HoldsUp

Michael Grandner

Michael Grandner is a researcher in behavioral sleep medicine and sleep health. His published research investigates the relationships between sleep, circadian rhythms, cardiovascular health, and cognitive decline. Additionally, his work explores the social determinants of sleep disparities, insomnia chronicity, and interventions to improve sleep apnea treatment adherence.

107 claims checked on air: 9 context 2 contradicted 5 overstated 78 supported 13 unverified

What they said on air

3 citing their own research

0:00:00supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Approximately one in three people in the United States experiences some form of sleep complaint or problem.

"One out of three people in the US has some sort of sleep complaint or problem." (said at 0:00:00)

Nationally representative surveillance data from the Centers for Disease Control and Prevention (CDC) confirm that approximately one in three adults in the United States experiences sleep problems or insufficient sleep. Analysis of the Behavioral Risk Factor Surveillance System (BRFSS, n = 444,306) showed that 65.2% of U.S. adults reported obtaining a healthy sleep duration (≥7 hours per 24-hour period), meaning more than one-third (34.8%) reported short sleep duration. Additional surveillance data show that 35.3% report sleeping less than 7 hours, 37.9% report unintentionally falling asleep during the day, and an estimated 50 to 70 million Americans have chronic sleep and wakefulness disorders.

0:00:09supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Untreated sleep apnea can lead to liver, kidney, and brain complications due to cellular oxygen stress.

"Untreated sleep apnea can lead to liver problems, kidney problems, brain problems because every cell that relies on oxygen starts getting stressed." (said at 0:00:09)

Untreated obstructive sleep apnea (OSA) involves repeated cycles of upper-airway obstruction leading to chronic intermittent hypoxia and reoxygenation. This process induces cellular oxidative stress via bursts of reactive oxygen species (ROS) that overwhelm antioxidant defenses, triggering systemic inflammation, endothelial dysfunction, and metabolic dysregulation. Extensive clinical and mechanistic literature links this oxygen deprivation and oxidative stress to end-organ pathology, including neurocognitive deficits and cerebrovascular injury (brain), nonalcoholic fatty liver disease / metabolic dysfunction (liver), and chronic renal impairment (kidney).

0:02:35supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Chronic insomnia disorder is clinically defined as persistent difficulty initiating or maintaining sleep or waking up too early occurring at least three nights per week for at least three months, with daytime impairment.

"So an insomnia disorder is defined as a persistent difficulty initiating or maintaining sleep or waking up too early. So it can happen anywhere in the night. The difficulty has to be there. Um, it has to occur at least three nights per week. It has to have gone on for at least 3 months to be considered chronic insomnia. It has to cause some sort of daytime functioning problem." (said at 0:02:35)

The speaker's statement precisely reflects the standard clinical diagnostic criteria for chronic insomnia disorder according to the major diagnostic classifications (including DSM-5, ICSD-3, and ICD-11). Diagnostic criteria require difficulty initiating sleep, difficulty maintaining sleep, or early-morning awakening with inability to return to sleep, occurring at least 3 nights per week, persisting for at least 3 months, and causing clinically significant daytime distress or functional impairment (despite adequate opportunity for sleep).

0:03:20unverifiedlowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

A sleep onset latency or wake after sleep onset of at least 30 minutes is a standard clinical threshold indicating potential insomnia disorder.

"a good rule of thumb we use is about 30 minutes. So, if it's taking you at least 30 minutes to fall asleep or you're awake for at least 30 minutes during the night trying to sleep and you can't, that's a good sign that maybe what you have is an insomnia disorder" (said at 0:03:20)

No published record matching the claim that a sleep onset latency or wake after sleep onset of at least 30 minutes is a standard clinical threshold indicating potential insomnia disorder was located; this does not prove the claim false.

0:11:13supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Sleep and wakefulness are regulated by separate neurobiological dimensions and signaling pathways that operate somewhat independently rather than along a single continuum.

"sleep-wake is not a unidimensional line where you're sleepy on one end and awake on the other end. There's actually two separate dimensions. Think of it like there's treble and there's bass. It's not just mono. There's treble and there's bass. You have a wakefulness signal and you have a sleep signal that are separate from each other. They're related, but they do function somewhat independently." (said at 0:11:13)

Published neurobiological research supports the concept that sleep and wakefulness are controlled by distinct, dedicated neural circuits rather than a passive single continuum. In the established 'flip-flop switch' model of sleep-wake regulation, distinct wake-promoting pathways (including orexinergic neurons in the lateral hypothalamus, monoaminergic nuclei, and subcortical glutamatergic/cholinergic projections) and sleep-promoting pathways (such as GABAergic/galaninergic neurons in the ventrolateral preoptic nucleus) mutually inhibit one another to generate discrete behavioral states. In addition, sleep propensity and alertness are shaped by distinct homeostatic (Process S, tracking sleep debt) and circadian (Process C, tracking biological time) mechanisms that operate somewhat independently.

0:12:52supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

The stimulus control therapy protocol for insomnia was first published in 1972.

"stimulus control was first published in 1972." (said at 0:12:52)

Richard R. Bootzin first published and presented the stimulus control therapy protocol for insomnia in 1972 (Bootzin, R. R., 'Stimulus control treatment for insomnia', Proceedings of the 80th Annual Convention of the American Psychological Association, 1972, 7, 395-396). Stimulus control remains recognized by major sleep medicine task forces as a core empirically supported behavioral intervention for chronic insomnia.

0:26:40needs contexthighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

In the original publication describing sleep restriction therapy, the intervention was called restriction of time in bed rather than sleep restriction therapy.

"if you actually look to the original publication, they didn't, they didn't even call it sleep restriction therapy. They called it restriction of time in bed, which is really what it is." (said at 0:26:40)

In the seminal 1987 paper describing the intervention by Arthur Spielman and colleagues, the article was titled 'Treatment of chronic insomnia by restriction of time in bed', emphasizing that the technique curtails time spent in bed rather than physiological sleep. However, contrary to the assertion that the original authors did not call it sleep restriction therapy, they explicitly introduced and used the term 'sleep restriction therapy' in the original publication and its abstract.

0:33:52unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Major medical and athletic organizations (including the NCAA and IOC) recommend Cognitive Behavioral Therapy for Insomnia (CBT-I) as the first-line treatment for insomnia.

"But if you look at every medical organization that has any recommendation around in how to treat insomnia, and for athletes, you know, this includes like NCAA and IOC who who've put out sleep-related materials, they all say CBT-I first" (said at 0:33:52)

No published record matching the claim that major medical and athletic organizations (including the NCAA and IOC) recommend Cognitive Behavioral Therapy for Insomnia (CBT-I) as the first-line treatment for insomnia was located; this does not prove the claim false.

0:34:15supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Cognitive Behavioral Therapy for Insomnia (CBT-I) is effective for treating insomnia in people with chronic pain, fibromyalgia, and cancer.

"Not only does it work reliably well, it works when you have other like, well, what about if you're in chronic pain? Like the pain is keeping you up. How is that—you don't have conditioned arousal, you have an active thing going on? Still works in works in fibromyalgia, works in chronic pain, works in cancer." (said at 0:34:15)

Multiple systematic reviews and meta-analyses of randomized controlled trials demonstrate that Cognitive Behavioral Therapy for Insomnia (CBT-I) is effective for treating insomnia comorbid with chronic pain, fibromyalgia, and cancer. A comprehensive 2025 meta-analysis in JAMA Internal Medicine evaluated 67 randomized trials of CBT-I across chronic medical conditions (including chronic pain and cancer) and found large, durable improvements in insomnia severity (Hedges' g = 0.98) and sleep efficiency (g = 0.77). Condition-specific meta-analyses consistently report significant benefits on sleep quality and insomnia severity in patients with chronic non-cancer pain, fibromyalgia, and cancer survivors.

0:34:36supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

CBT-I is effective for improving insomnia in patients with sleep apnea before their sleep apnea is treated.

"It works in sleep apnea. It works before your sleep apnea is even treated. It helps with your insomnia." (said at 0:34:36)

Randomized controlled trials evaluating comorbid insomnia and obstructive sleep apnea (COMISA) demonstrate that cognitive behavioral therapy for insomnia (CBT-I) administered prior to positive airway pressure (PAP/CPAP) therapy significantly improves insomnia severity, sleep parameters (such as sleep onset latency, wake after sleep onset, and sleep efficiency), and subsequent CPAP adherence.

0:34:55needs contexthighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

CBT-I removes sleep barriers in approximately 85% of cases.

"What it does is it removes some of those barriers about, again, about 85% of the time, not 100%." (said at 0:34:55)

Cognitive behavioral therapy for insomnia (CBT-I) is widely recognized as the first-line treatment for insomnia and demonstrates strong efficacy across systematic reviews and randomized controlled trials. Clinical response rates for CBT-I typically fall between 70% and 80%, with session completion rates for individual in-person CBT-I reaching approximately 84%. While an approximate 85% figure aligns well with the general magnitude of clinical benefit and high completion rates of structured CBT-I, exact response and remission percentages vary depending on the delivery format (e.g., individual vs. automated digital CBT-I) and the specific outcome criteria used.

0:38:00unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Approximately one in three people in the United States experiences some form of sleep complaint or disturbance.

"about one out of three people in the US has some sort of sleep complaint or problem or something, whether it's falling asleep, staying asleep, not feeling refreshed. That seems to be about a third of the population at least." (said at 0:38:00)

No published record matching the claim that approximately one in three people in the United States experiences some form of sleep complaint or disturbance was located; this does not prove the claim false.

0:38:17unverifiedlowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Approximately 10% of the US population meets the diagnostic criteria for an insomnia disorder.

"And it seems like about 1 in 10 people probably would meet the criteria for an insomnia disorder if you if you if you assessed them." (said at 0:38:17)

No published record matching the claim that approximately 10% of the US population meets diagnostic criteria for an insomnia disorder was located; this does not prove the claim false.

0:39:34supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Approximately 1 in 4 to 5 men over the age of 30 has sleep-related breathing issues, rising to about 50% for men with a BMI over 30.

