ByDarko Savic
How can people contribute to humanity's quest for biological immortality?
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Deru Xu Aug 26, 2020
How does sleep time affect aging? How to sleep better?
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With the development of society and science and technology, people have less and less sleep time, and the tendency to stay up late is on the rise. However, sleep is necessary to maintain normal physiological activities. Sleep refers to a natural physiological phenomenon of humans and animals. What is the relationship between sleep and aging?
First of all, we need to understand the benefits of sleep:
- Energy can be saved through sleep.Brain glycogen is the main energy reserve of the brain. As the time of awakening is extended, the level of brain glycogen gradually decreases, and the level of brain glycogen can be restored after sleep.
- Sleep can promote the excretion of metabolites.During the day, metabolites in the brain continue to accumulate, and during sleep, the brain can efficiently remove metabolites and restore brain vitality.
- Enhance immune function. Many people may have the experience that people will want to sleep when they have a cold, fever or other diseases. This is actually one of the body's protective reactions, because adequate sleep can enhance immunity and speed up the body's recovery.
- Sleep can promote growth and development. Slow wave sleep period is the main period that affects the secretion of growth hormone, so good sleep is the key to ensuring growth and development.
- Sleep can also enhance the ability of learning and memory. Sleep is one of the necessary conditions for long-term memory consolidation.
The University of California San Diego School of Pharmacy and the American Cancer Society conducted a six-year trial. They observed one million subjects between the ages of 30 and 102. The experiment took into account factors such as age, medical history, and health of the research subjects. They were compared with subjects whose physical condition was similar. Studies have found that people who sleep only 6 or 7 hours a day have a much lower mortality rate than those who sleep more than 8 hours or less than 4 hours a day. Among them, those who sleep 7 hours a day have the lowest mortality rate, and even those who sleep only 5 hours have a lower coefficient than those who sleep enough for 8 hours. Although the research institution said that more evidence is needed to prove the causal relationship between mortality and sleep time, but this undoubtedly gives us a new reminder: how long do we need to sleep?
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Irregular sleep is associated with but not causal to aging
A research group performed a meta-analysis of studies identifying an association between sleep duration and all-cause mortality. Most studies indicated an optimum sleep time of 7-8 hours. The results suggested that people who slept for less than 7 hours were 1.12 more likely to die during the follow-up period and those who slept for more than 8 hours were 1.3 times more likely to die compared to those who slept for 7 – 8 hours. [1]
A more recent study reported that 55% of the long-lived people (median age 97 years) studied slept more than 8 hours daily and 28% of them napped, when they were around 70 years old. Napping was associated with insulin resistance among the control subjects (aged 70 years), but not the offspring (aged 70 years) of the long-lived people. Also, the controls who napped were 2.79 times more likely to have hypertension, myocardial infarction, stroke, or diabetes compared to the offspring of the long-lived people. Moreover, there was no association between sleep duration and health in long-lived people. These results suggested that although the long-lived subjects slept more than 8 hours when they were 70, they are somehow protected from age-related diseases. [2] Another study provided evidence that prolonged sleep duration was associated with frailty in an elderly population aged 70 to 87 years. [3]
Overall, it seems that long-lived people are protected (against all-cause mortality) by mechanisms/ habits other than regular sleep patterns.
References:
1. Cappuccio FP, D’Elia L, Strazzullo P, Miller MA. Sleep Duration and All-Cause Mortality: A Systematic Review and Meta-Analysis of Prospective Studies. Sleep [Internet]. 2010 May;33(5):585–92. Available from: https://academic.oup.com/sleep/article-lookup/doi/10.1093/sleep/33.5.585
2. Klein L, Gao T, Barzilai N, Milman S. Association between Sleep Patterns and Health in Families with Exceptional Longevity. Front Med [Internet]. 2017 Dec 8;4. Available from: http://journal.frontiersin.org/article/10.3389/fmed.2017.00214/full
3. Sun X-H, Ma T, Yao S, Chen Z-K, Xu W-D, Jiang X-Y, et al. Associations of sleep quality and sleep duration with frailty and pre-frailty in an elderly population Rugao longevity and ageing study. BMC Geriatr [Internet]. 2020 Dec 6;20(1):9. Available from: https://bmcgeriatr.biomedcentral.com/articles/10.1186/s12877-019-1407-5
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The Amount of Sleep We Need May Depend on Our Genes
Ying-Hui Fu and colleagues looked at the genes of family members that could function normally on 4 ½ hours of sleep. It was found that these individuals had a mutation in the ADRB1 gene (A187V) which encodes adrenoceptor beta 1 (a beta-adrenergic receptor). Then Fu and colleagues bred rats with the ADRB1 gene mutation (A187V). It was found that these rats slept nearly 1 hour less each day compared to the controls! [1] So it seems that the mutation in the ADRB1 gene enhances alertness and individuals with this specific mutation can last on fewer hours of sleep!
