Complete Circadian Alignment Bundle (pre-order)

Complete Circadian Alignment Bundle (pre-order)

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1,500+ People Resetting Their Body Clock

Sleep Disruption Is a Timing Problem.

Measurable biomarker results within 7 nights.

The 3AM wakeup. 

Lying awake before sleep arrives. Waking exhausted after a full night in bed.

These are not random events. 

They are not inevitable signs of aging. 

They are measurable biomarker signals from a circadian clock that has drifted off its biological schedule.

Take the Free Circadian Alignment Quiz — 2 Minutes →

Identify the specific biomarker disruption driving the pattern. Personalized Circadian Drift Score delivered instantly.

*These statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, cure, or prevent any disease.

The Body Runs a 24-hour Biological Program. Most People Are Operating on a Drifted Clock and Don't Know It.

The human body does not simply "fall asleep" and "wake up." It runs a tightly sequenced 24-hour hormonal program governed by a central pacemaker in the brain called the suprachiasmatic nucleus, or SCN.

The SCN[1][2] coordinates the release and withdrawal of every major hormone across the day. Cortisol peaks in the first 30 minutes after waking[4][5]. Core body temperature rises through the morning, peaks in the early afternoon, and begins a gradual decline toward sleep. Melatonin production begins in the early evening, triggered by darkness and peaks during the night[6][7] before withdrawing ahead of the next morning's cortisol rise.

This is not a passive process. It is a precisely timed biological sequence. When the timing is accurate, the system operates invisibly. When it drifts, everything downstream degrades.

Circadian disruption is not insomnia. It is not a sleep disorder in the clinical sense. It is a
calibration problem — a shift in the timing of biological signals that moves the body's internal
clock out of alignment with the external environment.

The most common indicators of circadian drift are the patterns most people have normalized
as simply "the way things are":

Sleep latency — the body is in bed but the biological signal for sleep onset[6][7] has not yet arrived. The clock is running late.

WASO events — Wake After Sleep Onset. The circadian trough phase when sleep should be deepest, has lost stability[8][9]. The 3AM wakeup is not random. It is a timing failure.

Blunted morning energy — the Cortisol Awakening Response is firing at reduced amplitude[4][5][21][22]. The body arrives at morning without its primary activating signal.

Afternoon energy crashes — a severe circadian dip signals the morning CAR was insufficient to carry the system through the full day cycle.

Fatigue without restoration — 8 hours in bed without sufficient N3 deep sleep[8][10[11]. The hours are there. The sleep architecture is not.

None of these patterns are random. Each one maps to a specific point in the 24-hour sequence where a timing signal has arrived late, fired at insufficient amplitude, or been suppressed by a competing biological input.

Circadian disruption is a measurable calibration problem with a measurable biological cause. The patterns most people attribute to aging, stress, or genetics are frequently outputs of a clock that has drifted and a clock that has drifted can be recalibrated.

Stress Does Not Just Cause Poor Sleep. It Directly Suppresses the Biological Signal That Initiates It.

This is a documented hormonal mechanism, not a lifestyle observation.

The most commonly identified trigger for circadian disruption is stress. But the mechanism by which stress degrades sleep is specific and it is not the one most people assume.

Stress does not simply make the mind "too active to sleep." Stress activates the HPA axis[17][18] the hypothalamic-pituitary-adrenal system which responds by maintaining elevated cortisol levels into the evening hours.[17][20]

Cortisol and melatonin operate on a direct inverse relationship[19]. The body cannot run both simultaneously at full amplitude. As evening cortisol remains elevated, the pineal gland delays melatonin production DLMO shifts later.[6][7][19]

This single mechanism — elevated evening cortisol suppressing DLMO[17][19] — is the upstream cause of the majority of circadian disruption patterns that present as "sleep problems."

What this looks like in measurable biomarker terms:

DLMO (Dim Light Melatonin Onset) fires 60-90 minutes later than the biological optimum[6][7]. The body is in bed before the biological signal for sleep has arrived.

N3 slow-wave sleep compresses[8][10][11]. When DLMO is late, the body enters deep sleep later and exits it sooner. Cellular repair and immune consolidation are cut short.[10]

The circadian trough phase (approximately 2-4AM) becomes unstable[8][9]. This is the window when consolidated sleep should be deepest. When it is poorly anchored, WASO events occur.