"The most recent data I've seen estimates that about one out of four or five men over 30 probably has at least some sleep-related breathing issues, especially if if their BMI is over 30. It's more like 50/50." (said at 0:39:34)

Population-based epidemiologic data directly support the claim. In landmark findings from the Wisconsin Sleep Cohort Study, approximately 24% (roughly 1 in 4) of adult men aged 30 to 60 had sleep-disordered breathing defined by an apnea-hypopnea index (AHI) ≥ 5 events per hour. Obesity is a major causal driver: in men with a body mass index (BMI) over 30 kg/m², the prevalence of sleep-disordered breathing increases substantially, approaching or exceeding 50%. Updated analyses reflecting increasing population obesity indicate that rates of sleep-disordered breathing remain elevated across adult men.

0:39:51supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Sleep apnea affects approximately 1 in 15 to 20 women.

"Women get it less often, but it's also shockingly common in women, too. It might be more like one out of every 15 or 20 women." (said at 0:39:51)

Epidemiological cohort data support the estimate that obstructive sleep apnea / sleep-disordered breathing affects approximately 1 in 15 to 1 in 20 women (5% to 6.7%), with exact rates depending on age and severity criteria. Data from the Wisconsin Sleep Cohort Study showed that moderate-to-severe sleep-disordered breathing (apnea-hypopnea index ≥ 15) affects 3% of women aged 30–49 and 9% of women aged 50–70, averaging roughly 5–6% across middle-aged women.

0:41:26supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Having up to 4 or 5 breathing pauses per hour during sleep is clinically normal, with mild sleep apnea defined starting at 5 events per hour and moderate sleep apnea starting at 15 events per hour.

"it you can have four or five breathing pauses per hour in the night and be in the normal range. Sleep apnea doesn't begin at five is mild begin is the low end of mild, and it's not even till you get to 15 per hour that it becomes starts becoming moderate." (said at 0:41:26)

Standard clinical diagnostic criteria define sleep apnea severity using the Apnea-Hypopnea Index (AHI), which measures the average number of apnea and hypopnea events (breathing pauses or reductions) per hour of sleep. An AHI of fewer than 5 events per hour (<5/h) is classified as normal (no sleep apnea), mild obstructive sleep apnea is defined as an AHI of 5 to 14.9 events per hour, and moderate obstructive sleep apnea is defined as an AHI of 15 to 29.9 events per hour (with ≥30 events per hour classified as severe).

0:43:52supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Stage 2 sleep comprises more than 50% of total sleep time across the night in adults.

"It is more than 50% of the night. Most of the work that your brain does in sleep is done in stage two." (said at 0:43:52)

Normative polysomnographic sleep architecture demonstrates that stage 2 (N2) non-REM sleep constitutes the single largest fraction of total sleep time in healthy adults, typically accounting for approximately 45% to 55% (and commonly exceeding 50% with advancing adult age) of the night.

0:44:30supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Growth hormone is secreted primarily during stage 3 (N3 / slow-wave) non-REM sleep.

"This is for athletes. This is super important because this is when growth hormone is secreted in N3 sleep at stage three or non-REM stage three sleep." (said at 0:44:30)

Endocrine and sleep physiology literature firmly establishes that the primary nocturnal surge of growth hormone (GH) secretion is tightly coupled to non-REM stage 3 (N3) slow-wave sleep (SWS). Experimental enhancement or disruption of slow-wave sleep directly impacts GH secretion levels.

0:44:40supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Severe sleep apnea is clinically defined as having 30 or more respiratory events per hour.

"when you get the more severe sleep apnea of like 30 events per hour or more with with these other presentations" (said at 0:44:40)

Standard clinical guidelines established by the American Academy of Sleep Medicine (AASM) classify the severity of obstructive sleep apnea (OSA) using the Apnea-Hypopnea Index (AHI) or Respiratory Disturbance Index (RDI). An index of 5 to <15 events per hour is classified as mild, 15 to <30 events per hour as moderate, and 30 or more events per hour as severe.

0:46:01supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

During REM sleep, skeletal muscles are paralyzed because alpha motor neurons are hyperpolarized.

"your muscles are very relaxed, that's nothing compared to how relaxed your muscles are in REM sleep. Not because they're recovering, but because you're actively paralyzed. Uh your alpha motor neurons are hyperpolarized. You cannot move uh even if you wanted to." (said at 0:46:01)

The claim is accurate and supported by neurophysiological research. Intracellular recordings in animal models demonstrate that during REM sleep, spinal and cranial motor neurons (alpha motoneurons) undergo sustained tonic hyperpolarization driven by inhibitory GABAergic and glycinergic inputs from premotor circuitry (e.g., in the ventromedial medulla), which actively induces somatic muscle atonia and prevents motor execution during sleep.

0:46:50supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

The typical adult wakes up 10 times or more during the night without remembering most awakenings.

"Actually, the typical adult will wake up 10 times a night or more during the night. They just don't remember. It's very short." (said at 0:46:50)

Polysomnography and actigraphy studies show that healthy adults frequently experience brief nocturnal awakenings and EEG arousals throughout the night, far exceeding 10 occurrences across an entire sleep period, and generally do not recall them in the morning unless wakefulness lasts several minutes. In normal control subjects undergoing polysomnography, Rechtschaffen and Kales criteria showed a mean of 4 awakenings per hour of sleep (totaling roughly 20-30 per night), alongside a substantially higher frequency of brief EEG arousals (mean of 21 per hour). Furthermore, actigraphy and recall studies demonstrate that healthy adults do not form memories of brief nocturnal awakenings unless continuous wakefulness exceeds an average threshold of approximately 4 to 5 minutes.

0:48:21supportedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

During deep slow-wave sleep, the interstitial space between brain cells increases, allowing the clearance of waste products from the brain.

"the spaces between your brain cells actually increases and like sort of like a like actually like a filter it increases and actually waste products can start clearing out of your brain." (said at 0:48:21)

The claim accurately describes the mechanism of the glymphatic system discovered in rodent models. In vivo studies using two-photon imaging and real-time diffusion measurements demonstrated that natural sleep and anesthesia induce an approximately 60% expansion of the brain's interstitial space, facilitating the convective exchange of cerebrospinal fluid with interstitial fluid and accelerating the clearance of metabolic waste products such as amyloid-beta. Because direct real-time measurement of interstitial space volume expansion relies primarily on preclinical animal models, certainty for direct human translation is graded as very low.

0:53:26supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Hypnic jerks occur specifically during Stage 1 sleep.

"this is also where you get hypnic jerks in you. If you have one of those, you were in stage one sleep." (said at 0:53:26)

Hypnic jerks (also referred to as sleep starts or hypnagogic jerks) are benign, involuntary myoclonic twitches that characteristically occur during the sleep-wake transition, specifically during the onset of stage 1 (N1) non-rapid eye movement (NREM) sleep.

0:55:31supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Peak cerebral blood flow during sleep occurs during REM sleep.

"Peak blood flow in the brain is actually REM sleep. Like your brain is extremely active. It's actually more like waking than any other sleep stage." (said at 0:55:31)

Published neuroimaging and physiological research consistently demonstrates that cerebral blood flow (CBF) fluctuates markedly across sleep architecture and reaches its highest levels during rapid eye movement (REM) sleep. A 2024 systematic review and meta-analysis of 38 human studies found that CBF is lowest during non-REM (NREM) sleep and highest during REM sleep, reflecting the high metabolic activity and active neural processing characteristic of REM sleep.

0:57:01supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Slow-wave (deep) sleep facilitates synaptic pruning and synaptic homeostasis, whereas REM sleep facilitates synaptic strengthening and connection building.

"the main thing that seems to be happening in the deep sleep is synaptic pruning and synaptic homeostasis. And in REM sleep there's a lot of synaptic strengthening and connection building and those two things work in concert with each other." (said at 0:57:01)

The speaker accurately describes a prominent and well-supported neurobiological framework regarding sleep-dependent plasticity. Under the synaptic homeostasis hypothesis (pioneered by Tononi and Cirelli), wakefulness leads to a net increase in synaptic strength, and slow-wave (deep) sleep is characterized by generalized synaptic downscaling (pruning/weakening) to restore energetic and computational homeostasis. In contrast, rapid-eye-movement (REM) sleep, often in synergy with prior slow-wave sleep, has been shown to support selective synaptic potentiation, restructuring, and strengthening of memory-associated neuronal connections.

1:00:36supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Human sleep cycles repeat approximately every 90 minutes across the night.

"You cycle through them. And it's about every 90 minutes. Anyone can Google that, but it's not exact. They're different across the night." (said at 1:00:36)

Human sleep is well established to alternate between non-rapid eye movement (NREM) and rapid eye movement (REM) stages in ultradian cycles averaging approximately 90 to 110 minutes in length, typically recurring 4 to 6 times per night. As the speaker noted, cycle durations vary both between individuals and across the course of the night, with the proportion of slow-wave sleep predominating in early cycles and REM episodes lengthening toward the morning.

1:01:06contradictedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Waking up with dream recall occurs because the person woke directly out of REM sleep.

"But so if you woke up and you remember a dream, it's cuz you woke up out of REM. That's all that's all that means." (said at 1:01:06)

The assertion that recalling a dream upon waking implies that the individual woke directly out of REM sleep is contradicted by sleep physiology research. While dream reports are generally more frequent, vivid, and narrative-like following awakenings from REM sleep, substantial scientific evidence demonstrates that dreaming and successful dream recall also regularly occur upon awakening from non-rapid eye movement (NREM) sleep stages (N1, N2, and N3). Laboratory polysomnography studies show that awakening from NREM sleep yields dream recall in 40% to 70% of awakenings, sharing specific posterior cortical activation patterns with REM dreaming.

1:01:06needs contextmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Arousal thresholds are higher during slow-wave deep sleep than during stage 2 sleep or REM sleep, making it easier to awaken from stage 2 and REM.

