By Patrick Holford
Sleep is how the brain recovers. There is now overwhelming evidence that sleep is a ‘brain essential’ and just like Goldilocks, it seems we need just the right amount. Getting too much, or too little, increases our risk for cognitive decline.
The optimal amount of sleep for brain health appears to be a total of seven hours. This does not necessarily need to be in one uninterrupted stretch – a study found that napping after physical activity can reduce the risk of cognitive impairment (1).
However, those consistently getting less than seven hours of sleep may be doubling their risk of age-related cognitive decline (2). A UK study of Whitehall civil servants, which began in the 1980s, found that persistent short sleep at ages 50, 60, and 70 was associated with a 30% increased risk of dementia (3). Sleep loss does not just increase long-term dementia risk – it also reduces empathy, increases negative emotions, and impairs next-day functioning (4).
Think of sleep as the brain’s housekeeper. During sleep, circulation of blood and cerebrospinal fluid improves, helping to clear out waste products from brain metabolism (5). These include harmful oxidants and amyloid protein, the latter linked to Alzheimer’s and brain inflammation – which can begin accumulating after just one night of poor sleep (6).
One key agent in this nightly brain cleanse is melatonin. As night falls, our brains convert serotonin into melatonin, primarily in the pineal gland – referred to by Descartes as the seat of the soul, and known in yoga as the ‘third eye’ chakra.
Sensitive to light via receptors behind the eyes, the pineal gland is the only endocrine organ in direct contact with the external world. Darkness triggers melatonin production, while exposure to light – including screen use before bed – suppresses it.
Melatonin helps keep us in sync with the circadian cycle. Some frequent flyers even use melatonin supplements to overcome jet lag and adjust their sleep rhythms more easily (7).
More than just a sleep aid, melatonin acts as a powerful antioxidant – disarming damaging oxidants, restoring mitochondrial energy production, and acting as an anti-inflammatory. It has been used to support recovery in cancer, COVID-19, and cardiovascular conditions (8,9). Reduced brain melatonin levels and circadian disruption are also observed in individuals with cognitive decline.
Sleep isn’t just for rest – it’s a deeply active process. About 30 minutes after falling asleep, we enter deep sleep, marked by slower breathing, a reduced heart rate, and lower blood pressure. This phase restores and repairs bodily tissues. About 90 minutes in, we shift into REM (rapid eye movement) sleep – where most dreaming occurs.
REM sleep is critical for brain health. Each night, we cycle between deep, light, and REM sleep three to five times, with REM ideally making up about 25% of total sleep.
REM and deep sleep phases also see increased production of growth hormone, which supports tissue repair. Meanwhile, melatonin helps clear metabolic waste. However, under stress, cortisol levels rise and suppress REM sleep and growth hormone production, reducing the brain’s ability to recover. Sleep-deprived individuals tend to experience more REM when they finally do sleep, suggesting REM plays a key role in emotional processing.
One theory suggests that dreams help us metabolise suppressed emotions – fear, anger, sadness – stored during our busy days. If you have a vivid, emotional dream, it may be worth tracing it back to unresolved feelings from the previous day.
Chronic or intense stress – such as bereavement, illness, or financial strain – has been shown to increase the risk of cognitive decline and dementia (10). However, good sleep can help process a stressful day.
The perception of control matters, too. Studies show that high job demands combined with low control are strongly linked to an increased risk of depression and cognitive impairment (11). Examples might include caregiving for a loved one with dementia while navigating health services, or working in a high-stress job without the resources to make meaningful changes.
Two hormones mediate stress: adrenaline (short-acting) and cortisol (longer-acting). Adrenaline prepares you to act quickly – it’s the fight-or-flight hormone. Cortisol helps regulate energy and alertness throughout the day.
In the morning, cortisol naturally rises to get us going. It should fall in the evening to support sleep. But chronic stress disrupts this rhythm. If cortisol stays high at night, sleep is disturbed. If it’s too low in the morning, you may feel foggy and reach for caffeine.
Excess cortisol impairs memory, slows thinking, lowers social functioning, and raises the risk of dementia (12). What’s happening in the brain is that cortisol overstimulates the hippocampus, which is responsible for memory and emotional regulation. With prolonged stress, this feedback loop fails – the hippocampus shrinks, and cortisol levels remain elevated, accelerating brain ageing.
Oscar Ichazo described how we reach for compensations under stress. Unfortunately, many – like alcohol and sugar – backfire.
Alcohol temporarily boosts GABA, calming the nervous system and reducing adrenaline. But the effect is short-lived. Drinking too much reduces GABA receptor sensitivity the next day, leaving us more anxious. In the long term, alcohol is neurotoxic and increases dementia risk (12). It also disrupts sleep architecture, impairing the brain’s ability to repair itself.
Sugar triggers dopamine and activates the brain’s reward circuits, making us crave more. It also spikes the adrenal system, amplifying stress and cortisol levels (13). Fats and proteins do not have this effect – this is unique to sugar.
So, when we use sugar or alcohol to manage stress, we often wake up feeling more anxious and foggy. This leads us to reach for caffeine and more sugar, which spikes cortisol again, leaving us even more depleted by evening – creating a cycle of stress, poor sleep, and accelerated brain ageing.