The Cortisol Awakening Response (CAR) fires at reduced amplitude[4][5][22] the following morning. A night of fragmented sleep suppresses the quality of the next day's activating signal. The cycle compounds.

Heart Rate Variability (HRV) declines[15][16]. The nervous system is not completing the parasympathetic recovery cycle that consolidated sleep provides.

This is a closed biological loop. Each disrupted night sets up the conditions for the following disrupted night. The mechanism is upstream. The solution has to be upstream as well.

The patterns most commonly treated as sleep problems are frequently circadian calibration problems. The distinction is clinically significant because the intervention that addresses a calibration problem is fundamentally different from one that addresses a sedation problem.

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Magnesium Activates Gaba. Melatonin Delivers a Signal. Neither Restores the Clock That Generates It.

Two of the most widely used sleep supplements in the world address the symptom layer of sleep disruption.

Magnesium operates at the onset layer, it does not address WASO events in the second half of the night, stabilize the circadian trough phase, or restore the morning cortisol signal that anchors the following day's rhythm.

Melatonin introduces exogenous hormone into a system designed to produce that hormone endogenously. At the doses commonly sold over the counter, supplemental melatonin suppresses natural DLMO production over time[22][24]. The timing problem that generated the disruption remains unaddressed.

Dependence is a property of substitution. When the body receives a biological signal externally, it reduces its own production[23][24]. The clock does not recalibrate. It waits for the next dose.

75% of Circadia founding members had already tried magnesium or melatonin before the Reset Protocol. The reason those approaches produced inconsistent results is biological they were addressing the alarm, not the clock.

The Body Has a 24-hour Master Clock. When It Drifts, Every Downstream Biomarker Drifts With It.

Stress is the most common driver. Evening cortisol is the primary mechanism behind delayed sleep onset.

The SCN[1][2][3] (suprachiasmatic nucleus) is the central pacemaker of human biology. Every downstream process runs on timing signals it generates: hormone secretion, immune regulation, metabolic function, cognitive performance.

Sleep is one output of this system. Not the system itself.

The SCN synchronizes through two primary biological inputs called zeitgebers. The morning light signal initiates the Cortisol Awakening Response (CAR)[4][5][21][22]. The evening DLMO window[6][7] triggers the biological shift toward sleep.

When either signal drifts, the cascade follows a predictable biological sequence:

Chronic stress keeps cortisol elevated into the evening.[17][18]

Elevated evening cortisol suppresses melatonin onset. This is the cortisol-melatonin antagonism[19] — the primary mechanism behind delayed sleep onset.

DLMO fires late[6]. Sleep latency extends. The N3 deep sleep window compresses.[8][11]

The circadian trough phase destabilizes[8][9]. WASO events follow. The 3AM wakeup is not random it is a measurable clinical indicator.

Morning arrives without a calibrated CAR[4][22]. The day signal is blunted. Caffeine fills the gap, masking the biomarker rather than restoring it.

Evening cortisol remains elevated. The cycle repeats.

The five primary circadian biomarkers: DLMO timing[6][7], CAR amplitude[4][5], WASO frequency[8][9], N3 sleep architecture depth[8][10], and nighttime HRV[15][16][25]. All measurable via Oura, WHOOP, or Apple Watch.

Uninterrupted Sleep Requires Two Calibrated Timing Signals. Most Protocols Address Zero.

The circadian rhythm requires an accurate start signal and an accurate stop signal every single day to maintain synchronization.

The start signal - the Cortisol Awakening Response[4][5][21]. The sharp cortisol spike within 30 minutes of waking that anchors the biological day and determines when sleep pressure builds later that night.

The stop signal — DLMO[6][7]. The neurochemical event generated by the SCN that initiates the shift from wakefulness to consolidated sleep. When DLMO is delayed, sleep latency extends and sleep architecture fragments.

Standard interventions address neither signal at the source. The Circadia Reset Protocol was

built specifically around this gap.

AM Rise targets the morning CAR window. PM Drift targets the evening DLMO window.

Together they create the bookend signals the master clock requires.

The 30-Day AM + PM Circadian Reset Protocol

Two formulas. Two minutes a day. Two ends of the circadian rhythm addressed simultaneously.

The Circadia Reset Protocol is not a sleep supplement. It is a time-targeted circadian support system built around the biological architecture of the 24-hour rhythm.

The protocol runs for 30 days — the window the clinical literature identifies as required for meaningful circadian realignment in a drifted system.

