The Epworth Sleepiness Scale tool above takes about two minutes to complete. But it’s worth understanding what the Epworth Sleepiness Scale is actually measuring, why that measurement matters far more than most people initially appreciate, and what your score is telling you about your health. Because a number without context is just a number, and the context here turns out to be surprisingly important.

Most people who complete the Epworth Sleepiness Scale for the first time experience a version of the same mild surprise: either their score is higher than they expected, which raises questions they hadn’t thought to ask, or it’s lower, and they feel a quiet relief they didn’t realise they needed. What almost nobody expects is for an eight-question questionnaire to prompt genuine reflection about the quality of their daily life. And yet, consistently, it does, because it forces a question most of us have never directly confronted: “Is the way I feel during the day actually normal?” For a surprisingly large proportion of the population, the honest answer is no.

Tiredness and Sleepiness Are Not the Same Thing

The distinction between tiredness and sleepiness is the conceptual foundation of everything else in this article, and it’s one that even clinicians sometimes blur. Getting it right changes how you interpret your score and how seriously you take what your body is telling you.

Tiredness, in the physiological sense, refers to a state of physical or mental fatigue. This is the heaviness in your legs after a long run, the mental fog that settles after hours of concentrated work, the bone-deep weariness that follows a difficult emotional week. Tiredness is something you feel, but it doesn’t necessarily mean your body is primed to fall asleep. A highly stressed person can be profoundly tired and yet lie awake for hours; an anxious person can feel utterly exhausted and still be physiologically incapable of dropping off. This is why tiredness, on its own, is a relatively poor indicator of sleep health.

Sleepiness is a different and more specific phenomenon. It refers to the homeostatic pressure to actually fall asleep. It is a measurable physiological drive that builds with time awake and dissipates with sleep. When sleep researchers talk about sleepiness, they’re talking about something that can be objectively quantified: your ability to stay awake in a quiet, monotonous environment, the speed at which your brain transitions toward sleep states when you lie down, and the degree to which your alertness fluctuates across the day. The Epworth Sleepiness Scale measures the behavioural expression of this drive, by questioning the likelihood that you’d actually doze off across a range of everyday situations.

This matters because pathological sleepiness (sleepiness that exceeds what’s explainable by your current circumstances) is a symptom. It’s not a personality trait, not a character flaw, and not simply the inevitable consequence of a busy life, but a physiological signal worth investigating. The problem is that we’ve become extraordinarily good at rationalising it away. “I’m just not a morning person.” “Everyone my age feels this way.” “I’ve always been someone who needs a lot of sleep.” Sometimes those explanations are accurate. Often, they’re a form of learned helplessness and a way of accommodating a problem rather than addressing it.

The Epworth Sleepiness Scale cuts through this by anchoring sleepiness to concrete, observable behaviour rather than subjective feeling. It doesn’t ask how tired you feel; it asks how likely you are to fall asleep. That’s a more demanding and more clinically useful question.

The Science Behind the Scale: What Dr Murray Johns Actually Built

The Epworth Sleepiness Scale was developed by Australian sleep physician Dr Murray Johns and first published in the journal Sleep in 1991. Johns was working at the Epworth Hospital in Melbourne (hence the name) and was frustrated by the limitations of existing sleepiness measures, which tended to be either too complex for routine clinical use or too narrow in what they captured. He wanted a simple, self-administered tool that could reliably distinguish normal from pathological sleepiness across a general population.

What Johns created was elegant in its simplicity. The eight scenarios he chose were carefully selected to span a wide range of soporific (something that causes or tends to cause sleep) stimulus; from highly sedating (lying down to rest in the afternoon) through moderately passive (watching television, sitting quietly after lunch) to situations where falling asleep would be genuinely unusual in a healthy, alert person (sitting and talking to someone, stopped briefly in traffic). This gradient is the scale’s diagnostic power: someone who scores high only on the obviously soporific items is different, clinically, from someone who scores high across the board, including the more stimulating situations. The latter pattern is more suggestive of pathological sleepiness.

