Ghrelin and Leptin: The Hunger Hormones Explained, and How Sleep and Diet Change Them

Scroll through a feed for ten minutes and you will meet the hunger hormones. A creator holds up a jar of “leptin support” capsules; another promises to “reset” your leptin in a week; a third explains that ghrelin, not willpower, is why the kitchen calls at 10 p.m. The clips are everywhere as of spring 2025, riding the same wave of attention that newer appetite medicines have brought to the biology of fullness. Some of what they say is true. Most of it is a cartoon of the research.

The real story is more interesting than the cartoon. Leptin was identified in 1994 and upended the idea that fat tissue is inert padding; it is, in fact, an organ that talks to the brain. Ghrelin followed in 1999, discovered in the stomach lining and quickly nicknamed the hunger hormone.

Thirty years of trials, cohort studies and a handful of remarkable rare-disease cases have taught us what these signals do, what they cannot do, and why two short nights can change how much you want to eat tomorrow.

What is leptin, and what does it actually do?

A hormone is a chemical messenger made in one tissue that travels through the blood to change what another tissue does. Leptin is the messenger of fat. Fat cells, called adipocytes, release it in rough proportion to how much fat they hold, so a person with more stored fat generally has more leptin circulating than a person with less. The name comes from the Greek leptos, meaning thin, because mice that lack it become severely obese and giving it back slims them.

The main audience for leptin is the hypothalamus, a thumb-sized region at the base of the brain that governs appetite, body temperature and the stress and reproductive systems. When leptin arrives in adequate amounts, the hypothalamus reads the message as “energy stores are fine.” Appetite-stimulating neurons quieten, appetite-suppressing neurons speak up, and the body feels free to spend energy on things like fertility, immune activity and warmth.

What leptin does best is not shrink a body that has plenty; it is protect a body that is running low. Levels fall sharply within one to three days of fasting, well before meaningful fat is lost. That drop is the alarm: hunger rises, resting energy use dips a little, and reproductive hormones can retreat. Researchers now describe leptin as a starvation signal more than a satiety hormone, and that distinction explains most of the disappointments covered later in this article.

Two practical details matter for interpretation. Women typically carry higher leptin than men with the same amount of body fat, partly because of how fat is distributed and partly because of estrogen. Levels also follow a daily rhythm, peaking overnight, which is one reason sleep enters the conversation so quickly.

What is ghrelin, the hunger hormone that rises before meals?

Ghrelin is a small protein hormone made mostly by specialized cells in the lining of the stomach, with smaller amounts from the upper intestine and pancreas. It was found in 1999 by scientists looking for a substance that triggers growth hormone release, which it does; the name is built on “ghre,” a root word for growth. Its effect on appetite emerged almost immediately afterwards and became the headline.

The pattern of ghrelin across a day is what makes it feel personal. Levels climb in the hour or two before a habitual mealtime, peak just before you eat, and fall within an hour of a meal. People who eat lunch at noon every day develop a ghrelin surge around noon, which is why hunger can arrive on schedule even on a day you ate a late breakfast. The stomach, in other words, learns your timetable.

Ghrelin reaches the hypothalamus through the blood and through the vagus nerve, the long nerve that links gut and brain. There it activates the same appetite-stimulating neurons that leptin suppresses. The two hormones are not perfect opposites, but on this one circuit they pull in opposite directions.

Ghrelin has a second job that gets less attention. After intentional weight loss, average ghrelin levels rise and stay higher for months, a finding first reported in a 2002 study of dieters and repeatedly confirmed since. That upward drift is part of why maintaining a lower weight is often harder than reaching it. Interestingly, people who have had gastric bypass surgery tend to show lower ghrelin, which may contribute to the reduced appetite many report, though the surgery changes many hormones at once and ghrelin is only one actor.

How do the hunger hormones talk to the brain?

Picture the arcuate nucleus, a cluster of neurons deep in the hypothalamus, as a thermostat with two dials. One set of neurons, often abbreviated NPY/AgRP, drives hunger and conserves energy. The other set, called POMC neurons, promotes fullness and energy spending. Leptin turns the hunger dial down and the fullness dial up. Ghrelin does the reverse. Insulin, the pancreatic hormone that moves sugar into cells, nudges the dials in the same direction as leptin after a meal.