It pairs both formulas with two behavioral anchors: 15 minutes of morning light exposure during the AM Rise window, and a consistent wind-down period during the PM Drift window. The ingredients support the biology. The behavioral consistency is the entrainment mechanism.

AM Rise targets the morning CAR window. PM Drift targets the evening DLMO window.

Together they create the bookend signals the master clock requires.

The goal is not better sleep as a feeling. The goal is a master clock that runs accurately, and the measurable downstream biomarker outcomes that follow.

AM Rise — Morning Calibration Formula.

Supports the Cortisol Awakening Response and daytime circadian signal. Peach Tea. 30 Servings.

The morning signal determines the entire 24-hour rhythm. Not just the morning.

A calibrated CAR within the first 30 minutes of waking[4][5] initiates the hormonal cascade governing energy, cognitive activation, and metabolic function, and establishes the timing reference point from which DLMO will fire that evening.

One scoop in cold water. Consistent timing every morning.

L-Theanine (100mg)[26][27] — calm, focused alertness without overstimulation. Supports the natural morning cortisol rise.

Ashwagandha KSM-66 (300mg)[28][29] — supports healthy cortisol regulation throughout the day. Helps prevent cortisol from staying elevated into the evening, the primary upstream mechanism behind delayed DLMO.

Rhodiola Rosea (200mg, 3% rosavins)[30][31] — adaptogenic support for mental energy and stress resilience during the morning activation window.

Vitamin D3 (1000 IU)[32][33] — supports the photoreceptor pathways activated by morning light. Reinforces the biological day signal. Critical during low-light seasons in Canada and Australia.

Magnesium Glycinate (50mg)[38][40] — low morning dose for neuromuscular support and stress buffer. Distinct in dose and function from the PM formula.

Zinc (10mg)[34] — supports healthy cortisol and CAR amplitude. Zinc deficiency is directly linked to blunted morning biomarker output.[34]

Vitamin B6 P-5-P (25mg)[35] — cofactor in serotonin synthesis. A strong morning serotonin signal is required for healthy DLMO production later that evening.

Alpha GPC (150mg)[36][37] — supports morning cognitive activation and acetylcholine production. Addresses the morning fog pattern that follows fragmented or insufficiently deep sleep.

Take AM Rise within 30 minutes of waking. Mix one scoop in cold water. For optimal results, consume during 15 minutes of morning natural light exposure.

PM Drift — Evening Reset Formula.

Supports DLMO onset timing, cortisol wind-down, and N3 sleep architecture. Honey Citrus Chamomile. 30 Servings.

The night signal has a precise biological window. Most sleep interventions miss it entirely.

When DLMO fires at the correct time, the cortisol-melatonin transition occurs without resistance[6][19]. Sleep onset arrives on schedule. The trough phase stabilizes. WASO events reduce. N3 deep sleep, responsible for cellular repair and immune consolidation[10][11], is protected through the full cycle.

When DLMO is delayed, the sleep transition shifts later, the trough phase destabilizes, and the 3AM wakeup follows.

One scoop in water, 60-90 minutes before target sleep time.

Magnesium Glycinate (300mg elemental)[38][39][40] — primary evening ingredient. Activates GABA receptors to support neurological wind-down. Glycinate form maximizes absorption without digestive side effects.

L-Theanine (200mg)[26][27][41] — at double the AM dose, promotes alpha brain wave activity, the state of relaxed wakefulness that precedes natural sleep onset. Addresses the tired-but-wired pattern.

Lemon Balm Extract (300mg, 10:1)[42][43] — supports GABA activity and calm without sedation. OTC compliant across US, Canada, and Australia.

Ashwagandha KSM-66 (300mg)[28][29] — evening dosing targets the cortisol decline required for DLMO to fire on time. The direct intervention point in the cortisol-melatonin antagonism.

L-Glycine (2000mg)[44][45][46] — supports core body temperature reduction, the primary physiological trigger for sleep onset and N3 maintenance[44][45]. Strong clinical literature at this dose.

Apigenin (50mg)[47][48][49] — active compound in chamomile. Binds GABA-A receptors without dependency or tolerance development[47][48]. Does not suppress the body's own GABA production.

Tart Cherry Extract (200mg, Montmorency 10:1)[50][51] — food-derived melatonin precursor support. Does not introduce exogenous melatonin. Supports the body's own DLMO production pathway.

