The neuroscience of sleep: why D-hormone, acetylcholine and the microbiome matter

During deep sleep the space between brain cells expands and cerebrospinal fluid can flow through brain tissue. This flow flushes out metabolic waste and protein residue accumulated during waking hours — a process known as glymphatic clearance.

Crucially, this mechanism is tied mainly to deep, slow-wave sleep. If the deep phase is shortened by late alcohol, a late meal, an overly warm room or chronic strain, the clearance isn't completed — even when total time in bed looks perfectly normal.

The term "vitamin D" is a historical misnomer. It's a steroid prohormone that the body primarily synthesises in the skin with sufficient exposure to the UVB part of sunlight, and which is then activated by the liver and kidneys.

Receptors for D-hormone (VDR) are also present in brainstem regions involved in regulating the switch between wakefulness and sleep, and in circadian rhythm. Low levels are therefore often associated with poorer sleep quality and longer time to fall asleep.

For much of the year at our latitude, sunlight isn't strong enough for adequate synthesis. So it makes sense to measure the level and interpret it together with a physician, rather than guessing from generic recommendations.

Acetylcholine is a neurotransmitter central to attention, learning and memory. Notably, its activity during REM rises to levels comparable with wakefulness — the brain is highly active while the muscles stay relaxed.

In this state the brain links new information to existing networks: this is the phase in which daily experience is converted into usable knowledge and the emotional content of the day is processed.

Because REM phases cluster in the second half of the night, they're hit hardest by interrupted or shortened morning sleep. Regularly cutting the last two hours systematically reduces exactly the part of the night that matters most for memory and mood.

The gut microbiome communicates with the central nervous system along several routes: via the vagus nerve, via immune signalling, and via metabolites produced when fibre is broken down. These metabolites participate in regulating inflammatory processes and, indirectly, sleep quality.

A large share of serotonin, the precursor of melatonin, is produced in the digestive tract. So dietary pattern, the timing of the last meal and fibre diversity aren't a side topic when we talk about sleep — they're part of the same system.

In practice this means sleep analysis often doesn't end at the sensor on your wrist, but also takes in your dietary pattern and, where needed, laboratory parameters.

These four mechanisms interact. Low D-hormone can worsen sleep onset, alcohol can both shorten deep sleep and suppress REM, a late meal can raise night-time heart rate and reduce recovery. A single intervention rarely turns things around — it makes sense to start from measurement.

At HUMAX we therefore begin with a baseline: sleep structure from a sensor, selected laboratory parameters, and a review of daily patterns. The interpretation is handled by the appropriate specialist, while we take care of organising and tracking it over time.