Short-term and long-term signals layer on top of one another. Ghrelin, GLP-1 and a hormone called PYY are meal-to-meal messengers; they rise and fall within hours and tell the brain whether food has just arrived. Leptin is the slow background signal that reports the size of the reserve tank over days and weeks. The brain integrates both, then adjusts appetite, the pleasure you get from food, and even how much you fidget.

This layered design is why one skipped meal is uncomfortable but not dangerous, while weeks of under-eating produce a coordinated defense: ghrelin up, leptin down, thyroid hormone slightly reduced, and a quieter sympathetic nervous system. The body has no equivalent alarm for too much stored energy. Leptin rises with fat gain, but the brain’s response to abundance is weak compared with its response to scarcity. Evolution built a smoke detector for famine and a dim indicator light for feast.

Understanding that asymmetry reframes the whole topic. The hunger hormones are not villains to outwit. They are a conservative accounting department, and sleep and diet are two of the few levers that adjust their ledgers without a prescription.

What changed recently in leptin research and the public conversation

Three threads braided together to put leptin and ghrelin back in the headlines. The first is the arrival of GLP-1 receptor agonist medicines such as semaglutide and tirzepatide, which made millions of people curious about appetite hormones in general and prompted a flood of “natural alternative” content built around leptin. Clinic education pages from major academic health systems updated or expanded their leptin and ghrelin explainers in 2022 and 2023 in response to that search demand.

The second thread is older but newly rediscovered online: the sleep studies. In 2004, a small crossover trial published in the Annals of Internal Medicine restricted twelve healthy young men to four hours in bed for two nights and found leptin fell about 18 percent, ghrelin rose about 28 percent, and self-rated hunger increased by about 24 percent compared with ten-hour nights. The same year, an analysis of roughly a thousand adults in the Wisconsin Sleep Cohort linked five hours of habitual sleep with about 15 percent lower leptin and 15 percent higher ghrelin than eight hours. Both papers are now quoted in short videos, usually without their caveats.

The third thread is the quiet maturing of leptin as a medicine. Metreleptin, a laboratory-made version of leptin sold under the brand name Myalept, has been approved in the United States since 2014 for people with generalized lipodystrophy, a rare condition in which the body cannot store fat normally and leptin runs extremely low. It is given only under specialist supervision through a restricted program, and it is not approved for common obesity. Research into whether leptin can be combined with other agents to help weight maintenance continues at an early stage, with small studies and no approval. That gap between a real approved use and a viral promise is where most confusion now lives.

Does lack of leptin cause weight gain?

In the strict sense, yes, and the proof is dramatic. Congenital leptin deficiency is an inherited condition in which a fault in the leptin gene means the body makes little or no working hormone. Children with it are born at a normal weight, then develop intense, constant hunger and severe obesity within the first months of life, along with delayed puberty and frequent infections. MedlinePlus Genetics describes it as extremely rare; fewer than a hundred cases have been reported worldwide. Daily injections of replacement leptin, given under specialist care, transform these children’s appetite and weight, one of the clearest hormone-replacement success stories in modern medicine.

That rarity is the key qualifier. In the ordinary population, a true lack of leptin is almost never the explanation for weight gain. The opposite is the rule: people who carry more body fat have higher leptin, because more fat cells are making it. Measuring leptin in a routine blood test is therefore uncommon and rarely useful, since the result mostly restates what a tape measure already shows.

Where “low leptin” does show up in everyday life is after weight loss. Lose ten percent of your weight and your leptin falls by more than ten percent, because fat cells shrink and because they release less hormone per unit of fat when energy is scarce. The brain reads that as a shortage, and hunger, food preoccupation and a slightly lower metabolic rate follow. Small controlled studies led at Columbia University found that restoring leptin to pre-diet levels in weight-reduced volunteers partly reversed those changes. Those trials involved a few dozen people and a research protocol, not a treatment anyone can request, but they support the idea that falling leptin is one biological reason regain is common.

What is leptin resistance, and is it real?

Leptin resistance is the term for a state in which leptin is high but the brain acts as though it were low: hunger persists and energy spending does not rise despite ample stores. The concept is real and has been studied for decades, mostly in animals. Mice fed rich diets develop high leptin and stop responding to extra doses. Proposed mechanisms include reduced transport of leptin across the protective barrier between blood and brain, cellular braking proteins that switch off the leptin receptor’s signal, and low-grade inflammation in the hypothalamus.