Zinc (5mg)[34][52] — supports the enzymatic conversion of serotonin to melatonin in the pineal gland[34][52]. Targets the body's own DLMO generation at the source.

Take PM Drift 60-90 minutes before target sleep time. Dim overhead lighting. Minimize bright screen exposure. The environmental reduction in light and the formula operate as a combined DLMO-supporting signal.

Two Minutes a Day. Two Ends of the 24-Hour Rhythm. One Synchronized Clock.

The protocol is simple by design. The master clock synchronizes through repeated, predictable timing signals. Complexity undermines consistency. Consistency is the entrainment mechanism.

Morning: AM Rise within 30 minutes of waking. One scoop in cold water. 15 minutes of natural light exposure. The same time every day.

Evening: PM Drift 60-90 minutes before target sleep time. One scoop in water. Lights

dimmed. Screens reduced. The same time every night.

Both actions take under two minutes. The ritual itself is a circadian reinforcement signal the body learns to anticipate the wind-down sequence with the same biological predictability it uses to anticipate sunrise.

No stacking. No complex supplement schedule. Two products. Two windows. The full 24-hour rhythm addressed from both ends simultaneously.

What a Synchronized Clock Produces and When

Circadian realignment is measurable, not subjective. Track results via Oura, WHOOP, or Apple Watch.

  • DAY 7

  • DAY 14

  • DAY 30

  • DAY 90

Measurable reduction in WASO events and sleep latency.[8][9]

  • DLMO window begins shifting earlier.[6][7]
  • Sleep onset arrives sooner. 
  • Nighttime wakeup frequency begins declining. 
  • Detectable in the first week of tracking data.

Measurable recovery in nighttime Heart Rate Variability.[15][16][25]

HRV is a direct biomarker of autonomic nervous system regulation and circadian alignment.

Improvement at day 14 indicates the master clock is beginning to synchronize its downstream hormonal outputs.

Restored N3 deep sleep architecture[8][10][11] and improved sleep efficiency.

  • Sleep cycles complete without fragmentation. 
  • The trough phase holds stability through the full night.
  • The master clock is no longer drifting.

Reduced systemic inflammatory biomarkers.

Chronic circadian disruption is linked in peer-reviewed literature to elevated CRP and IL-6.[12][13][14][53]

As the clock stabilizes, these inflammatory markers begin declining. 

A synchronized clock is a systemic health architecture, not just a sleep intervention.

The goal is not better sleep. The goal is a clock that runs accurately, and the compounding downstream biomarker outcomes that follow. Track the data. The protocol is measurable.

A Reset Protocol and a Nightly Supplement Are Not the Same Mechanism.

This is not a supplement designed to be taken indefinitely. It is a protocol with a finish line.

Dependence is a property of substitution. When the body receives a biological signal from an external source, it reduces its own production of that signal. This is standard physiological adaptation.

Substitution provides the signal the body should be generating and bypasses the system that generates it.

Entrainment reinforces the timing inputs the master clock uses to synchronize, restoring the body's own capacity to generate the signal on schedule.

Every ingredient in PM Drift is selected on this principle. L-Glycine supports thermoregulation[44][45]. Tart Cherry provides melatonin precursors, not melatonin itself.[50][51] Apigenin binds GABA-A receptors without suppressing the body's own GABA production[47][48]. Ashwagandha supports the cortisol decline that allows natural DLMO to fire on time.[28][29]

The 30-day protocol provides consistent timing reinforcement until the master clock has rebuilt its own entrainment capacity. Then the protocol is complete.

The goal is a biological clock that operates independently, not one that requires nightly intervention to maintain function.

What Happens When the Clock Starts Running on Time.

"After years of 3AM wakeups and nightly melatonin, the realization that changed everything was not a new product, it was a different

understanding of the problem. Within the first week of the protocol, the nighttime wakeups stopped. By week two, the morning fog was gone. Waking up before the alarm, not because of discipline, because the clock was finally running on schedule."

— Carolyn R., 54 — Ontario, Canada

"The Oura data told the story. HRV up 22% at day 14. Deep sleep from 9% to 17% over 30 days. Those are not subjective impressions. Those are biomarker measurements. Magnesium and melatonin never produced a number that could be pointed to. This did."

