The Physiology of Sleep and the Physical and Psychological Harms of Chronic Insomnia
How sleep works, what goes wrong in chronic insomnia, and what months of broken sleep actually do to the body and mind.
A deep dive companion to our Insomnia condition guide. For symptoms, diagnosis and treatment, start there.
Key fact: Sleep is not a passive state. It is an active, highly structured process during which the brain clears metabolic waste, consolidates memory, regulates hormones and repairs tissue. Chronic insomnia disrupts that architecture, and the consequences extend well beyond feeling tired — into cardiovascular risk, metabolic health, immune function and mood.
90 min
length of a single sleep cycle
4–6
cycles per night in a healthy adult
2x
increased depression risk with chronic insomnia
The physiology of normal sleep
Sleep is not a single uniform state. It is a cycle of distinct stages that repeat roughly every 90 minutes, four to six times a night, and each stage does different work. Understanding this makes it clear why how you sleep matters as much as how long.
The two broad types of sleep
Sleep divides into non-REM and REM sleep, and non-REM itself has three stages.
| Stage | What happens | What it does |
|---|---|---|
| N1 — light transition | Brief, a few minutes. Muscle tone relaxes, breathing slows. Easily woken. | The gateway from wakefulness to sleep |
| N2 — light sleep | Heart rate and body temperature fall. Sleep spindles and K-complexes appear on EEG. | Makes up around half of total sleep. Consolidates motor memory and protects sleep continuity. |
| N3 — deep slow-wave sleep | Delta waves dominate. Growth hormone is released. Very difficult to wake. | Physical restoration, tissue repair, immune function, and clearance of metabolic waste from the brain. |
| REM — dreaming sleep | Brain activity rises to near-waking levels. Eyes move rapidly. Voluntary muscles are paralysed. Heart rate and breathing become irregular. | Emotional memory processing, consolidation of procedural skills, and creative problem-solving. |
The sleep cycle through the night
Deep slow-wave sleep is concentrated in the first half of the night. REM sleep is concentrated in the second half, in the hours before waking. This is why the two most common patterns of insomnia produce different consequences:
- Difficulty falling asleep — cuts into deep slow-wave sleep, so the physical restoration is lost
- Waking in the small hours or early morning — cuts into REM sleep, so emotional processing and memory consolidation are lost
- Frequent awakenings throughout — fragments the cycle, so neither stage completes properly
Why architecture matters: Two people can both sleep six hours and feel entirely different the next day. One has six hours of well-structured sleep, with normal cycles and adequate deep and REM sleep. The other has six hours of fragmented sleep with frequent arousals, and almost no deep sleep. The second is more damaging, and it is the more common pattern in chronic insomnia.
Waste clearance during sleep
One of the more striking discoveries in sleep science is that the brain appears to clear metabolic waste far more efficiently while asleep. In animal studies, the fluid-filled space between brain cells expands considerably during sleep, increasing the flow of cerebrospinal fluid through brain tissue and the clearance of by-products of daytime neural activity, including amyloid-beta.
This is the most plausible mechanism linking long-term poor sleep with cognitive decline, though the human evidence remains an area of active research rather than settled fact.
The systems that regulate sleep
Two processes govern when and how well you sleep, and both are disrupted in chronic insomnia.
Sleep pressure (Process S)
Adenosine accumulates in the brain the longer you are awake, creating a growing biological drive to sleep. It is discharged by sleep. Caffeine works by blocking adenosine receptors, which is why it delays sleep onset and reduces deep sleep even when you do fall asleep.
Circadian rhythm (Process C)
The body clock in the suprachiasmatic nucleus runs on a roughly 24-hour cycle, driven by light exposure. It controls the timing of melatonin release, core body temperature, and cortisol. Shift work and jet lag are problems of this system rather than of sleep pressure.
When the two align — high sleep pressure and a circadian signal for night — sleep is deep and consolidated. When they are misaligned, or when one is blunted, sleep becomes shallow, fragmented and unrefreshing.
This is why the classic insomnia compensations backfire. Going to bed early, lying in and napping all discharge sleep pressure without adding sleep. Less pressure means shallower sleep the following night. The behaviour that feels most sensible is the one that most reliably makes the problem worse, which is exactly the mechanism sleep restriction therapy exploits in reverse.