The scale has been validated in dozens of studies across multiple populations and languages, and it performs well as a screening instrument. It correlates meaningfully with objective measures of sleepiness, including the Multiple Sleep Latency Test (MSLT), which measures how quickly someone falls asleep in standardised nap conditions and is considered the gold standard for objective sleepiness assessment. It’s sensitive to change over time, meaning it can track whether an intervention (such as treating sleep apnoea, improving sleep habits, adjusting medication) actually improves daytime alertness. And it’s simple enough to be completed anywhere, which is part of why it’s remained in widespread clinical use for over three decades. Unfortunately, not a lot of people are aware of it in the general public, and certainly not a lot of health and fitness coaches are aware of it, despite how helpful it is for those who offer lifestyle coaching as part of their service. 

The total score runs from 0 to 24 (eight questions, each scored 0 to 3) and falls into four clinical bands. Scores of 0-10 are considered normal, with most healthy adults clustering between 4 and 8. Scores of 11-12 represent mild excess sleepiness; 13-17 moderate excess sleepiness; and 18-24 severe excess sleepiness. These thresholds aren’t arbitrary: they were derived from Johns’ original research comparing patient populations with known sleep disorders against healthy controls, and have been broadly replicated and refined in subsequent work.

It’s also important to understand what the scale is not, as well as what it is. It’s a self-report tool, which means it’s subject to the limitations of self-assessment. So people who have adapted to chronic sleepiness may underestimate it because it’s become their baseline. It doesn’t tell you why you’re sleepy; it tells you the degree of your sleepiness. And it’s a screening instrument rather than a diagnostic one. A high score is a flag that warrants further investigation, not a diagnosis in itself. Keeping these caveats in mind helps you use the tool intelligently rather than either over-interpreting or dismissing your result.

Why We Normalise Dangerous Sleepiness

Unfortunately, there’s a particular kind of cultural permission we’ve granted ourselves to be exhausted, and it’s worth exploring, because it’s one of the main reasons pathological sleepiness goes unaddressed for so long.

In most industrialised societies, busyness has become a status symbol, and sleep has been reframed as something you earn rather than something you need. The person who announces they got four hours last night and still made it to the gym is performing a kind of productivity virtue, and this performance is so normalised that we’ve stopped questioning whether it represents a choice worth admiring or a habit worth worrying about. Meanwhile, the person who admits they fell asleep in a meeting or needed a nap every afternoon is more likely to feel embarrassed than to wonder whether their body is trying to tell them something important.

This normalisation has real consequences. The most immediate and quantifiable is driving safety. The research here clearly shows that driving while significantly sleep-deprived impairs reaction time and judgment to a degree comparable to being over the legal alcohol limit, and people who are chronically sleepy are often the worst judges of their own impairment. The same way someone who’s been awake for 24 hours frequently rates their own performance as fine when objective testing shows it’s severely degraded (you can do this yourself with our Sleep Deprivation Reaction Time Test). Studies examining road traffic accidents and ESS scores have found substantially elevated accident risk in drivers with scores above 10, and a landmark analysis by Sassani and colleagues estimated that treating obstructive sleep apnoea alone (one of the primary drivers of elevated ESS scores) could prevent thousands of traffic fatalities and tens of thousands of injuries annually.

Beyond driving, cognitive impairment from chronic sleepiness is both pervasive and insidious. It affects working memory (your ability to hold and manipulate information in the moment). It degrades executive function (your capacity to plan, prioritise, and make sound decisions). It blunts emotional regulation (making you more reactive, less patient, and less able to manage interpersonal complexity with the grace you’d prefer). And because these effects accumulate gradually, they become your new normal: you forget what it felt like to think clearly, to have sustained energy through an afternoon, to navigate a difficult conversation without snapping. You stop realising what you’re missing.

The other reason chronic sleepiness persists is perhaps the most psychologically interesting: we are genuinely poor at accurately assessing our own sleepiness, and this incapacity worsens as sleep deprivation accumulates. Research by Hans Van Dongen and David Dinges at the University of Pennsylvania demonstrated this with disturbing clarity. When subjects were restricted to six hours of sleep per night for two weeks, their cognitive performance (measured objectively) continued to deteriorate across the entire study period, reaching levels equivalent to two days of total sleep deprivation. But their subjective ratings of their own sleepiness plateaued after a few days. They thought they’d adapted. They hadn’t. They’d simply lost the ability to accurately perceive their own impairment. This is why “I’ve always been fine on six hours” is one of the least reliable things a person can say about their sleep.

What’s Actually Making You Sleepy? Understanding the Causes

The Epworth Sleepiness Scale measures the degree of your sleepiness. Understanding its source is a separate and equally important question, because the causes are meaningfully different and require different responses.