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2 Bubu OM, Brannick M, Mortimer J, Umasabor-Bubu O, Sebastião YV, Wen Y, Schwartz S, Borenstein AR, Wu Y, Morgan D, Anderson WM. Sleep, Cognitive impairment, and Alzheimer’s disease: A Systematic Review and Meta-Analysis. Sleep. 2017 Jan 1;40(1). doi: 10.1093/sleep/zsw032. PMID: 28364458.
3 Sabia S, Fayosse A, Dumurgier J, van Hees VT, Paquet C, Sommerlad A, Kivimäki M, Dugravot A, Singh-Manoux A. Association of sleep duration in middle and old age with incidence of dementia. Nat Commun. 2021 Apr 20;12(1):2289. doi: 10.1038/s41467-021-22354-2. PMID: 33879784; PMCID: PMC8058039.
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56 Xie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, O’Donnell J, Christensen DJ, Nicholson C, Iliff JJ, Takano T, Deane R, Nedergaard M. Sleep drives metabolite clearance from the adult brain. Science. 2013 Oct 18;342(6156):373-7. doi: 10.1126/science.1241224. PMID: 24136970; PMCID: PMC3880190.
6 Shokri-Kojori E, Wang GJ, Wiers CE, Demiral SB, Guo M, Kim SW, Lindgren E, Ramirez V, Zehra A, Freeman C, Miller G, Manza P, Srivastava T, De Santi S, Tomasi D, Benveniste H, Volkow ND. β-Amyloid accumulation in the human brain after one night of sleep deprivation. Proc Natl Acad Sci U S A. 2018 Apr 24;115(17):4483-4488. doi: 10.1073/pnas.1721694115. Epub 2018 Apr 9. PMID: 29632177; PMCID: PMC5924922.
7 Herxheimer A, Petrie KJ. Melatonin for the prevention and treatment of jet lag. Cochrane Database Syst Rev. 2002;(2):CD001520. doi: 10.1002/14651858.CD001520. PMID: 12076414.
8 Keithahn C, Lerchl A. 5-hydroxytryptophan is a more potent in vitro hydroxyl radical scavenger than melatonin or vitamin C. J Pineal Res. 2005 Jan;38(1):62-6. doi: 10.1111/j.1600-079X.2004.00177.x. PMID: 15617538.
9 Chitimus DM, Popescu MR, Voiculescu SE, Panaitescu AM, Pavel B, Zagrean L, Zagrean AM. Melatonin’s Impact on Antioxidative and Anti-Inflammatory Reprogramming in Homeostasis and Disease. Biomolecules. 2020 Aug 20;10(9):1211. doi: 10.3390/biom10091211. PMID: 32825327; PMCID: PMC7563541; regarding covid see also Tan DX, Reiter RJ. Mechanisms and clinical evidence to support melatonin’s use in severe COVID-19 patients to lower mortality. Life Sci. 2022 Apr 1;294:120368. doi: 10.1016/j.lfs.2022.120368. Epub 2022 Jan 30. PMID: 35108568; PMCID: PMC8800937.; see also Begum R, Mamun-Or-Rashid ANM, Lucy TT, Pramanik MK, Sil BK, Mukerjee N, Tagde P, Yagi M, Yonei Y. Potential Therapeutic Approach of Melatonin against Omicron and Some Other Variants of SARS-CoV-2. Molecules. 2022 Oct 16;27(20):6934. doi: 10.3390/molecules27206934. PMID: 36296527; PMCID: PMC9609612.; regarding cancer see Reiter RJ, Rosales-Corral SA, Tan DX, Acuna-Castroviejo D, Qin L, Yang SF, Xu K. Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis. Int J Mol Sci. 2017 Apr 17;18(4):843. doi: 10.3390/ijms18040843. PMID: 28420185; PMCID: PMC5412427.
10 Franks KH, Bransby L, Saling MM, Pase MP. Association of Stress with Risk of Dementia and Mild Cognitive Impairment: A Systematic Review and Meta-Analysis. J Alzheimers Dis. 2021;82(4):1573-1590. doi: 10.3233/JAD-210094. PMID: 34366334.
11 Wang HX, Wahlberg M, Karp A, Winblad B, Fratiglioni L. Psychosocial stress at work is associated with increased dementia risk in late life. Alzheimers Dement. 2012;8(2):114-20. doi: 10.1016/j.jalz.2011.03.001. PMID: 22404853; see also Gonzalez-Mulé, E., & Cockburn, B. S. (2021). This job is (literally) killing me: A moderated-mediated model linking work characteristics to mortality. Journal of Applied Psychology, 106(1), 140–151. https://doi.org/10.1037/apl0000501; see also Gonzalez-Mulé E, Kim MM, Ryu JW. A meta-analytic test of multiplicative and additive models of job demands, resources, and stress. J Appl Psychol. 2021 Sep;106(9):1391-1411. doi: 10.1037/apl0000840. Epub 2020 Sep 21. PMID: 32955269.
12 Ouanes S, Popp J. High Cortisol and the Risk of Dementia and Alzheimer’s Disease: A Review of the Literature. Front Aging Neurosci. 2019 Mar 1;11:43. doi: 10.3389/fnagi.2019.00043. PMID: 30881301; PMCID: PMC6405479.13 Gonzalez-Bono E, Rohleder N, Hellhammer DH, Salvador A, Kirschbaum C. Glucose but not protein or fat load amplifies the cortisol response to psychosocial stress. Horm Behav. 2002 May;41(3):328-33. doi: 10.1006/hbeh.2002.1766. PMID: 11971667.
