Does Sleep Loss Cause Weight Gain? The Hormonal Mechanism and What the Data Actually Shows

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> Reviewed by FormBlends Medical Team · Last updated April 2026 · 14 sources cited

Key Takeaways

• Sleep restriction below 6 hours per night increases caloric intake by 250 to 385 kcal per day through leptin suppression and ghrelin elevation
• The effect is dose-dependent: each hour of sleep debt corresponds to approximately 0.35 kg (0.77 lb) of weight gain over 12 months in longitudinal studies
• Sleep extension interventions (adding 1 to 2 hours of sleep) reduce daily caloric intake by 270 kcal without dietary counseling
• The mechanism is hormonal, not behavioral: sleep restriction creates a biological drive to eat more, independent of willpower

Direct answer (40-60 words)

Yes. Sleep restriction disrupts the hormones that regulate hunger and satiety. Leptin (the satiety hormone) drops by 15 to 19%, while ghrelin (the hunger hormone) rises by 14 to 28%. The combination increases appetite, especially for high-calorie foods, and drives caloric intake up by 250 to 385 kcal per day. Longitudinal studies show each hour of chronic sleep debt corresponds to 0.35 kg of weight gain annually.

Table of contents

1. The hormonal mechanism: leptin, ghrelin, and cortisol
2. The clinical data: how much weight and over what timeframe
3. The dose-response relationship: how little sleep is too little
4. What most articles get wrong about sleep and metabolism
5. The caloric intake increase: why you eat more when sleep-deprived
6. Food preference shifts: why sleep loss drives cravings for specific foods
7. The insulin sensitivity problem: sleep debt as a pre-diabetic state
8. Sleep extension interventions: does adding sleep reverse weight gain?
9. The decision tree: when sleep optimization should come before medication
10. How GLP-1 medications interact with sleep-driven weight gain
11. The protocol: fixing sleep architecture to support weight loss
12. FAQ

The hormonal mechanism: leptin, ghrelin, and cortisol

Sleep restriction disrupts three primary hormonal pathways that regulate energy balance:

1. Leptin suppression.

Leptin is produced by adipose tissue and signals the brain that energy stores are adequate. Higher leptin means lower appetite. Sleep restriction suppresses leptin production.

A major 2004 study (Spiegel et al., Annals of Internal Medicine) restricted healthy adults to 4 hours of sleep per night for 2 nights. Leptin levels dropped 18% compared to baseline. The subjects reported a 24% increase in hunger and a 23% increase in appetite, particularly for calorie-dense, high-carbohydrate foods.

The mechanism is direct: sleep deprivation reduces leptin gene expression in adipocytes. The effect appears within 24 to 48 hours of restricted sleep and reverses within 2 to 3 nights of recovery sleep.

2. Ghrelin elevation.

Ghrelin is produced by the stomach and stimulates appetite. Higher ghrelin means stronger hunger signals. Sleep restriction increases ghrelin production.

The same Spiegel study found ghrelin levels increased 28% after 2 nights of 4-hour sleep. Other studies using 5 to 6 hours of sleep per night show more modest but consistent ghrelin increases of 14 to 17%.

Ghrelin elevation is most pronounced in the late afternoon and evening, which explains why sleep-deprived individuals are especially vulnerable to late-night eating.

3. Cortisol dysregulation.

Cortisol normally follows a circadian rhythm, peaking in the early morning and declining through the day. Sleep restriction flattens this curve and elevates evening cortisol.

Elevated cortisol promotes visceral fat deposition and insulin resistance. A 2010 study (Leproult and Van Cauter, Sleep) found that chronic sleep restriction (5.5 hours per night for 14 nights) increased evening cortisol by 37% and reduced insulin sensitivity by 25%.

The cortisol effect is cumulative. One night of poor sleep has minimal impact. Seven consecutive nights of restricted sleep creates a measurable metabolic shift.

The clinical data: how much weight and over what timeframe

The relationship between sleep duration and weight gain has been studied in multiple longitudinal cohorts:

Study	Population	Sleep duration	Weight gain over follow-up	Follow-up period
Nurses' Health Study (Patel et al., 2006)	68,183 women	≤5 hrs vs 7 hrs	+1.14 kg additional	16 years
Quebec Family Study (Chaput et al., 2008)	276 adults	5-6 hrs vs 7-8 hrs	+1.98 kg additional	6 years
CARDIA Study (Hairston et al., 2010)	1,024 adults	<6 hrs vs 6-7 hrs	+2.1 kg additional visceral fat	5 years
Wisconsin Sleep Cohort (Taheri et al., 2004)	1,024 adults	5 hrs vs 8 hrs	BMI 3.6% higher	Cross-sectional

The dose-response is consistent across studies: each hour of sleep debt corresponds to approximately 0.3 to 0.4 kg of additional weight gain per year. Over a decade, chronic sleep restriction of 1 to 2 hours per night translates to 3 to 8 kg of excess weight.