What goes wrong in chronic insomnia
Chronic insomnia is not a simple inability to fall asleep. It is a state of hyperarousal, in which the systems that should quieten at night stay activated.
Three physiological changes are consistently seen in people with chronic insomnia:
1
Raised sympathetic nervous system activity
Heart rate, blood pressure and body temperature remain higher than normal across the 24-hour cycle, not just at night. This is measurable even during the day, when the person feels relatively normal.
2
Elevated cortisol
Cortisol should fall to its lowest level in the evening. In chronic insomnia the hypothalamic-pituitary-adrenal axis stays more activated, which opposes the sleep drive and fragments sleep architecture.
3
Altered brain activity
Neuroimaging shows increased activity in the arousal and salience networks, and reduced connectivity in the networks that normally promote sleep. The brain is behaving as if it needs to stay alert.
This hyperarousal explains several things that otherwise seem paradoxical. It explains why people with insomnia are exhausted but cannot nap. It explains why sleep often comes easily when they are away from home, or on the sofa, and then does not come at all in their own bed. And it explains why the treatment with the best evidence is behavioural rather than pharmacological: the arousal is being driven and maintained by patterns that need to be unlearned.
The three Ps model: Clinicians often describe chronic insomnia in terms of predisposing, precipitating and perpetuating factors. Some people are predisposed to hyperarousal by temperament or genetics. A precipitating event — illness, bereavement, a new baby — starts the insomnia. What perpetuates it is the set of compensations: longer time in bed, napping, worrying about sleep, checking the clock. By the time it is chronic, the perpetuating factors are the problem, and they are what CBT-I targets.
The physical harms of sleep loss
The consequences of chronic insomnia are not confined to feeling tired. Sustained sleep loss and fragmented sleep architecture affect almost every physiological system, and the effects are cumulative.
Cardiovascular system
Sleep is when blood pressure normally dips by around 10 to 20 per cent — the "nocturnal dip" that gives the heart and blood vessels a nightly rest. Insomnia can raise night-time blood pressure and reverse that dipping pattern, and night-time blood pressure is a stronger predictor of cardiovascular outcomes than readings taken in a clinic.
Large prospective cohort studies and meta-analyses consistently associate insomnia symptoms and diagnosed insomnia with:
- Hypertension
- Myocardial infarction and coronary heart disease
- Stroke
- Heart failure
- Cardiovascular mortality
The associations are stronger in people whose insomnia comes with genuinely short sleep duration, and in those whose insomnia persists rather than resolving. Mendelian randomisation studies involving millions of participants further support a likely causal link, rather than insomnia simply travelling alongside other risk factors.
The mechanisms combine: sustained sympathetic activation and HPA axis activation raise resting heart rate and blood pressure; low-grade inflammation promotes plaque formation; the blood pressure profile across 24 hours is adverse; and the metabolic changes described below add further risk.
One important confounder. Insomnia is a heterogeneous condition and frequently coexists with other sleep disorders, obstructive sleep apnoea in particular. Sleep apnoea carries substantial cardiovascular risk of its own, and it can present looking very much like insomnia. Some of the association between insomnia and heart disease is likely to reflect undiagnosed apnoea, which is a strong argument for getting snoring, gasping or witnessed pauses in breathing properly assessed rather than treated as insomnia.
Metabolic and endocrine effects
Sleep loss disrupts the hormones that regulate appetite, blood sugar and fat storage.
| Hormone or measure | Effect of sleep loss | Consequence |
|---|---|---|
| Leptin | Falls | Reduced feeling of satiety after eating |
| Ghrelin | Rises | Increased hunger, particularly for high-calorie and carbohydrate-rich foods |
| Cortisol | Stays elevated in the evening | Promotes abdominal fat storage and insulin resistance |
| Insulin sensitivity | Falls | Raised blood sugar, contributing to type 2 diabetes |
| Growth hormone | Reduced (released mainly in deep sleep) | Impaired tissue repair and muscle maintenance |
These effects have been demonstrated experimentally rather than merely observed. Healthy young men restricted to short nights show falling leptin, rising ghrelin, and measurably increased hunger and appetite; sleep restriction over a single week produces measurable reductions in glucose tolerance. Over months and years, this contributes to weight gain, metabolic syndrome and type 2 diabetes, independent of diet and physical activity.