What is far less settled is how to measure leptin resistance in a person, or whether it is a cause of weight gain, a consequence of it, or simply a normal ceiling on how much appetite suppression leptin can deliver. There is no clinical blood test that diagnoses it. A single leptin level cannot distinguish a brain that is ignoring the signal from a brain that is receiving it and has nothing further to do. Many endocrinologists prefer the phrase “reduced leptin sensitivity” and treat it as a description rather than a diagnosis.

The online version of leptin resistance borrows the scientific label and attaches a program: eliminate certain foods, take certain supplements, and your “resistance” will “reverse.” No randomized trial has shown that any food, supplement or schedule restores leptin sensitivity in humans in a way that produces meaningful weight change. What does reliably lower leptin and modestly improve its signaling is losing fat by any method, which is circular advice for someone trying to lose fat.

Honest summary: the biology is credible, the diagnosis does not exist in the clinic, and the fixes being sold are unproven. Treat the phrase as a research hypothesis, not as a label for yourself.

How does sleep change leptin and ghrelin?

Sleep is the lever with the best human evidence, and it is a lever most people can actually pull. The 2004 crossover trial mentioned earlier is small, but its design is strong: the same twelve men served as their own controls, eating identical meals under identical conditions, with only time in bed changed. After two four-hour nights, appetite for calorie-dense, high-carbohydrate foods such as sweets and salty snacks rose by roughly a third, and the size of each man’s leptin drop tracked how hungry he reported feeling.

Population data point the same way. In the Wisconsin cohort, body mass index followed a U-shaped curve with sleep duration, and the shortest sleepers had both the hormonal profile you would expect, lower leptin and higher ghrelin, and a higher average BMI. Mayo Clinic’s expert answer on sleep and weight summarizes the broader literature: short sleepers tend to eat more, and the hormonal shift is one plausible route, alongside more waking hours in which to snack and more fatigue-driven choices.

Mechanistically, the overnight leptin peak is partly driven by sleep itself, so cutting sleep short truncates the peak. Ghrelin, meanwhile, appears to be released in response to extended wakefulness, perhaps as a signal that an awake body needs fuel. Later studies have been mixed on the exact size of the ghrelin effect, especially when participants are allowed to eat freely, but the direction of travel for hunger and intake is consistent.

The practical implication is not that one bad night ruins anything. It is that chronic short sleep, below the seven hours most adults need according to the CDC, biases your hormonal baseline toward eating more and feeling less satisfied. Protecting sleep is appetite management that happens while you are unconscious.

How does diet change leptin and ghrelin?

Diet reaches the hunger hormones in three ways: through what a meal contains, through how processed it is, and through how much total energy you take in over time. The first two act within hours. The third acts over weeks and is the strongest.

Meal composition changes the ghrelin curve. Meals higher in protein suppress ghrelin for longer and raise fullness hormones more than meals dominated by refined carbohydrate, a finding repeated across many small feeding studies. Fiber slows stomach emptying and sustains the fall in ghrelin. Fructose, the sugar abundant in sweetened drinks, produces smaller insulin and leptin responses than glucose in acute studies, which may mean sweet liquids register weakly as food. These are consistent, modest, short-term effects on how satisfied a given meal leaves you.

Processing level matters independently of nutrients. In a 2019 inpatient trial at the National Institutes of Health, twenty adults spent two weeks each on an ultra-processed diet and a minimally processed diet matched for calories offered, sugar, fat, fiber and sodium, and were allowed to eat as much as they liked. On the ultra-processed diet they ate about 500 more calories a day and gained weight; on the minimally processed diet, ghrelin was lower and the fullness hormone PYY higher. Twenty people is a small sample, but the control was unusually tight.

Energy balance over time is the heavyweight. Sustained calorie restriction lowers leptin and raises ghrelin regardless of the food used to achieve it, which is the body defending its reserves. Intermittent fasting patterns produce the same hormonal responses as continuous restriction when total intake is matched, so there is no evidence that meal timing tricks the hormones in a way that bypasses the arithmetic. What a thoughtful diet can do is make a given calorie level feel less hungry. That is worth a lot.