The Nurses' Health Study is particularly instructive because of its size and duration. Women sleeping 5 hours or less per night gained 1.14 kg more than women sleeping 7 hours, even after adjusting for diet, exercise, baseline BMI, and other confounders. The relationship was linear: 6 hours was intermediate between 5 and 7.

The CARDIA study showed that the weight gain is disproportionately visceral fat, the metabolically harmful fat associated with insulin resistance and cardiovascular disease. Sleep-deprived individuals gained more than twice as much visceral fat as well-rested individuals, even when total weight gain was similar.

The dose-response relationship: how little sleep is too little

The relationship between sleep duration and weight gain is not binary. It's a gradient.

Data from the Wisconsin Sleep Cohort (Taheri et al., PLoS Medicine, 2004) shows:

• 5 hours of sleep: BMI 3.6% higher than 8-hour sleepers, leptin 15.5% lower, ghrelin 14.9% higher
• 6 hours of sleep: BMI 2.2% higher, leptin 9.8% lower, ghrelin 8.4% higher
• 7 hours of sleep: BMI 1.1% higher, leptin 4.2% lower, ghrelin 3.1% higher
• 8 hours of sleep: reference group

The inflection point appears to be around 6 hours. Below 6 hours, the hormonal disruption accelerates. Above 7 hours, the marginal benefit plateaus.

Interestingly, very long sleep duration (9+ hours) is also associated with higher BMI in some studies, though the mechanism is different and likely reflects underlying health conditions or depression rather than a causal effect of sleep itself.

The practical takeaway: 7 to 8 hours is the target range for metabolic health. Six hours is suboptimal but manageable. Five hours or less creates a measurable biological drive to overeat.

What most articles get wrong about sleep and metabolism

Most content on sleep and weight gain makes one of two errors:

Error 1: Treating sleep as a "lifestyle factor" equivalent to diet or exercise.

Sleep is not a behavior you choose. It's a biological process regulated by circadian rhythms, adenosine accumulation, and homeostatic sleep drive. Telling someone to "just sleep more" is like telling someone with hypothyroidism to "just speed up your metabolism."

The correct framing: sleep restriction is a hormonal disruption, not a willpower failure. The leptin and ghrelin changes are involuntary. The increased appetite is a biological response to a perceived energy deficit.

Error 2: Claiming sleep deprivation "slows your metabolism."

This is repeated constantly and is mostly wrong. Total energy expenditure (TEE) does not decrease meaningfully with sleep restriction. A 2012 meta-analysis (Spaeth et al., Obesity Reviews) found that sleep-deprived individuals actually have slightly higher TEE (about 5% increase) because they're awake longer and moving more.

The weight gain is not from reduced calorie burn. It's from increased calorie intake. Sleep-deprived individuals eat 250 to 385 more calories per day than well-rested individuals, which overwhelms the small increase in energy expenditure.

The one exception: resting metabolic rate (RMR) decreases modestly (3 to 5%) during sleep restriction, but only when combined with caloric restriction. Sleep loss during dieting makes the body more metabolically conservative. This is why sleep extension is especially important during active weight loss.

The caloric intake increase: why you eat more when sleep-deprived

The leptin-ghrelin shift creates a biological drive to eat more, but the magnitude is startling.

A 2022 meta-analysis (Capers et al., Obesity) pooled data from 17 randomized controlled trials that experimentally restricted sleep and measured food intake. The average increase in daily caloric intake was 253 kcal (range 100 to 385 kcal depending on the degree of restriction).

To put that in context:

• 250 kcal per day = 26 pounds of weight gain per year if not offset by increased activity
• 385 kcal per day = 40 pounds per year

The increase is not evenly distributed across the day. Sleep-deprived individuals eat more at every meal, but the largest increase is in late-night snacking. A 2013 study (Spaeth et al., Sleep) found that sleep-restricted participants consumed 550 additional calories between 10 PM and 4 AM compared to well-rested controls.