— James T., 61 — Phoenix, Arizona

"The standard in any credible health intervention is ingredient source

disclosure, third-party testing, and a mechanistic explanation that holds up to scrutiny. Circadia provided all three before purchase. Deep sleep moved from 11% to 19% over 30 days."

— Michelle K., 47 — Seattle, Washington

The Reason Prior Approaches Did Not Hold Is Biological, Not Personal.

Magnesium, melatonin, and sleep hygiene protocols are effective at what they are designed to do. The limitation is not quality it is the layer of the problem they address.

When the master clock has drifted significantly, the disruption has moved upstream of what surface-layer interventions can correct. The clock is the upstream variable. Everything else is downstream of it.

The Circadia Reset Protocol addresses six biological metrics that standard approaches do not reach:

Upstream Master Clock (SCN) — targeted through timed AM and PM formulas that reinforce entrainment signals at both ends of the 24-hour cycle.

Natural DLMO Timing — supported through cortisol reduction and the melatonin precursor pathway. The body generates its own DLMO signal rather than receiving it externally.

N3 Deep Sleep Architecture — protected through L-Glycine's temperature reduction mechanism and stabilized trough phase through the full night.

Morning CAR Activation — supported within the critical 30-minute post-waking window. The morning signal that determines the quality of the following night.

WASO Event Reduction — addressed through trough phase stabilization, not onset sedation.

Biological Entrainment — the clock learns to run on an accurate schedule without requiring ongoing external input to maintain it.

Prior protocols produced inconsistent results because the intervention was applied at the symptom layer of a problem that originates at the timing layer. Addressing the alarm without addressing the clock produces temporary relief. Addressing the clock produces durable outcomes.

One Protocol. One Purchase. No Subscription Required.

The pre-order is a single transaction. No automatic subscription. No recurring billing. No cancellation system to navigate.

$1 holds a founding member kit. $79.99 is charged at shipment only. Cancel any time before shipping for a full $1 refund.

The reset model is built around a 30-day protocol with a defined endpoint. If a subsequent cycle is desired after reviewing the results, that decision is made by the person who completed the protocol with full biomarker data in hand.

The Last Plan You'll Ever Need to Achieve Circadian Alignment

With a consistent personalised routine and based on your answers; early improvements often show up in 3–7 days, with noticeably steadier sleep timing in 4–6 weeks. The goal is reliability and stability, not perfection.

Week 1
Week 2
Week 3
Week 4
Week 6
Week 8

What this means: the biggest change usually comes from aligning signals (morning light, consistent wake time, and dim evenings). Supplements can support the routine, but the signals steer the timing.

Educational only. Individual results vary based on schedule consistency, light exposure, stress, and habits.

Reserve a Founding Member Kit for $1.

200 founding member slots. 147 reserved.

$1 holds the kit. $79.99 charged at shipment. Cancel before shipping — full $1 refund.

The founding member kit includes:

AM Rise

Morning Calibration Formula. Peach Tea. 30 servings.

PM Drift

Evening Reset Formula. Honey Citrus Chamomile. 30 servings.

Foundations of Human Circadian Rhythm

the complete reference guide to the biology behind the protocol.

4-Week Personal Circadian Alignment Program

structured week-by-week guide built from the quiz results profile.

Circadia Canister

complimentary with founding member orders.

Circadia Orbit Bottle

Bonus: for founding members

Hold My Founding Member Kit for $1 →

Non-habit forming | Every dose disclosed | Cancel before shipment for full refund

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Circadia Reset supports healthy circadian rhythm function. It is not a treatment for insomnia, sleep apnea, or any medical sleep disorder. Consult a qualified healthcare provider before use if pregnant or breastfeeding, if a hormone-sensitive condition or thyroid disorder is present, or if prescription medications including antidepressants or MAO inhibitors are currently in use. Individual results vary. Results depend on consistent daily use in accordance with the full AM/PM protocol. Contains no melatonin. Non-habit forming. OTC compliant in the United States, Canada, and Australia.