"and that's also why it's easier to wake up out of stage two and REM than deep sleep." (said at 1:01:06)

The claim is broadly accurate for stage 2 sleep and tonic REM sleep, but requires qualification regarding REM sleep substates. Polysomnographic arousal studies show that auditory arousal thresholds (AATs) are significantly higher during slow-wave sleep (stage 3/4 deep sleep) compared to stage 2 sleep, making stage 2 easier to awaken from. However, arousal thresholds during REM sleep vary substantially by substate: during tonic REM sleep, arousal thresholds are low and comparable to stage 2 sleep, whereas during phasic REM sleep (episodes with rapid eye movements), arousal thresholds are elevated to levels comparable to slow-wave deep sleep.

1:06:15supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Sleep apnea reliably and dramatically reduces slow-wave deep sleep.

"Sleep apnea is one of the few things that can artificially, reliably, dramatically reduce your slow-wave deep sleep because it it prevents you because you can't detach because your body keeps trying to get your attention." (said at 1:06:15)

Published polysomnographic research confirms that sleep apnea causes frequent respiratory-related arousals and sleep fragmentation, which significantly reduces the amount and continuity of slow-wave sleep (N3 deep sleep) while increasing lighter non-REM sleep stages. Relief of airway obstruction (e.g., via surgery or positive airway pressure) restores sleep architecture and leads to a substantial increase in slow-wave sleep percentage.

1:06:39supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Sleep apnea dramatically increases stage 1 sleep and reduces REM sleep.

"The other thing it does is it dramatically increases it can dramatically increase stage one... The other thing it can do, it can dramatically reduce your REM sleep because remember what I said about muscles in REM sleep." (said at 1:06:39)

Polysomnographic studies demonstrate that obstructive sleep apnea (OSA) alters sleep architecture by increasing sleep fragmentation, significantly elevating the proportion of time spent in light stage 1 (N1) sleep, and reducing time spent in rapid eye movement (REM) sleep compared to individuals without OSA.

1:07:09supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Snoring is worse during REM sleep and toward the end of the night because respiratory muscles lose tone and REM sleep is concentrated later in the sleep period.

"Even your respiratory muscles get weaker. That's why snoring is worse in REM and or worse at the end of the night because you have more REM at the end of the night." (said at 1:07:09)

During rapid eye movement (REM) sleep, physiological muscle atonia involves the suppression of upper airway dilator and accessory respiratory muscle tone. This reduction in muscle activity increases upper airway resistance and collapsibility, exacerbating snoring and obstructive respiratory events. Because normal sleep architecture concentrates REM sleep predominantly in the second half and towards the end of the night, sleep-disordered breathing events and upper airway collapsibility are typically more pronounced during these later periods.

1:07:52supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Untreated sleep apnea is an established risk factor for neurodegeneration.

"Untreated sleep apnea is a known risk factor for neurodegeneration, especially when it's more severe." (said at 1:07:52)

Extensive meta-analyses of prospective cohort studies confirm that obstructive sleep apnea (OSA) and sleep-disordered breathing are established risk factors for cognitive impairment, all-cause dementia, and neurodegenerative conditions such as Alzheimer's disease. Pooled analyses indicate that individuals with OSA have a significantly increased risk of developing Alzheimer's disease (hazard ratio ~1.45) and all-cause dementia/cognitive decline (hazard ratio ~1.33 to 1.52). Furthermore, OSA is associated with increased blood and cerebrospinal fluid biomarkers of Alzheimer's pathology (including amyloid-beta and tau) and cerebral small vessel disease.

1:08:00supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Severe sleep apnea is defined clinically as 30 or more respiratory events per hour.

"Severe sleep apnea—and that's 30 events or more an hour—seems very reliably tied to bad outcomes." (said at 1:08:00)

Standard clinical sleep medicine guidelines, including those established by the American Academy of Sleep Medicine (AASM), define severe obstructive sleep apnea (OSA) by an Apnea-Hypopnea Index (AHI) of 30 or more respiratory events per hour. An AHI of 5 to 14.9 events/hour indicates mild OSA, 15 to 29.9 indicates moderate OSA, and 30 or more indicates severe disease, which is consistently associated with adverse cardiometabolic outcomes and increased mortality.

1:08:40supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Intermittent hypoxia in sleep apnea causes cells to release reactive oxygen species, generating chronic oxidative stress.

"It's not really the hypoxia, it's the intermittent hypoxia... all of these cells are releasing reactive oxygen species every time this happens. So, you're releasing these reactive oxygen species. This oxidative stress is happening and then it's quelled, and then it's stressed" (said at 1:08:40)

Extensive clinical and mechanistic research confirms that intermittent hypoxia and subsequent reoxygenation cycles in obstructive sleep apnea (OSA) trigger recurrent surges of reactive oxygen species (ROS) from leukocytes and endothelial cells, leading to systemic oxidative stress.

1:10:00supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Untreated sleep apnea can cause damage and dysfunction in the liver, kidneys, brain, heart, and immune system.

"So that's why not just sleep deprivation, but also untreated sleep apnea can lead to liver problems, kidney problems, brain problems, heart issues, you know, immune system problems, because every cell that relies on oxygen starts getting stressed" (said at 1:10:00)

The speaker's statement accurately reflects the established pathophysiology and clinical epidemiology of obstructive sleep apnea (OSA). Recurrent upper airway obstruction causes chronic intermittent hypoxia, sleep fragmentation, oxidative stress, and sympathetic hyperactivity. These systemic insults contribute to multiorgan dysfunction and disease, including cardiovascular disease (hypertension, arrhythmias, coronary artery disease, heart failure), neurovascular and cognitive issues (stroke, brain structural changes), nonalcoholic fatty liver disease (steatohepatitis, fibrosis), chronic renal injury via the cardio-renal axis, and immune/inflammatory dysregulation (systemic inflammation, endothelial dysfunction).

1:10:33supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

When sleep is impaired by deprivation or fragmentation, vigilant attention is the first cognitive domain to deteriorate.

"When your sleep is poor, whether it's sleep deprivation or sleep apnea or fragmentation or whatever, the first brain function to go is vigilant attention, your ability to maintain focus, especially when whatever you're focusing on isn't super exciting." (said at 1:10:33)

Extensive experimental sleep literature demonstrates that vigilant attention (sustained attention/vigilance, typically assessed using tasks such as the Psychomotor Vigilance Test [PVT]) is the most sensitive cognitive function affected by acute sleep deprivation, chronic sleep restriction, and sleep fragmentation. Impairments in vigilant attention manifest as slowed reaction times and attentional lapses, and form a fundamental substrate underlying deficits across higher-order cognitive processes.

1:15:52supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Playing the didgeridoo strengthens upper airway muscles through circular breathing and helps reduce mild sleep apnea.

"there's very famous work done with like people who play the didgeridoo, where they have to do the cyclical breathing. It ends up strengthening certain muscles that even when you're asleep, they're a little stronger and they can maintain a little more tone. So sometimes that can help, especially for more mild apnea cases." (said at 1:15:52)

A landmark randomized controlled trial published in the BMJ evaluated didgeridoo playing (which requires circular breathing) for training upper airway muscles in patients with obstructive sleep apnea syndrome. In the trial of 25 patients with moderate sleep apnea, 4 months of regular practice (approximately 25 minutes daily) led to statistically significant reductions in the apnea-hypopnea index (difference of -6.2 events per hour) and daytime sleepiness compared to a waitlist control group. Subsequent systematic reviews have confirmed this benefit while noting that evidence is derived from limited sample sizes.

1:15:52supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Daytime intraoral neuromuscular electrical stimulation of the tongue (such as eXciteOSA) improves upper airway muscle tone during sleep to reduce mild obstructive sleep apnea and snoring.

"There's a device called eXciteOSA, where you put it on your tongue when you're awake and it sort of electrically stimulates your tongue muscle. So then you go to bed, it keeps a little—it's like a TENS unit kind of, where it stimulates your tongue muscles so that when you go to bed, there's a little more muscle tone in there. That seems to work okay." (said at 1:15:52)

Daytime intraoral neuromuscular electrical stimulation (NMES) devices, such as eXciteOSA, are used during wakefulness (typically 20 minutes daily for 6 weeks) to increase tongue muscle tone (particularly the genioglossus) and prevent upper airway collapse during sleep. Clinical studies, including prospective cohort trials and a double-blind sham-controlled randomized trial, demonstrate that this therapy significantly reduces objective and subjective snoring time (by approximately 40% to 50%) and reduces the apnea-hypopnea index (AHI) or respiratory event index (REI) by approximately 30% to 52% in patients with primary snoring and mild obstructive sleep apnea.

1:16:04supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Indoor bedroom lighting provides a couple hundred lux, whereas outdoor daylight provides thousands of lux.

"I'm talking about daylight. I'm talking about like outdoor light, not just "turn on a light in my bedroom" light—that's a couple hundred lux. Step outside, it's thousands of lux of light." (said at 1:16:04)

Standard physical measurements of ambient illuminance consistently demonstrate that typical indoor residential lighting provides approximately 100 to 300 lux (a couple hundred lux), whereas outdoor daylight ranges from thousands of lux on overcast days to well over 100,000 lux in direct sunlight.

1:16:22supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Implantable hypoglossal nerve stimulation devices (such as Inspire) electrically stimulate upper airway muscles when airway obstruction is detected to maintain airway patency during sleep.

"There's a new device people have maybe seen commercials called Inspire, which just means "breathe in," but it's sort of like a pacemaker that they install. So it's an implantable electrical device that they do surgery, but it's a sort of a pacemaker for your tongue muscle. And so what it does is when it detects that your tongue is falling back, it zaps it to open it up." (said at 1:16:22)

Hypoglossal nerve stimulation systems (such as the FDA-approved Inspire device) are implantable neurostimulator devices ('pacemaker-like' systems) designed to treat moderate-to-severe obstructive sleep apnea in patients who cannot tolerate continuous positive airway pressure (CPAP). The system includes an implantable pulse generator, a respiratory sensing lead to detect breathing effort, and a stimulation lead placed on branches of the hypoglossal nerve (cranial nerve XII). When synchronized with respiration during sleep, the device delivers mild electrical pulses to activate upper airway dilator muscles (primarily the genioglossus), advancing the tongue and maintaining airway patency.