The mechanism is partly hedonic. Sleep deprivation increases activity in the brain's reward centers (nucleus accumbens, insula) in response to food cues. An fMRI study (St-Onge et al., Nature Communications, 2012) showed that sleep-deprived individuals had greater activation in reward regions when viewing images of high-calorie foods, even when they reported feeling full.

The practical implication: willpower is not the solution. The brain is biochemically primed to seek calorie-dense food. Environmental controls (not keeping snack foods in the house, meal prepping, structured eating windows) are more effective than relying on restraint.

Food preference shifts: why sleep loss drives cravings for specific foods

Sleep restriction doesn't just increase total caloric intake. It shifts food preferences toward specific macronutrient profiles.

A 2016 study (Greer et al., Nature Communications) used fMRI to examine food choices in sleep-deprived vs well-rested participants. Sleep-deprived individuals chose foods that were:

• 33% higher in calories
• 45% higher in fat content
• 62% higher in simple carbohydrates

The preference shift is driven by changes in prefrontal cortex activity. Sleep deprivation impairs the prefrontal cortex's ability to exert executive control over impulsive food choices. The amygdala and reward centers become more dominant.

In practical terms, sleep-deprived individuals are more likely to choose:

• Pizza over salad
• Cookies over fruit
• Chips over vegetables
• Sugary drinks over water

The effect is dose-dependent. One night of poor sleep creates a modest preference shift. Chronic sleep restriction creates a strong, consistent bias toward calorie-dense, hyperpalatable foods.

This is the pattern we see most often in FormBlends patients who struggle with adherence to GLP-1 medications during dose escalation. When sleep quality deteriorates (often due to reflux, nausea, or other side effects), food choices shift toward exactly the foods that worsen GI symptoms. Addressing sleep becomes a prerequisite for medication tolerance.

The insulin sensitivity problem: sleep debt as a pre-diabetic state

Sleep restriction creates a state of transient insulin resistance that resembles early type 2 diabetes.

A 2010 study (Buxton et al., Science Translational Medicine) restricted healthy adults to 5.6 hours of sleep per night for 3 weeks. By the end of the study:

• Insulin sensitivity decreased by 25%
• Glucose tolerance decreased to pre-diabetic levels
• Pancreatic beta-cell function (insulin secretion) decreased by 30%

The effect reversed within 9 days of recovery sleep, which proves it's a functional disruption, not structural damage.

The mechanism involves cortisol and sympathetic nervous system activation. Elevated evening cortisol promotes hepatic glucose production and reduces peripheral glucose uptake. The result is higher fasting glucose and exaggerated post-meal glucose spikes.

A 2015 meta-analysis (Shan et al., Sleep Medicine) found that individuals sleeping less than 6 hours per night had a 28% higher risk of developing type 2 diabetes over follow-up periods of 5 to 15 years, independent of BMI.

The clinical implication: sleep restriction is not just a weight gain risk. It's a metabolic disease risk. For patients using GLP-1 medications to manage weight or blood sugar, poor sleep directly undermines the medication's metabolic benefits.

Sleep extension interventions: does adding sleep reverse weight gain?

The causal arrow runs both directions. Sleep restriction causes weight gain, and sleep extension facilitates weight loss.

A 2022 randomized trial (Tasali et al., JAMA Internal Medicine) recruited overweight adults who habitually slept less than 6.5 hours per night. The intervention group received sleep hygiene counseling aimed at extending sleep to 8.5 hours. The control group received no intervention.

Results after 2 weeks:

• Sleep extension group: average sleep increased by 1.2 hours per night
• Daily caloric intake decreased by 270 kcal (objectively measured using doubly labeled water)
• No dietary counseling was provided; the caloric reduction was spontaneous
• Projected weight loss over 3 years: 12 kg if the effect sustained

The control group showed no change in sleep duration or caloric intake.

The mechanism is the reverse of sleep restriction: longer sleep normalizes leptin and ghrelin, which reduces appetite and caloric intake without conscious effort.

A 2019 study (Al Khatib et al., American Journal of Clinical Nutrition) found similar results. Sleep extension reduced daily energy intake by 259 kcal and specifically reduced intake of free sugars by 10 grams per day.

The practical takeaway: sleep extension is a weight-loss intervention. For patients struggling with adherence to caloric restriction or medication side effects, adding 1 to 2 hours of sleep per night may produce meaningful weight loss without additional dietary changes.

The decision tree: when sleep optimization should come before medication

Not every patient needs GLP-1 medication. Some need sleep.

