@sleepdiplomat @foundmyfitness This is something I’ve often wondered: all these studies about the “optimal hours of sleep”, do the normalize by the time people *spend in bed* or the time *they are actually sleeping*?
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etc (bio/acc)
1K posts
etc (bio/acc)
@__modeerf__
automation, health, self improvement.
Beigetreten Eylül 2015
1K Folgt111 Follower
@foundmyfitness And if you use the median of that range, and assume high sleep efficiency numbers (i.e., strong, healthy sleepers), the amount of time needed to be in bed to obtain that median essential amount of sleep looks like this, as best I can tell.
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The sleep "sweet spot" for biological aging isn't 8 hours per night.
6.4-7.8 hours was associated with the lowest biological age gaps across 23 organ-specific clocks including the brain, liver, pancreas, skin, and adipose tissue.
Short (<6 hours) and long (>8 hours) sleep were both associated with higher biological aging, but likely for different reasons.
Short sleep may directly cause aging, while long sleep may reflect underlying disease or pathology - something that causes someone to require more sleep due to fatigue, recovery, or poor sleep quality.
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I gave selegiline a try because I saw it in this post, and dopamine breakdown, I think, has been an issue for me. (Specifically, l-tyrosine, a few coffees, and the selegiline)
Dopaminergics hit me well enough, but always leave much to be desired when it comes to duration of the effects.
What a wild feeling to finally have it last.
My brother is in town, and he’s even worse than me. Cannot focus for the life of him. Might have something to do with the amphetamines he was given starting at the age of 7.
He also tried it and was able to focus unlike I think I’ve ever seen from him.
I’m not an expert on this. It might be a horrible idea for you to take it. All I did was a little bit of reading and then down the hatch to see what it’s really about.
I’m pretty blown away.
Lawrence Elliot@LawrenceElliots
Cognition slows when synaptic transmission becomes inefficient, white matter integrity degrades + cortical networks lose plastic adaptability Here are a few of the many ‘agents’ that support sharper decision-making: 1. Cerebrolysin acts upstream of neurotransmitters by: •enhancing synaptogenesis •improving dendritic spine density •stabilising glutamatergic signalling •increasing neuronal survival under metabolic stress 2. Uridine Raw material for synapse construction. Uridine contributes to: •phosphatidylcholine synthesis •synaptic membrane formation •neurite outgrowth In combination with DHA + choline, it directly supports synaptic density and efficiency 3. Nicotine Demonised. useful if implemented strategically. It will: •tightens attentional bandwidth •reduces mind-wandering •improves rapid decision latency nicotine reliably improves reaction time, vigilance tasks, working memory speed 4. Bromantane Upregulates tyrosine hydroxylase and dopamine transporter expression over time, improving dopaminergic tone without phasic overstimulation. 5. Pitolisant Disinhibits histamine neurons leading to improved cortical arousal and executive vigilance. Histamine is chronically underexploited in nootropic design. 6. TAAR1 Partial Agonists Trace amine–associated receptor 1 modulates monoamine firing patterns by stabilising dopaminergic firing + improving signal precision Several pharma candidates exist but none appear in the mainstream. 7. 9-ME-BC Dopaminergic neuroplasticity agent. Won’t provide acute speed, but longer-term increases in dopaminergic efficiency - often described as clearer thinking + faster mental transitions. 8. Methylene Blue (low-dose) Mitochondrial redox cycling - enhances electron transport chain efficiency, increases ATP availability in neurons. 9. DSIP (Delta Sleep–Inducing Peptide) (indirect cognitive enhancer) improves sleep architecture, growth hormone pulsatility, neural recovery. Not for speed during use but speed via recovery. DSIP improves next-day reaction time and mental clarity indirectly. 10. MOTS-c Enhances mitochondrial biogenesis and glucose utilisation - improving metabolic efficiency in neurons. 11. Low-dose Selegiline (micro-dose range) increases mental sharpness and speed consistency, especially in high-output individuals MOA-B inhibition = reduced dopamine breakdown = improved baseline dopaminergic tone 12. Adenosine A2A Antagonists This pathway governs psychomotor speed and decision latency. Modulating a2a receptors in striatum improves dopamine efficiency 13. Creatine monohydrate Worthy of mention as brain energy buffer - improves attention time and information processing speed, especially under stressors (sleep loss, high demand)
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If you are highly optimized for longevity, walking 20,000 steps a day - let alone intense endurance cardio, can be counter productive and possibly shorten lifespan.
For me, simply staying active and combining with a few short 30 second bursts a week on a bike is optimal.
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The stack continues to recalibrate …
Tadalifil 5mg daily
Telmisartan 20mg daily
NAC 600mg MWF
VitC 250mg daily
DIM 100mg daily
Ubiquinol 100mg daily
Urolithin A 1000mg daily
Nattokinase 12,000FU daily
Fish Oil 2.8g daily
Citicoline 250mg daily
Phosphatidylserine 100mg daily
Pregnenolone 100mg EON
Once weeklies:
A, D, K, E, methyfolate, zinc
If I’m feeling a bit run down with the above:
B1, B2, B3, and B12
I take Saturdays off of the pills.
