Evidence map›Paper›PMID 35778957›Full record

ReviewAging cell2022

Human age reversal: Fact or fiction?

Adiv A Johnson, Bradley W English, Maxim N Shokhirev, David A Sinclair, Trinna L Cuellar

Open access · goldAbstract readReview
In one paragraph

Review in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Adiv A JohnsonLongevity Sciences, Inc. (dba Tally Health), Greenwich, Connecticut, USA.ORCID 0000-0002-4740-2635
Bradley W EnglishBlavatnik Institute, Department of Genetics, Paul F. Glenn Center for Biology of Aging Research, Harvard Medical School, Boston, Massachusetts, USA.
Maxim N ShokhirevLongevity Sciences, Inc. (dba Tally Health), Greenwich, Connecticut, USA.
David A SinclairBlavatnik Institute, Department of Genetics, Paul F. Glenn Center for Biology of Aging Research, Harvard Medical School, Boston, Massachusetts, USA.
Trinna L CuellarLongevity Sciences, Inc. (dba Tally Health), Greenwich, Connecticut, USA.
Longevity Biotech (United States) · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although chronological age correlates with various age-related diseases and conditions, it does not adequately reflect an individual's functional capacity, well-being, or mortality risk. In contrast, biological age provides information about overall health and indicates how rapidly or slowly a person is aging. Estimates of biological age are thought to be provided by aging clocks, which are computational models (e.g., elastic net) that use a set of inputs (e.g., DNA methylation sites) to make a prediction. In the past decade, aging clock studies have shown that several age-related diseases, social variables, and mental health conditions associate with an increase in predicted biological age relative to chronological age. This phenomenon of age acceleration is linked to a higher risk of premature mortality. More recent research has demonstrated that predicted biological age is sensitive to specific interventions. Human trials have reported that caloric restriction, a plant-based diet, lifestyle changes involving exercise, a drug regime including metformin, and vitamin D3 supplementation are all capable of slowing down or reversing an aging clock. Non-interventional studies have connected high-quality sleep, physical activity, a healthy diet, and other factors to age deceleration. Specific molecules have been associated with the reduction or reversal of predicted biological age, such as the antihypertensive drug doxazosin or the metabolite alpha-ketoglutarate. Although rigorous clinical trials are needed to validate these initial findings, existing data suggest that aging clocks are malleable in humans. Additional research is warranted to better understand these computational models and the clinical significance of lowering or reversing their outputs.

Indexed as

DNA MethylationEpigenesis, GeneticAgingCaloric RestrictionHumansLife Styleaging clockbiological ageepigenetic agehealthspanlifespanlongevitymachine learningmortality

Identifiers

PMID35778957
PMCPMC9381899
OpenAlexW4283783381

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.