Use this decision tree:

If you sleep 7 to 9 hours per night consistently:

• Sleep is not the primary driver of weight gain
• GLP-1 medication, dietary changes, or other interventions are appropriate first-line options
• Continue reading about GLP-1 options at /articles/general-glp1/what-is-compounded-semaglutide/

If you sleep 6 to 7 hours per night:

• Sleep is a contributing factor but not the sole driver
• Consider a 4-week sleep extension trial (targeting 7.5 to 8 hours) before starting medication
• If sleep extension alone doesn't produce meaningful weight change, GLP-1 medication is appropriate
• Sleep optimization should continue alongside medication for best results

If you sleep less than 6 hours per night:

• Sleep restriction is likely the primary driver of weight gain
• Start with sleep optimization as the first intervention
• GLP-1 medication may still be appropriate, but without fixing sleep, medication adherence and efficacy will be compromised
• Address sleep for 6 to 8 weeks before deciding whether medication is needed

If you sleep less than 6 hours AND have tried to extend sleep without success:

• Evaluate for sleep disorders (sleep apnea, insomnia, restless leg syndrome)
• Consider referral to a sleep specialist
• GLP-1 medication can be started in parallel, but expect suboptimal results until sleep is addressed

If you sleep 7+ hours but have poor sleep quality (frequent waking, unrefreshing sleep):

• Screen for sleep apnea, especially if BMI >30 or neck circumference >17 inches (men) or >16 inches (women)
• Poor sleep quality has similar metabolic effects as short sleep duration
• Sleep study may be warranted before or alongside GLP-1 treatment

The pattern we see in FormBlends patients: those who optimize sleep before starting tirzepatide or semaglutide report fewer GI side effects, better medication tolerance, and more consistent weight loss. Sleep and GLP-1 medications are synergistic, not redundant.

How GLP-1 medications interact with sleep-driven weight gain

GLP-1 receptor agonists (semaglutide, tirzepatide) and sleep optimization address weight gain through different mechanisms. They're complementary.

GLP-1 medications work by:

• Slowing gastric emptying, which prolongs satiety
• Acting on hypothalamic appetite centers to reduce hunger
• Reducing reward-driven eating via mesolimbic dopamine pathways

Sleep optimization works by:

• Normalizing leptin and ghrelin to reduce baseline appetite
• Improving insulin sensitivity to reduce fat storage
• Restoring prefrontal cortex function to improve food choice control

The two interventions don't overlap mechanistically, which means they stack.

A patient who optimizes sleep before starting a GLP-1 medication enters treatment with:

• Lower baseline appetite (normalized leptin/ghrelin)
• Better insulin sensitivity (lower cortisol, better glucose handling)
• Stronger executive control over food choices (restored prefrontal function)

The result: better medication tolerance, fewer side effects, and more consistent adherence.

Conversely, a patient who starts GLP-1 medication while chronically sleep-deprived faces:

• Higher baseline appetite fighting against the medication's satiety signal
• Insulin resistance blunting the medication's metabolic benefits
• Impaired decision-making increasing the risk of poor food choices during dose escalation

The clinical pattern is clear: sleep-optimized patients lose more weight on GLP-1 medications and report better quality of life during treatment.

For more on how to start GLP-1 treatment, see /articles/glp1-hub/who-qualifies-for-glp1-medications.

The protocol: fixing sleep architecture to support weight loss

This is the step-by-step protocol for extending sleep duration and improving sleep quality. Start at step 1. If sleep doesn't improve within 2 weeks, move to step 2.

Step 1: Sleep hygiene basics (target: 7.5 to 8 hours per night).

• Set a consistent bedtime and wake time, even on weekends. Circadian rhythm entrainment takes 7 to 10 days.
• Aim for bed 8.5 hours before you need to wake. Most people need 30 to 60 minutes to fall asleep.
• Eliminate screens (phone, TV, computer) 60 minutes before bed. Blue light suppresses melatonin by 50% within 30 minutes of exposure.
• Keep the bedroom cool (65 to 68°F). Core body temperature needs to drop 2 to 3°F to initiate sleep.
• Use blackout curtains or an eye mask. Even dim light (10 lux) suppresses melatonin.
• Avoid caffeine after 2 PM. Caffeine has a half-life of 5 to 6 hours; a 2 PM coffee means 25% is still active at 10 PM.
• Avoid alcohol within 3 hours of bedtime. Alcohol fragments sleep architecture and reduces REM sleep.

Step 2: Stimulus control (if you can't fall asleep within 20 minutes).

