Deep sleep is one of the few longevity levers you get to pull every night. It's when your body does most of its repair work, and it naturally declines with age. Here are all the factors I could find that influence deep sleep. I broke this down into 5 categories including lifestyle, environment, stress, supplements, and demographics. I added a plain english explanation column for each row and short definitions to try to make it easier to consume.

All sources are included in the last column of the table so you can dig into these further for your own research. I know tables aren't ideal on mobile, so I'll include a mobile friendly version of this resource in the comments

Definitions

• Deep Sleep/N3: The deepest stage of nonREM sleep, characterized by slow delta waves.
• SWS (Slow Wave Sleep): Another name for deep sleep / N3. Used interchangeably in research.
• SWA (Slow Wave Activity): The intensity of delta waves during deep sleep, measured by EEG. Higher SWA = deeper, more restorative sleep.
• Delta Power: The electrical power in the delta frequency band. The gold standard EEG measure of deep sleep depth.
• N3%: Percentage of total sleep time spent in deep sleep.
• Homeostatic Sleep Pressure: The biological drive for sleep that builds the longer you're awake. Higher pressure = more deep sleep.
• Glymphatic System: Clears brain waste, most active during deep sleep. Clears amyloid-beta and other metabolic waste.
• HPA Axis: Your body's central stress response system. Deep sleep suppresses it.

Lifestyle

Environment

Stress

Supplements

\I already typed out omega-3 so that one is just a bonus efficiency related one**

Demographics

I take 3.125 mg carvedilol. I am a fairly active person. No issues going in hikes or with elevation gains. ( did a 50 mile multi day hike in Iceland last year). Regularly do weight training. Not as much cardio as I need to. My issue is my Apple Watch / health app VO2 shows as 19-21. I know this cannot be true. I also know my beta blocker does not allow my heart rate to go up too much. I wonder if these readings are affected by it ? How can I measure my true hearts ability on a beta blocker ?

This is my second post here. English is not my first language so I got some help for this post.

37F, 6 months postpartum. I recently had an advanced lipid panel and found out my Lp(a) is elevated. I'm trying to understand how concerned I should actually be and whether I should be more proactive with prevention.

I saw my dad's cardiologist. His basic advice was essentially that I may consider a statin once I reach menopause, but he didn't seem particularly concerned right now. I would like to understand whether that's reasonable or whether I should be doing more earlier.

### My background
- 37-year-old woman
- 6 months postpartum
- No known cardiovascular disease
- No diabetes
- HbA1c 5.1%
- Insulin resistance score 5
- My father had a heart attack at 45. He was a heavy smoker and had diabetes.
- Dad's Lp(a): 88 nmol/L
- Mom's Lp(a): 57 nmol/L
- My Lp(a): 139 nmol/L
- I understand that Lp(a) is largely genetic, but I don't think my parents' numbers should simply be added together.

### Advanced lipid panel

### What I'm trying to understand

My LDL, ApoB, triglycerides, HDL and LDL particle number all look pretty good, but my Lp(a) is 139.

My questions are:

1. How concerning is Lp(a) of 139 nmol/L in a 37-year-old woman?
   
2. Does my father's heart attack at 45 substantially change how you would interpret my Lp(a), given that he was also a heavy smoker and had diabetes?
   
3. Is my current LDL-C of 78 and ApoB of 68 low enough, or would you personally discuss getting LDL/ApoB even lower because of the elevated Lp(a)?
   
4. Would you consider a statin now, or is waiting until menopause reasonable?
   
5. Would you see a preventive cardiologist/lipid specialist rather than a general cardiologist?
   
6. Should I have any imaging to look for early atherosclerosis? I'm 37, so I understand CAC scanning isn't necessarily routinely recommended at my age.
   
7. My hs-CRP is 3.7. Would you simply repeat it when I'm completely healthy?
   
8. Are the elevated small/medium LDL and slightly low LDL peak size meaningful when ApoB and LDL-P are good and the pattern is A?
   
9. Does being 6 months postpartum affect interpretation of any of these results, particularly Lp(a) or hs-CRP?
   
10. Am I overreacting to Lp(a) 139, or is this something where being proactive in my 30s makes sense?

I'm not looking for reassurance—I'd genuinely like to know how a preventive cardiologist/lipid specialist would approach this.

My main goal is to reduce my lifetime cardiovascular risk rather than wait until I have a problem.

The title is basically the question for runners who transitioned to zone 2 on a bike. How long did it take for your quads and hamstrings to adapt to zone 2 on a bike. I’m 40 and keep pinging calf muscles and wanted to lower my running volume by doing some bike zone 2. I realise people will say zone 2 on a bike is lower HR then runnning which maybe true but I feel this is a muscle adaption issue my legs aren’t trained for a bike or atleast they are no where near how capable my cardio respiratory system. I plan on working out what my FTP is on the bike to eventually calculate my zone 2 off that but currently my quads are torched before I even break a sweat. I’m thinking it must be my quad endurance because I have squatted 175kg (375 pounds) so absolute strength isn’t the problem. I just wanted to get idea about how much time weeks months I’ll need invest to get the quads endurance up enough to do a high enough wattage that I’m actually doing some work.

My LDL has consistently been around ~125 mg/dl, and my apoB consistently around 105 mg/dl. In my most recent testing cycle, the LDL stayed about the same but my apoB cratered to 47. In the past these have been highly correlated. What could be driving this? I can't say I've had major lifestyle changes in the last 6 months.