Insufficient sleep duration is the most straightforward and most common explanation. The evidence on sleep need is now robust: the vast majority of adults require between seven and nine hours of sleep per night for optimal cognitive and physical function, and a small genetic minority (probably less than 3% of the population) can genuinely thrive on less. Everyone else who claims to function well on six hours is either accumulating a sleep debt they’ve adapted to, or confusing “getting by” with “functioning optimally.” Chronic short sleep (consistently getting an hour or two less than your individual requirement) has a cumulative effect on daytime alertness that doesn’t fully reverse with a single recovery night. If your ESS score is elevated and you’re regularly getting fewer than seven hours, this is almost certainly the primary driver, and the intervention is exactly as unsexy as it sounds: go to bed earlier and protect your sleep opportunity more aggressively.

Poor sleep quality is the second major category, and it’s trickier because it can produce significant daytime sleepiness even in people who appear to be getting adequate hours. Sleep isn’t a homogeneous state, as it cycles through distinct stages with different physiological functions. Slow-wave sleep (stages 3 and 4 of non-REM sleep) is primarily restorative for the body: it’s when growth hormone is secreted, tissue repair occurs, immune function is consolidated, and the clearance of metabolic waste products from the brain (via the glymphatic system) is most active. REM sleep serves different but equally critical functions: emotional memory processing, creative integration of information, and the consolidation of procedural and associative memories. When sleep architecture is disrupted (for example, by alcohol, by a sleep disorder, by environmental factors, or by certain medications), you can spend eight hours in bed and emerge feeling profoundly unrefreshed, because you’ve been denied adequate time in the stages that actually do the restorative work.

Circadian misalignment is a less commonly discussed but increasingly recognised contributor. Your circadian rhythm (the roughly 24-hour biological clock regulated primarily by light exposure) determines not just when you feel sleepy and alert, but the quality of your sleep at any given time. Sleeping against your natural chronotype (the night owl forced to rise at 6am for work; the extreme morning type who regularly stays up until midnight for social reasons) produces sleep that’s architecturally inferior regardless of its duration. Shift workers experience the most extreme version of this, and their elevated rates of metabolic disease, cardiovascular disease, and mental health difficulties are at least partly attributable to chronic circadian disruption. But even among people with conventional schedules, weekend social jetlag (staying up two hours later and sleeping two hours later on Friday and Saturday nights) creates a minor but meaningful form of circadian disruption that affects Monday morning alertness.

Obstructive sleep apnoea deserves its own section, which I will discuss more below.

Medical and psychiatric conditions round out the major categories. Hypothyroidism (underactivity of the thyroid gland) is one of the most common medical causes of excessive daytime sleepiness and is frequently missed, particularly in women. Anaemia, especially iron deficiency anaemia, is another common culprit. Depression produces both a strong subjective experience of fatigue and often genuine disruption to sleep architecture. Certain medications (antihistamines, beta-blockers, benzodiazepines, many antidepressants, anticonvulsants, and others) have sleepiness as a direct pharmacological effect. Restless legs syndrome and periodic limb movement disorder can fragment sleep significantly without the person being aware of it. And rarer conditions like narcolepsy (characterised by sudden, irresistible sleep attacks, often with cataplexy) can produce severely elevated ESS scores and require specialist assessment.

The practical implication of this complexity is that if you have an elevated ESS score and no obvious lifestyle explanation (i.e. adequate sleep, reasonable habits, and no obvious stressors) it’s worth approaching the question systematically rather than simply concluding you’re tired and moving on.

Obstructive Sleep Apnoea

Obstructive sleep apnoea deserves particular attention because it’s far more common than most people realise, it’s frequently missed for years or decades, it has serious health consequences when untreated, and it’s one of the primary clinical contexts in which the Epworth Sleepiness Scale is used as a screening tool.

OSA occurs when the muscles of the upper airway (the tongue, soft palate, and surrounding tissues) relax excessively during sleep and cause the airway to collapse, partially or completely. When the airway collapses completely, breathing stops. The brain detects the resulting drop in oxygen saturation and generates a brief arousal (just enough to restore muscle tone and reopen the airway) before the person returns to sleep, often without any conscious awareness of the interruption. In moderate to severe OSA, this cycle can repeat dozens or hundreds of times per night.