Immune function
Deep sleep is when much of the immune system does its work. T-cell proliferation, cytokine production and the formation of immunological memory are concentrated in the sleeping hours.
- Reduced natural killer cell activity — these cells are part of the first-line defence against viral infection and tumour cells
- Lower antibody response to vaccination — studies of influenza and hepatitis vaccines show reduced protection in people who slept poorly in the nights around vaccination
- Increased susceptibility to infection — as in the rhinovirus study above
- Slower wound healing — demonstrated in controlled studies of skin barrier disruption
Pain and inflammatory conditions
Sleep loss and pain reinforce each other. Poor sleep lowers the pain threshold, increases sensitivity to painful stimuli, and reduces the effectiveness of the body's endogenous pain control. Chronic pain conditions — musculoskeletal disorders, fibromyalgia, arthritis and headaches — are consistently worse in people with insomnia, and treating the sleep often reduces the pain.
Low-grade inflammation is also elevated in chronic insomnia, with higher levels of C-reactive protein and interleukin-6. This is thought to be one of the mechanisms linking poor sleep to cardiovascular disease and metabolic dysfunction.
Longer-term risk
The evidence is strongest for cardiovascular and metabolic outcomes, but chronic insomnia has also been associated with:
- Cognitive decline and dementia — the association is consistent, though whether insomnia causes the decline or is an early marker of it remains debated
- Certain cancers — the evidence is weaker and confounded by shift work, but the immune and hormonal changes provide a plausible mechanism
- Overall mortality — meta-analyses show a modest increase in all-cause mortality in people with chronic insomnia, after adjustment for other risk factors
The size of the effect matters. These are associations from population studies, not proof that any one person with insomnia will develop heart disease or diabetes. The risk is increased, not inevitable, and the majority of the increase is likely mediated by the same lifestyle and physiological factors that CBT-I and sleep hygiene address.
The psychological harms of sleep loss
The psychological effects of chronic insomnia are at least as significant as the physical ones, and in the shorter term they are more apparent.
Mood and emotion
Sleep loss does not simply make people tired and grumpy. It produces measurable changes in how the brain processes emotional information.
In a landmark imaging study, healthy volunteers kept awake for around 35 hours showed roughly 60 per cent greater amygdala activation to negative images than rested controls, and a threefold increase in the volume of amygdala tissue activated. At the same time, the connection between the amygdala and the medial prefrontal cortex — the region that normally applies the brakes — was significantly weaker, while connectivity to brainstem arousal centres was stronger.
- Increased amygdala reactivity — the brain's threat-detection centre responds more strongly to negative images and situations
- Reduced prefrontal regulation — the region that normally dampens emotional responses has weaker connectivity with the amygdala, so the reaction is less controlled
- Blunted response to positive stimuli — the reward system responds less to things that are enjoyable, which is why sleep-deprived people often feel flat rather than simply tired
- Irritability and reduced frustration tolerance — the threshold for becoming annoyed is lower
The result is a person who reacts more strongly to negative events, less strongly to positive ones, and has less capacity to regulate the response. This is not a matter of character or willpower. It is the predictable effect of sleep loss on the emotional brain.
Depression and anxiety
Insomnia is one of the strongest prodromal symptoms of a depressive episode — it often appears before low mood does. It is also a strong predictor of relapse in people who have had depression. Anxiety disorders show a similar pattern: insomnia frequently precedes them, and chronic insomnia substantially increases the risk of developing one.
The relationship with bipolar disorder is particularly important. Sleep loss can trigger a manic or hypomanic episode in people with bipolar disorder, which is one reason that sleep restriction therapy — a component of CBT-I — needs to be supervised and adapted in this group.
Cognition and performance
The cognitive effects of sleep loss are broad and clinically significant.
| Domain | Effect of chronic sleep loss |
|---|---|
| Attention and vigilance | Reduced sustained attention; more lapses; slower reaction times. This is the domain most affected by sleep loss, and the one most relevant to driving. |
| Working memory | Reduced capacity to hold and manipulate information in mind |
| Long-term memory | Impaired consolidation of new memories, because consolidation happens during sleep |
| Executive function | Reduced planning, problem-solving and cognitive flexibility |
| Decision-making | Increased risk-taking and reduced ability to weigh consequences |
| Creativity | Reduced ability to make novel connections, which depends on REM sleep |
People with chronic insomnia are often poor at judging their own impairment. Performance on objective tests declines more than subjective ratings do, which is why someone who feels "fine" after months of poor sleep may still be making more errors, driving less safely, and functioning below their true capacity.