1:16:35supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Receiving strong bright light at a predictable time in the morning cues the circadian clock so the body expects to sleep about 16 to 17 hours later.

"Getting that strong daytime signal in the morning at a predictable time starts a clock... if you have a strong morning signal with some bright light at a predictable time, about 16 to 17 hours later, your body will expect to be ready for sleep." (said at 1:16:35)

The claim is supported by established chronobiological principles. The central circadian pacemaker (the suprachiasmatic nucleus) is entrained to the 24-hour environmental cycle primarily through light exposure. Exposure to bright light in the morning produces a circadian phase advance according to the human light phase response curve (PRC), anchoring the timing of physiological rhythms. In an entrained 24-hour cycle, this morning signal aligns the circadian rhythm of melatonin production and core body temperature such that dim-light melatonin onset (DLMO) and physiological sleep propensity predictably peak approximately 14 to 17 hours after morning wakefulness and light exposure.

1:17:36supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Higher exposure to bright outdoor daylight during the day reduces susceptibility to circadian disruption caused by light exposure at night.

"the more outdoor light, the more bright light—but it mostly means outdoor light—the more light you get during the day, it inoculates you against light at night. Because if you got a really strong daytime signal, you can get all kinds of light from screens or whatever at night, and it actually won't matter for most people." (said at 1:17:36)

Human controlled experimental studies demonstrate that prior photic history significantly influences the sensitivity of the circadian pacemaker and acute melatonin suppression. Exposure to brighter light during the day reduces sensitivity to subsequent light-induced melatonin suppression and phase shifts compared to dimmer prior light exposure. Additionally, experimental trials show that daytime bright light exposure attenuates or abolishes the disruptive effects of evening light from self-luminous screens on pre-sleep melatonin levels and sleep parameters.

1:20:08supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Morning light exposure accelerates the natural morning decline and suppression of melatonin.

"So melatonin naturally—your natural melatonin will drop in the morning down to like from its peak to almost nothing. Light suppresses melatonin naturally. That's what it does. And so the earlier—if your melatonin is still kind of high and it's dropping, by getting that light, you accelerate its ability to drop." (said at 1:20:08)

The speaker's statement accurately reflects human circadian physiology. Melatonin is synthesized by the pineal gland during the biological night under the control of the suprachiasmatic nucleus, declining naturally toward daytime baseline levels in the morning. Ocular light exposure acutely inhibits pineal melatonin production and accelerates the suppression and termination of circulating melatonin levels, as well as advancing the circadian timing of the melatonin rhythm.

1:31:40supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Adenosine levels in the body are lowest upon waking and accumulate across the day.

"Adenosine builds across the day, and you're at your lowest levels as soon as you wake up." (said at 1:31:40)

The statement accurately reflects the established neurobiological model of sleep homeostasis. Extracellular adenosine in key brain regions (particularly the basal forebrain and cortex) progressively accumulates as a byproduct of cellular energy consumption and neuronal activity during sustained wakefulness across the day, generating homeostatic sleep pressure, and is progressively cleared during sleep, reaching baseline (lowest) levels upon waking.

1:31:55unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Natural sleep inertia wears off within 10 to 60 minutes after waking for most people.

"for most people, that natural sleep inertia will wear off within 10 to 60 minutes as soon as they wake up." (said at 1:31:55)

No published record matching the claim that natural sleep inertia wears off within 10 to 60 minutes after waking for most people was located; this does not prove the claim false.

1:33:43supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Peak alertness effects of caffeine occur approximately 30 minutes after ingestion.

"caffeine doesn't reach its peak effects for at least like a half an hour after you ingest it, and then it'll last for a few hours afterwards." (said at 1:33:43)

Standard immediate-release caffeine is rapidly absorbed from the gastrointestinal tract, reaching peak plasma concentrations (Tmax) between 30 and 60 minutes after oral ingestion (typically around 0.5 to 1 hour), with an elimination half-life generally ranging from 3 to 7 hours, supporting the statement that peak effects occur at least 30 minutes post-ingestion and persist for several hours.

1:34:08supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Melatonin administered as an adjunct therapy during COVID-19 infection improved clinical recovery outcomes.

"It was seen as an adjunct treatment during COVID that didn't conflict with any of the other treatments, but actually made illness recovery better." (said at 1:34:08)

Multiple systematic reviews and meta-analyses of randomized controlled trials (RCTs) confirm that melatonin administered as an adjunctive treatment in patients with COVID-19 significantly improves clinical recovery outcomes, shortens hospital length of stay, and reduces inflammatory markers such as C-reactive protein (CRP). For example, a meta-analysis by Lan et al. (2022) found a higher clinical recovery rate in melatonin-treated COVID-19 patients compared to controls (OR: 3.67; 95% CI: 1.21-11.12), and an RCT by Farnoosh et al. (2022) showed significantly improved symptoms and shorter time to discharge when 3 mg melatonin three times daily was added to standard care. A meta-analysis by Farhoodi et al. (2023) further confirmed that adjunctive melatonin increased clinical improvement rates (OR: 5.09; 95% CI: 2.60-9.96) and shortened hospital stays.

1:34:59supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Exposure to light during the night acutely suppresses endogenous melatonin levels.

"light suppresses it. So even if you're at peak levels during the night, turn on a bright bathroom light, plummets." (said at 1:34:59)

Extensive experimental and clinical research demonstrates that exposure to light during the biological night acutely suppresses circulating melatonin levels in humans. Controlled dose-response studies show that acute melatonin suppression occurs rapidly upon light exposure, with even moderate domestic indoor illuminance (around 100 lux) producing roughly half of the maximal suppression seen with bright light (~9,000 lux), and higher light intensities leading to profound, rapid decreases in circulating concentrations.

1:35:09supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Aging leads to a natural decline in endogenous melatonin production.

"the way to stop producing natural melatonin would be aging. That reduces it." (said at 1:35:09)

The claim that aging leads to a decline in endogenous melatonin production is well supported by scientific literature. Systematic reviews and clinical observational studies confirm that pineal melatonin secretion and nocturnal peak concentrations decline significantly with advancing age in humans. A systematic review of physiological melatonin levels in older adults (PMID: 27302542) demonstrated a significant decline in maximal nocturnal peak concentrations from younger to older age groups (participants aged 65–70 years vs. ≥75 years). Studies measuring salivary and plasma melatonin (PMID: 12485366, PMID: 15066050) similarly report an age-related reduction in the circadian amplitude and peak melatonin levels beginning as early as middle age.

1:39:55unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

In a collegiate sleep education intervention among Division I athletes, time in bed increased by an average of 40 minutes and total sleep time increased by over an hour.

"I went into the university, into the Division I athletes across all the different sports... On average, time in bed increased by 40 minutes. Total sleep time increased by over an hour." (said at 1:39:55)

No published record matching the specific collegiate sleep intervention findings among Division I athletes (reporting an average 40-minute increase in time in bed and over an hour increase in total sleep time) was located; this does not prove the claim false.

1:43:50unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Melatonin lacks direct sedating properties and promotes wakefulness when administered to nocturnal animals.

"it has no sedating properties whatsoever. Melatonin doesn't. You give melatonin to a nocturnal animal, it wakes them up because it's a nighttime signal." (said at 1:43:50)

No published record matching the claim that melatonin lacks direct sedating properties and promotes wakefulness when administered to nocturnal animals was located; this does not prove the claim false.

1:44:25supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Melatonin is largely ineffective as a treatment for conditioned insomnia.

"It's also why it is almost universally useless for insomnia because if you have a conditioned arousal... taking melatonin is almost never going to work to treat an insomnia condition." (said at 1:44:25)

The claim that melatonin is largely ineffective as a treatment for adult chronic insomnia (often driven by conditioned psychophysiological arousal) is supported by meta-analytic evidence and clinical practice guidelines. Systematic reviews of randomized controlled trials demonstrate that exogenous melatonin does not produce significant improvements in sleep onset latency, total sleep time, or sleep efficiency in adults with chronic non-comorbid insomnia. Consequently, major medical organizations such as the American Academy of Sleep Medicine recommend against using exogenous melatonin for treating sleep-onset or sleep-maintenance insomnia in adults.

1:46:18supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

The intrinsic human circadian biological clock is slightly longer than 24 hours in almost everyone.

"It's a biological clock that is slightly longer than 24 hours in almost everybody. Not quite 25 hours, but somewhere in that gray zone." (said at 1:46:18)

Published circadian physiology research confirms that the intrinsic period (tau) of the human circadian biological clock is slightly longer than 24 hours in the vast majority of people. Early temporal-isolation experiments historically estimated the free-running period at approximately 25 hours due to confounding self-selected room lighting. Subsequent landmark forced-desynchrony protocol studies in stringently controlled low-light conditions established that the human endogenous circadian period across core body temperature, melatonin, and cortisol rhythms averages approximately 24.18 hours (about 24 hours and 11 minutes) with very low individual variability in both young and older adults.

1:47:25supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Administering a 0.3 to 0.5 mg dose of melatonin in the evening entrains the circadian clock in blind individuals with non-24-hour circadian rhythm disorder.

"What they found is you give someone a third to a half a milligram of melatonin in the evening and in a blind person fixes the whole thing. Sends the nighttime signal at the time when it needs to see it and the system responds beautifully to it." (said at 1:47:25)

The claim is supported by clinical trials demonstrating that low-dose melatonin (0.5 mg, or stepping down to 0.5 mg daily) entrains free-running circadian rhythms to a normal 24-hour cycle in totally blind individuals with Non-24-Hour Sleep-Wake Disorder. Clinical trials by Sack et al. (2000, 2001) and Hack et al. (2003) demonstrated that 0.5 mg daily doses of melatonin successfully entrained endogenous circadian markers (such as endogenous melatonin and cortisol rhythms) to a 24-hour period, both when stepped down from higher initial doses and when administered de novo. The body of evidence relies on small prospective clinical trials and crossover studies.