It is great that these individuals can last on fewer hours of sleep, but I do wonder what the consequences of this are on their overall health. Does the ADRB1 mutation (A187V) have any impact on their lifespan?! What does their epigenetic age look like? I haven’t seen any research studies using this specific mutation for lifespan studies yet.
1. Shi, Guangsen, et al. "A rare mutation of β1-Adrenergic receptor affects sleep/wake behaviors." Neuron 103.6 (2019): 1044-1055.
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Impact of Aging on Sleeping Behaviours
Non-pathological changes in sleep occur across the normal aging process. Older adults experience shorter total sleep time (TST) than younger adults, with total sleep time decreasing until about age 60, then stabilizing through the later decades of life. This may be due to a combination of physiological changes in sleep, changes in sleep-related habits, and increased rates of sleep disorders. [1]
In addition to changes in sleep architecture that occur as we age, other factors affecting sleep are the circadian rhythms that coordinate the timing of our bodily functions, including sleep. For example, older people tend to become sleepier in the early evening and wake earlier in the morning compared to younger adults. [2] This pattern is called advanced sleep phase syndrome. The sleep rhythm is shifted forward so that 7 or 8 hours of sleep are still obtained but the individuals will wake up extremely early because they have gone to sleep quite early. The reason for these changes in sleep and circadian rhythms as we age is not clearly understood. Many researchers believe it may have to do with light exposure and treatment options for advanced sleep phase syndrome typically include bright light therapy. [3]
The prevalence of insomnia is also higher among older adults. According to NSF’s (National Sleep Foundation ) 2003 Sleep in America poll, 44% of older persons experience one or more of the nighttime symptoms of insomnia at least a few nights per week or more.[4] Insomnia may be chronic (lasting over one month) or acute (lasting a few days or weeks) and is oftentimes related to an underlying cause such as a medical or psychiatric condition.[5]
Across the aging process, normal changes to sleep occur, including shorter night time total sleep time, decreased time in slow-wave and REM ( Rapid Eye Movement) sleep, increased sleep-onset latency, and increased arousals following sleep onset. Daytime napping is also increased. Melatonin secretion is reduced, and the circadian rhythm becomes weaker and advances.[6] Although these changes are non-pathological, sleep apnea, insomnia, circadian rhythm sleep-wake disorders, and parasomnias are frequently observed in this population. Because many sleep disturbances are attributable to underlying conditions and medications in older adults, medical evaluation and treatment of identified contributing factors is necessary. Thorough sleep history is important in the assessment of all sleep disorders. A sleep diary, supplemented with actigraphy or caregiver report, provides information helpful in diagnosing insomnia and circadian rhythm disorders, and a sleep study is needed to diagnose sleep apnea, PLMD (Periodic Limb Movement Disorder ) , and RBD (REM behaviour Disorder ), which must be completed with EEG ( Electro Encephalo Gram ) and EMG ( Electromyography ). HSAT( Home Sleep Apnea Test ) may be used but may require follow-up PSG ( Polysomnography ) , particularly in this population who may have difficulty using HSAT ( Home Sleep Apnea Test ). [7]
PAP therapy, along with behavioral changes specific to the individual's sleep habits, is recommended for sleep apnea. Insomnia is treated with sleep restriction, or sleep compression in individuals susceptible to adverse events resulting from increased daytime sleepiness, stimulus control, sleep hygiene, and other behavioral and cognitive techniques based on the patient’s presentation. Few treatments are well-studied in CRSWD ( Circadian Rhythm Sleep-Wake Disorder ) in older adults, but evening light therapy may be helpful in delaying circadian rhythms. RLS is treated pharmacologically and may improve with lifestyle changes. There is little evidence to support treatments for PLMD (Periodic Limb Movement Disorder ), but identification and treatment of underlying conditions and discontinuation of certain medications may improve symptoms. Behavioral interventions to increase safety in combination with clonazepam or melatonin are the primary treatment approaches to RBD. [8]
References
1: Adler CH, Thorpy MJ. Sleep issues in Parkinson's disease. Neurology. 2005;64(12 suppl):S12–20.
2: Alessi C, Martin JL, Fiorentino L, Fung CH, Dzierzewski JM, Rodriguez Tapia JC, Song Y, Josephson K, Jouldjian S, Mitchell MN. Cognitive behavioral therapy for insomnia in older veterans using nonclinician sleep coaches: randomized controlled trial. J Am Geriatr Soc. 2016;64(9):1830–8. PMC5351772
3: Alessi CA, Martin JL, Webber AP, Kim EC, Harker JO, Josephson KR. Randomized controlled trial of a nonpharmacological intervention to improve abnormal sleep/wake patterns in nursing home residents. J Am Geriatr Soc. 2005;53(5):619–26.
