ReviewAging and disease2017
Aging, Metabolism, and Cancer Development: from Peto's Paradox to the Warburg Effect.
Review in Aging and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Pooled it
- Cholesterol sulfate replenishment rejuvenates aged hematopoietic stem cell phenomes.Theranostics · 2026Article
- The hippo pathway: a molecular bridge between environmental cues and pace of life.BMC ecology and evolution · 2025Review
- The mammalian longevity associated acetylome.Nature communications · 2025Article
- Systemic Rejuvenating Interventions: Perspectives on Neuroinflammation and Blood-Brain Barrier Integrity.Neurochemical research · 2025Review
- Older adults with cancer and common comorbidities-challenges and opportunities in improving their cancer treatment outcomes.Journal of the National Cancer Institute · 2024Article
- PTEN is both an activator and a substrate of chaperone-mediated autophagy.The Journal of cell biology · 2023Article
- Cell size, body size and Peto's paradox.BMC ecology and evolution · 2022Review
- Peroxiredoxin, Senescence, and Cancer.Cells · 2022Review
- Article
- [Detection of DNA methylation ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Article
- Editorial: Genomic alteration landscapes of aging, metabolic disorders, and cancer: Emerging overlaps and clinical importance.Frontiers in genetics · 2022Article
- Mutation or not, what directly establishes a neoplastic state, namely cellular immortality and autonomy, still remains unknown and should be prioritized in our research.Journal of Cancer · 2022Review
- A novel perspective suggesting high sustained energy expenditure may be net protective against cancer.Evolution, medicine, and public health · 2022Article
- Regulatory insights into progression of cancer and Alzheimer's disorder from autophagy perspective.Molecular biology reports · 2021Review
- Senescence marker protein 30 inhibits tumor growth by reducing HDAC4 expression in non-small cell lung cancer.Translational lung cancer research · 2021Article
- Protective Effects of Flavonoids Against Mitochondriopathies and Associated Pathologies: Focus on the Predictive Approach and Personalized Prevention.International journal of molecular sciences · 2021Review
- Noncanonical functions of glucocorticoids: A novel role for glucocorticoids in performing multiple beneficial functions in endometrial stem cells.Cell death & disease · 2021Article
- Remodeling the Epigenetic Landscape of Cancer-Application Potential of Flavonoids in the Prevention and Treatment of Cancer.Frontiers in oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Medical advances made over the last century have increased our lifespan, but age-related diseases are a fundamental health burden worldwide. Aging is therefore a major risk factor for cardiovascular disease, cancer, diabetes, obesity, and neurodegenerative diseases, all increasing in prevalence. However, huge inter-individual variations in aging and disease risk exist, which cannot be explained by chronological age, but rather physiological age decline initiated even at young age due to lifestyle. At the heart of this lies the metabolic system and how this is regulated in each individual. Metabolic turnover of food to energy leads to accumulation of co-factors, byproducts, and certain proteins, which all influence gene expression through epigenetic regulation. How these epigenetic markers accumulate over time is now being investigated as the possible link between aging and many diseases, such as cancer. The relationship between metabolism and cancer was described as early as the late 1950s by Dr. Otto Warburg, before the identification of DNA and much earlier than our knowledge of epigenetics. However, when the stepwise gene mutation theory of cancer was presented, Warburg's theories garnered little attention. Only in the last decade, with epigenetic discoveries, have Warburg's data on the metabolic shift in cancers been brought back to life. The stepwise gene mutation theory fails to explain why large animals with more cells, do not have a greater cancer incidence than humans, known as Peto's paradox. The resurgence of research into the Warburg effect has given us insight to what may explain Peto's paradox. In this review, we discuss these connections and how age-related changes in metabolism are tightly linked to cancer development, which is further affected by lifestyle choices modulating the risk of aging and cancer through epigenetic control.
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What OpenQuestion holds
Registered trials
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.