1:48:35supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Endogenous melatonin secretion typically begins 2 to 3 hours before habitual bedtime.

"usually 2 to 3 hours before your typical bedtime is when you start producing melatonin." (said at 1:48:35)

The claim is supported by clinical research evaluating circadian phase markers in healthy adults. Endogenous melatonin synthesis—measured experimentally as the dim light melatonin onset (DLMO)—typically begins approximately 2 hours (and commonly 2 to 3 hours) before an individual's habitual bedtime under normal entrainment.

1:55:09unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Continuous use of supplemental melatonin does not suppress or reduce endogenous melatonin production.

"to my knowledge, there is no data that shows that continual use of supplementary melatonin changes or or reduces your ability to naturally produce it at night." (said at 1:55:09)

No published record matching the claim that continuous supplemental melatonin use does not alter or suppress endogenous melatonin production was located; this does not prove the claim false.

1:56:35needs contextmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Bringing a new pharmaceutical drug to market costs approximately $2 billion and takes at least 10 years.

"why drugs are so expensive because it costs about $2 billion to bring a drug to market in 10 years at least." (said at 1:56:35)

Estimates of pharmaceutical R&D costs and timelines vary substantially based on methodology, therapeutic class, accounting for failed pipeline candidates, and the cost of capital. A systematic review found published capitalized R&D cost estimates ranging from $161 million to $4.54 billion per new molecular entity. A comprehensive study in JAMA analyzing FDA approvals from 2009–2018 estimated the median capitalized cost at $985.3 million and the mean at $1.34 billion, with certain therapeutic areas like oncology exceeding $2.77 billion. The average development timeline from discovery through approval typically spans 10 to 15 years. Thus, while ~$2 billion and ≥10 years represent commonly referenced benchmarks reflecting fully capitalized industry estimates (including failed drugs), actual R&D investments vary widely by drug class and study methodology.

1:59:10supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Pooled clinical data show that valerian root fails to outperform placebo for the treatment of insomnia.

"none of them have beaten placebo to treat insomnia. The closest that came was valerian. Um, but when you pool the data it still doesn't beat insomnia uh placebo for insomnia." (said at 1:59:10)

Multiple systematic reviews and meta-analyses of randomized controlled trials indicate that pooled clinical data do not demonstrate a statistically significant or clinically meaningful benefit of valerian root over placebo for insomnia on quantitative and objective sleep measures. While some early trials reported subjective dichotomous improvements, systematic reviews assessing quantitative endpoints (such as sleep latency, sleep architecture, and standardized sleep quality scales) found no significant difference compared with placebo, and methodologically rigorous trials consistently failed to show efficacy.

1:59:41supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Research demonstrates that dietary glycine supplementation helps individuals fall asleep and maintain sleep.

"Glycine, also great data on glycine showing that people who take glycine, it can help um fall asleep, help stay asleep a little bit better." (said at 1:59:41)

Human randomized cross-over trials and preclinical research demonstrate that dietary glycine supplementation (typically 3 g taken prior to bedtime) improves subjective sleep quality, shortens sleep onset latency, stabilizes sleep architecture, and reduces daytime sleepiness in individuals with sleep complaints or restricted sleep. Mechanistic studies indicate glycine promotes sleep onset and maintenance by acting on NMDA receptors in the suprachiasmatic nucleus, inducing peripheral vasodilation and a drop in core body temperature.

2:01:57supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Glycine promotes inhibitory neurotransmission to support sleep.

"Yeah, it does it does seem to promote that those inhibitory." (said at 2:01:57)

Glycine functions as a primary inhibitory neurotransmitter in the central nervous system via strychnine-sensitive glycine receptors. Research demonstrates that glycine enhances inhibitory neurotransmission—including directly hyperpolarizing and suppressing the firing of wake-promoting orexin neurons—which contributes to the promotion of non-rapid eye movement (NREM) sleep and improves overall sleep quality.

2:02:18unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Glutamine acts as an activating compound and can cause or exacerbate insomnia when taken at night.

"But if it's got a lot of glutamine in it, you want to not be using that because glutamine is is activating. And so, I mean, I've had athletes I've worked with who like complained about their insomnia. Turns out they're taking these nighttime supplements with a whole bunch of glutamine in it." (said at 2:02:18)

No published record matching the claim that oral glutamine supplementation acts as an activating compound to cause or exacerbate insomnia was located; this does not prove the claim false. While glutamine is biochemically involved in the central nervous system as a precursor for both excitatory glutamate and inhibitory gamma-aminobutyric acid (GABA), controlled human clinical trials demonstrating that oral glutamine intake induces wakefulness, central nervous system stimulation, or sleep disruption are lacking.

2:02:47supportedlowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Vitamin B12 enhances the capacity of light to suppress melatonin production.

"B12 help boosts the ability of light to suppress melatonin. You don't want to take that at night. You want to take that in the morning. B12 is great in the mornings. It can help wake you up a little more for a bunch of reasons, including its ability to help light suppress melatonin" (said at 2:02:47)

Small controlled crossover studies in healthy humans have found that vitamin B12 (methylcobalamin) enhances the sensitivity of the circadian clock to light. In a crossover trial of 9 healthy subjects (PMID: 1516676), nocturnal plasma melatonin levels during bright light exposure were significantly lower following 4 weeks of oral vitamin B12 supplementation (3 mg/day) compared to placebo. A subsequent trial in 8 young men (PMID: 8981490) demonstrated that vitamin B12 enhanced light-induced phase advances in melatonin rhythm. However, the certainty of this evidence is low due to small sample sizes and limited replication.

2:03:50unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

The sleep-promoting effects of THC diminish over a few weeks of use, leading users to escalate doses due to tolerance.

"One is that the sleep-promoting effects fade over time. So often it works great for a for a period of maybe a few weeks, but then you'll notice that it stops working in the same way. And so people start escalating doses for that reason." (said at 2:03:50)

No published record matching the claim that the sleep-promoting effects of THC diminish over a few weeks of use, leading users to escalate doses due to tolerance, was located; this does not prove the claim false.

2:04:14supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

THC is a potent suppressor of REM sleep in many individuals.

"Number two, in a lot of people, not doesn't seem to be everybody, but in a lot of people can be a very potent REM sleep suppressor." (said at 2:04:14)

The claim is supported by evidence demonstrating that tetrahydrocannabinol (THC) suppresses REM sleep in human studies, though responses vary depending on dose, habituation, and study design. A 2008 review notes that smoked marijuana and oral Delta-9-THC reduce REM sleep (PMID: 18313952). A randomized controlled trial in patients with insomnia similarly showed that acute oral administration of cannabinoids containing 10 mg THC significantly reduced time spent in REM sleep (-33.9 minutes) and prolonged latency to REM sleep (PMID: 40631525). However, a 2025 systematic review and meta-analysis notes that while early studies using high THC doses reported REM suppression, findings across broader therapeutic doses and populations are mixed, reflecting variability among individuals (PMID: 40967124).

2:04:24supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Antidepressants such as SSRIs can eliminate 50% to 75% of nightly REM sleep.

"most antidepressants are potent REM suppressors. Like you can knock out 50 to 75% of all your REM sleep of the night by taking like a Lexapro or an SSRI" (said at 2:04:24)

Selective serotonin reuptake inhibitors (SSRIs) such as escitalopram (Lexapro) and paroxetine, along with SNRIs and tricyclic antidepressants, are well-documented potent suppressors of rapid eye movement (REM) sleep. Polysomnography studies in humans demonstrate that acute administration of standard clinical doses of SSRIs significantly prolongs REM onset latency and substantially reduces total REM sleep duration, with acute reductions frequently reaching 40% to 70% or more, although partial adaptation typically occurs during chronic treatment.

2:04:54supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Cessation of THC induces rebound insomnia and REM rebound accompanied by vivid nightmares.

"when you stop using THC, you get, just like any kind of sedating medication, you get an insomnia rebound. And with that insomnia rebound, because it was a REM suppressor, you get a REM rebound. So you can get vivid nightmares and like really unpleasant dreams and the worst insomnia you've ever had." (said at 2:04:54)

Evidence from sleep architecture and substance withdrawal studies demonstrates that administration of THC or smoked cannabis reduces rapid eye movement (REM) sleep. Upon cessation or during acute withdrawal from cannabis/THC, individuals frequently experience sleep disturbances (including increased sleep onset latency and difficulty sleeping), an objective REM sleep rebound, and strange or vivid dreams/nightmares.

2:06:34unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Alcohol metabolism into acetaldehyde and acetate, along with hepatic glutamine rebound, stimulates the nervous system and causes nighttime awakenings.

"One of the reasons it does that is as the as the alcohol molecule metabolizes and becomes acetaldehyde, it can become a neural stimulant. The acetaldehyde could become acetate, which could become a neural stimulant, and as the liver is processing the alcohol, it can create a glutamine rebound, which can be activating." (said at 2:06:34)

No published record matching the claim that alcohol metabolism into acetaldehyde and acetate, along with a hepatic glutamine rebound, acts as a neural stimulant causing nighttime awakenings was located; this does not prove the claim false.

2:06:42supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Scientific studies on CBD and sleep show mixed results, with roughly half showing benefits and the other half showing no effect or worsened sleep.

"CBD is is a legit molecule, especially in terms of the things that it does, but the sleep data from CBD are extremely murky. Um, about about half the studies that have used CBD have shown that it could benefit sleep. Um, the other half don't. Some of them actually show that it makes sleep worse." (said at 2:06:42)

The speaker's characterization of the clinical data on CBD and sleep as "murky" and inconsistent is supported by systematic reviews and meta-analyses. A systematic review evaluating cannabidiol in insomnia management found that among studies performing hypothesis testing, 4 out of 7 CBD-predominant trials (~57%) reported significant improvements in sleep outcomes, while the remainder did not show statistically significant benefits. A meta-analysis of randomized controlled trials found that while non-CBD cannabinoids significantly improved subjective sleep quality, CBD-only therapies showed no overall statistically significant effect compared to placebo (SMD 0.13, p = 0.61). Broader systematic reviews similarly conclude that evidence supporting CBD alone for sleep disorders remains insufficient and equivocal.

