Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (564 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A state of insufficient flesh on the body usually defined as having a body weight less than skeletal and physical standards, such as body mass index, and dependent on age, sex, and genetic background.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Leanness; Underweight.
Where it fits in the MeSH classification
- Broader topics
- Body Weight
- Narrower topics
- Cachexia; Emaciation
- See also
- Emaciation
Related concepts
Research landscape
PubMed indexes 16,874 records tagged with the MeSH heading “Thinness” (counts retrieved 2026-10-31). 4,894 of them (29.0%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 6,046 records.
Reviews account for 2,518 records (14.9%) and meta-analyses for 258. Randomized controlled trials number 503 (3.0%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,911 |
| 2000-2009 | 3,023 |
| 2010-2019 | 6,046 |
| 2020 onward | 4,894 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,518 | 14.9% |
| Meta-analyses | 258 | 1.5% |
| Randomized controlled trials | 503 | 3.0% |
Method: PubMed query "Thinness"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Hepatic gluconeogenesis and PDK3 upregulation drive cancer cachexia in flies and mice | 2025 | Research article Design not recorded in structured metadata | 40 | cc by PMID 40275022 · DOI · PMC12021660 |
| Cancer cachexia: molecular basis and therapeutic advances | 2026 | Review article Design not recorded in structured metadata | 32 | cc by PMID 41526343 · DOI · PMC12795897 |
| Cancer therapy and cachexia | 2025 | Review article Design not recorded in structured metadata | 28 | cc by PMID 40759570 · DOI · PMC12321403 |
Hepatic gluconeogenesis and PDK3 upregulation drive cancer cachexia in flies and mice [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Cachexia, a severe wasting syndrome characterized by tumour-induced metabolic dysregulation, is a leading cause of death in people with cancer, yet its underlying mechanisms remain poorly understood.
- Closing excerpt
- This study highlights the conserved nature of tumour-induced metabolic disruptions and identifies potential therapeutic targets to mitigate cachexia in people with cancer.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (146 words)
Cachexia, a severe wasting syndrome characterized by tumour-induced metabolic dysregulation, is a leading cause of death in people with cancer, yet its underlying mechanisms remain poorly understood. Here we show that a longitudinal full-body single-nuclei-resolution transcriptome analysis in a Drosophila model of cancer cachexia captures interorgan dysregulations. Our study reveals that the tumour-secreted interleukin-like cytokine Upd3 induces fat-body expression of Pepck1 and Pdk, key regulators of gluconeogenesis, disrupting glucose metabolism and contributing to cachexia. Similarly, in mouse cancer cachexia models, we observe IL-6-JAK-STAT-signalling-mediated induction of Pck1 and Pdk3 expression in the liver. Increased expression of these genes in fly, mouse, and human correlates with poor prognosis, and hepatic expression of Pdk3 emerges as a previously unknown mechanism contributing to metabolic dysfunction in cancer cachexia. This study highlights the conserved nature of tumour-induced metabolic disruptions and identifies potential therapeutic targets to mitigate cachexia in people with cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40275022 · DOI · PMC12021660
Cancer cachexia: molecular basis and therapeutic advances [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The dynamic interplay between neoplastic cells and the host has been increasingly recognized as important players in the pathogenesis of cancer cachexia, a syndrome affecting ~50-80% of cancer patients with various incidences of different types of malignancies.
- Closing excerpt
- Notably, targeting the multifaceted interplay of organismal metabolic remodeling and cancer-associated inflammation holds great promise for clinical translation, as illustrated by a series of innovative therapeutic strategies and ongoing clinical trials aimed at mitigating cachexia in cancer patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (216 words)
The dynamic interplay between neoplastic cells and the host has been increasingly recognized as important players in the pathogenesis of cancer cachexia, a syndrome affecting ~50-80% of cancer patients with various incidences of different types of malignancies. Despite its prevalence, a comprehensive understanding of cancer cachexia progression, with a holistic view at the cross-organismal, cellular and molecular levels, remains elusive. In this review, we undertake an in-depth exploration of the relevant target organs and their regulatory roles in cancer cachexia, with a particular focus on macroenvironmental interactions via various organismal crosstalk axes. Moreover, we highlight how systemic metabolic remodeling, a hallmark of cancer cachexia, plays essential roles in modulating the inflammatory responses of immune and stromal cells in the tumor microenvironment (TME). These cellular responses, in turn, disrupt energy metabolism in distant organs and perturb organismal homeostasis by secreting a variety of mediators that activate specific signaling pathways, thereby fostering a vicious cycle that exacerbates cancer cachexia. We comprehensively summarize these complex cellular and molecular networks that constitute reciprocally regulatory dynamics between systemic metabolic reprogramming and inflammatory cascades. Notably, targeting the multifaceted interplay of organismal metabolic remodeling and cancer-associated inflammation holds great promise for clinical translation, as illustrated by a series of innovative therapeutic strategies and ongoing clinical trials aimed at mitigating cachexia in cancer patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41526343 · DOI · PMC12795897
Cancer therapy and cachexia [3]
Abstract reading summary — source excerpts
- Opening excerpt
- A central challenge in cancer therapy is the effective delivery of anticancer treatments while minimizing adverse effects on patient health.