Scientific References with Verified Sources

CIRCADIAN BIOLOGY & SCN

[1] Colwell, C.S. (2011) 'Linking neural activity and molecular oscillations in the SCN', Nature Reviews Neuroscience, 12(10), pp. 553–569. PubMed PMID 21886186

[2] Hastings, M.H., Maywood, E.S. and Brancaccio, M. (2018) 'Generation of circadian rhythms in the suprachiasmatic nucleus', Nature Reviews Neuroscience, 19(8), pp. 453–469. PubMed PMID 29934559

[3] Saper, C.B., Scammell, T.E. and Lu, J. (2005) 'Hypothalamic regulation of sleep and circadian rhythms', Nature, 437(7063), pp. 1257–1263. PubMed PMID 16251950

CORTISOL AWAKENING RESPONSE (CAR)

[4] Fries, E., Dettenborn, L. and Kirschbaum, C. (2009) 'The cortisol awakening response (CAR): facts and future directions',

Neuroscience & Biobehavioral Reviews, 33(7), pp. 1045–1053. PubMed PMID 18854200

[5] Stalder, T. et al. (2016) 'Assessment of the cortisol awakening response: expert consensus guidelines', Psychoneuroendocrinology, 63, pp. 414–432. PubMed PMID 26563991

DIM LIGHT MELATONIN ONSET (DLMO)

[6] Pandi-Perumal, S.R. et al. (2007) 'Dim light melatonin onset (DLMO): a tool for the analysis of circadian phase', Progress in Neuro-Psychopharmacology and Biological Psychiatry, 31(1), pp. 1–11. DOI: 10.1016/j.pnpbp.2006.06.020

[7] Lewy, A.J. et al. (2006) 'Circadian uses of melatonin in humans', Chronobiology International, 23(1–2), pp. 403–412. DOI: 10.1080/07420520500521657

N3 DEEP SLEEP ARCHITECTURE & WASO

[8] Dijk, D.J. (2009) 'Regulation and functional correlates of slow wave sleep', Journal of Clinical Sleep Medicine, 5(2 Suppl), pp. S6–S15. PMC2824213

[9] Ohayon, M.M. et al. (2004) 'Meta-analysis of quantitative sleep parameters across the human lifespan', Sleep, 27(7), pp. 1255–1273. DOI: 10.1093/sleep/27.7.1255

CELLULAR REPAIR & GLYMPHATIC CLEARANCE

[10] Xie, L. et al. (2013) 'Sleep drives metabolite clearance from the adult brain', Science, 342(6156), pp. 373–377. PubMed PMID 24136970

[11] Tasali, E. et al. (2008) 'Slow-wave sleep and the risk of type 2 diabetes in humans', Proceedings of the National Academy of Sciences, 105(3), pp. 1044–1049. PubMed PMID 18172212

INFLAMMATION — CRP & IL-6

[12] Irwin, M.R., Olmstead, R. and Carroll, J.E. (2016) 'Sleep disturbance, sleep duration, and inflammation: a systematic review and meta-analysis', Biological Psychiatry, 80(1), pp. 40–52. PubMed PMID 26140821

[13] Meier-Ewert, H.K. et al. (2004) 'Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk', Journal of the American College of Cardiology, 43(4), pp. 678–683. PubMed PMID 14975479

[14] Wright, K.P. Jr. et al. (2015) 'Influence of sleep deprivation and circadian misalignment on cortisol, inflammatory markers, and cytokine balance', Brain, Behavior, and Immunity, 47, pp. 24–34. PubMed PMID 25640603

HEART RATE VARIABILITY (HRV)

[15] Stein, P.K. and Pu, Y. (2012) 'Heart rate variability, sleep and sleep disorders', Sleep Medicine Reviews, 16(1), pp. 47–66. PubMed PMID 21658979

[16] Boudreau, P. et al. (2013) 'Circadian variation of heart rate variability across sleep stages', Sleep, 36(12), pp. 1919–1928. PubMed PMID 24293767

HPA AXIS & CORTISOL-MELATONIN ANTAGONISM

[17] Vgontzas, A.N. et al. (2001) 'Chronic insomnia is associated with nyctohemeral activation of the hypothalamic-pituitary-adrenal axis', Journal of Clinical Endocrinology & Metabolism, 86(8), pp. 3787–3794. DOI: 10.1210/jcem.86.8.7778

[18] Balbo, M., Leproult, R. and Van Cauter, E. (2010) 'Impact of sleep and its disturbances on hypothalamo-pituitary-adrenal axis activity', International Journal of Endocrinology, 2010, 759234. PMC2895944 (Open Access)

[19] Kellner, M. et al. (1997) 'Corticotropin-releasing hormone inhibits melatonin secretion in healthy volunteers', Neuroendocrinology, 65(4), pp. 284–290. PubMed PMID 9143000