Leptin vs ghrelin vs GLP-1: how the signals compare

Because so much current interest comes from GLP-1 medicines, it helps to put the three hormones side by side. GLP-1, short for glucagon-like peptide-1, is a hormone released by cells in the intestine after eating; it slows stomach emptying, helps the pancreas release insulin and signals fullness to the brain. Natural GLP-1 lasts only minutes in the blood. The medicines are long-acting look-alikes that keep that signal switched on. Leptin is a different molecule, from a different tissue, with a different timescale, and it is not what GLP-1 medicines contain or mimic.

Feature	Leptin	Ghrelin	GLP-1
Made by	Fat cells	Stomach lining	Intestinal cells
Main message	How much energy is stored	Time to eat	Food has just arrived
Effect on appetite	Lowers (weakly when stores are high)	Raises	Lowers
Timescale	Days to weeks	Hours, meal to meal	Minutes to hours
With weight loss	Falls	Rises	Little consistent change
Short sleep	Falls	Rises	Mixed data
Approved medicine	Metreleptin, for lipodystrophy only	None	Several, for type 2 diabetes and obesity

The table makes one point starkly. The hormone with the strongest intuitive story for treating obesity, leptin, has the narrowest approved use, while GLP-1, a short-lived gut signal, became the basis for widely used medicines. The reason is the asymmetry described earlier: boosting a satiety signal the brain still responds to works better than adding more of a signal that is already abundant. Any decision about a GLP-1 medicine belongs with a prescribing clinician who knows your history; the table is for understanding, not for choosing.

Can I take leptin to lose weight?

For almost everyone, no, and the reasons are instructive. Leptin is a protein. Swallowed, it is digested like any other protein in food, so there is no such thing as an oral leptin pill, and products labeled “leptin” or “leptin support” on supplement shelves contain herbs, fiber or green tea extract rather than the hormone. They are not regulated as medicines and have not been shown in controlled trials to change leptin signaling or body weight.

Injected leptin has been tested directly in people with common obesity. A 1999 trial published in JAMA randomized adults to daily injections of a recombinant leptin or placebo for several months. Average weight loss at the higher exposure levels was modest, and the spread of results was enormous: some participants lost meaningful weight while others lost none. Injection-site reactions were common. The conclusion drawn by the field, confirmed in later studies, was that people with obesity already have high leptin and adding more does little, exactly what the starvation-signal model predicts.

The exceptions are the deficiency states. Congenital leptin deficiency and generalized lipodystrophy are the two conditions in which leptin levels are genuinely very low, and in both, replacement with metreleptin produces large benefits under specialist supervision. Metreleptin is prescription-only, dispensed through a restricted safety program because of risks including antibody formation and a rare association with lymphoma in people with a related condition, and it is not approved or recommended for weight loss in the general population.

A more promising direction is leptin as a maintenance aid after weight loss, when levels have fallen below what the body expects. The supporting trials are small and no product is approved for this purpose. If you are curious whether any leptin-related treatment applies to you, that conversation belongs with your doctor, who can check for the rare conditions where it genuinely does.

Is it better to have high leptin or low leptin?

Neither, in isolation. The right question is whether your leptin matches your body and whether your brain is responding to it. A high level in a person with a lot of body fat is expected, not a bonus; it reflects more fat tissue reporting in, and it is often accompanied by the reduced sensitivity discussed above. High leptin has also been associated in observational studies with inflammation and cardiovascular risk markers, though in those studies it is hard to separate the hormone’s own effects from the effects of the fat mass producing it.

A low level is desirable only when it matches low fat stores in someone who is well nourished and healthy. When leptin is low because of under-eating, over-training or an eating disorder, the consequences can be serious: menstrual periods may stop, bone density can fall, and immune function may weaken. Research in women athletes with missing periods has shown that these changes track with low leptin, and in small studies leptin replacement restored some reproductive and bone markers. That work remains experimental.

For most readers, a leptin number is not something you will ever see, and that is fine. Clinicians rarely order it outside endocrinology referrals because it adds little to what body composition and symptoms already tell them. If a test is done, interpretation requires knowing sex, fat mass, recent weight change, fasting state and time of day, because all of these shift the value.

Think of leptin as a thermostat reading rather than a score. A reading of 72 degrees is neither good nor bad; it depends on whether you are trying to heat or cool the room and whether the furnace is listening.