4: Allen RP, Chen C, Garcia-Borreguero D, Polo O, DuBrava S, Miceli J, Knapp L, Winkelman JW. Comparison of pregabalin with pramipexole for restless legs syndrome. N Engl J Med. 2014;370(7):621–31.
4: Ancoli-Israel S, Martin JL, Blackwell T, Buenaver L, Liu L, Meltzer LJ, Sadeh A, Spira AP, Taylor D, Owens J, Smith M. The SBSM guide to actigraphy monitoring: clinical and research applications. J Behav Sleep Med. 2015;13(Suppl. 1):S4–S38.
5: Aronsohn RS, Whitmore H, Van Cauter E, Tasali E. Impact of untreated obstructive sleep apnea on glucose control in type 2 diabetes. Am J Respir Crit Care Med. 2010;181(5):507–13.
6: Association AP. Diagnostic and statistical manual of mental disorders. 5th ed. Washington DC: American Psychiatric Association; 2013.
7: Auger RR, Burgess HJ, Emens JS, Deriy LV, Thomas SM, Sharkey KM. Clinical practice guideline for the treatment of intrinsic circadian rhythm sleep-wake disorders: advanced sleep-wake phase disorder (ASWPD), delayed sleep-wake phase disorder (DSWPD), non-24-hour sleep-wake rhythm disorder (N24SWD), and irregular sleep-wake rhythm disorder (ISWRD). An update for 2015: an American Academy of sleep medicine clinical practice guideline. J Clin Sleep Med. 2015;11(10):1199–236.
8: Ayalon L, Ancoli-Israel S, Stepnowsky C, Marler M, Palmer BW, Liu L, Loredo JS, Corey-Bloom J, Greenfield D, Cooke J. Adherence to continuous positive airway pressure treatment in patients with Alzheimer's disease and obstructive sleep apnea. Am J Geriatr Psychiatry. 2006;14(2):176–80.
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Folic acid protects from abnormal sleep-induced telomere damage or loss
Folic acid is a water-soluble vitamin with the molecular formula C19H19N7O6, also known as vitamin B9. It is a basic compound involved in many important biochemical processes :
- participates in the metabolism of genetic material and proteins;
- affects animal reproductive performance;
- affects animal pancreatic secretion
- promotes growth;
- improves immunity.
Possible causes of folic acid deficiency include insufficient intake, increased demand, intestinal malabsorption, vitamin C deficiency, use of folic acid antagonists, liver disease, etc.
According to reports, due to the high citrulline content of telomeres, it is considered to be a fragile site in the genome. After being attacked by ROS, chemicals, ionizing radiation (IR), etc., it causes telomere dysfunction, which makes the genome unstable and causes cell aging. Researchers found that ultrashort telomeres were detected in those with folate deficiency with insufficient sleep, indicating that abnormal sleep rhythms may cause telomere damage or loss other than telomere shortening. They found that folic acid supplementation can improve telomere dysfunction . Folic acid treatment inhibited the secretion of senescence-related cytokines (especially TNF-α) and telomere shortening/damage only affected mice with insufficient sleep. Folic acid can help resolve aging-related phenotypic changes caused by sleep deprivation.
[1]Yang Y, Wang C, Jiao B. Research Progress of Folic Acid. Processing of agricultural products. Academic Journal, 2006(5): 31-35.
[2]Zhang X,Wang Y,Zhao R,et al. Folic Acid Supplementation Suppresses Sleep Deprivation-Induced Telomere Dysfunction and Senescence-Associated Secretory Phenotype (SASP)[J]. Oxidative medicine and, cellular longevity, 2019, 2019(7, article e1544):1-14.
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App that stops nightmares and helps you sleep better
FDA recently approved a "prescription app" called NightWare that uses Apple Watch sensors to track your sleep. When an algorithm detects that the user is experiencing a nightmare, the device vibrates to disrupt their sleep just enough to stop the nightmare and not to wake the user up .
That way, people experiencing PTSD-caused nightmares have an option to get a night of better sleep and affect their general health.