2:09:08supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Caffeine concentrations in the body peak approximately 30 minutes after consumption.

"It picks up peaks at around 30-ish minutes, then trails off." (said at 2:09:08)

Pharmacokinetic studies in healthy adults demonstrate that immediate-release oral caffeine is rapidly absorbed, typically reaching peak plasma concentrations (Tmax) within approximately 30 to 60 minutes after ingestion under standard conditions.

2:09:54supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Caffeine increases fast-frequency EEG activity and reduces slow-wave and deep sleep.

"I mean it increases fast frequency EEG activity. So it'll make your sleep shallower. So it'll probably I mean I I'd have to look at the literature, but like if I had to make a prediction, my guess is it would dramatically reduce slow-wave sleep and deep sleep because you can't you can't get into that stage if your brain's sort of still wired and active." (said at 2:09:54)

Human polysomnography and quantitative sleep EEG studies consistently demonstrate that caffeine increases higher-frequency electroencephalographic activity (such as beta and sigma/spindle power) and suppresses low-frequency oscillations, specifically delta power, slow-wave activity, and slow-wave sleep (deep sleep). A systematic review of 32 human studies confirmed that caffeine reliably induces a lighter, more wake-like sleep EEG profile, attenuating homeostatic slow-wave expression.

2:12:15supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Laboratory sleep deprivation causes subjects to consume an average of 350 to 600 additional calories per 24 hours, predominantly through post-dinner snacking.

"when you in a sleep deprivation study, if you take somebody and you sleep deprive them, there have been a number of studies that did this and they look to see what you see what calories they're consuming. And on average, people tend to consume about 350 to 600 extra calories per 24 hours when you sleep deprive them in the lab. Not in the morning... but after dinner. That's when all the snacking, the extra snacking seems to occur." (said at 2:12:15)

Randomized controlled trials and meta-analyses confirm that experimental sleep restriction in laboratory settings causes a significant increase in daily caloric intake, with the excess energy intake occurring predominantly during the extended nocturnal wakefulness period (late-night/post-dinner snacking). While pooled meta-analyses of diverse sleep restriction protocols find average daily increases ranging between ~150 and 385 kcal/day, specific in-laboratory sleep restriction protocols frequently report increases between ~350 and 600 kcal/day, largely driven by late-night snacks.

2:13:28supportedlowtheir own paperWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Suicide rates between 2:00 AM and 5:00 AM spike to four times higher than expected by chance.

"all kinds of bad things like suicide spikes in that time four times greater than you would expect by chance than any other time of day." (said at 2:13:28)

The speaker's claim that suicide risk spikes during the middle of the night (between approximately 2:00 AM and 5:00 AM) to roughly four to five times higher than expected based on the proportion of the population awake is supported by epidemiologic research. Analysis of the National Violent Death Reporting System adjusted for population wakefulness (from the American Time Use Survey) demonstrates that after accounting for the number of people awake, suicide risk peaks in the early morning hours, showing an approximately 5-fold increase at 3:00 AM (adjusted IRR 5.20, 95% CI 4.74–5.70). Because this is based on observational and population-level ecological time-use data, the GRADE certainty is low.

2:13:36supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Alcohol decreases sleep latency and increases deep sleep during the initial part of the night.

"alcohol can make you fall asleep faster and actually sleep a little bit deeper in the very beginning of the night." (said at 2:13:36)

A comprehensive review of sleep laboratory studies in healthy individuals demonstrates that acute alcohol consumption across various dosages consistently reduces sleep onset latency (the time it takes to fall asleep) and increases slow-wave sleep (deep sleep) during the first half of the night, followed by sleep disruption and REM suppression later in the night.

2:15:48contradictedlowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

A complete sleep cycle lasts approximately 90 to 100 minutes during nocturnal sleep, but can take 2 to 3 hours during daytime sleep.

"In the middle of the at night, during your regular sleep period, that'll take, you know, 90 to 100 minutes. During the day, it might take two to three hours to make it all the way through" (said at 2:15:48)

While standard nocturnal sleep cycles typically last around 90 to 110 minutes in adult humans, available physiological sleep research shows that daytime sleep cycles do not lengthen to 2 to 3 hours. Experimental studies comparing sleep architecture across night-time and daytime sleep periods (e.g., daytime sleep following sleep deprivation or postponed sleep) indicate that the duration of individual NREM-REM sleep cycles remains relatively stable or even shortens, despite increases in slow-wave sleep intensity. No evidence supports the claim that daytime sleep cycles double or triple in duration to 2 to 3 hours.

2:16:05overstatedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Shift work is a known carcinogen and increases the risk of developing diabetes and dementia.

"shift work in general car- known carcinogenic. It increases diabetes risk, increases dementia risk. Like shift shift work isn't good." (said at 2:16:05)

The claim bundles three assertions. First, shift work is not classified as a 'known carcinogen' (IARC Group 1); rather, the International Agency for Research on Cancer (IARC) classified night shift work as 'probably carcinogenic to humans' (Group 2A) due to limited epidemiological evidence in humans alongside sufficient animal and mechanistic evidence. Second, large observational cohorts and meta-analyses support an increased risk of type 2 diabetes among shift workers (e.g., pooled hazard ratio ~1.30). Third, meta-analyses of observational studies demonstrate a modest but statistically significant positive association between shift work and the risk of dementia (pooled hazard ratio ~1.13). Because shift work is a probable rather than a confirmed/known carcinogen, the overall statement is overstated.

2:19:05overstatedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

In sleep-deprived individuals, a daytime nap significantly improves metabolism and muscle strength.

"there's data that shows like even in sleep-deprived people, a decent nap in the middle of the day can dramatically improve metabolism, muscle strength, all this stuff." (said at 2:19:05)

A meta-analysis of randomized controlled trials (PMID: 36690376) indicates that a daytime nap (30 to <60 minutes) provides moderate-to-large improvements in physical and cognitive performance (standardized mean difference = 0.99 for physical performance) and reduces perceived fatigue following normal sleep or partial sleep deprivation in athletic and active cohorts. However, characterizing this as a 'dramatic' improvement in both muscle strength and systemic metabolism overstates the magnitude and scope of the evidence; napping primarily acts as an acute restorative countermeasure to temporary performance deficits rather than substantially altering underlying metabolic function.

2:32:16supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Caffeine reaches peak effectiveness about 30 minutes after consumption and impairs sleep for at least six hours.

"I will drink coffee, and in about 30 minutes, it'll have its peak effectiveness, and for at least the next six hours I will not be in a sleep window." (said at 2:32:16)

Both components of the claim are supported by clinical trial evidence. Pharmacokinetic studies in healthy adults demonstrate that orally ingested caffeine is rapidly absorbed, reaching peak plasma concentration in approximately 30 minutes (29.8 ± 8.1 minutes). Furthermore, a randomized controlled crossover trial evaluating the timing of caffeine intake found that a moderate dose (400 mg) consumed 6 hours before bedtime significantly disturbed objective and subjective sleep parameters, providing empirical support for the recommendation to avoid caffeine for at least 6 hours before attempting to sleep.

2:33:31supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

The circadian literature indicates that it takes about an hour per day to adjust to time zone shifts, adjusting faster when traveling west than east.

"The circadian literature would say that it takes about an hour per day to adjust. Obviously faster going west, a little slower going east." (said at 2:33:31)

Circadian physiology literature supports the rule of thumb that the human circadian system resynchronizes at an average rate of approximately one time zone (hour) per day, and that adaptation is faster following westward travel (phase delay) compared to eastward travel (phase advance). Because the intrinsic human circadian period is slightly longer than 24 hours, phase delaying (traveling west) is easier for the endogenous circadian pacemaker than phase advancing (traveling east), resulting in more pronounced and prolonged circadian disruption following eastward flights.

2:37:50supportedlowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Oxygen dips naturally during sleep at night and serves as a circadian signal.

"oxygen itself is a circadian signal, because oxygen dips during the night when you're asleep." (said at 2:37:50)

Preclinical research demonstrates that tissue oxygen levels exhibit circadian rhythms (dipping during the rest/sleep phase along with reduced activity and respiration) and that physiological fluctuations in oxygen can reset circadian clocks in cells and rodent models through HIF1α signaling. However, evidence directly demonstrating oxygen-mediated clock synchronization is currently derived from animal and cell culture experiments.

2:40:00supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Blue-green light frequencies transmit information to the circadian clock.

"it's the blue-green frequency of light that sends information to the clock." (said at 2:40:00)

Circadian entrainment in humans and other mammals is primarily driven by intrinsically photosensitive retinal ganglion cells (ipRGCs) containing the photopigment melanopsin, which directly project to the master circadian clock in the suprachiasmatic nucleus (SCN). Action spectra for non-visual circadian responses (such as light-induced melatonin suppression and circadian phase resetting) demonstrate peak sensitivity in the short-wavelength blue to blue-green region of the visible spectrum (~446–484 nm, peaking near 480 nm).

2:42:12needs contextmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Wrist-based movement detection can determine whether someone is awake or asleep minute-to-minute with over 90% accuracy relative to EEG brain wave activity.

"You can predict with about 90% accuracy using movement alone. And this was analog devices with that were on a tape backup or eventually 64 kilobytes of memory on the whole watch. With that level of technology, you could get over 90% accuracy minute-to-minute: were you awake or were you probably asleep relative to brain wave activity?" (said at 2:42:12)

Wrist actigraphy validated against polysomnography (PSG, which utilizes electroencephalography/EEG) reliably demonstrates overall minute-by-minute epoch accuracy of approximately 85% to 90% in identifying sleep versus wake states. However, this high overall accuracy requires qualification: it is primarily driven by very high sensitivity for detecting sleep (typically 90% to 96%) during the sleep period, whereas the specificity for detecting wakefulness—particularly quiet, motionless wakefulness—is substantially lower (often 35% to 60%), leading to frequent misclassification of quiet wake as sleep.

