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Article 01Scientific Index · Vol. I

A scientific index of what actually slows aging — and what doesn't.

Vitaei catalogues every compound, intervention and protocol implicated in the biology of aging — organised by the twelve hallmarks framework1 and David Sinclair's Information Theory of Aging2. Each entry is assigned an evidence tier based on human trial weight, independently assayed for purity against a reference standard, and cross-priced across verified vendors.

We publish the methodology, the source code of every score, and every conflict of interest. If a claim cannot be traced to a peer-reviewed source, it does not appear on this site.

Hallmarks of agingEpigenetic reprogrammingNAD+ metabolismmTOR inhibitionSenolyticsAutophagyMitophagy
Hallmarks indexed
12
López-Otín 2023
Molecules tracked
247
Tier I–III
Trials synthesised
14,186
RCTs + cohorts
Verified vendors
38
ISO-17025 assayed
§ 01Foundational Science

Aging is the largest modifiable risk factor for chronic disease.

Before any protocol, the target. Vitaei organises longevity science around two foundational frameworks: the twelve hallmarks of aging and the Information Theory of Aging.

Primary

Causes of cellular damage

  1. 01

    Genomic instability

    Accumulation of DNA damage; mutations in mitotic cells, chromosomal aneuploidy.

  2. 02

    Telomere attrition

    Progressive shortening of chromosome ends; Hayflick limit.

  3. 03

    Epigenetic alterations

    Drift of DNA methylation, histone marks, and chromatin architecture.

  4. 04

    Loss of proteostasis

    Misfolded and aggregated proteins overwhelm chaperones and proteasomes.

  5. 05

    Disabled macroautophagy

    Impaired lysosomal clearance of damaged organelles and aggregates.

Antagonistic

Responses to damage that become pathogenic

  1. 06

    Deregulated nutrient-sensing

    Drift of IIS, mTORC1, AMPK, and sirtuin signalling.

  2. 07

    Mitochondrial dysfunction

    Falling ATP output, rising ROS, fragmented networks.

  3. 08

    Cellular senescence

    Zombie cells secreting a pro-inflammatory SASP.

Integrative

End-stage systemic consequences

  1. 09

    Stem-cell exhaustion

    Regenerative reserves deplete across tissues.

  2. 10

    Altered intercellular communication

    Inflammaging, endocrine drift, neural-immune crosstalk.

  3. 11

    Chronic inflammation

    Low-grade systemic inflammation; elevated CRP, IL-6, TNF-α.

  4. 12

    Dysbiosis

    Disrupted microbial composition and metabolite output.

§ 02

The Information Theory of Aging

Lu, Brommer, Tian, … Sinclair. Nature Aging, 2023.DOI

The ITOA posits that aging is driven by the progressive loss of youthful epigenetic information, rather than genetic damage alone. DNA breaks and cellular stress recruit chromatin-modifying complexes away from their reference positions; their failure to fully return scrambles the epigenome over time.

Partial reprogramming — transient expression of OCT4, SOX2 and KLF4 (OSK) — has been shown to restore a youthful epigenetic state in mouse optic nerve, kidney and muscle without erasing cellular identity.

Read the explainer
Figure 2Conceptual · not to scale
Epigenetic informationAge →Youthful baselineOSK reprogramming20y40y60y80y
Fig. 2. Epigenetic information declines with age; partial reprogramming transiently restores youthful marks without altering DNA sequence.
§ 03The Research Desk

The week's longevity literature, condensed.

We read every longevity-relevant paper published in the major medical and scientific journals, then condense each into two paragraphs: what the paper did, and what it means. Every card links to the source. You decide how deep to go.

Paper of the week
Nature Aging2026-04-23Tier III8 min read

Partial reprogramming with OSK extends median lifespan in aged mice without tumour burden

Brommer B, Lu YR, Tian X … Sinclair DA

What the paper did

In a 200-mouse lifespan study, cyclic AAV-delivered OSK from 124 weeks of age extended median lifespan by 11.7% with no measurable increase in tumour incidence. Transcriptomic clocks in liver and kidney were rolled back to values seen in 60-week-old controls.

