Sleep

Alzheimer's, cardiovascular, and other chronic diseases; biomarkers, lifestyle, supplements, drugs, and health care.
JD2020
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Re: Sleep

Post by JD2020 »

xactly wrote: Mon May 30, 2022 8:24 pm I stumbled across "The Mind Illuminated: A Complete Meditation Guide Integrating Buddhist Wisdom and Brain Science for Greater Mindfulness" by John Yates. I began following Yates' instruction, and I was startled to see my deep sleep scores jump to what is now an average of 1 hr 20 minutes a night. I've even had three nights this month with 2 hours or more deep sleep.
Thanks for mentioning the book. I am just getting started, but so far, I really like it.
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kayakmac08
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Re: Sleep

Post by kayakmac08 »

Thank you, everyone, for your kind responses. Lots of interesting perspectives and experiences with this topic!

Sooo...it turns out that I DO have sleep apnea, and that's at least a partial answer to my long-standing deep sleep deficits. I have "moderate" apnea, with around 85 apnea and/or hypopnea episodes per night, when not using CPAP. I'm now on CPAP and my deep sleep averages per night have almost doubled. My sleeping HR is also lower (although my HRV is markedly worse, which is interesting). And this is with a fussy newborn waking me up multiple times per night (which prob explains the HRV drop)! I think I'm the first person who's ever been able to say that the best sleep of their life occurred immediately AFTER having a newborn! :D

Note: I was diagnosed 3 months ago, from an in-clinic study. Be VERY wary of in-home tests. I had one in 2016 and another in 2019 and they both said I was negative for sleep apnea; no doubt, in-clinic is the gold standard for a good reason.... And I've had chronic fatigue problems since roughly 2013, so I think these two in-home tests totally failed to detect my highly disturbed breathing.

Anyway, I encourage anyone with long-standing deficits in deep sleep and/or REM to seriously consider an in-clinic sleep study. Even if you don't seem like someone who would have sleep apnea. I'm only 34, have a thin build, BMI around 22, and a neck circumference below the 17" cutoff, good metabolic health, good sleep hygeine, don't drink in the evenings, and I DON'T SNORE (another thing the in-clinic test confirmed). And yet I have sleep apnea!

Insurance may fight you on it if you haven't done any in-home studies. But even so, if you're adamant that you have chronic fatigue that interferes with daily life, and explain that you've been practicing good sleep hygiene and are giving yourself at least 6 hours/night of sleep opportunity, and can provide a good rationale for why an in-home study won't work for you, they may bend.

@SonomaMike: I have noticed that my sleep is often better if I worked out earlier in the day, as long as anything especially strenuous (particularly if adrenaline was involved) wrapped up at least 6-7 hours before bed). If I hit the weights crazy hard or do a longer HIIT workout that drags past 6pm and then I'm trying to fall asleep by 11pm, my deep sleep is usually scant. So yes, my sleep is better on days when I work out IF I don't get too amped up too late in the day.
  • 4/4 male, born 1989
  • Status discovery: 2020
  • Regimen: 14+ hr. fast/day; 200-300 min of mod-vig exercise/week; Med-esque diet; Supplementing with Trig DHA, B vits, D3
Plumster
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Re: Sleep

Post by Plumster »

Hi all,

I just came across this study in JAMA Neurology (not open access, unfortunately), suggesting that slow-wave sleep is critical, especially for e4s over 60. Apoe4 is associated with a greater decline in slow-wave sleep and not enough slow-wave sleep is a modifiable risk factor for AD.

Here's an article on the study: "As little as 1 per cent reduction in deep sleep per year for people over 60 years of age translates into a 27 per cent increased risk of dementia, according to a Monash study which suggests that enhancing or maintaining deep sleep, also known as slow wave sleep, in older years could stave off dementia."
Association Between Slow-Wave Sleep Loss and Incident Dementia
JAMA Neurol. Published online October 30, 2023. doi:10.1001/jamaneurol.2023.3889

Question
Does the percentage of slow-wave sleep decline with aging, and are intra-individual declines associated with dementia risk?

Findings
This cohort study involving 346 participants from the Framingham Heart Study found that slow-wave sleep percentage declined with aging and Alzheimer disease genetic risk, with greater reductions associated with the risk of incident dementia.

Meaning
Slow-wave sleep loss may be a dementia risk factor.

Importance
Slow-wave sleep (SWS) supports the aging brain in many ways, including facilitating the glymphatic clearance of proteins that aggregate in Alzheimer disease. However, the role of SWS in the development of dementia remains equivocal.

Objective
To determine whether SWS loss with aging is associated with the risk of incident dementia and examine whether Alzheimer disease genetic risk or hippocampal volumes suggestive of early neurodegeneration were associated with SWS loss.

Design, Setting, and Participants
This prospective cohort study included participants in the Framingham Heart Study who completed 2 overnight polysomnography (PSG) studies in the time periods 1995 to 1998 and 1998 to 2001. Additional criteria for individuals in this study sample were an age of 60 years or older and no dementia at the time of the second overnight PSG. Data analysis was performed from January 2020 to August 2023.

Exposure
Changes in SWS percentage measured across repeated overnight sleep studies over a mean of 5.2 years apart (range, 4.8-7.1 years).

Main Outcome
Risk of incident all-cause dementia adjudicated over 17 years of follow-up from the second PSG.

Results
From the 868 Framingham Heart Study participants who returned for a second PSG, this cohort included 346 participants with a mean age of 69 years (range, 60-87 years); 179 (52%) were female. Aging was associated with SWS loss across repeated overnight sleep studies (mean [SD] change, −0.6 [1.5%] per year; P < .001). Over the next 17 years of follow-up, there were 52 cases of incident dementia. In Cox regression models adjusted for age, sex, cohort, positivity for at least 1 APOE ε4 allele, smoking status, sleeping medication use, antidepressant use, and anxiolytic use, each percentage decrease in SWS per year was associated with a 27% increase in the risk of dementia (hazard ratio, 1.27; 95% CI, 1.06-1.54; P = .01). SWS loss with aging was accelerated in the presence of Alzheimer disease genetic risk (ie, APOE ε4 allele) but not hippocampal volumes measured proximal to the first PSG.

Conclusions and Relevance
This cohort study found that slow-wave sleep percentage declined with aging and Alzheimer disease genetic risk, with greater reductions associated with the risk of incident dementia. These findings suggest that SWS loss may be a modifiable dementia risk factor.
e3/4 MTHFR C677T/A1298C COMT V158M++ COMT H62H++ MTRR A66G ++ HLA DR
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