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Here are the results from the recent CR and Sleep Survey, as a follow-up to the General CR Survey conducted a couple weeks ago, whose results are available here. This time where were 20 respondents, with 70% men and 30% women. The age distribution was skewed much younger than the first survey. Here is the data (click to enlarge): There was also a greater proportion of people with higher BMIs this time: and with fewer years of CR under their belt, although we had a good contingent of veterans as well: Overall, CRers reported sleeping about 6.8 hours per night on average. Here is the distribution: Overall, CRers reported sleeping about 0.8 hours less per night on average since starting CR. Here is the distribution: CRers reported that by far the most common sleep problem was "early waking". Here is the distribution of sleep difficulties: Here are some interesting interactions between CR practices and sleep characteristics that showed up in the data. As usual, the numbers are small and so these should be taken as trends and with a grain of salt: While the number of reported nightly hours of sleep did not differ based on duration of CR, CR veterans (> 10 years) reported a greater reduction in sleep time than people who've been practicing less than 10 years (-0.91 vs. -0.21 hours, respectively). People who waited 2-4 hours between their last meal/snack and their bedtime reported less of a decrease in their time spent sleeping than either people who waited less than 2 hours, or greater than 4 hours before going to bed (-0.25 vs. -0.9 hours, respectively). So if you want to lose less sleep as a result of CR, it appears best to wait a moderate time between eating and going to sleep. The biggest impact on sleep seemed to be the result of BMI. People with a BMI less than 20 reported sleeping 40min less than those with a BMI > 20 (6.47 vs. 7.14 hours respectively). The skinnier folks also report that this was "too little" sleep more often than the heavier people (63% vs. 9%). In summary, it appears that CR tends to decrease the amount of time people sleep, with people practicing CR for more years, and more severe CR (as measured by BMI) tend to experience a greater decrease, and "early waking" seems to be the most common cause of this sleep reduction. Thanks to everyone who participated! --Dean
I've suffered from early waking insomnia all my life. Until a few years ago, it was fairly minor, and manageable. But a few years ago, in connection with some other andropause-like changes I went through, I started to wake and not get back to sleep after 4-5 hours of sleep instead of 6-7 (8 hours is optimal for me). I was also losing weight, though I don't think I was eating less. I think I moved into an aged phenotype all at once. (Long story there.) Regardless of the strange changes that took place a few years ago, the early waking, which was always a problem, became worse. I've had my early morning cortisol tested several times over the last few years, and it's always been above the reference range. This is no big surprise for a person on CR: low blood sugar causes an increase in cortisol (which keeps blood sugar from falling "too low"). It's not that I'm tense, it's not that I'm hungry (well, I am, but I always am). I'm just awake. Well, my 2:1 diet plan has yielded some interesting results. The night after Feast Day 2, I sleep beautifully! The night after Feast Day 1, I often sleep fairly well. The night after the fasting day (right now around 700 calories/day), I sleep worse than ever. I wake too early, and can't get back to sleep. I'm happy, non-tense, not really hungry even. Just really awake. So now I'm thinking I might take timed-release zolpidem or something on fasting days before going to bed. But I'm wondering if anyone else has tried any cortisol lowering strategies that have helped with sleep. A lot of supplements that supposedly lower cortisol seem to do so (if they work at all...) by lowering stress. I'm not stressed. Phosphatidylserine blunts the post-exercise cortisol spike, but it’s not clear it would help with low glucose-induced cortisol. Suvorexant might be a better choice than timed-release zolpidem (or one of the other Z-drugs), but I haven't studied the relation between orexin and cortisol enough to know whether it would help me. Any CR folks with early morning insomnia have any strategies they'd like to share?
