Why sleep changes after 60, and which changes are worth treating

Sleep architecture changes with age in ways that are consistent, well documented and largely normal. Deep slow-wave sleep declines from early adulthood onward, substantially so by the sixties. Total sleep time falls modestly. Sleep becomes more fragmented, with more brief awakenings that may not be remembered. And the circadian rhythm advances — the whole cycle shifts earlier, so sleepiness arrives sooner in the evening and waking comes sooner in the morning.

That last change explains a great deal of what gets reported as insomnia. A person who used to sleep from eleven to seven now becomes sleepy at nine, dozes in front of the television, goes to bed at ten and wakes fully at half past four. They have had six and a half hours, which is close to what they need, distributed inconveniently. That is a scheduling problem, not a sleep disorder, and it responds to light and timing rather than to sedatives.

What counts as an actual problem

The clinical definition of insomnia disorder requires difficulty initiating or maintaining sleep, occurring at least three nights a week for at least three months, and causing daytime impairment. That last clause is doing important work. Sleeping less than you used to, without feeling impaired during the day, is not a disorder.

Daytime impairment means fatigue, poor concentration, mood disturbance, or falling asleep unintentionally. It does not mean being annoyed about lying awake, though that is genuinely unpleasant and worth addressing.

The conditions that hide behind "poor sleep"

Several distinct problems present identically to the patient and require completely different treatment. Getting the diagnosis right matters more than any sleep hygiene advice.

Obstructive sleep apnoea becomes substantially more common with age and is heavily under-diagnosed in older adults, partly because the classic picture — overweight, middle-aged, loud snoring — leads clinicians to look past thin elderly women who have it. Suspect it if there is witnessed pausing in breathing, morning headache, unrefreshing sleep despite adequate hours, or heavy daytime sleepiness. It is treatable and it matters, being associated with hypertension, atrial fibrillation and cognitive impairment.

Restless legs syndrome — an irresistible urge to move the legs, worse in the evening, relieved by movement. Often associated with low ferritin, which is worth checking because it is correctable.

REM sleep behaviour disorder — acting out dreams, sometimes violently. This one deserves specific attention because it is strongly associated with later development of Parkinson's disease and related conditions. It needs a neurological assessment, not a sleeping tablet.

Nocturia. Getting up three times to pass urine is a urological problem presenting as a sleep complaint.

Depression. Early morning waking with low mood is a classic pattern and treating the sleep alone will not resolve it.

What CBT-I actually involves

It is not relaxation and it is not sleep hygiene leaflets. The two effective components are behavioural and initially counter-intuitive.

Stimulus control re-establishes the association between bed and sleep. Bed is for sleeping. If you are awake for more than about twenty minutes, you get up, go elsewhere, and return when sleepy. No reading in bed, no television, no lying there resolving to sleep.

Sleep restriction — better named sleep consolidation — deliberately reduces time in bed to match actual sleep time, then extends it as efficiency improves. Someone spending nine hours in bed to obtain six hours of broken sleep is instructed to spend six and a half hours in bed. The sleep consolidates. It is unpleasant for the first fortnight and it is the most effective single component.

This is worth doing with guidance, and it is not appropriate for everyone — it needs care in people with bipolar disorder, epilepsy, or a high falls risk who may be unsteady during a period of increased sleepiness.

Light, which is under-used

Because the underlying change is often circadian, light timing is a genuine lever. Bright light in the late afternoon or early evening delays the body clock and pushes both sleep onset and waking later — useful for the person falling asleep at nine and waking at four. Getting outside in the morning has the opposite effect and is more useful for someone whose rhythm has drifted late.

Older eyes transmit less light to the retina — the lens yellows and the pupil is smaller — so the exposure needed is larger than in a younger person. Outdoors on an overcast day still delivers vastly more than a well-lit room.

About sleeping tablets

Benzodiazepines and z-drugs reduce time to sleep onset by an average of around twenty minutes and increase total sleep by roughly half an hour in trials. Against that, in adults over sixty they are associated with falls, fractures, cognitive impairment and next-day sedation, and tolerance develops within weeks. Multiple guidelines advise against routine use in this age group.

Sedating antihistamines, widely sold over the counter for sleep, are anticholinergic and appear on every list of drugs to avoid in older adults. Melatonin has a modest effect on sleep onset, a good safety profile, and is licensed in prolonged-release form for over-55s in several countries — it is the most defensible pharmacological option, and it is not a sedative in any meaningful sense.

If you are already on a sleeping tablet and have been for years, that is worth a conversation about tapering rather than a decision to stop. Withdrawal insomnia is real and temporary, and getting through it usually requires a plan and some support.