slowing down your experience of time via increased mindfulness is the best longevity technology we have by a large margin. at least 2-5x possible
There’s Jhourney. There’s reading @nickcammarata twitter.
the FIRST thing to do is to supplement all brain deficiencies (get an ION panel, see your L-tyrosine and HVA levels). Get selegiline. Get plasmalogens. Maybe try ISRIB A15. Get apigenin/dried parsley to block NAD-deactivating enzymes. You can’t meditate unless your brain is healthy and plastic enough to do it. ADHD people might find it exponentially more difficult
Then there are those who have tried - Shinzen Young [wants to find a category-theoretic formulation of meditation/brain changes/IChing], Jay Sangiamuetti, Rob Burbea, Jhourney [which Kathern Devaney used to be on but left b/c she wanted something that more maximized her neuroscience PhD skills]. Not everyone is going to provide the best instructions for meditation (tbh Nick Cammarata’s tweets are probably best, esp b/c they’re easiest to remember)
You can just meditate without any supplements or medications or technologies, and you should. The other things help I am sure.
Do it daily, even if just 5 minutes. The point is to focus on your breath, and if you notice yourself getting lost in thoughts then go back to your breath. That’s a very easy method of meditation. There are also free and paid phone apps that have guided meditations, a free one I use is Insight Timer.
What I was doing for a while was taking a high dose of melatonin and then meditating in darkness. I just meditate without melatonin because the high dose interrupted my sleep a bit. But I found it was very relaxing.
like @AustraliaLongevity said … or count your exhalations slowly from one to ten over and over focusing on each number and letting everything else go. When (not if) you loose track, start at one again. Two good methods.
the closest life has to a cheat code I know of is that all things are made of sensory phenomena and you can learn to dissolve any sensory phenomena at will
Here’s the best-supported omics picture so far for a “successful” (alert, neuroplastically engaged) response to meditation versus an unsuccessful/no-response pattern. I’m grouping by assay and highlighting directions of change that show up across randomized trials, longitudinal retreats, and monk cohorts.
Lipidomics (and lipid-linked metabolites)
Consistent “responder” signals
Endocannabinoid tone upregulation (or proxies):
• ↑ N-acyl glycines (e.g., capryloyl- and N-lauroyl-glycine) after brief mindfulness training; these are eCB-related fatty-acid amides. (Nature)
• After an 8-day Samyama retreat, ↑ acylglycines and ↓ atherogenic lipids (TAG, DAG, cholesteryl esters), ↓ acylcarnitines, ↓ many PCs/PEs (including some plasmalogens). Authors interpret acylglycines as linked to higher cellular anandamide levels. (Retreat included a vegan diet, so treat as meditation+diet.) (PubMed)
• Independent work shows yoga/meditation acutely raise AEA and 2-AG, the canonical endocannabinoids. (PMC)
Sphingolipids and complex glycosphingolipids: Brief RCT (IBMT vs relaxation) reports ↑ tetrahexosylceramide and N-acylsphingosine with mindfulness relative to control at post-test. (Nature)
Pathway-level shifts after mindfulness (IBMT RCT): enrichment for sphingolipid metabolism, linoleic/α-linolenic acid metabolism, and fatty-acid β-oxidation enzymes; specific between-group differences include higher PC(17:1/0), PE(13:0/22:6), PS(16:0/20:5) in IBMT. (Nature)
Why this plausibly aligns with “healthy/younger” biology: independent population work links parts of the lipidome (e.g., high TAG/low HDL, some CE species) to accelerated epigenetic aging; thus meditation-linked drops in TAG/CE plausibly point in a favorable direction. (Mechanistic tie-in to your Aging Cell paper.) (BioMed Central, PMC)
“Non-responder” lipid pattern (by contrast):
Little/no change in eCB-related acylglycines; no consistent reduction in TAG/DAG/CE or acylcarnitines; no enrichment of fatty-acid oxidation/sphingolipid pathways versus control. (In the IBMT RCT, the relaxation arm showed no significant metabolite shifts after training.) (Nature)
Small-molecule metabolomics (non-lipid)
Responder signals
Central energy/redox tilt consistent with alert engagement: In the IBMT RCT, post-IBMT vs baseline shows ↓ pyruvate, ↓ lactate, ↑ fumarate, plus ↑ glutamate and histidine; pathway hits include pyruvate/TCA, histidine, nitrogen/sulfur metabolism, with ↓ sulfate/thiosulfate. (Nature)
No FDR-significant pre/post change (as above for relaxation control), or inconsistent shifts that don’t cluster in central carbon, lipid, or sulfur pathways. (Nature)
Brain-facing neurochemistry (links to “alertness” / plasticity)
Responder signals
Anterior cingulate cortex (ACC) glutamate ↑ after ~10 h of mindfulness training (MRS), interpreted as heightened excitatory throughput in a control/attention hub (fits the “alert but calm” profile). (PubMed)
Non-responder pattern
No ACC glutamate change from baseline; absent coupling of peripheral metabolite shifts with central measures.