Disturbed sleep patterns are known to be associated with cognitive impairment and Alzheimer's disease. But it isn't entirely clear whether Alzheimer's disease is caused by sleep disturbances or the other way around. This popular press article: http://www.kurzweilai.net/sleep-disruptions-similar-to-jet-lag-linked-to-memory-and-learning-problems on a new study  in mice helps to shed some light on the issue. They disrupted the sleep of both normal mice and mice breed to exhibit a mice-model of Alzheimer's disease by altering the day/night pattern of light they were exposed to every three days to simulate jet lag. They found the cognition (Morris water maze performance) of both types of mice were impaired by the disturbed sleep schedule. The impairment to learning was more pronounced in the Alzheimer's mice, and that the degree of impairment was proportional to the reduction of the endogenous antioxidant glutathione (GSH) in the brains of the mice, with Alzheimer's mice showing a greater reduction in GSH than the normal mice. This would seem to emphasize the importance of maintaining good sleep patterns in order to avoid cognitive decline and Alzheimer's disease with aging. --Dean ---------  Journal of Alzheimer's Disease, vol. Preprint, no. Preprint, pp. 1-16, 2015; DOI: 10.3233/JAD-150026 Circadian Disruption Reveals a Correlation of an Oxidative GSH/GSSG Redox Shift with Learning and Impaired Memory in an Alzheimer’s Disease Mouse Model. LeVault, Kelsey, Tischkau, Shelley, Brewer, Gregory. It is unclear whether pre-symptomatic Alzheimer’s disease (AD) causes circadian disruption or whether circadian disruption accelerates AD pathogenesis. In order to examine the sensitivity of learning and memory to circadian disruption, we altered normal lighting phases by an 8 h shortening of the dark period every 3 days (jet lag) in the APPSwDI NOS2–/– model of AD (AD-Tg) at a young age (4-5 months), when memory is not yet affected compared to non-transgenic (non-Tg) mice. Analysis of activity in 12-12 h lighting or constant darkness showed only minor differences between AD-Tg and non-Tg mice. Jet lag greatly reduced activity in both genotypes during the normal dark time. Learning on the Morris water maze was significantly impaired only in the AD-Tg mice exposed to jet lag. However, memory 3 days after training was impaired in both genotypes. Jet lag caused a decrease of glutathione (GSH) levels that tended to be more pronounced in AD-Tg than in non-Tg brains and an associated increase in NADH levels in both genotypes. Lower brain GSH levels after jet lag correlated with poor performance on the maze. These data indicate that the combination of the environmental stress of circadian disruption together with latent stress of the mutant amyloid and NOS2 knockout contributes to cognitive deficits that correlate with lower GSH levels.
All, It has long been known that CR can influence circadian rhythms in animals (e.g. ), and there is anecdotal evidence that CR impacts sleep in people too. I've created a new short survey on "CR and Sleep" to investigate the relationship between CR and sleep as part of the CR Society "citizen science" efforts. Please take a few minutes to fill out the survey: https://www.surveymonkey.com/r/SZDBFC3 I'll report back in a week or so with the results. Thanks! --Dean -------------  Brain Research Volume 1057, Issues 1–2, Pages 1-198 (28 September 2005) Influence of long-term food restriction on sleep pattern in male rats Tathiana A.F. Alvarenga, Monica L. Andersen, Ligia A. Papale, Isabela B. Antunes, Sergio Tufik Abstract The present purpose was to determine the effects of different schedules of long-term food restriction (FR) applied to rats from weaning to the 8th week. Rats were distributed into FR and ad libitum groups at weaning and fed at 7 am, at 7 pm, and finally, restricted rats fed ad libitum. The restricted rats started with 6 g/day and the food was increased by 1 g per week until reaching 15 g/day by adulthood. The rats were implanted with electrodes to record electrocorticogram/eletromyogram signals. Their wake–sleep cycles were monitored over 3 consecutive days (72 h of recording). The FR group fed at 7 am showed an increase in awake time, and decrease in slow wave sleep (SWS) and paradoxical sleep (PS) during the three light periods compared with the control recordings whereas in the dark periods, these sleep parameters were the opposite. The restricted group fed in the evening showed no statistical significances at diurnal periods; however, a significant decrease was observed in the dark recordings for awake time, but the SWS and PS were increased in relation to controls. The analysis of the 24-h period demonstrated that both FR groups presented increase in SWS time. After being FR, the rats were fed ad libitum and their sleep was monitored for 3 additional days. During the first dark recording, the decrease in awake time and increase in SWS were still present; however, as ad libitum food continued, these sleep parameters returned to control values, reestablishing the normal sleep pattern. These results suggest that dietary restriction, regardless to the feeding schedule, caused increase in total sleep time, during the active period. doi:10.1016/j.brainres.2005.07.024