The consequence is a catastrophically fragmented sleep architecture. The person with severe untreated OSA may spend eight or nine hours in bed but be physiologically prevented from sustaining the deep slow-wave sleep and REM sleep that make those hours restorative. They wake unrefreshed, struggle through the morning, rely heavily on caffeine, perhaps feel more alert by mid-afternoon, and then collapse with exhaustion again by evening. Many have lived with this pattern for so long that they’ve simply accepted it as their constitution. Some are aware they snore heavily, or that they wake with headaches, or that their partner has noticed them stopping breathing during sleep; all of which are important clinical flags. Others have no symptoms beyond the sleepiness itself.

The scale of the problem is significant. Estimates vary depending on diagnostic criteria and study population, but large epidemiological studies suggest that clinically significant OSA affects somewhere between 10% and 30% of the adult population, with higher rates in men, in older adults, and in people who are overweight (although it’s worth noting that OSA occurs in people of all body types, including lean individuals with certain craniofacial anatomies). More importantly, the vast majority of cases remain undiagnosed. A frequently cited figure from US research suggested that around 80-90% of people with moderate-to-severe OSA hadn’t been diagnosed at the time of the study.

In terms of health consequences, untreated OSA is not a benign condition. The repeated nocturnal oxygen desaturations and sympathetic nervous system activations associated with apnoea events drive significant cardiovascular strain. OSA is independently associated with hypertension, atrial fibrillation, heart failure, and stroke. There’s strong evidence linking it to insulin resistance and type 2 diabetes. It’s associated with elevated markers of systemic inflammation. And the cognitive and mood effects (like impaired executive function, depression, irritability, and reduced libido) are substantial and frequently misattributed to other causes.

The Epworth Sleepiness Scale doesn’t diagnose OSA, as that requires polysomnography (an overnight sleep study in a laboratory) or home sleep apnoea testing, but it performs reasonably well as a screening instrument. At a cut-off score of 10, the ESS has a sensitivity of approximately 65-75% for moderate-to-severe OSA in clinical populations. Its specificity is lower, meaning there are meaningful numbers of false positives (people who score above 10 for other reasons). This is why the ESS is typically used alongside other screening instruments, particularly the STOP-BANG questionnaire, which assesses eight clinical risk factors: Snoring, Tiredness, Observed apnoeas, blood Pressure, BMI, Age, Neck circumference, and Gender. A high score on both the ESS and STOP-BANG represents a meaningfully elevated pre-test probability of OSA and a strong indication for formal sleep assessment.

One important caveat: some people with significant OSA score in the normal range on the Epworth Sleepiness Scale. This can happen because they’ve adapted to their sleepiness and underestimate it, because they have a naturally aroused sympathetic nervous system that keeps them alert despite fragmented sleep, or because their primary symptoms are cardiovascular or cognitive rather than somnolence. If you have a partner reporting heavy snoring or observed breathing pauses, or if you consistently wake unrefreshed despite adequate time in bed, those are clinically significant signals regardless of your ESS score, and worth raising with your GP.

Treatment of OSA depends on severity and patient preference. Continuous positive airway pressure (CPAP) therapy (a mask that maintains positive airway pressure throughout the night, preventing airway collapse) is the most effective treatment for moderate-to-severe OSA and produces dramatic improvements in daytime alertness, cognitive function, mood, and cardiovascular risk markers in many patients. Mandibular advancement devices (custom-made dental appliances that reposition the jaw during sleep) are effective for mild-to-moderate OSA and are preferred by many patients who struggle with CPAP compliance. Weight loss (where relevant) can significantly reduce OSA severity, sometimes resolving it entirely. And positional therapy (sleeping on your side rather than your back) can be effective for positional OSA, where apnoea events occur predominantly when supine.

Understanding Your Score: What Each Band Actually Means for Your Life

Now, I understand that numbers on a scale are abstract until you translate them into something you can feel and act on. Here’s how to think about each band:

0-10: Normal Alertness

The majority of healthy, well-rested adults score between 4 and 8, which means there’s meaningful variation within the normal range. A score of 2 or 3 suggests you’re genuinely well-rested and highly alert during the day; this is what good sleep looks like behaviourally. A score of 8 or 9 is still within normal limits but sits at the upper end; it might reflect mild chronic sleep debt, a mildly disrupted week, or simply natural variation in sleepiness. There’s no clinical concern at this level, but it might prompt you to ask whether you’re consistently protecting your sleep as well as you could be.