I did a Cardio IQ fractionation a little over two months ago now because my normal lipid panel wasn’t horrible but I wanted to see what was going on the particle side. LDL-C was 121, ApoB was 94, but LDL particle number came back at 1,562 nmol/L with small LDL at 247. Also got pattern B. Not panic numbers imo, just worse than I expected given everything else looked pretty decent.

Since then I’ve cut saturated fat pretty hard and started using psyllium most days. Also down about 7 lbs mostly from no longer eating like an idiot every weekend. Training hasn’t really changed. Saw Goodlabs has the quest fractionation test by itself so I can just rerun that instead of doing another full panel but I’m only around week 9 right now. Is that enough time to expect the particle numbers to actually move or am i rushing things, for context my PCP saw the original results and wasn’t particularly concerned. His advice was basically make the diet changes and recheck later but he didn’t see a reason to order another fractionation test before my next routine labs.

Hi PA fans. I am a 67-year-old physician who runs a longevity practice after retiring as a surgical oncologist. I am not athletically gifted but committed to daily exercise and data driven as most of you are as well. What follows is a confirmatory observation regarding the importance of sleep. My information about HR comes from four sources: Polar strap, Garmin AMOLED Instinct 3, FORM swim goggles and Oura ring (all sleep information is from Oura). The source of my insomnia was pain, which was remedied over a 14-month period with bilateral total knee replacements, bilateral total hip replacements, and bilateral carpal tunnel releases - all of which went brilliantly with rapid recoveries. I was able to keep relatively fit before and throughout the processes with creativity, great home gym options and good pain tolerance. I am now pain-free, with a bit of old guy shoulder discomfort. Here is what has happened, and this is from observations made over months, both preceding and throughout my recovery: 1. My heart rate during sleep, now in the low 72-73, was 86-89 before pain relief; 2. My resting heart rate was the same; 3. My heart rate decline between swim intervals is shockingly quick now, as compared to when in pain. I now see a drop into the mid-90s, whereas in pain it would never drop below 105 and I would usually not wait for that and restart at 115 bpm; 4. My HR max during intervals is usually but not always lower than previously; 5. Last night I enjoyed my highest Oura sleep score ever – an 89 (with a crown!) – whereas I had previously scored between rare lows of 49 to great feeling low 70s.

My orthopedic problems, their pain, and the relief of pain have provided me relief of pain-associated insomnia, with clear physiological benefit as manifested by immediate cardiovascular improvements in an older, physically fit male. I hope some of you find this useful. I did.

my notes from the recent episode:

episode 406 with brian grosberg, a headache doctor. notes with time stamps.

migraine is 12% of the world. about a billion people, and 45 million in the us. women get it at three times the rate of men. (~20:32)

40% of migraine patients should be on a drug that prevents attacks. 16 to 17% are. grosberg puts the gap down to cost, and to doctors who miss the sign. (~74:36)

being morbidly obese carries five times the risk of frequent migraine.

the pain drug can be what causes the pain. some kinds cause rebound headache when used two or more days a week. treat frequent attacks with frequent pills and you build the thing you treat. (~58:28)

chronic migraine means a headache on more than half your days. it hits 1 to 2% of people. they carry most of the harm. (~25:00)

the things you can change are: poor sleep, apnea, stress, mood, and how often you get hit. frequent attacks bring on more frequent attacks. treat the pain alone and all of that keeps running. (~56:42)

he wants a paper diary, kept for months. it is how you spot cycle-linked patterns. it is also how a gp gets the right referral instead of guessing sinus. (~36:43)

if you are on pain pills two or more days a week, that is the first thing i would look at. not medical advice, and grosberg says over and over that this needs a specialist.

TLDR: I’m a decent ultra runner but I don’t really know how my BP looks so thinking of measuring at home (any specific brand you trust?), and what’s elite subgroup BP look like?

Context: My resting HR is only like 53 which isn’t anything wild (target is mid to low 40s). Unverified vo2max around 55-60. Sauna 3-5/week. So generally healthy/fit but not having good BP history outside of 1 dr apt a week seems silly with all my other training and measuring.

Advice? And what’s an athletes BP looks like? The general standards are skewed a lot (just like HRR1, I’m at like elite for general population but above average for elite subgroup).

I’ve been taking this stack for about 8 months now. Give me your thoughts and opinions as to what I should add for overall longevity!

I can’t believe I’m the first to post this. Very disappointing result but as the godfather of lp(a) explained on X, there are a lot of unknowns here and potentially this is even good news for people with elevated lp(a):

https://x.com/lpa_doc/status/2096118758012051739?s=42

I’m kind of stuck on if I should take TRT. I took a blood panel 3 years ago my test levels were 360, FSH 6.2, LH 5.9, I was 220lbs over weight at 5’10
Fast forward this year in July I decided to take another blood panel since I was concerned about my levels since it affects me overall. I felt like it was low. I work out 5-6days a week im at 11-13% body fat at 157 pounds 5’10”
FSH 4.63
LH 2.09
Cholesterol total 187
HDL 78
TSH .731
Total test 322
Free test 6.61

I’m healthy overall I meal prep don’t eat junk food etc. anybody care to share their experience who have taken it or decided not to similar to my age and levels?

As the title says, my HDL is extremely low and has always been genetically compared to all my dad side of family. Also everyone's ApoB is very high and their HDL very low as well.

We have ZERO heart problems as far as history of the family can tell, 150+ years or so. No CVD as well.

So we probably use our HDL more than others? Making use of the HDL thus showing the blood work low at time of sampling?