What the evidence actually says about leptin, ghrelin, sleep and diet

Evidence comes in grades. Randomized controlled trials, where people are assigned by chance to different conditions, are the strongest for cause and effect. Observational studies, which track what people already do, show associations but cannot rule out other explanations. Expert opinion and animal work sit below both. Here is how the main claims in this article stack up.

• Leptin deficiency causes severe obesity and replacement reverses it: strong, from genetic case series and treatment responses in rare patients; the number of patients is tiny but the effect is unmistakable.
• Leptin injections help common obesity: randomized trials exist and show modest, inconsistent effects; the evidence is strong that it does not work well.
• Short sleep lowers leptin and raises ghrelin: small randomized crossover trials plus large observational cohorts agree on direction; moderate strength, with uncertainty about the size of the ghrelin effect.
• Short sleep increases food intake: multiple controlled feeding studies; moderate to strong.
• Protein and fiber suppress ghrelin more than refined carbohydrate: many small randomized meal studies; moderate, with short-term outcomes only.
• Ultra-processed food raises intake and alters gut hormones: one tightly controlled randomized trial of twenty adults; promising but limited.
• Leptin resistance drives human weight gain: strong in animals, weak and indirect in humans; expert hypothesis level.
• Supplements or specific diets reverse leptin resistance: no randomized human evidence.

The pattern is consistent. The further a claim moves from the clinic toward the marketplace, the thinner the evidence beneath it. The best-supported actions for everyday life are unglamorous: sleep roughly seven to nine hours, build meals around protein, fiber and minimally processed foods, and expect hunger to rise during weight loss because the hormones are doing their job. Any personal medical question, especially about medicines that touch these pathways, belongs with your clinician.

Common myths about leptin and the hunger hormones

Myth: a supplement can raise or “fix” your leptin. No over-the-counter product contains leptin, because the hormone would be digested, and none has shown in a randomized trial that it changes leptin signaling or weight. Labels using the word are marketing, not pharmacology.

Myth: people with obesity have low leptin. Almost always the reverse. More fat cells make more leptin. True deficiency is confined to rare genetic and lipodystrophy conditions that are diagnosed by specialists.

Myth: you can reset leptin in seven days. Leptin responds within days to under-eating by falling, which is the opposite of what the programs promise. There is no evidence that any short protocol restores sensitivity; the only reliable way to change the baseline is sustained fat loss.

Myth: ghrelin is a flaw to be suppressed. Ghrelin times meals, protects against starvation and helps release growth hormone. Suppressing it entirely is neither possible without surgery nor desirable. The goal is a ghrelin rhythm that matches regular, satisfying meals.

Myth: eating after 8 p.m. spikes ghrelin and causes fat gain. Ghrelin rises before habitual mealtimes, whenever those are. Late eating is linked with higher intake mainly because it adds eating occasions and often pairs with short sleep, not because the clock changes the hormone’s chemistry.

Myth: GLP-1 medicines work by raising leptin. They mimic a different gut hormone. Leptin typically falls on these medicines as fat is lost, the same as with any weight loss.

Myth: a high leptin level means your metabolism is strong. It means you have more fat tissue reporting in, and often that the brain is responding less to each unit. The number is a reflection of body composition, not a performance score.

When to see a doctor

Most hunger is ordinary and needs no medical attention. Certain patterns, though, point to something worth evaluating, and hormones including leptin and ghrelin may be part of that evaluation when a specialist judges it useful. Make an appointment if any of the following apply.

• A child shows intense, constant hunger and rapid, severe weight gain in the first years of life, especially with delayed growth or frequent infections; rare genetic appetite disorders are diagnosable and treatable, and early referral matters.
• You have lost a noticeable amount of fat from your limbs or face while fat accumulates elsewhere, or you have been told your triglycerides or blood sugar are unusually hard to control; these can be features of lipodystrophy.
• Menstrual periods have stopped for three months or more without pregnancy, particularly alongside heavy exercise, restricted eating or weight loss; low leptin is one marker of insufficient energy availability, and bone health is at stake.
• Hunger feels relentless and out of character, you wake at night to eat, or weight is changing quickly without a clear reason; thyroid, blood sugar and medication effects should be checked.
• You are losing weight without trying, or have persistent nausea, early fullness, vomiting, difficulty swallowing, blood in stool or black stools, or abdominal pain; these are red flags for conditions unrelated to appetite hormones and need prompt assessment.
• Sleep is consistently under six hours despite enough time in bed, you snore loudly or stop breathing in sleep, or you fall asleep during the day; sleep disorders are treatable and affect appetite regulation.