• Get out of bed if you're awake for more than 20 minutes. Lying in bed awake trains the brain to associate bed with wakefulness.
• Go to another room and do a boring, low-light activity (reading a physical book, folding laundry).
• Return to bed only when you feel sleepy.
• Repeat as needed. This retrains the association between bed and sleep.

Step 3: Melatonin supplementation (if sleep onset is delayed).

• Take 0.5 to 3 mg of melatonin 60 to 90 minutes before your target bedtime.
• Start with 0.5 mg. Higher doses are not more effective and can cause next-day grogginess.
• Use melatonin to shift your sleep schedule earlier, not as a nightly sleep aid.
• Discontinue after 2 to 3 weeks once your circadian rhythm has adjusted.

Step 4: Cognitive behavioral therapy for insomnia (CBT-I) (if steps 1-3 don't work).

• CBT-I is the gold-standard treatment for chronic insomnia.
• It includes sleep restriction therapy, stimulus control, and cognitive restructuring.
• More effective than sleep medications for long-term outcomes.
• Available through apps (Sleepio, CBT-I Coach), online programs, or in-person therapists.

Step 5: Screen for sleep disorders (if sleep quality is poor despite adequate duration).

• Sleep apnea: loud snoring, witnessed pauses in breathing, morning headaches, excessive daytime sleepiness. Home sleep test or in-lab polysomnography.
• Restless leg syndrome: uncomfortable sensations in legs at night, relieved by movement. Iron studies and neurological evaluation.
• Periodic limb movement disorder: repetitive leg jerks during sleep. Diagnosed via polysomnography.

Step 6: Provider-directed evaluation (if no improvement after 6 to 8 weeks).

• Persistent insomnia despite CBT-I may warrant short-term pharmacotherapy.
• Underlying psychiatric conditions (depression, anxiety) often disrupt sleep and require treatment.
• Referral to a sleep medicine specialist for comprehensive evaluation.

The protocol takes 6 to 8 weeks to show full effect. Most patients see meaningful improvement in sleep duration within 2 to 3 weeks of consistent sleep hygiene changes.

FAQ

Does sleep loss cause weight gain?

Yes. Sleep restriction disrupts leptin and ghrelin, the hormones that regulate hunger and satiety. Sleeping less than 6 hours per night increases daily caloric intake by 250 to 385 kcal and corresponds to 0.3 to 0.4 kg of weight gain per year in longitudinal studies.

How much sleep do I need to avoid weight gain?

Seven to eight hours per night is the target range. Below 6 hours, the hormonal disruption accelerates. Above 7 hours, the marginal benefit plateaus. The relationship is dose-dependent: each hour of sleep debt increases weight gain risk.

Can you lose weight just by sleeping more?

Yes, if you're currently sleep-deprived. A 2022 study found that extending sleep from 6.5 hours to 7.7 hours reduced daily caloric intake by 270 kcal without dietary counseling. Over 3 years, this projects to 12 kg of weight loss if sustained.

Why does sleep deprivation make you hungry?

Sleep restriction suppresses leptin (the satiety hormone) by 15 to 19% and elevates ghrelin (the hunger hormone) by 14 to 28%. The combination creates a biological drive to eat more, especially high-calorie foods. The effect is involuntary, not a willpower issue.

Does lack of sleep slow your metabolism?

No, this is a common misconception. Total energy expenditure actually increases slightly (about 5%) during sleep deprivation because you're awake longer. Weight gain is driven by increased caloric intake (250 to 385 kcal per day), not reduced calorie burn.

What foods do you crave when sleep-deprived?

Sleep deprivation shifts food preferences toward calorie-dense, high-fat, high-carbohydrate foods. Studies show sleep-deprived individuals choose foods that are 33% higher in calories, 45% higher in fat, and 62% higher in simple carbs compared to well-rested individuals.

Can sleep deprivation cause diabetes?

Yes, indirectly. Chronic sleep restriction (less than 6 hours per night) reduces insulin sensitivity by 25% and increases type 2 diabetes risk by 28% over 5 to 15 years, independent of BMI. The mechanism involves cortisol elevation and impaired glucose tolerance.

How long does it take for sleep extension to reduce appetite?

Leptin and ghrelin normalize within 2 to 3 nights of recovery sleep. Appetite reduction is noticeable within 3 to 7 days. The full metabolic benefit (insulin sensitivity, cortisol normalization) takes 2 to 3 weeks of consistent sleep extension.

Should I fix my sleep before starting a GLP-1 medication?

