Nutrition and cellular-senescence biomarkers: a systematic review of 27 human trials
Across 27 human trials with 3811 participants, nutritional interventions most often changed circulating inflammatory and secretory senescence-associated markers, while cell-cycle-arrest markers and telomere length were largely unchanged or variable. [1]
Automatic summary · not editorially reviewed
The key findings
The review included 29 articles covering 27 human trials with 3811 participants and searched four databases to 10 September 2024. [1]
Calorie restriction produced the most recurrent reductions in circulating inflammatory and secretory SASP-panel factors and senescence-associated transcriptomic signatures. [1]
Because SASP factors and circulating cytokines are heterogeneous and not specific to senescent cells, the authors interpret findings as possible modulation of senescence-associated markers, not definitive effects on senescence burden. [1]
The source at a glance
- Study type / format
- Systematic review of interventional human studies (abstract)
- Population / context
- Participants in 27 interventional human studies (3811 participants) assessing nutritional strategies and cellular-senescence biomarkers.
- Summary based on
- Study abstract
- Original publication
- July 4, 2026
Senescence biomarkers in 27 human nutrition trials
The review asked whether nutritional strategies affect biomarkers of cellular senescence in humans. Cellular senescence is described as stable cell-cycle arrest plus a pro-inflammatory secretory phenotype. The authors searched four databases from inception to 10 September 2024 and included interventional human studies reporting senescence biomarkers: cell-cycle-arrest markers, DNA damage, telomere length, transcriptomic signatures and senescence-associated secretory phenotype (SASP) factors. They included 29 articles covering 27 trials and 3811 participants.
Supporting source [1]
Calorie restriction and SASP markers; supplements limited
Nutritional interventions changed several senescence biomarkers to varying degrees. Calorie restriction produced the most recurrent reductions in circulating inflammatory and secretory factors commonly included in SASP panels, and in senescence-associated transcriptomic signatures. Classical cell-cycle-arrest markers such as CDKN2A/p16 and CDKN1A/p21 and telomere length were largely unchanged or highly variable. Calorie-restriction mimetics, particularly metformin and rapamycin, showed context-dependent effects, most evident under metabolic or physiological stress. Among supplements, n-3 polyunsaturated fatty acids may modulate selected inflammatory/SASP-related circulating markers, but supplement evidence remains limited and heterogeneous.
Supporting source [1]
Markers may shift without lower senescence burden
The authors conclude that nutritional interventions may preferentially affect senescence-associated inflammatory and secretory biomarker profiles, particularly SASP-related mediators, rather than markers more directly tied to senescent cell abundance. Because SASP factors and circulating cytokines are heterogeneous and not specific to senescent cells, they read these findings as possible modulation of senescence-associated markers, not definitive effects on senescence burden. They recommend multi-marker, functionally relevant endpoints in future clinical studies on biological ageing. This is an abstract; the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The review covers interventional human studies, but the abstract gives no per-trial sample sizes, follow-up durations or effect sizes. SASP factors and circulating cytokines are heterogeneous and not specific to senescent cells, so marker changes do not establish reduced senescence burden.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Lin Y, Altulea A, Demaria M. · europepmc.org · July 4, 2026