A sleeping baby looks peaceful. But what is happening inside that small brain is anything but passive. The brain is growing, neural connections are forming, memories are being laid down, and growth hormone is being released. Sleep is not a pause in life, sleep is a large part of living itself.

For newborns, this is especially true. In the first year of life, a baby spends more than half of her time asleep. For preterms in their first weeks born, this can even be up to 90% of the day. That is not a biological coincidence. It is a signal of how fundamental sleep is during this period. Because at that time, when the brain is growing at a pace it will never match again, many critical developmental processes happen while sleeping.

The sleeping brain is not off. It is busy building.

During active sleep, the early precursor to what later becomes REM sleep, connections between neurons are formed and strengthened. This process is critical for the maturation of the visual system, the motor system, and the broader neural plasticity of the brain.

A review published in Pediatric Research in 2024 describes sleep as one of the central driving forces behind brain development, both before and after birth.

A separate review by Lokhandwala and Spencer, published in Developmental Cognitive Neuroscience in 2022, analysed studies in both humans and animals. Disruptions to active or REM sleep in early life are associated in animal models with reduced neural plasticity, particularly in the maturation of the visual system and motor circuits.

The fact that babies sleep so much is not a sign of weakness or fatigue. It is the biological programme of a brain running at full capacity.

Babies learn during sleep. That may sound surprising, but it is scientifically established.

Researchers at Ruhr University Bochum and the University of Sheffield showed 6- and 12-month-old babies new actions, after which half the group slept and the other half stayed awake.

The result was clear: babies who slept for at least 30 minutes within four hours of learning retained the new behaviours significantly better, 4 to 24 hours later, than babies who remained awake. Babies who did not sleep after learning showed almost no retention.

The researchers concluded that babies depend on frequent naps for the formation of long-term memories. Memory consolidation, the process by which new information is stored, is active in the first year of life and is inseparably linked to sleep.

Every nap is therefore more than recovery. It is the moment when the brain processes, organises, and stores the day.

Sleep is closely connected to several body systems that are still developing in early life. One example is growth hormone, which is essential for physical growth, muscle development, and tissue repair. In children, its release is strongly linked to deep sleep, especially the first deep sleep episode after falling asleep.

This connection is also visible in infant growth patterns. A study published in SLEEP in 2011 found that periods of longer sleep and increased naps were followed by greater increases in body length in babies.

Sleep and immune development are connected as well. During sleep, the body produces cytokines, proteins that help fight infections and inflammation. Sleep disruption can affect this system, likewise illness can affect how and how much a baby sleeps.

A longitudinal cohort study in children aged 2 to 5 found that children who consistently slept less than their peers had higher blood levels of IL-6 and TNF-alpha at age five. These markers are linked to elevated immune activity and low-grade inflammation. Together, these findings do not prove simple causality, but they do show why sleep is relevant far beyond rest alone.

A review published in Nursing for Women's Health states that growing evidence indicates sleep quality is essential for the development of the central nervous system and is associated with long-term neurodevelopmental outcomes.

Research shows this has measurable consequences. A study of 34 preterm infants found an association between noise reduction via silicone earplugs and better scores on the mental development index at 18 to 22 months, with sleep identified as the mediating factor.

Researchers at UMC Utrecht published a study in the Journal of Neuroscience in 2024 in which machine learning was used to measure active sleep in preterm infants based on routinely recorded heart rate and respiratory signals. The finding: a higher percentage of active sleep during the preterm period, 29 to 32 weeks postmenstrual age, was significantly associated with greater white matter volume at term-equivalent age.

White matter is the network of connections in the brain that enables communication between regions. This finding does not prove causality, but it does show that active sleep is not just background behaviour: it may carry important information about early brain development in preterm infants.

During active sleep, the brain is not only consolidating what it learned. It is also physically forming new neural connections. Synaptogenesis, the creation of new synapses, is closely tied to active sleep in early development. This is part of why active sleep dominates so completely in the newborn and preterm period: the brain is quite literally under construction.

As the brain matures, sleep takes on an additional role. The Synaptic Homeostasis Hypothesis, developed by Tononi and Cirelli at the University of Wisconsin, proposes that deep sleep also scales back synapses that are no longer needed. Connections that are used are preserved; weaker ones are pruned. This refining process improves efficiency and signal quality across childhood and adolescence.

In autism spectrum disorder, this refining process appears less effective in some studies. Research on postmortem brain tissue shows that autistic brains retain higher axon density in areas associated with communication and social processing, consistent with reduced pruning over time. Immunological research points to impaired microglial function as a possible mechanism: these are the cells responsible for identifying and removing surplus synapses.

Whether disrupted sleep in early life contributes to this pattern in humans has not been established. Animal studies show that sleep deprivation impairs the microglial pruning mechanism, but direct evidence in infants is lacking. What is established is that the amount of active sleep during the preterm period is associated with white matter volume at term-equivalent age, one measurable marker of how the developing brain is building its connection infrastructure.

Preterm birth is a well-established risk factor for neurodevelopmental outcomes. A meta-analysis based on 52 studies found autism features in 20% of preterm populations using screening tools, compared to 1-2% in the general population. A 2025 review confirms elevated ADHD rates across all preterm subgroups.

But preterm ADHD is not simply more ADHD. Research describes a distinct preterm behavioral phenotype: predominantly inattentive rather than hyperactive, less associated with conduct difficulties, and more closely linked to structural brain differences, particularly white matter abnormalities in frontal-limbic tracts, than to the dopamine dysregulation that characterises ADHD in the general population. These are different problems at a structural level, and that distinction matters for how children may respond to interventions.

White matter alterations in preterm-born children are measurable into adolescence and adulthood, and are associated with poorer performance on sustained attention and processing speed tasks. The connection to sleep is the same one described in the prematurity section above: active sleep during the NICU period is associated with white matter volume at term-equivalent age. Structural brain development, sleep quality, and later neurodevelopmental profiles are connected, though the direction and magnitude of those relationships is still being mapped.

A prospective longitudinal study by Begum-Ali and colleagues, published in the Journal of Child Psychology and Psychiatry in 2023, followed 164 infants from 5 to 14 months. Lower night sleep scores in infancy were associated with a later autism diagnosis at age three, reduced cognitive abilities, and changes in social attention. Whether poor sleep is an early signal of a neurodevelopmental difference, a contributing factor, or both remains an active area of research.

Scientific honesty belongs in this conversation.

We do not yet know exactly how much sleep a preterm infant needs at each gestational age. We do not know which type of sleep disruption has the greatest impact on which aspect of development. And we cannot say with certainty whether better sleep in the NICU leads to measurably better cognitive outcomes in the long term, let alone that it prevents autism or ADHD.

The causality question is complex: sleep difficulties can be both an early signal of a neurodevelopmental difference and a contributing factor to it. In all likelihood, it is both, depending on the child and the context.

That does not mean sleep is unimportant. It means we are honest about what we know and what is still being studied. The mechanisms are plausible, the associations are demonstrable, but making definitive claims would take the science further than it has gone.

Taken together, sleep research points in one direction: sleep is biologically fundamental, early sleep patterns are associated with developmentally relevant outcomes, and making sleep more visible and actionable should support parents and caregivers in protecting an important part of early development.