[20] Leproult, R. et al. (1997) 'Sleep loss results in an elevation of cortisol levels the next evening', Sleep, 20(10), pp. 865–870. DOI: 10.1093/sleep/20.10.865

EXOGENOUS MELATONIN & ENDOGENOUS SUPPRESSION

[21] Clow, A. et al. (2010) 'The cortisol awakening response in context', International Review of Neurobiology, 93, pp. 153–175. PubMed PMID 20970005

[22] Thosar, S.S. et al. (2022) 'The circadian system modulates the cortisol awakening response in humans', Frontiers in Neuroscience, 16, 932354. PubMed PMID 3640839

[23] Buscemi, N. et al. (2006) 'Efficacy and safety of exogenous melatonin for secondary sleep disorders: meta-analysis', BMJ, 332(7538), pp. 385–393. PMC1370968 (Open Access)

[24] Vural, E.M., van Munster, B.C. and de Rooij, S.E. (2014) 'Optimal dosages for melatonin supplementation therapy in older adults', Drugs & Aging, 31(6), pp. 441–451. DOI: 10.1007/s40266-014-0178-0

[25] Shaffer, F., McCraty, R. and Zerr, C.L. (2014) 'A healthy heart is not a metronome: an integrative review of heart rate variability', Frontiers in Psychology, 5, 1040. PMC4179748 (Open Access)

L-THEANINE

[26] Nobre, A.C., Rao, A. and Owen, G.N. (2008) 'L-theanine, a natural constituent in tea, and its effect on mental state', Asia Pacific Journal of Clinical Nutrition, 17(Suppl 1), pp. 167–168. PubMed PMID 18296328

[27] Hidese, S. et al. (2019) 'Effects of L-theanine administration on stress-related symptoms and cognitive functions in healthy adults: a randomized controlled trial', Nutrients, 11(10), 2362. PMC6836118 (Open Access)

ASHWAGANDHA KSM-66 (WITHANIA SOMNIFERA)

[28] Chandrasekhar, K., Kapoor, J. and Anishetty, S. (2012) 'A prospective, randomized double-blind placebo-controlled study of ashwagandha root in reducing stress and anxiety', Indian Journal of Psychological Medicine, 34(3), pp. 255–262. PubMed PMID 23439798

[29] Lopresti, A.L. et al. (2019) 'An investigation into the stress-relieving and pharmacological actions of an ashwagandha (Withania somnifera) extract', Medicine, 98(37), e17186. PubMed PMID 31517876

RHODIOLA ROSEA

[30] Panossian, A. and Wikman, G. (2010) 'Effects of adaptogens on the central nervous system', Pharmaceuticals, 3(1), pp. 188–224. PMC3991026 (Open Access)

[31] Darbinyan, V. et al. (2000) 'Rhodiola rosea in stress induced fatigue — a double blind cross-over study', Phytomedicine, 7(5), pp. 365–371. DOI: 10.1016/S0944-7113(00)80055-0

VITAMIN D3

[32] Gominak, S.C. and Stumpf, W.E. (2012) 'The world epidemic of sleep disorders is linked to vitamin D deficiency', Medical Hypotheses, 79(2), pp. 132–135. PubMed PMID 22583560

[33] Majid, M.S. et al. (2018) 'The effect of vitamin D supplement on sleep quality in 20–50 year-old people with sleep disorders', Nutritional Neuroscience, 21(7), pp. 511–519. DOI: 10.1080/1028415X.2017.1317395

ZINC & VITAMIN B6 (P-5-P)

[34] Sandyk, R. and Anastasiadis, P.G. (1990) 'Is zinc deficiency related to pineal dysfunction?', International Journal of Neuroscience, 54(3–4), pp. 357–369. PubMed PMID 2203916

DIET, SEROTONIN & SLEEP

[35] Peuhkuri, K., Sihvola, N. and Korpela, R. (2012) 'Diet promotes sleep duration and quality', Nutrition Research, 32(5), pp. 309–319. DOI: 10.1016/j.nutres.2012.03.009

ALPHA-GPC

[36] Parker, A.G. et al. (2015) 'The effects of alpha-glycerylphosphorylcholine on markers of mood, cognitive function, power, speed, and agility', Journal of the International Society of Sports Nutrition, 12(Suppl 1), P41. DOI: 10.1186/1550-2783-12-S1-P41

