edmund P. Joyce, C.S.C., Professor of Anthropology, pioneered the first behavioral and electro-physiological studies documenting differences between mothers and infants sleeping together and apart. He has become known worldwide for his work in promoting studies of breastfeeding and mother-infant cosleeping. A biological anthropologist, McKenna began his career studying the social behavior and development of monkeys and apes, with an emphasis on parenting behavior and ecology, and has published over 140 articles and six books including Sleeping With Your Baby: A Parents’ Guide To Cosleeping, and a co-edited volume Evolution and Health: New Perspectives (Oxford University Press, 2008). He won the prestigious Shannon Award (with Dr. Sarah Mosko) from the National Institutes of Child Health and Development for his SIDS research and is the nation’s foremost authority and spokesperson to the national press on issues pertaining to infant and childhood sleep problems, sleep development, and breastfeeding. Most recently he has published a new paper with Lee Gettler proposing a new concept, “breastsleeping,” to promote the idea that breastfeeding and infant sleep are part of the same inextricable adaptive system that makes studying either normal healthy infant sleep, or normal breastfeeding patterns separate from each other inaccurate and/or invalid.


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