- Closing excerpt
- Such integrative approaches may better capture therapeutic efficacy while preserving patient well-being.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (202 words)
A central challenge in cancer therapy is the effective delivery of anticancer treatments while minimizing adverse effects on patient health. The potential dual impact of therapy is clearly illustrated in cancer-associated cachexia, a multifactorial syndrome characterized by involuntary weight loss, systemic inflammation, metabolic dysregulation, and behavioral alterations such as anorexia and apathy. While cachexia research often focuses on tumor-driven mechanisms, the literature indicates that cancer therapies themselves, particularly chemotherapies and targeted treatments, can initiate or exacerbate the biological pathways driving this syndrome. Here, we explore how therapeutic interventions intersect with the pathophysiology of cachexia, focusing on key organ systems including muscle, adipose tissue, liver, heart, and brain. We highlight examples such as therapy-induced upregulation of IL-6 and growth-differentiation factor 15, both contributing to reduced nutrient intake and a negative energy balance via brain-specific mechanisms. At the level of nutrient release and organ atrophy, chemotherapies also converge with cancer progression, for example, activating NF-κB in muscle and PKA/CREB signaling in adipose tissue. By examining how treatment timing and modality align with the natural trajectory of cancer cachexia, we underscore the importance of incorporating physiological endpoints alongside tumor-centric metrics in clinical trials. Such integrative approaches may better capture therapeutic efficacy while preserving patient well-being.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40759570 · DOI · PMC12321403
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Global prevalence, incidence, and outcomes of non-obese or lean non-alcoholic fatty liver disease: a systematic review and meta-analysis [4]
- Research article The effect of experimental presentation of thin media images on body satisfaction: a meta-analytic review [5]
- Research article BMI and all-cause mortality in older adults: a meta-analysis [6]
- Research article Cancer cachexia in adult patients: ESMO Clinical Practice Guidelines☆ [7]
- Research article The Spectrum of Malnutrition/Cachexia/Sarcopenia in Oncology According to Different Cancer Types and Settings: A Narrative Review [8]
- Research article Cancer cachexia and its pathophysiology: links with sarcopenia, anorexia and asthenia [9]
References
- Liu Y, Dantas E, Ferrer M, Miao T, Qadiri M, Liu Y, et al.. Hepatic gluconeogenesis and PDK3 upregulation drive cancer cachexia in flies and mice. . 2025. PMID 40275022 · DOI · PMC12021660
- Tan Y, Xue R, Pan Y, He Z, Hu X, Li Y, et al.. Cancer cachexia: molecular basis and therapeutic advances. . 2026. PMID 41526343 · DOI · PMC12795897
- Thakir TM, Wang AR, Decker-Farrell AR, Ferrer M, Guin RN, Kleeman S, et al.. Cancer therapy and cachexia. . 2025. PMID 40759570 · DOI · PMC12321403
- Ye Q, Zou B, Yeo YH, Li J, Huang DQ, Wu Y, et al.. Global prevalence, incidence, and outcomes of non-obese or lean non-alcoholic fatty liver disease: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2020. PMID 32413340 · DOI
- Groesz LM, Levine MP, Murnen SK. The effect of experimental presentation of thin media images on body satisfaction: a meta-analytic review. Int J Eat Disord. 2002. PMID 11835293 · DOI
- Winter JE, MacInnis RJ, Wattanapenpaiboon N, Nowson CA. BMI and all-cause mortality in older adults: a meta-analysis. Am J Clin Nutr. 2014. PMID 24452240 · DOI
- Arends J, Strasser F, Gonella S, Solheim TS, Madeddu C, Ravasco P, et al.. Cancer cachexia in adult patients: ESMO Clinical Practice Guidelines☆. ESMO Open. 2021. PMID 34144781 · DOI · PMC8233663
- Bossi P, Delrio P, Mascheroni A, Zanetti M. The Spectrum of Malnutrition/Cachexia/Sarcopenia in Oncology According to Different Cancer Types and Settings: A Narrative Review. Nutrients. 2021. PMID 34207529 · DOI · PMC8226689
- Peixoto da Silva S, Santos JMO, Costa E Silva MP, Gil da Costa RM, Medeiros R. Cancer cachexia and its pathophysiology: links with sarcopenia, anorexia and asthenia. J Cachexia Sarcopenia Muscle. 2020. PMID 32142217 · DOI · PMC7296264
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.