It’s also worth noting that a score of 0 (a seemingly perfect result) occasionally reflects not exceptional alertness but a tendency to underestimate sleepiness, particularly in people who’ve spent years accommodating chronic fatigue. If you scored very low but also know you rely heavily on caffeine, struggle on mornings after poor nights, or feel a clear afternoon energy slump most days, those are worth paying attention to even if your ESS score doesn’t reflect them.

11-12: Mild Excess Sleepiness

This band sits just above the normal threshold and is, in some ways, the most interesting because it’s the range where people are most likely to dismiss their result. “Eleven isn’t that bad.” And in isolation, that’s true: mild excess sleepiness isn’t an emergency. But it does represent a measurable departure from normal alertness, and in a large population study of people scoring in this range, you’d find a meaningful proportion with early or mild OSA, a larger proportion with chronic mild sleep debt, and a smaller proportion with other medical contributors.

If you scored 11-12, the most useful first question is: Am I consistently getting seven or more hours of sleep on school nights? If the honest answer is no, that’s your starting point; not supplements, not sleep trackers, not elaborate biohacking protocols, but simply protecting more time in bed. If you’re getting adequate hours and still scoring in this range, the second question is about sleep quality: do you wake feeling genuinely refreshed, or is your morning alertness poor even after a full night? If the latter, it’s worth discussing with a GP rather than simply shrugging it off.

13-17: Moderate Excess Sleepiness

At this level, the science is fairly clear that your cognitive performance is being meaningfully impaired, even if you’ve adapted to the impairment enough that you no longer notice it acutely. Research using objective cognitive testing on people with ESS scores in this range consistently documents reduced processing speed, impaired working memory, poorer sustained attention, and slower reaction times compared to people in the normal range. These aren’t subtle laboratory effects — they translate into real-world consequences in complex tasks, decision-making under pressure, and activities that require sustained concentration.

A score of 13–17 warrants action rather than monitoring. If you haven’t already, start with the fundamentals: consistent sleep and wake times, adequate sleep opportunity, alcohol reduction, and caffeine discipline. If your habits are already reasonable and your score is still in this range, the probability of an underlying sleep disorder increases meaningfully. In particular, if you are male, middle-aged or older, carry any excess weight, snore, or wake unrefreshed, the clinical suspicion for OSA should be high enough to warrant formal evaluation. Speak to your GP and be specific about your score and your symptoms.

18-24: Severe Excess Sleepiness

A score in this range is significantly above what any lifestyle explanation is likely to account for on its own, and the research associations are sobering. Large studies of untreated sleep apnoea patients show mean ESS scores in the 14–18 range, which means a score of 18 or above places you at the severe end of what’s seen even in known sleep disorder populations. This isn’t cause for panic, but it is cause for prompt medical attention.

At this level, the impairment to daily functioning is substantial, and the health risks are meaningful. Driving is a particular concern, and the research on accident risk at ESS scores above 16 is clear enough that some sleep medicine clinicians advise patients in this range to avoid driving pending further evaluation. This advice is worth taking seriously, as it keeps both you and the rest of the road users safer.

The pathway forward is a GP appointment, a conversation about your symptoms, and a likely referral for sleep studies (either a home sleep apnoea test or laboratory polysomnography). If OSA is confirmed and treated, the improvements in alertness are often dramatic and rapid: many people who’ve lived with untreated severe OSA describe the experience of successful CPAP treatment as transformative, a qualitative shift in how they feel that makes them realise, retrospectively, how compromised their function had become.

Building Better Sleep

Whatever your score, the foundations of healthy sleep are worth understanding and implementing, because they’re the most powerful levers available to most people before any clinical intervention is necessary.

Sleep consistency is, in the view of most sleep scientists, the single most impactful behavioural change most people can make. Your circadian rhythm is anchored primarily by your wake time. The consistent signal of morning light and activity resets your biological clock each day. Waking at the same time every day, including weekends, stabilises your circadian rhythm, regulates adenosine build-up (the sleep-pressure chemical that accumulates with wakefulness), and over time produces more consistent, higher-quality sleep. The weekend lie-in is appealing but counterproductive: sleeping two hours later on Saturday and Sunday is equivalent to flying to a different time zone for the weekend, and the resulting circadian disruption (social jetlag) contributes meaningfully to Monday morning grogginess. If you do nothing else, set a consistent wake time and protect it.