If you take any medicine that affects weight or appetite, including GLP-1 agents, do not change or stop it based on something you read, including this article. Report side effects such as severe abdominal pain, persistent vomiting or signs of dehydration to your prescriber promptly. Every decision about testing, treatment or medication adjustment rests with the clinician who knows your full history.

Frequently asked questions

Can I take leptin to lose weight?

Not for ordinary weight loss. Leptin cannot be taken by mouth because it is digested, and injected leptin produced only modest, inconsistent results in randomized trials of people with obesity, who already have high levels. The approved form, metreleptin, is reserved for rare deficiency conditions such as generalized lipodystrophy and is prescribed only by specialists. Ask your doctor if you suspect a deficiency disorder.

Is it better to have high leptin or low leptin?

Neither is better on its own. Leptin should match your body fat and your brain should respond to it. High leptin usually reflects more fat tissue and often reduced sensitivity. Low leptin is healthy only when it reflects low fat stores in a well-nourished person; when it results from under-eating or over-training it can disrupt periods, bone health and immunity.

Does lack of leptin cause weight gain?

Yes in the rare condition called congenital leptin deficiency, where a gene fault leaves the body with little or no working hormone and children develop severe early obesity. In the general population, lack of leptin is almost never the cause of weight gain; levels are typically high in people with more body fat. Leptin does fall after weight loss, which increases hunger and contributes to regain.

Is GLP-1 the same as leptin?

No. GLP-1 is a short-lived hormone released by the intestine after eating that slows stomach emptying and signals fullness; medicines such as semaglutide mimic it. Leptin comes from fat cells and reports long-term energy stores over days to weeks. GLP-1 medicines do not contain or raise leptin; leptin typically falls on them as fat is lost.

What is ghrelin and why do I feel hungry at the same time every day?

Ghrelin is a hormone made mainly by the stomach lining that rises in the hour or two before your usual mealtimes and falls after eating. The stomach learns your schedule, so hunger arrives on cue even if you ate recently. Regular meals built around protein and fiber keep the ghrelin rhythm predictable and the dips longer.

How does sleep affect the hunger hormones?

Short sleep lowers leptin and raises ghrelin, shifting the balance toward hunger. A controlled trial of two four-hour nights found an 18 percent leptin drop, a 28 percent ghrelin rise and stronger cravings for sweet and starchy foods. Large population studies show the same direction, with the shortest sleepers having higher average body mass index. Most adults need at least seven hours.

Is leptin resistance a real diagnosis?

It is a real research concept, well documented in animals, describing a brain that responds weakly to high leptin. In people there is no clinical test for it and no proven treatment to reverse it. Products and programs marketed to fix leptin resistance lack randomized trial evidence. The only reliable way to lower leptin and improve its signaling is sustained fat loss.

Which foods lower ghrelin and increase fullness?

Meals higher in protein suppress ghrelin for longer than meals dominated by refined carbohydrate, and fiber extends the effect by slowing stomach emptying. Minimally processed foods also appear to leave ghrelin lower and fullness hormones higher than ultra-processed versions with similar nutrients. These effects are modest and short-term, but they make a given calorie intake feel more satisfying.

Does intermittent fasting change leptin and ghrelin differently from regular dieting?

Not in any way the evidence can detect. When total calorie intake is matched, fasting schedules produce the same falls in leptin and rises in ghrelin as continuous restriction, because the hormones respond to energy deficit rather than the clock. Ghrelin does adapt to a new eating window within days, so hunger at skipped mealtimes usually fades.

Why am I hungrier after losing weight?

Because the hunger hormones are defending your previous weight. Leptin falls more than fat mass does, and ghrelin rises and stays elevated for months, while resting energy use dips slightly. These are normal physiological responses, not a sign of failure. Adequate sleep, protein and fiber can blunt the hunger; if appetite feels unmanageable, discuss options with your clinician.

References

• Cleveland Clinic: Leptin and Leptin Resistance
• Cleveland Clinic: Ghrelin
• MedlinePlus Genetics: Congenital leptin deficiency
• NHS: Why lack of sleep is bad for your health

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.