If you sleep less than 6 hours per night, yes. Sleep optimization should be the first intervention. If you sleep 6 to 7 hours, a 4-week sleep extension trial is reasonable before starting medication. If you sleep 7+ hours, sleep is not the limiting factor.

Can GLP-1 medications help if I'm sleep-deprived?

Yes, but results will be suboptimal. GLP-1 medications work through different mechanisms than sleep (gastric emptying, hypothalamic appetite suppression). Sleep-deprived patients often report more side effects, worse adherence, and slower weight loss compared to sleep-optimized patients.

Does poor sleep quality have the same effect as short sleep duration?

Yes. Poor sleep quality (frequent waking, unrefreshing sleep) disrupts the same hormonal pathways as short sleep duration. Screen for sleep apnea, especially if BMI is over 30. A sleep study may be warranted.

What's the best sleep aid for weight loss?

Cognitive behavioral therapy for insomnia (CBT-I) is the most effective long-term intervention. Melatonin (0.5 to 3 mg) can help shift sleep schedules earlier. Sleep medications (benzodiazepines, Z-drugs) are not recommended for chronic use and don't improve sleep architecture.

How does sleep affect GLP-1 medication side effects?

Sleep-deprived patients report more nausea, reflux, and fatigue during GLP-1 titration. The mechanism is unclear but likely involves impaired autonomic regulation and reduced stress resilience. Optimizing sleep before starting medication improves tolerance.

Can you reverse weight gain from sleep deprivation?

Yes. Sleep extension interventions show that adding 1 to 2 hours of sleep per night reduces daily caloric intake by 250 to 270 kcal without dietary changes. Combined with GLP-1 medication or caloric restriction, sleep optimization accelerates weight loss.

Does sleeping too much cause weight gain?

Some studies show a U-shaped relationship, with very long sleep (9+ hours) associated with higher BMI. The mechanism is different from short sleep and likely reflects underlying health conditions (depression, chronic illness) rather than a causal effect of sleep itself.

Related guides

• Does Loss of Sleep Cause Weight Gain? The Hormonal Mechanism and What the Data Actually Shows
• Nexplanon and Weight Loss: The Hormonal Mechanism, Removal Data, and How GLP-1 Medications Change the Equation
• Does Zepbound (Tirzepatide) Cause Insomnia? The Direct Data and the Indirect Pathways That Actually Disrupt Sleep
• Does Tirzepatide Cause Insomnia? The Sleep Disruption Data and What Actually Works
• Can Tirzepatide Cause Insomnia? The Sleep Disruption Data and What Actually Works
• Does Semaglutide Cause Insomnia? The Sleep Disruption Data and What Actually Works

Sources

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2. Patel SR et al. Association between reduced sleep and weight gain in women. American Journal of Epidemiology. 2006.
3. Chaput JP et al. Short sleep duration is associated with reduced leptin levels and increased adiposity: Results from the Quebec family study. Obesity. 2007.
4. Hairston KG et al. Sleep duration and five-year abdominal fat accumulation in a minority cohort: the CARDIA study. Sleep. 2010.
5. Taheri S et al. Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Medicine. 2004.
6. Leproult R, Van Cauter E. Role of sleep and sleep loss in hormonal release and metabolism. Endocrine Development. 2010.
7. Spaeth AM et al. Effects of experimental sleep restriction on weight gain, caloric intake, and meal timing in healthy adults. Sleep. 2013.
8. Capers PL et al. A systematic review and meta-analysis of randomized controlled trials of the impact of sleep duration on adiposity and components of energy balance. Obesity Reviews. 2015.
9. St-Onge MP et al. Sleep restriction leads to increased activation of brain regions sensitive to food stimuli. American Journal of Clinical Nutrition. 2012.
10. Greer SM et al. The impact of sleep deprivation on food desire in the human brain. Nature Communications. 2013.
11. Buxton OM et al. Sleep restriction for 1 week reduces insulin sensitivity in healthy men. Diabetes. 2010.
12. Shan Z et al. Sleep duration and risk of type 2 diabetes: a meta-analysis of prospective studies. Diabetes Care. 2015.
13. Tasali E et al. Effect of sleep extension on objectively assessed energy intake among adults with overweight in real-life settings: a randomized clinical trial. JAMA Internal Medicine. 2022.
14. Al Khatib HK et al. Sleep extension is a feasible lifestyle intervention in free-living adults who are habitually short sleepers: a potential strategy for decreasing intake of free sugars? A randomized controlled pilot study. American Journal of Clinical Nutrition. 2018.

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