Mental health and safety
- Increased risk of accidents — both at work and on the road, through reduced vigilance and slower reaction times
- Increased risk of suicidal ideation — independent of depression, in some studies
- Psychotic experiences — in people with underlying vulnerability, severe sleep loss can precipitate hallucinations or delusional thinking
- Worsening of existing mental health conditions — including PTSD, ADHD and substance use disorders
- Substance use — alcohol and sedatives are often used to self-treat, which worsens sleep architecture and creates a second problem
Seek urgent medical advice if insomnia comes with thoughts of self-harm or suicide. This is a medical emergency, and it is treatable. Do not drive if you feel sleepy, and inform the DVLA if excessive sleepiness is affecting your driving.
What chronic insomnia actually is
Chronic insomnia is difficulty getting to sleep, staying asleep, or getting restorative sleep, occurring on three or more nights a week, lasting three months or more, despite having adequate opportunity to sleep, and causing impaired daytime functioning.
By the time it becomes chronic, the original trigger is usually gone. What maintains it is a set of learned behaviours and beliefs about sleep — the compensations and anxiety described earlier in this article. That is why treatment is behavioural rather than pharmacological: the mechanisms are learned, and they can be unlearned.
For symptoms, diagnosis, and how chronic insomnia differs from short-term insomnia, see our full insomnia condition guide.
How much of this is reversible?
Reading a list of harms like the one above is unsettling, and it would be a poor article that left it there. So it is worth stating the other side plainly.
Almost everything described here is a consequence of ongoing poor sleep, not a permanent injury. The hyperarousal that maintains chronic insomnia is a learned state, and it is the specific target of the treatment with the best evidence. When sleep consolidates, the physiology follows: sympathetic tone falls, the blood pressure profile improves, appetite regulation normalises, and mood and cognition recover.
- The mood and cognitive effects improve relatively quickly once sleep consolidates — often within weeks
- The metabolic changes seen in short-term sleep restriction studies reverse when normal sleep is restored
- Cardiovascular risk is cumulative and probabilistic rather than a switch that has been thrown; it is one risk factor among several, all of which are modifiable
- Treating insomnia improves depression outcomes, which is why the relationship running in both directions is good news rather than bad
The practical point: the risks described in this article are reasons to treat chronic insomnia properly, not reasons to worry about it at 3am. Worry about sleep is itself one of the perpetuating factors, so if this article has made you anxious about your sleep, the most useful response is to act on it rather than to dwell on it.
Where to get treatment
If you have read this far and recognise chronic insomnia in yourself, the useful next step is to have it assessed properly.
For anything lasting three months or more, the first-line treatment in UK guidance is cognitive behavioural therapy for insomnia (CBT-I) — not a tablet. Our guide to CBT-I explains what the programme involves and how to access it. If CBT-I has been tried and has not worked, or is unavailable where you live, a prescriber can review whether a licensed medication such as daridorexant is appropriate.
Before any of that, one question is worth answering: do you snore loudly, gasp or choke at night, or has anyone witnessed you stop breathing? If so, get assessed for obstructive sleep apnoea first. It causes broken, unrefreshing sleep that looks like insomnia, carries cardiovascular risk of its own, and sedatives can make it worse.
Speak to a Prescriber About Your Sleep
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View Insomnia Treatments →Frequently Asked Questions
What are the stages of sleep?
Sleep divides into non-REM and REM sleep, cycling roughly every 90 minutes, four to six times a night. Non-REM has three stages. N1 is a brief light transition from wakefulness. N2 is light sleep and makes up around half of total sleep, consolidating motor memory and protecting sleep continuity. N3 is deep slow-wave sleep, when growth hormone is released and physical restoration, tissue repair, immune work and clearance of metabolic waste from the brain happen. REM is dreaming sleep, when brain activity rises to near-waking levels and emotional memory processing and creative problem-solving occur.
Why does the quality of sleep matter as much as the hours?
