Evidence map›Paper›PMID 23860844›Full record

ArticleBiogerontology2013

Assessing biological aging: the origin of deficit accumulation.

Arnold Mitnitski, Xiaowei Song, Kenneth Rockwood

Abstract read
In one paragraph

Article in Biogerontology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

82 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Does lifestyle intervention lower clinically significant cognitive impairment risk?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Trial
  5. Frailty Change and Major Osteoporotic Fracture in the Elderly: Data from the Global Longitudinal Study of Osteoporosis in Women 3-Year Hamilton Cohort.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016
    Trial
  6. Trial
  7. Embracing non-linearity in human ageing.Nature reviews. Genetics · 2026
    Review
  8. Review
  9. FI-CGA and eFI-CGA in Frailty Care: a Scoping Review.Canadian geriatrics journal : CGJ · 2026
    Review
  10. Article
  11. Neural embedding of frailty in cognitively unimpaired aging and dementia across Latin America.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Observational
  17. Frailty in Critically Ill Patients with COVID-19: The Lessons Learned.Advances in experimental medicine and biology · 2024
    Review
  18. Review
  19. Article
  20. Genetic and Environmental Influences on Longitudinal Frailty Trajectories From Adulthood into Old Age.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023
    Article

22 more citing papers are in PubMed but not listed here.

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

3 authors.

Arnold MitnitskiDepartment of Medicine, Dalhousie University, Suite 229-5790 University Ave., Halifax, NS, B3H 1V7, Canada, arnold.mitnitski@dal.ca.
Xiaowei Song
Kenneth Rockwood

Funding

Canadian Institutes of Health Research MOP24388
6 · The paper itself

Abstract

The health of individuals is highly heterogeneous, as is the rate at which they age. To account for such heterogeneity, we have suggested that an individual's health status can be represented by the number of health deficits (broadly defined by biological and clinical characteristics) that they accumulate. This allows health to be expressed in a single number: the frailty index (FI) is the ratio of the deficits present in a person to the total number of deficits considered (e.g. in a given database or experimental procedure). Changes in the FI characterize the rate of individual aging. The behavior of the FI is highly characteristic: it shows an age specific, nonlinear increase, (similar to Gompertz law), higher values in females, strong associations with adverse outcomes (e.g., mortality), and a universal limit to its increase (at FI ~0.7). These features have been demonstrated in dozens of studies. Even so, little is known about the origin of deficit accumulation. Here, we apply a stochastic dynamics framework to illustrate that the average number of deficits present in an individual is the product of the average intensity of the environmental stresses and the average recovery time. The age-associated increase in recovery time results in the accumulation of deficits. This not only explains why the number of deficits can be used to estimate individual differences in aging rates, but also suggests that targeting the recovery rate (e.g. by preventive or therapeutic interventions) will decrease the number of deficits that individuals accumulate and thereby benefit life expectancy.

Indexed as

AgingHealth StatusModels, BiologicalAgedAged, 80 and overAge FactorsAnimalsFemaleFrail ElderlyGeriatric AssessmentHumansMaleRecovery of FunctionStochastic ProcessesStress, PhysiologicalTime Factors

Identifiers

PMID23860844
PMCPMC3847281

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.