[1]https://www.dailymail.co.uk/sciencetech/article-8929837/NightWare-app-Apple-Watch-wins-FDA-approval-treatment-PTSD-related-nightmares.html
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The relationship between telomere length, sleep and aging
Telomere length, which is a marker of cellular aging, is one of the research hotspots that has attracted much attention. Telomere refers to the special curved cap-like structure at the end of the chromosome of eukaryotic cells. It is a nucleus composed of DNA repeats containing TTAGGG and telomere binding protein. Protein complex. Telomere length determines the number of cell divisions and survival period, and is a biological marker of cell aging. Telomere length is regulated by genes and affected by various external factors. Normal human cells divide indirectly, and the length of telomeres will be shortened accordingly. When a certain critical value is reached, the cells are prevented from dividing further, leading to cell senescence and death. Senescence is a gradual process. As the risk of injury or disease increases, Healthy individuals can gradually become unhealthy individuals and eventually die [1]. The length of telomeres can reflect the number of cell divisions, suggesting the relationship between actual age and physiological aging. Researchers believe that telomere length is the regulation of biological aging-related processes, and sleep is one of the physiological processes most affected by aging [2] There are currently some studies on the potential connection between telomere length and sleep and aging, sleep quality and Sleep rhythm is deeply affected by aging. Initial observations have found that sleep loss such as sleep deprivation (SD), sleep restriction or sleep fragmentation and increased oxidative stress damage, abnormal cellular immunity, stress response, inflammatory response, homeostasis Various pathophysiological processes such as imbalance and unfolded protein response [3] are related to [4-5]. The above-mentioned mechanisms may be involved in the cell aging process, and studies have confirmed that there is a significant correlation between white blood cell telomere length and cell aging [6] Sleep disorders are very common in the elderly, such as insomnia, obstructive sleep apnea (OSA) [7], restless legs syndrome (RLS) [8] or rapid eye movement sleep behavior disorder (RBD) [9-10] With age, sleep physiology changes, the incidence of sleep disorders and other age-related diseases gradually increases, and the telomere length, a marker of cellular aging, also decreases. Recent cross-sectional studies and case-control studies have shown that telomere length is particularly It is the average white blood cell telomere length (LTL) that is related to reduced sleep time and sleep dysfunction [11]. Therefore, some scholars suggest that white blood cell telomere length should be used as a potential marker for age-related sleep disorders. Recognizing biological markers of aging can not only reflect the degree of aging in the biological process, but also evaluate the risk of age-related diseases [12].
Reference:
[1]Fathi E, Charoudeh HN, Sanaat Z, Farahzadi R. Telomere shortening as a hallmark of stem cell senescence［J］. Stem Cell Investig, 2019, 6:7.
[2]Mander BA, Winer JR, Walker MP. Sleep and human aging［J］.Neuron, 2017, 94:19-36.
[3]Anafi RC, Pellegrino R, Shockley KR, Romer M, Tufik S, Pack AI. Sleep is not just for the brain: transcriptional responses to sleep in peripheral tissues［J］. Bmc Genomics, 2013, 14:362.
[4]Tufik S, Andersen ML, Bittencourt LR, Mello MT. Paradoxical sleep deprivation:
neurochemical, hormonal and behavioral alterations. Evidence from 30 years of research[J]. An Acad Bras Cienc, 2009, 81:521-538.
[5]Han F, Xiao FL. Focus on interoperation between sleep medicine and neurology［J］. Zhongguo Xian Dai Shen Jing Ji Bing Za Zhi, 2017, 17:705-707.
[6]Saretzki G. Telomeres, telomerase and ageing［J］. Subcell Biochem, 2018, 90:221-308.
[7]Hongyo K, Ito N, Yamamoto K, Yasunobe Y, Takeda M, Oguro R, Takami Y, Takeya Y, Sugimoto K, Rakugi H. Factors associated with the severity of obstructive sleep apnea in older adults[J]. Geriatr Gerontol Int, 2017, 17:614⁃621.
[8]Çurgunlu A, Döventas A, Karadeniz D, Erdinçler DS, Oztürk AK, Karter Y, Yaldiran A, Sipahioglu F, Beger T. Prevalence and characteristics of restless legs syndrome (RLS) in the
elderly and the relation of serum ferritin levels with disease severity: hospital-based study from Istanbul, Turkey[J]. Arch Gerontol Geriatr, 2012, 55:73-76.
[9]Tufan A, Ilhan B, Bahat G, Karan MA. An under -diagnosedgeriatric syndrome: sleep disorders among older adults［J］. Afr Health Sci, 2017, 17:436-444.
[10]Jung Y, St Louis EK. Treatment of REM sleep behavior disorder[J].Curr Treat Options Neurol, 2016, 18:50.
[11]Tempaku PF, Mazzotti DR, Tufik S. Telomere length as a marker of sleep loss and sleep disturbances: a potential link between sleep and cellular senescence[J]. Sleep Med, 2015, 16:559-563.
[12]Turner KJ, Vasu V, Griffin DK. Telomere biology and human phenotype［J］. Cells, 2019, 8:E73.
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