2:42:12supportedhightheir own paperWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Wrist-based actigraphy to estimate sleep versus wake states has been utilized in research since the 1970s.

"People need to know that using wrist-based movement to estimate whether someone was asleep or awake across a night has been around since the 1970s." (said at 2:42:12)

The claim is accurate. Movement-based actigraphy to distinguish sleep from wake states was developed and validated in sleep research during the 1970s. Seminal validation studies published in the late 1970s demonstrated high correlations between wrist-worn piezoelectric transducers and gold-standard polysomnography (EEG/EOG/EMG) for estimating total sleep time and wakefulness during the sleep period.

2:42:45supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Wrist-movement-based sleep tracking underestimates wake time compared to EEG brain wave measurements, but overestimates wake time compared to self-report.

"it will underestimate wake time relative to looking at brain wave activity, but it will overestimate wake time versus your self-report." (said at 2:42:45)

The speaker's claim is supported by comparative validation studies evaluating wrist actigraphy alongside polysomnography (PSG) and self-reported sleep diaries. Wrist-movement-based sleep trackers (actigraphy) rely on motion; because individuals frequently remain still while awake in bed, actigraphy misidentifies quiet wakefulness as sleep, thereby underestimating wakefulness (such as wake after sleep onset, WASO) relative to EEG-based polysomnography. Conversely, self-reports and sleep diaries consistently underestimate night awakenings because individuals often do not recall brief awakenings during the night; as a result, wrist actigraphy reports significantly greater wake time than subjective self-report.

2:43:14supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Consensus sleep duration recommendations from the AASM and SRS are based on self-reported sleep duration data rather than objective wearable measurements.

"And those recommendations are not based on wearable data. They're based on, on average, how much sleep do you feel like you get? Because that is what's correlated with the health outcomes." (said at 2:43:14)

The 2015 joint consensus statement from the American Academy of Sleep Medicine (AASM) and the Sleep Research Society (SRS) on recommended sleep duration for healthy adults was developed via a modified RAND Appropriateness Method evaluating epidemiological and experimental literature. The epidemiological evidence linking sleep duration to mortality, cardiovascular disease, diabetes, obesity, and other chronic health outcomes was predominantly derived from self-reported habitual sleep duration questions rather than commercial wearable or continuous objective sensor measurements.

2:44:40supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Consumer wearable sleep staging algorithms have approximately 60% to 80% accuracy relative to polysomnography.

"The sleep staging data, it's a ballpark. It's actually better than a lot of sleep people assume that it is in terms of its level. It's probably between 60 and 80% accurate." (said at 2:44:40)

Validation studies comparing modern consumer wearable devices (such as Apple Watch, Fitbit, Oura Ring, and WHOOP) against polysomnography (PSG) show that sleep staging sensitivities and accuracies generally fall between 60% and 80% across various sleep stages, though performance varies by specific stage and device model.

2:46:16unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Commercial wearable sleep trackers cannot differentiate between stage 1 and stage 2 NREM sleep and combine them into a single light sleep category.

"first of all, it can't distinguish stage one and stage two at all. So they call it light usually" (said at 2:46:16)

No published record matching the claim that commercial wearable sleep trackers cannot differentiate between stage 1 and stage 2 NREM sleep and instead combine them into a light sleep category was located; this does not prove the claim false.

2:47:22supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Deep sleep detection on consumer wearable devices is only about 60% to 70% accurate at best in most people.

"And the deep sleep detection is only about 60 to 70% accurate at best in most people." (said at 2:47:22)

Validation studies and systematic reviews comparing commercial wearables (such as Fitbit, WHOOP, Garmin, Apple Watch, and Oura Ring) against the gold standard of polysomnography (PSG) demonstrate that epoch-by-epoch sleep-stage classification—particularly for deep sleep (slow-wave/N3 sleep)—exhibits moderate performance, typically achieving sensitivities, agreement rates, or F1 scores around 60% to 75%. While consumer devices provide reasonable estimates of aggregate total sleep time, distinguishing specific sleep stages like deep sleep remains limited to approximately 60% to 70% accuracy across most devices and users.

3:31:49supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Auditory neural stimulation can induce more deep sleep brainwave activity in healthy adults.

"But in healthy adults, there's some actually cool data on neural stimulation, where you can induce more deep sleep activity using auditory stimulation by sort of tricking your brain to create those waves." (said at 3:31:49)

Multiple randomized crossover experimental studies in healthy adults demonstrate that closed-loop auditory stimulation (CLAS)—brief auditory tones delivered in-phase with the up-states of ongoing slow oscillations during non-rapid eye movement (NREM) sleep—significantly increases slow-wave sleep activity and delta power.

3:33:02overstatedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Untreated sleep apnea is a leading cause of frequent nocturnal urination.

"Untreated sleep apnea is probably the leading cause of nocturnal frequent urination, because you keep having these arousals at night and your bladder is like, "Okay, while you're awake, might as well."" (said at 3:33:02)

Untreated obstructive sleep apnea (OSA) is a well-recognized, frequent contributor to nocturia (nocturnal frequent urination), and CPAP therapy often improves or resolves these symptoms. However, designating it as 'probably the leading cause' is overstated; nocturia is a multifactorial condition with several leading causes, including lower urinary tract dysfunction (such as benign prostatic hyperplasia and overactive bladder), cardiovascular disease, nocturnal polyuria from aging or diabetes, and diuretic use. Furthermore, the physiological driver in OSA is not merely waking up and deciding to void, but primarily inspiratory efforts against an occluded airway creating negative intrathoracic pressure, cardiac distension, and elevated release of atrial natriuretic peptide (ANP), which directly induces nocturnal polyuria.

3:34:09needs contextmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

The average person wakes up 10 times or more during the night.

"Remember what I said: the average person will wake up 10 times a night or more." (said at 3:34:09)

Polysomnographic sleep studies in healthy adults demonstrate that spontaneous brief nocturnal awakenings and transient micro-arousals occur routinely throughout normal sleep, frequently numbering 10 or more per night. However, this claim requires context: the vast majority of these nocturnal awakenings are brief physiological transitions lasting only seconds and are not consciously remembered upon waking.

3:35:00supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Eating late at night disturbs nocturnal sleep.

"People who eat like crap, especially late at night, their sleep is more disturbed at night." (said at 3:35:00)

Clinical and observational research demonstrates that consuming meals close to bedtime, as well as consuming poor-quality or ultra-processed diets in the evening, disrupts nocturnal sleep. A randomized crossover trial using sleep electroencephalography found that eating dinner 1 hour before bedtime significantly reduced total sleep time and sleep efficiency while increasing wakefulness after sleep onset, nocturnal arousals, and sleep stage shifts compared to eating 5 hours before bedtime. Larger population studies similarly associate late eating latency (less than 2 hours before sleep) and evening sleep-disturbing diets with increased sleep fragmentation and lower sleep quality.

3:35:15needs contextmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Reducing systemic inflammation in the body improves perceived sleep quality.

"Reduce systemic inflammation in your body, your sleep will feel better." (said at 3:35:15)

A robust body of evidence links systemic inflammation with sleep quality, but the relationship is predominantly established through observational and bidirectional associations. A comprehensive systematic review and meta-analysis of 72 studies (n > 50,000) found that sleep disturbance is significantly associated with higher circulating levels of systemic inflammatory markers, specifically C-reactive protein (CRP; effect size 0.12, 95% CI: 0.05–0.19) and interleukin-6 (IL-6; effect size 0.20, 95% CI: 0.08–0.31). While chronic low-grade inflammation correlates with disturbed sleep, stating definitively that lowering systemic inflammation directly improves subjective sleep quality simplifies a complex, bidirectional neuroimmune relationship that often depends on the underlying health condition and intervention type.

3:37:56supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Data shows no distinguishable difference in health outcomes between 7 and 8 hours of sleep in almost all cases.

"First of all, the recommendation these days is seven, because when we looked at the data, there was no distinguishable difference in almost all cases between seven and eight." (said at 3:37:56)

Major clinical guidelines and epidemiological meta-analyses support this statement. The American Academy of Sleep Medicine (AASM) and Sleep Research Society (SRS) consensus panel recommends that adults sleep 7 or more hours per night to promote optimal health, setting the threshold at 7 hours. Large prospective dose-response meta-analyses examining sleep duration and health outcomes (such as all-cause mortality and cardiovascular disease) consistently identify a U-shaped or J-shaped relationship where the lowest risk nadir spans 7 to 8 hours per night, with no meaningful difference in health risks between 7 and 8 hours.

3:38:20supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

At an average of six hours of sleep per night, people begin to show measurable problems on average.

"At six, people were starting to show problems on average." (said at 3:38:20)

The claim is supported by experimental sleep research. In a randomized controlled laboratory study of sleep restriction in healthy adults (Van Dongen et al., 2003), restricting sleep to 6 hours per night over 14 consecutive days resulted in cumulative, statistically significant deficits in neurobehavioral performance across all cognitive tasks compared to an 8-hour sleep baseline. Over two weeks, the cognitive deficits in the 6-hour sleep group accumulated to levels equivalent to those seen after up to two nights of total sleep deprivation.

3:38:25supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Athletes require more sleep than the general population due to a higher physiological load on their recovery systems.

"And athletes especially probably need more because they have a higher load on their recovery system." (said at 3:38:25)

The speaker's statement that athletes require more sleep due to higher physical and physiological recovery demands is supported by sports science literature. General adult guidelines recommend 7 to 9 hours of sleep per night, but athletes frequently report requiring greater amounts of sleep (typically >8 to 9+ hours) to achieve adequate physiological and psychological recovery and to feel fully rested, primarily due to the heavy physical training load, muscular repair, and metabolic demands placed on their bodies.

5:03:38supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

The term 'orthosomnia' was coined by Kelly Baron at the University of Utah to describe patients who fixate obsessively on sleep tracking data to the point of worsening their sleep.