Light exposure is the circadian clock’s primary zeitgeber (the environmental cue it uses to calibrate its timing). Getting bright natural light into your eyes within the first 30 to 60 minutes of waking is one of the most powerful signals you can send to your biological clock: it advances your circadian phase, stimulates the cortisol awakening response (a healthy morning alerting mechanism), and sets the downstream timing of your melatonin onset in the evening. This doesn’t require sunshine, and even the diffuse natural light of an overcast morning in Ireland is significantly brighter than indoor artificial lighting, but it does require stepping outside rather than turning on the kitchen lights. Conversely, in the evening, bright artificial light and blue-rich screen light suppress melatonin production and delay circadian phase, which is why the advice to dim lights and reduce screen exposure in the two hours before bed is super important.

Caffeine timing is something most people think they have figured out, but the pharmacokinetics are worth understanding more precisely. Caffeine works by competitively blocking adenosine receptors in the brain; it doesn’t actually reduce adenosine levels, it simply prevents adenosine from signalling. When caffeine is eventually metabolised, the accumulated adenosine floods back in, which is partly why the caffeine crash can be disproportionately unpleasant. The half-life of caffeine varies substantially between individuals (as genetics play a significant role) but averages around five to seven hours. A coffee consumed at 3pm still has roughly half its stimulatory effect at 8 or 9pm. Beyond delaying sleep onset, late caffeine intake also reduces slow-wave sleep depth even in people who don’t notice difficulty falling asleep. 

Alcohol and sleep is perhaps the most commonly misunderstood relationship in everyday sleep hygiene. Alcohol is an effective anxiolytic and sedative at moderate doses, and many people find it helps them fall asleep, which is true. But the downstream effect on sleep architecture is consistently negative. Alcohol is metabolised at approximately one unit per hour, which means that drinks consumed in the evening are being broken down in the early hours of the morning, when their stimulatory metabolic effects fragment the second half of the night and suppress REM sleep. The result is frequent early-morning waking, reduced dream sleep, and morning fatigue that’s disproportionate to the number of hours spent in bed. Regular evening drinking doesn’t just impair single nights; it disrupts circadian rhythm regulation over time and progressively degrades baseline sleep quality. This is worth knowing because alcohol is one of the most common unrecognised contributors to elevated ESS scores in people with otherwise reasonable habits.

Sleep environment is genuinely important rather than merely nice to have. Core body temperature needs to drop by approximately 1°C for sleep initiation to occur, which is why a cool bedroom (ideally between 16 and 19°C) facilitates both sleep onset and the maintenance of deep slow-wave sleep. Many people sleep in rooms that are simply too warm, particularly in winter with central heating, and this alone can degrade sleep quality. Darkness also matters because even low levels of ambient light can suppress melatonin production and increase sleep fragmentation; blackout blinds or a sleep mask are cheap and evidence-backed interventions that really do help here. And noise, even noise that doesn’t wake you consciously, can reduce slow-wave sleep depth, which is why white noise or earplugs are worth experimenting with if your environment is not reliably quiet.

Exercise has a bidirectional relationship with sleep. Regular aerobic exercise, particularly when done consistently and not within two to three hours of bedtime, is one of the most robustly supported non-pharmacological interventions for sleep quality. It increases slow-wave sleep depth, reduces sleep onset latency, improves sleep continuity, and attenuates the subjective and objective effects of sleep restriction. The mechanism involves multiple pathways: adenosine build-up from physical exertion increases sleep pressure, regular exercise stabilises circadian rhythms, and the anti-inflammatory effects of habitual exercise improve the neurobiological environment for restorative sleep. People who go from sedentary to regularly active typically see meaningful improvements in sleep quality within weeks, often more pronounced than they’d anticipated.

Stress and sleep have a relationship that’s vicious when it goes wrong: stress activates the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, suppressing melatonin, elevating cortisol, and producing a state of physiological arousal that’s directly incompatible with sleep onset and maintenance. Chronic stress, whether from work pressure, relationship difficulties, financial anxiety, or unresolved psychological strain, is one of the most common drivers of insomnia and degraded sleep quality. Managing this isn’t simply a matter of “relaxing more”; it often requires addressing the sources of stress directly, developing more sophisticated cognitive and behavioural responses to it, and sometimes working with a therapist trained in cognitive behavioural therapy for insomnia (CBT-I), which is now the first-line recommended treatment for chronic insomnia over pharmacological sleep aids.