Testosterone is now EOD.
Peptides (not daily) in rotation or PRN:
HCG. Tirz. BPC157, Tb4, KPV, GHK-cu, Ta1
I was able to drop the statin when I started running. Neat. Running is medicine.
I’ll finish my bottle of urolithin A and be done with that for awhile. Maybe use it twice per year. Idk.
I’ve finished two weeks of selank/semax. Not sure what I think.
The neuronal support is new. And I think mechanistically makes sense with androgens, caffeine, and stessful work. They will be given a solid three months.
NAC has switched to a lower and pulsed dosing that I think is more inline with optimal glutathione production. I don’t think “cycled” is the right approach. I continue to recommend 1200mg daily while using any oral anabolic.
Pregnenolone helps me sleep better. Also backfills upstream precursors for adrenal hormones.
I’ve been able to actually reduce a lot of my supplements and pills. And I’m using my peptides in a much more targeted fashion.
Every lever you pull has a cascade of effects. Also just pulling big on a lever doesn’t, surprisingly to intuition, often net bigger results. And can often have longer term unintentional or unwanted net negative effects.
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the new instant model in chatgpt is so good damn
if you have been thinking-model-only for awhile, give it a try!
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Codex完全勝利だな
・知能ナンバーワン
・リミットも寛大
・ネイティブMacアプリが秀逸
・ハーネスはOSS
・App Serverはサブスクで使える
OpenAIの名前に恥じない中身を伴ってきた
しかし誰であれ一強で気が緩むは良くないので
AnthropicやCursorには頑張ってほしい
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wow y'all love 5.5
we should think of something nice to do to celebrate!
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You really shouldn’t many pre-determined parts of any steroid cycle.
If the goal is to achieve X goal by Y date, that’s one thing.
But things like predetermined AI dosing, overall dose increases, cycle duration, and other interventions should be used only according to your goal.
For example, let’s say Jeff has a lot of size to build before he reaches his goal physique. We’re talking 30lbs+.
Jeff is super lean, and ready to begin his next blast.
Instead of “okay I’m gonna run 500 test and 200 primo for 16 weeks”
It should be, “I’m going to start test and primo high enough above cruise dosages to elicit growth, I’m going to increase food intake at plateaus, and I will add just enough extra gear to keep continue growing once added food seems to make me fat much more than it drives performance”
Then, watch biomarkers the whole time, and end the cycle when it actually makes sense, vs after a random time allotment.
If you’re staying healthy, growing like a weed, milking those incremental increases, and loving life, there really isn’t any reason to just stop.
Long, slow, off-seasons/bulks are always going to be more fruitful and more healthy than random blasting because you want to look like a geared out dude with a bunch of veins and no muscle.
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@OpenAI @Miles_Brundage If you add /remote-control I’ll never use Claude again
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Introducing GPT-5.5
A new class of intelligence for real work and powering agents, built to understand complex goals, use tools, check its work, and carry more tasks through to completion. It marks a new way of getting computer work done.
Now available in ChatGPT and Codex.
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@goodalexander @theo I’m beginning to worry there will be monopoly. GPT codex is far above the rest
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1. Javokhir Sindarov
2. Fabiano Caruana
3. Magnus Carlsen
4. Nodirbek Abdusattorov
5. Anish Giri
6. Pragg
7. Vincent Keymer
8. Arjun Erigaisi
9. Wei Yi
10. Hans Niemann
Anish Giri@anishgiri
Give me your list of 10 strongest chess players right now, classical time control. I want your (highly objective) opinion.
Català
@AbudBakri @CoffeeBlackMD By this logic, almost no drugs are longevity drugs. Outside of maybe the ones in the ITP like rapamycin. GLPs appear to reduce all cause mortality, although it’s difficult to distinguish the effects.
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@CoffeeBlackMD They aren’t longevity drugs until proven otherwise
The problem is people are already claiming they are based on obese and diabetic data sets
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GLP-1s aren’t longevity drugs
Obesity is just an anti longevity drug
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Please don't use kelly for trading. It is not suitable.
I see so many people posting about kelly this and kelly that related to trading.
Kelly was originally designed for gambling. Gambling has fixed rules that typically favour the house but in some cases you can find an edge. Because the rules and the environment are fixed, the edge can be calculated. In trading you have volatility clustering and fat tails and everchanging environmental chaos from both external event, varying participants and market internals.
Kelly assumes fixed and known constants. In trading NONE of these is true:
- Environment is known and constant
- Ratio of wins/losses is constant and known
- Payout is constant and known
You can get much better results via backtesting with decent sample size + monte carlo uncertainties.
/rant
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