Arete

Aging & longevity

How old you really are — and how fast you're aging. The bedrock metric and the twelve mechanisms beneath it.

The bedrock metric

Aging is a rate, not a number — and a rate can be slowed.

Arete's primary biological target is the pace of aging itself, measured against the twelve hallmarks the longevity field is organised around.

Biological AgeEpigenetics — the bedrock metric

DNA-methylation clocks read patterns in your DNA to calculate biological age. Horvath predicts chronological age; PhenoAge tracks disease phenotype; GrimAge is the most mortality-predictive; and DunedinPACE is the speedometer — it measures your rate of aging, not your age. Bryan Johnson's ~0.69 means he ages ~8 months per 12. TruDiagnostic's TruAge runs every clock from one blood draw; SYMPHONYAge breaks the result down per organ system, so we can see which modalities move which organs. The challenge is latency — epigenetic tests run only every 3–6 months, so we build a daily proxy from HRV, resting HR, sleep consistency and VO₂max, calibrated against the quarterly ground truth.

DunedinPACEGrimAgePhenoAgeTelomere length
How does the Arete experience shift DunedinPACE over 90 days?

The four aging clocks

ClockWhat it readsBest for
HorvathDNA methylation across tissuesThe original chronological-age clock
PhenoAgeMethylation tuned to disease phenotypeMorbidity & mortality risk
GrimAgeMethylation + plasma protein surrogatesThe most mortality-predictive
DunedinPACERate of methylation changeThe speedometer — pace of aging

DunedinPACE — the speedometer

Most clocks tell you how old your body looks; DunedinPACE tells you how fast it is aging right now. Bryan Johnson's ~0.69 means his body ages roughly 8 months for every 12 calendar months. A value under 0.80 is the headline number the app exists to move — and the one a 90-day Arete membership is designed to shift.

SYMPHONYAge — a biological age per organ

Organ systemPrimary Arete lever
CardiovascularInfrared sauna — heat as a cardiovascular stressor
Metabolic & immuneCold exposure — brown fat, anti-inflammatory shift
MusculoskeletalThe fitness floor — load and progressive overload
BrainSleep architecture + breathwork

Telomeres — the proof-of-rejuvenation number

Telomeres are the protective caps on chromosomes that shorten with each cell division. Johnson reported a 2.6% telomere extension (10.3 → 11.4 kb) after his HBOT protocol, with telomerase activity comparable to a 12-year-old. Tested bi-annually, it is one of the most legible 'younger than last time' numbers a member can receive.

The latency problem — bridging the gap with daily proxies

Epigenetic tests can only run every 3–6 months. The R&D work is the calibration study: build a daily biological-age proxy from continuous signals — HRV trend, resting heart rate, sleep consistency and VO₂max trajectory — and tune the weighting against real TruAge results until the proxy tracks the ground truth. The weighting isn't uniform: sleep and HRV dominate for sedentary members; VO₂max and RHR for athletes who already sleep well.

PhenoAge from a standard panel — the middle tier

Between the daily proxy and the bi-annual epigenetic test sits a measure most protocols overlook. PhenoAge can be computed from nine standard blood markers — albumin, creatinine, glucose, hsCRP, lymphocyte %, mean cell volume, red-cell distribution width, alkaline phosphatase and white-blood-cell count. Every member doing the quarterly panel gets a PhenoAge reading at no extra cost; its trajectory becomes a meaningful intermediate outcome.

The 12 hallmarks of agingLópez-Otín · Cell 2023
PrimaryHallmarks 1–4

The initiating causes of cellular damage — they happen first.

  • 01Genomic instability
  • 02Telomere attrition
  • 03Epigenetic alterations
  • 04Loss of proteostasis
AntagonisticHallmarks 5–8

The body's responses to damage — protective at first, harmful when chronic.

  • 05Disabled macroautophagy
  • 06Deregulated nutrient sensing
  • 07Mitochondrial dysfunction
  • 08Cellular senescence
IntegrativeHallmarks 9–12

The downstream consequences that produce the tissue dysfunction of aging.

  • 09Stem-cell exhaustion
  • 10Altered intercellular communication
  • 11Chronic inflammation (inflammaging)primary target
  • 12Dysbiosis