Because deep and REM sleep are not distributed evenly through the night and they do different jobs. Deep slow-wave sleep is concentrated in the first half of the night, and REM sleep in the second half. Two people can both sleep six hours and feel completely different: one with well-structured sleep and normal cycles, the other with six fragmented hours full of brief arousals and almost no deep sleep. The second is considerably more damaging, and it is the pattern typical of chronic insomnia. This is also why trouble falling asleep and early morning waking cause different problems.
What is hyperarousal in insomnia?
Hyperarousal is the state that maintains chronic insomnia, in which the systems that should quieten at night stay switched on. Three changes are consistently found: raised sympathetic nervous system activity, so heart rate, blood pressure and body temperature stay higher across the whole 24 hours rather than just at night; activation of the hypothalamic-pituitary-adrenal axis, so cortisol does not fall as it should in the evening; and altered brain activity, with increased activity in arousal networks. It explains why people with insomnia are exhausted but cannot nap, and why sleep often comes easily on the sofa but not in their own bed.
What are the three Ps of insomnia?
Predisposing, precipitating and perpetuating factors. Some people are predisposed to hyperarousal by temperament or genetics. A precipitating event such as illness, bereavement or a new baby starts the insomnia. What perpetuates it is the set of compensations that follow: spending longer in bed, napping, lying in, worrying about sleep and checking the clock. By the time insomnia is chronic the original trigger has usually gone and the perpetuating factors are the problem, which is why treatment targets those behaviours rather than the original event.
Does chronic insomnia increase the risk of heart disease?
Large prospective cohort studies and meta-analyses consistently associate insomnia with increased risk of hypertension, myocardial infarction, stroke, heart failure and cardiovascular mortality, with stronger associations where insomnia comes with genuinely short sleep or persists over time. Mendelian randomisation studies support a likely causal link rather than mere association. Mechanisms include sustained sympathetic activation, HPA axis activation, low-grade inflammation, and loss of the normal 10 to 20 per cent overnight dip in blood pressure. One important caveat is that insomnia often coexists with obstructive sleep apnoea, which carries cardiovascular risk of its own.
How does poor sleep affect weight and blood sugar?
Sleep loss disrupts the hormones regulating appetite and glucose. Leptin, which signals fullness, falls; ghrelin, which drives hunger, rises; and measured appetite increases, particularly for high-calorie carbohydrate-rich foods. Cortisol stays elevated in the evening, promoting abdominal fat storage and insulin resistance, and insulin sensitivity itself falls. Growth hormone, released mainly during deep sleep, is reduced. These effects have been shown experimentally in healthy volunteers within a week of restricted sleep, and over months and years they contribute to weight gain, metabolic syndrome and type 2 diabetes independent of diet and exercise.
Does lack of sleep weaken your immune system?
Yes, and this has been demonstrated under controlled conditions. In one study, 164 healthy adults had their sleep measured objectively by wrist actigraphy for a week, then were quarantined and given nasal drops containing rhinovirus. Those sleeping under six hours a night were around four times more likely to develop a genuine cold than those sleeping more than seven. Sleep loss also reduces natural killer cell activity, lowers the antibody response to influenza and hepatitis vaccination when sleep is poor around the time of the jab, and slows wound healing.
How does sleep loss affect mood and emotions?
It changes how the brain processes emotional information, measurably. In a landmark imaging study, volunteers kept awake around 35 hours showed roughly 60 per cent greater amygdala activation to negative images than rested controls, along with a threefold increase in the amount of amygdala tissue activated. At the same time the connection between the amygdala and the medial prefrontal cortex, which normally applies the brakes, was significantly weaker. The result is stronger reactions to negative events, blunted responses to positive ones, and less capacity to regulate either. This is a predictable physiological effect, not a failure of character or willpower.
Does insomnia cause depression?
Insomnia roughly doubles the likelihood of going on to develop depression. A meta-analysis of 21 longitudinal studies of people who were not depressed at the outset found around a two-fold increase in risk. Insomnia is one of the strongest early symptoms of a depressive episode, often appearing before low mood does, and it is a strong predictor of relapse in people who have had depression before. The relationship runs in both directions, which is encouraging rather than discouraging: treating the insomnia often improves the depression, and treating the depression often improves the sleep.
Is the damage from chronic insomnia permanent?