When to Seek Professional Help, and What to Expect

Knowing when to move from self-management to professional assessment is an important decision that many people get wrong in both directions, either seeking help prematurely for mild, addressable sleepiness, or delaying far too long when the signals clearly warrant investigation.

As a rough guide: if you have a score of 11 or above on the Epworth Sleepiness Scale and it doesn’t respond to genuine, sustained improvements in sleep hygiene over four to six weeks, a GP conversation is warranted. If you have a score of 15 or above, regardless of your habits, then a formal evaluation is appropriate. If you have a score of 18 or above, don’t wait; make the appointment now.

When you speak to your GP, be specific. Tell them your Epworth Sleepiness Scale score. Describe your typical sleep schedule: when you go to bed, when you wake, how long it takes to fall asleep, and whether you wake during the night. Mention any relevant symptoms: snoring (or ask a bed partner), observed apnoeas, unrefreshing sleep, morning headaches, nocturia (waking to use the toilet, which can be a sign of OSA), restless legs, or mood changes. The more specific and concrete you can be, the easier it is for your GP to triage the clinical priority appropriately.

Depending on the picture, your GP may order basic blood tests (stuff like thyroid function, full blood count, iron studies, HbA1c) to rule out medical contributors. They may refer you for a home sleep apnoea test, which involves wearing a simple monitoring device overnight and can diagnose OSA without the need for a laboratory sleep study in most cases. Or they may refer you directly to a sleep specialist or respiratory physician if the picture is complex.

If OSA is diagnosed, don’t worry, it’s an extremely treatable condition. The pathway from diagnosis to effective treatment is now well-established, and the health and quality-of-life improvements that follow successful treatment can be substantial. Many people who’ve lived for years with untreated OSA describe the experience of getting their first good night’s sleep on CPAP as genuinely life-changing.

Sleep Is Not a Passive State, It’s When Your Body Does Its Most Important Work

Unfortunately, there’s a persistent cultural metaphor that frames sleep as the absence of waking life, and merely the downtime between the meaningful stuff. This framing is not only scientifically wrong; it’s actively harmful, because it encourages us to treat sleep as the first thing to sacrifice when time is short and the last thing to invest in when we’re optimising our health.

What actually happens during sleep is extraordinary. Your glymphatic system (a network of channels around brain blood vessels) becomes dramatically more active, flushing out the metabolic waste products that accumulate during waking cognition, including the amyloid-beta and tau proteins whose accumulation is associated with Alzheimer’s disease. Your immune system consolidates its responses and produces cytokines critical to fighting infection. Growth hormone (which is not just essential for children’s development but for tissue repair, muscle protein synthesis, and metabolic regulation in adults) is secreted primarily during slow-wave sleep. Your hippocampus transfers the day’s experiences into long-term cortical memory. Your prefrontal cortex resets its emotional regulatory capacity. Your cardiovascular system gets a period of reduced sympathetic tone that’s critical for heart health.

When you chronically shortchange this process, whether through insufficient duration, poor quality, or untreated sleep disorders, you’re not just accumulating tiredness. You’re systematically impairing the biological maintenance that determines how well your body and brain function across decades. The relationship between sleep and long-term health is not peripheral or speculative; it sits at the centre of almost every domain of health.

As with everything, there is always more to learn, and we haven’t even begun to scratch the surface with all this stuff. However, if you are interested in staying up to date with all our content, we recommend subscribing to our newsletter and bookmarking our free content page. We do have a lot of content on sleep in our sleep hub.

If you would like more help with your training (or nutrition), we do also have online coaching spaces available.

We also recommend reading our foundational nutrition articles, along with our foundational articles on exercise and stress management, if you really want to learn more about how to optimise your lifestyle. If you want even more free information on sleep, you can follow us on Instagram, YouTube or listen to the podcast, where we discuss all the little intricacies of exercise.

Finally, if you want to learn how to coach nutrition, then consider our Nutrition Coach Certification course. We do also have an exercise program design course, if you are a coach who wants to learn more about effective program design and how to coach it. We do have other courses available too, notably as a sleep course. If you don’t understand something, or you just need clarification, you can always reach out to us on Instagram or via email.

This article and tool was created by Paddy Farrell.