[37] De Jesus Moreno Moreno, M. (2003) 'Cognitive improvement in mild to moderate Alzheimer's dementia after treatment with choline alfoscerate', Clinical Therapeutics, 25(1), pp. 178–193. DOI: 10.1016/S0149-2918(03)90023-3

MAGNESIUM GLYCINATE

[38] Abbasi, B. et al. (2012) 'The effect of magnesium supplementation on primary insomnia in elderly', Journal of Research in Medical Sciences, 17(12), pp. 1161–1169. PubMed PMID 23853635

[39] Lopresti, A.L. et al. (2025) 'Magnesium bisglycinate supplementation in healthy adults reporting poor sleep: a randomized, placebo-controlled trial', Nature and Science of Sleep, 17, pp. 163–173. PubMed PMID 40918053

[40] Arab, A. et al. (2023) 'The role of magnesium in sleep health: a systematic review', Biological Trace Element Research, 201(1), pp. 121–128. DOI: 10.1007/s12011-022-03162-1

LEMON BALM (MELISSA OFFICINALIS)

[41] Lyon, M.R. et al. (2011) 'The effects of L-theanine on objective sleep quality in boys with ADHD', Alternative Medicine Review, 16(4), pp. 348–354. PubMed PMID 22214254

[42] Kennedy, D.O., Little, W. and Scholey, A.B. (2004) 'Attenuation of laboratory-induced stress in humans after acute administration of Melissa officinalis', Psychosomatic Medicine, 66(4), pp. 607–613. PubMed PMID 15272110

L-GLYCINE

[43] Cases, J. et al. (2011) 'Pilot trial of Melissa officinalis leaf extract in volunteers suffering from mild-to-moderate anxiety and sleep disturbances', Mediterranean Journal of Nutrition and Metabolism, 4(3), pp. 211–218. DOI: 10.3233/s12349-010-0045-4

[44] Bannai, M. and Kawai, N. (2012) 'New therapeutic strategy for amino acid medicine: glycine improves the quality of sleep', Journal of Pharmacological Sciences, 118(2), pp. 145–148. PubMed PMID 22293292

[45] Kawai, N. et al. (2015) 'The sleep-promoting and hypothermic effects of glycine are mediated by NMDA receptors in the suprachiasmatic nucleus', Neuropsychopharmacology, 40(6), pp. 1405–1416. PubMed PMID 25533534

[46] Bannai, M. et al. (2012) 'The effects of glycine on subjective daytime performance in partially sleep-restricted healthy volunteers', Frontiers in Neurology, 3, p. 61. PubMed PMID 22529837

APIGENIN & CHAMOMILE

[47] Avallone, R. et al. (2000) 'Pharmacological profile of apigenin, a flavonoid isolated from Matricaria chamomilla', Biochemical Pharmacology, 59(11), pp. 1387–1394.

PubMed PMID 10751547

[48] Braun, L.S. et al. (2024) 'Apigenin: a natural molecule at the intersection of sleep and aging', Frontiers in Nutrition, 11, 1359176. PubMed PMID 38476603

[49] Zick, S.M. et al. (2011) 'Preliminary examination of the efficacy and safety of a standardized chamomile extract for chronic primary insomnia', BMC Complementary and Alternative Medicine, 11, p. 78. PMC3198755 (Open Access)

TART CHERRY (PRUNUS CERASUS)

[50] Howatson, G. et al. (2012) 'Effect of tart cherry juice (Prunus cerasus) on melatonin levels and enhanced sleep quality', European Journal of Nutrition, 51(8), pp. 909–916. PubMed PMID 22038497

[51] Burkhardt, S. et al. (2001) 'Detection and quantification of the antioxidant melatonin in Montmorency and Balaton tart cherries', Journal of Agricultural and Food Chemistry, 49(10), pp. 4898–4902. PubMed PMID 11600041

MELATONIN PATHWAY & PINEAL FUNCTION

[52] Zhdanova, I.V. et al. (2001) 'Melatonin treatment for age-related insomnia', Journal of Clinical Endocrinology & Metabolism, 86(10), pp. 4727–4730. DOI: 10.1210/jcem.86.10.7901

SYSTEMIC CONSEQUENCES OF SLEEP DEPRIVATION

[53] Mullington, J.M. et al. (2009) 'Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation', Progress in Cardiovascular Diseases, 51(4), pp. 294–302. PMC3428710 (Open Access)

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