Almost everything described in this article is a consequence of ongoing poor sleep rather than a permanent injury. The hyperarousal that maintains chronic insomnia is a learned state and it is the specific target of CBT-I. When sleep consolidates, the physiology follows: sympathetic tone falls, the blood pressure profile improves, appetite regulation normalises, and mood and cognition recover, often within weeks. The metabolic changes seen in sleep restriction studies reverse when normal sleep is restored. Cardiovascular risk is cumulative and probabilistic rather than a switch that has been thrown, and it is one modifiable risk factor among several.
How much sleep do I actually need?
There is no standard figure and the amount needed varies between individuals and changes with age, so the familiar seven-to-nine-hour guidance for adults is an average rather than a target. The practical test is whether you wake feeling reasonably rested and can perform well during the day. It is also normal for sleep to become lighter and more broken with age, with more awakenings and less total sleep time. Expecting the sleep you had at twenty-five to continue at sixty-five sets up a target you will keep missing, and worry about sleep is itself one of the factors that perpetuates insomnia.
Should I worry about these health risks if I have insomnia?
The risks described here are reasons to treat chronic insomnia properly rather than reasons to lie awake worrying about it. They come from population studies and describe increased risk, not certainty, and much of that increase is mediated by factors that treatment addresses. Worry about sleep is itself one of the things that maintains insomnia, so if reading this has made you anxious about your sleep, the most useful response is to act on it. For anything lasting three months or more, ask about CBT-I, and get snoring, gasping or witnessed pauses in breathing assessed for sleep apnoea first.
Where a licensed treatment is clinically appropriate, these are the options available through Access Doctor following an online consultation reviewed by a prescriber.
Insomnia · Rx
Quviviq (Daridorexant) 50mg
For long-term insomnia where CBT-I has been tried and has not worked.
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Circadin 2mg Prolonged-Release Melatonin
For primary insomnia with poor sleep quality in adults aged 55 and over.
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Snoring, gasping, restless legs and untreated reflux all produce broken sleep that looks like insomnia but needs different treatment. A GPhC-registered pharmacist independent prescriber will review your consultation and tell you what fits. Regulated UK pharmacy #9011198, nothing issued without clinical assessment.
Read the Full Insomnia Guide →References
- NICE Clinical Knowledge Summaries. Insomnia. Last revised June 2026. cks.nice.org.uk
- Pengo MF, et al. Insomnia and Cardiovascular Disease: Untangling a Complex Relationship. Journal of Sleep Research, 2026. onlinelibrary.wiley.com
- Prather AA, Janicki-Deverts D, Hall MH, Cohen S. Behaviorally Assessed Sleep and Susceptibility to the Common Cold. Sleep, 2015;38(9):1353–1359. pubmed.ncbi.nlm.nih.gov
- Baglioni C, et al. Insomnia as a predictor of depression: a meta-analytic evaluation of longitudinal epidemiological studies. Journal of Affective Disorders, 2011;135(1–3):10–19. pubmed.ncbi.nlm.nih.gov
- Yoo SS, Gujar N, Hu P, Jolesz FA, Walker MP. The human emotional brain without sleep — a prefrontal amygdala disconnect. Current Biology, 2007;17(20):R877–R878. pubmed.ncbi.nlm.nih.gov
- Spiegel K, Tasali E, Penev P, Van Cauter E. Brief communication: sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Annals of Internal Medicine, 2004;141(11):846–850. pubmed.ncbi.nlm.nih.gov
- Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on metabolic and endocrine function. The Lancet, 1999;354(9188):1435–1439. pubmed.ncbi.nlm.nih.gov
- Xie L, et al. Sleep drives metabolite clearance from the adult brain. Science, 2013;342(6156):373–377. pubmed.ncbi.nlm.nih.gov
- National Institute for Health and Care Excellence. Daridorexant for treating long-term insomnia (TA922). 18 October 2023. nice.org.uk
- National Institute for Health and Care Excellence. Sleepio to treat insomnia and insomnia symptoms (MTG70). 20 May 2022. nice.org.uk
- NHS. Insomnia. nhs.uk
- Driver and Vehicle Licensing Agency. Assessing fitness to drive: a guide for medical professionals. gov.uk
Medical disclaimer: This article is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional for diagnosis and treatment. In a medical emergency, call 999.