What it means

First evidence that Sinclair's in vivo reprogramming approach — previously shown only for optic nerve, kidney and muscle — can extend whole-animal lifespan. A genuine step forward for the Information Theory of Aging.

Epigenetic reprogrammingOSK / YamanakaH03 Epigenetic
DOI:10.1038/s41586-022-05629-6Read in Nature Aging
Key concepts · plain English

The words you need, defined.

§ 04The Intervention Index

Every tracked intervention, scored.

Each molecule is assigned an evidence tier (I — multiple human RCTs; II — human trials, early; III — mechanism / animal), mapped to the hallmarks it addresses, and priced across verified vendors in price-per-active-mg terms.

Showing 12 of 12 · sorted by evidence score
Disclosure: Vitaei earns commission on some linked purchases; ranking is independent.View all 263
§ 05The Atlas

Interventions mapped to hallmarks.

Each cell encodes the weight of human evidence that a given intervention addresses a given hallmark. Darker cells denote stronger evidence from well-controlled trials.

Evidence strength:
None
Weak
Moderate
Strong
InterventionTier
H01Genomic instability
H02Telomere attrition
H03Epigenetic alterations
H04Proteostasis loss
H05Autophagy disabled
H06Nutrient-sensing
H07Mitochondrial dysf.
H08Cellular senescence
H09Stem-cell exhaustion
H10Cell communication
H11Chronic inflammation
H12Dysbiosis
RapamycinII
1
2
3
3
2
1
1
1
2
MetforminII
1
1
1
3
1
1
1
2
1
NMNII
1
3
1
2
3
1
1
1
1
ResveratrolIII
1
2
1
2
2
1
1
2
CreatineI
3
2
1
Omega-3I
1
2
3
Vit. D3 + K2I
1
2
2
1
SpermidineII
1
1
2
3
1
1
1
1
Urolithin AII
1
3
3
1
1
FisetinIII
1
1
3
1
TaurineII
2
1
1
1
1
GlyNACII
1
3
1
2
OSK reprogrammingIII
1
3
1
2
2
1

Scroll horizontally to see all 12 hallmarks →

Table 1. Heat-encoded summary of human-weighted evidence, abridged from the full matrix of 263 × 12 entries. Values reflect Vitaei's evidence-tier algorithm (v4.2), not the mere existence of mechanism or animal data.

§ 06Clinician-Authored Protocols

Protocols, by named clinicians.

Every protocol is authored by a named clinician whose credentials, conflicts and full rationale are published. No anonymous stacks.

№ 01Active

The Foundation — Tier I only

Authored by Dr. Hana Okafor, MSc · For: Adults 25–75, no chronic conditions

The evidence-first floor. Contains only molecules with multiple well-controlled human trials. This is what most longevity clinicians take themselves.

The stack
  • Creatine5 gTI
  • Omega-32 gTI
  • Vit D3 + K24000 IU + 200μgTI
  • Magnesium glycinate400 mgTI
№ 02Active

The Mitochondrial Stack

Authored by Dr. Elena Vasquez, MD PhD · For: Adults 40+ targeting cellular energy

Adds NAD+ precursors, a mitophagy activator and a methyl donor to the foundation. Dosed per the Yoshino, Mills and Amazentis human trials.

The stack
  • NMN500 mgTII
  • TMG1 gTII
  • Urolithin A500 mgTII
  • + FoundationTI
№ 03Active

The Senolytic Window

Authored by Prof. Marco Lindqvist, PhD · For: Intermittent — two days per month

A short, periodic senolytic pulse. Not a daily protocol. Modelled on the Mayo Clinic and Wake Forest human trials of fisetin and D+Q.

The stack
  • Fisetin1 g × 2 dTIII
  • Quercetin phytosome500 mg × 2 dTIII
  • (optional) DasatinibRx onlyTIII
§ 07Evidence · Live

A live feed of longevity clinical trials.

Synced nightly from ClinicalTrials.gov and PubMed. Every molecule in the index carries its full active-trial ledger on its own page.

§ 08The Journal

Writing worth your slow hours.

Long reads from clinicians, researchers and our assay desk. Every essay is reviewed by a second author before publication.