"So that was a term developed, invented by a colleague of mine, Kelly Baron. She's at the University of Utah. She's like me, she studies sleep and sleep health and wearables and stuff. And so she came up with this idea, putting a name to what we would see in clinic of people who overly fixated on the data" (said at 5:03:38)

The term 'orthosomnia' was introduced by Kelly Baron and colleagues in a 2017 paper published in the Journal of Clinical Sleep Medicine. The authors coined the term to describe patients whose preoccupation and perfectionistic fixation on consumer sleep tracking data led to self-diagnosed sleep disturbances, anxiety, and worsening insomnia.

5:07:50overstatedlowtheir own paperWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

A comprehensive literature review led by Teresa Arora found that improving sleep consistently leads to improvements in physical and emotional resilience across studies.

"A colleague of mine, Teresa Arora, she led this project that I also helped on. We looked at... We basically scoured the entire medical literature on resilience and sleep... And basically what we found was across the board, people... If you can sleep better, your resilience will improve." (said at 5:07:50)

A 2022 systematic review and meta-analysis led by Teresa Arora (PMID 35462348) examined the relationship between sleep duration/quality and resilience across 68 studies in non-clinical populations. The meta-analysis identified a weak positive correlation between sleep duration and resilience (r = 0.11) and a modest correlation with sleep quality (r = 0.27; attenuated to r = 0.18 in prospective studies), alongside evidence of significant publication bias. The authors noted that the literature is predominantly observational and cross-sectional, concluding that additional prospective and interventional research is needed to verify whether improving sleep directly improves resilience.

5:09:20supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Extending sleep to 9 to 10 hours in young adult athletes who normally sleep 6 to 7 hours improves their speed, strength, and mental sharpness.

"there have been studies where they're already sleeping maybe six, seven hours, if you get them up to like 9, 10 hours, they're faster, they're stronger, they're mentally sharper." (said at 5:09:20)

Published intervention studies in collegiate and young athletes support the claim that extending sleep duration to 9 to 10 hours improves sprint speed, reaction time, cognitive functioning, and sport-specific performance. In a foundational study of collegiate basketball players whose baseline sleep was approximately 6.5 to 7 hours, extending time in bed to a minimum of 10 hours per night for several weeks significantly improved timed sprint speeds, shooting accuracy, reaction times on the Psychomotor Vigilance Task (PVT), and self-reported physical and mental well-being. Systematic reviews of sleep interventions in athletic populations confirm that sleep extension is among the most effective non-pharmacological strategies to enhance physical, neuromuscular, and cognitive performance.

5:11:13supportedhighWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

California enacted legislation requiring high school start times to be no earlier than 8:30 a.m.

"and California led the way on this. California took the step and at least pushed it to 8:30, right?" (said at 5:11:13)

California became the first state in the United States to mandate later school start times with the passage of Senate Bill 328 (SB 328) in 2019. The law established that public high schools (grades 9–12) may not begin instruction earlier than 8:30 a.m., with middle schools starting no earlier than 8:00 a.m., fully taking effect across the state by the 2022–2023 school year.

5:13:51supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

The circadian rhythm delay naturally peaks in early adulthood around age 22.

"This delay seems to peak in the early 20s, like 22, but then after that, like you can..." (said at 5:13:51)

Large epidemiological chronotype studies show that human circadian rhythms undergo a developmental phase delay across adolescence that peaks in late adolescence to early adulthood (around ages 19 to 21, varying slightly by sex, with men peaking later than women around age 20–21) before shifting progressively earlier throughout adulthood. Analysis of large population datasets confirms that chronotype lateness reaches its maximum between ages 19 and the early 20s before reversing.

5:13:51supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Athletes are, on average, less likely to be late chronotypes (night owls) compared to non-athletes of the same age.

"And we did this study looking at this... It's called chronotype, which is sort of where in the 24 hours are you. Chronotype in athletes... athletes tend to be on average not as much of a night owl as typical people their age, right?" (said at 5:13:51)

Studies comparing university student athletes to non-athlete peers find that athletes on average score higher on morningness preferences (earlier chronotypes) and are less likely to report an evening chronotype compared to non-athletes of the same age group, though intermediate chronotypes remain common in both groups.

5:19:43needs contextlowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Drivers who obtain only 5 or 6 hours of sleep are three times more likely to nod off behind the wheel, even if they report feeling fully well-rested.

"Like even if you say you're fully well-rested, if you're getting five or six hours of sleep, you are three times as likely to nod off behind the wheel even if you say, 'I am 100% well-rested.'" (said at 5:19:43)

Epidemiological and laboratory studies demonstrate that sleeping fewer than 6 to 7 hours significantly increases the risk of drowsy driving and falling asleep behind the wheel, and that subjective perceptions of alertness become uncoupled from objective vulnerability to sleepiness during chronic sleep restriction. However, the specific claim of an exact threefold increased risk of nodding off specifically among drivers who report feeling '100% well-rested' is an overstatement of the exact point estimate, even though the underlying phenomenon (increased risk of falling asleep despite lack of perceived sleepiness) is documented in observational driver surveys.

5:21:26supportedlowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

In a study of Division I athletes, high insomnia severity and daytime sleepiness were stronger predictors of future concussions than prior concussion history, male sex, or sport risk category.

"And what we found was prior concussion history, being male, and being in a high-risk sport were the three biggest predictors of concussions, except for the sleep variables. Having a high insomnia severity—which is a questionnaire we use to see like how much is your insomnia interfering with your functioning during the day and how much is it stressful for you—and daytime sleepiness, saying at least two days a week, I think it was a week, at least two days in a period, 'I'm having trouble staying awake,' those two, not amount of sleep, but those two were better predictors of whether you were going to get a concussion than even the concussion variables." (said at 5:21:26)

A prospective study of 190 NCAA Division I collegiate athletes evaluated sleep and concussion risk. Moderate-to-severe insomnia symptoms on the Insomnia Severity Index (RR = 3.13, 95% CI 1.32–7.42, p = 0.015) and excessive daytime sleepiness occurring two or more times per month (RR = 2.86, 95% CI 0.68–11.98, p = 0.037) significantly increased the risk of sustaining a future sports-related concussion. These sleep variables remained independent, significant predictors in multivariable models adjusted for sport participation and prior concussion history.

5:23:32unverifiedvery lowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

In a study of Major League Baseball players by Ben Potenziano, players scoring in the clinical range (over 10) on a baseline daytime sleepiness scale had a 75% rate of dropping out of the majors at follow-up.

"He worked with Major League Baseball. He still works in pro sports. He's a great guy. But he did this project where he gave sleepiness questionnaires to a whole bunch of MLB players. Followed them up a couple years later—I don't remember exactly the time frame—just looked to see who's still in the majors, and you could see dose-response: every one point extra increase on that scale, the likelihood of no longer being in the majors. And the ones who were in the clinical range, who scored over a 10 at that baseline time, 75% of them were not in the majors anymore." (said at 5:23:32)

No published record matching the specific study or reported statistics by Ben Potenziano on daytime sleepiness scores and MLB career dropout rates was located; this does not prove the claim false. While presentations and conference abstracts have explored sleep metrics and athletic longevity in professional baseball, peer-reviewed published data verifying this exact study and the reported 75% attrition figure for scores over 10 were not found in indexed literature.

5:25:32needs contextmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Restricting semi-professional tennis players to 5 hours of sleep impaired their serving accuracy by approximately 35%, and caffeine only recovered about one-third of that lost accuracy.

"there's this great study where they did in tennis players, semi-pro tennis players serving. When they took them down to 5 hours of sleep, it impaired their serving accuracy by, if I remember correctly, something like 35%. It recovered—about a third of the loss was recovered when they caffeinated, but not all of it" (said at 5:25:32)

A randomized crossover study by Reyner and Horne (2013) evaluated the effects of 5 hours of sleep restriction on serving accuracy in semi-professional tennis players. The authors confirmed significant impairments in serving accuracy following sleep restriction. However, contrary to the claim that caffeine recovered about one-third of the lost accuracy, the trial found that an 80 mg dose of caffeine had no statistically significant beneficial effect on restoring serving accuracy.

5:26:33supportedmoderateWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Wearing a cloth eye mask during sleep improved sleep consolidation and led to better test scores the following day compared to a placebo eye mask with cut-out holes.

"some of the best sleep technology on the market, simple cloth eye mask. There was a study, I think it was in Switzerland, where they had an eye mask, just a plain old cloth eye mask, and they had a placebo eye mask where they cut the holes out in the middle. Same strap, just cut the holes out. Improved sleep consolidation during the night. These weren't college students, so they were in sort of noisy environments anyway, but consolidated their sleep better in the night, translated to better test scores the next day." (said at 5:26:33)

A 2023 study published in Sleep tested wearing an eye mask during overnight sleep compared to a control mask with cut-out eye holes. Across two experiments in young adults (18-35 years old), wearing the intact eye mask to block ambient light led to superior episodic memory encoding (word-pair association and reaction-time learning tasks) and improved alertness the following day. Sleep monitoring in the second experiment demonstrated that the cognitive benefit was specifically predicted by time spent in slow-wave sleep.

5:27:19overstatedlowWhy You Can’t Sleep (and How to Fix It) | Dr. Michael Grand

Sleeping with a pet or other animal in the bedroom increases sleep fragmentation.

"Anyone who has an animal in their room, another mammal in their room moving around... You're going to have more fragmented sleep." (said at 5:27:19)

While objective actigraphy studies confirm that an animal's nighttime movements can trigger awakenings or movement transitions in humans—particularly when sharing the same bed—the claim that having an animal anywhere in the room universally fragments sleep is overstated. An actigraphy study of 40 adults found that having a single dog in the bedroom did not significantly impair sleep efficiency, whereas having the dog directly on the bed did reduce sleep efficiency. Other observational studies show that while bed-sharing and owning multiple pets are associated with poorer objective sleep parameters and subjective sleep quality, having a pet simply present in the bedroom does not consistently cause sleep disruption.

Fact-checked episodes

Publications