Proteomics
Responder signals (long-term practitioners)
Tibetan monk cohort shows a “protective plasma proteome”: signatures consistent with decreased atherosclerosis risk, enhanced glycolysis, and enhanced oxygen release—interpreted as resilience in the heart–brain axis despite cardiometabolic risk factors. (Protein-level specifics vary, but pathway-level effects are robust.) (PubMed, Directory of Open Access Journals)
Non-responder pattern
No coherent shift toward glycolysis/oxygen-release pathways; persistent pro-atherogenic/inflammatory profile relative to controls.
Endocrine/ANS readouts that tend to co-move with “successful” response
(Not lipids/proteins per se, but useful for discriminating alert engagement vs stress/drowsiness.)
Cortisol: Meta-analyses and trials generally find reductions with mindfulness programs (though not universally across all designs/populations). (Taylor & Francis Online, PMC, MDPI)
Salivary α-amylase (sAA; sympathetic/NE proxy): several studies show decreases across mindfulness programs, particularly alongside reduced perceived stress in daily-life sampling. (Wiley Online Library, ResearchGate)
HRV: experienced meditators often show higher HF power (vagal tone) vs novices; novice patterns can be mixed until skills consolidate. (BioMed Central)
Put together: a practical “responder vs non-responder” omics snapshot
No significant rise in acylglycines/eCBs; no drop in TAG/DAG/CE; no coherent pathway enrichment vs active control; no ACC glutamate rise; endocrine/ANS markers unchanged (or stress-tilted). (This is exactly what the relaxation-only arm showed in the IBMT RCT.) (Nature)
Notes & caveats you’ll care about
Retreat studies often include dietary confounds (e.g., vegan prep for Samyama), so interpret lipid shifts (TAG/CE/acylcarnitines) as meditation + diet unless isolated in RCTs. (PubMed)
Population links between lipids and epigenetic age exist (e.g., high TAG/low HDL → faster clocks), which is conceptually consistent with meditation-linked TAG/CE drops—but Aging Cell’s clock–lipid relationships are species-level and complex across many lipid classes; don’t overfit single species. (BioMed Central, PMC)
If you want a minimal, targeted panel to distinguish responders (pre/post):
Targeted lipidomics (LC-MS/MS):
N-acyl glycines (C8:0-, C12:0-).
eCBs: AEA, 2-AG (plus FAA/monoacylglycerols if possible).
Neutral/transport lipids: TAG, DAG, CE (with FA composition).
Acylcarnitines: short/medium/long chain.
Sphingolipids: ceramides, hexosylceramides/ tetrahexosylceramide; a few PE/PS/PC species used in the IBMT RCT. (Nature, PubMed)
Proteomics (plasma, pathway-focused): panels capturing glycolysis, oxygen-release/erythrocyte-related pathways, and atherogenesis/inflammation. (The monk study motivates these axes.) (PubMed)
Coupling readouts:salivary cortisol & sAA (awakening response and diurnal slope), HRV (HF power); optional MRS ACC glutamate if you have access. (MDPI, Wiley Online Library, PubMed)
Quick link you shared (Aging Cell e13934)
That paper maps lipid classes against DNA-methylation aging clocks at population scale; it’s useful context for interpreting whether your meditation-linked lipid shifts tilt “younger.” Use it to annotate your lipid panel rather than to predict individuals one-to-one. (PMC)
If you want, I can turn this into a checklist order form (targets, specimen, instrument notes, QC) you could hand to a lipidomics/metabolomics core.
Are you still meditating? I’ve moved up to 8.5 minutes daily. If ADHD type distractibility were a muscle you could strengthen and improve endurance, meditation is the number 1 exercise for that purpose.
I don’t do it out of any sense of kindness. I’ve found a logical reason to do it and it helps me get out of my own head (which is way too logical.) I’ve found myself becoming a bit more “kind” or just open to more social experiences that I might have been too rigid or stoic to allow myself to experience before.
I will check out your link.
By the way if you struggle just set out a 5 minute time every day you make yourself do it. Even if you were endlessly distracted the entire time it is a good exercise. Give that a go for a month and report back how you feel.