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: 4 complete abstracts (721 words), 10 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
The totality of characteristics of reproductive structure, functions, phenotype, and genotype, differentiating the MALE from the female organism.
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: Genotypic Sex; Sex, Genotypic; Phenotypic Sex; Sex, Phenotypic.
Where it fits in the MeSH classification
- Broader topics
- Reproductive Physiological Phenomena
- See also
- Libido; Psychosexual Development; Religion and Sex; Sexual Behavior; Sex Characteristics; Sex Determination Analysis
Related concepts
- Phenotype
- Genotype
- Female
Research landscape
PubMed indexes 7,786 records tagged with the MeSH heading “Sex” (counts retrieved 2026-10-31). 132 of them (1.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 6,663 records.
Reviews account for 409 records (5.3%) and meta-analyses for 8. Randomized controlled trials number 23 (0.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 6,663 |
| 2000-2009 | 643 |
| 2010-2019 | 348 |
| 2020 onward | 132 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 409 | 5.3% |
| Meta-analyses | 8 | 0.1% |
| Randomized controlled trials | 23 | 0.3% |
Method: PubMed query "Sex"[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 |
|---|---|---|---|---|
| Waning sexual function--the most important disease-specific distress for patients with prostate cancer | 1996 | Research article Design not recorded in structured metadata | 123 | cc by PMID 8645589 · DOI · PMC2074472 |
| How oxygen gave rise to eukaryotic sex | 2018 | Review article Design not recorded in structured metadata | 35 | cc by PMID 29436502 · DOI · PMC5829205 |
| Inflammatory Cytokine Pattern Is Sex-Dependent in Mouse Cutaneous Melanoma Experimental Model | 2017 | Research article Design not recorded in structured metadata | 32 | cc by PMID 29318162 · DOI · PMC5727748 |
| There is No Consensus on Biological Sex | 2026 | Research article Design not recorded in structured metadata | 13 | cc by PMID 41786319 · DOI · PMC12962796 |
Waning sexual function--the most important disease-specific distress for patients with prostate cancer [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The objective was to investigate how prostate cancer and its treatment affects sexual, urinary and bowel functions and to what extent eventual complications cause distress.
- Closing excerpt
- A decline in sexual functions was the most common cause of disease-specific distress in men with prostate 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 (194 words)
The objective was to investigate how prostate cancer and its treatment affects sexual, urinary and bowel functions and to what extent eventual complications cause distress. A questionnaire was sent to 431 men aged 50-80 years with prostate cancer diagnosed in 1992 in the Stockholm area (Sweden) and 435 randomly selected men with a similar age distribution. Sexual function, as compared with their youth, was diminished in a majority of all men. The prostate cancer patients were, however, more likely to report low frequency and/or intensity in all aspects of sexual function. A majority of the men were distressed by a waning sexual capacity. The proportion of men with prostate cancer who were severely distressed owing to a decline in sexual function was larger than in the reference group. The willingness to trade off an intact sexual function for long-term survival varied considerably among the men in the reference group. Urinary and bowel symptoms were less common than a waning sexual function in both groups, and few appeared to be severely distressed by urinary or bowel symptoms. A decline in sexual functions was the most common cause of disease-specific distress in men with prostate cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 8645589 · DOI · PMC2074472
How oxygen gave rise to eukaryotic sex [2]
Abstract reading summary — source excerpts
- Opening excerpt
- How did full meiotic eukaryotic sex evolve and what was the immediate advantage allowing it to develop?
- Closing excerpt
- Here, we discuss the relevant observations underpinning this model.
- 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 (207 words)
How did full meiotic eukaryotic sex evolve and what was the immediate advantage allowing it to develop? We propose that the crucial determinant can be found in internal reactive oxygen species (ROS) formation at the start of eukaryotic evolution approximately 2 × 109 years ago. The large amount of ROS coming from a bacterial endosymbiont gave rise to DNA damage and vast increases in host genome mutation rates. Eukaryogenesis and chromosome evolution represent adaptations to oxidative stress. The host, an archaeon, most probably already had repair mechanisms based on DNA pairing and recombination, and possibly some kind of primitive cell fusion mechanism. The detrimental effects of internal ROS formation on host genome integrity set the stage allowing evolution of meiotic sex from these humble beginnings. Basic meiotic mechanisms thus probably evolved in response to endogenous ROS production by the 'pre-mitochondrion'. This alternative to mitosis is crucial under novel, ROS-producing stress situations, like extensive motility or phagotrophy in heterotrophs and endosymbiontic photosynthesis in autotrophs. In multicellular eukaryotes with a germline-soma differentiation, meiotic sex with diploid-haploid cycles improved efficient purging of deleterious mutations. Constant pressure of endogenous ROS explains the ubiquitous maintenance of meiotic sex in practically all eukaryotic kingdoms. Here, we discuss the relevant observations underpinning this model.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29436502 · DOI · PMC5829205
Inflammatory Cytokine Pattern Is Sex-Dependent in Mouse Cutaneous Melanoma Experimental Model [3]
Abstract reading summary — source excerpts
- Opening excerpt
- We present the evaluation of inflammatory cytokines in mouse cutaneous melanoma experimental model, as markers of disease evolution.
- Closing excerpt
- Various serum cytokines correlated with the disease evolution in cutaneous melanoma mouse model.
- 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 (195 words)
We present the evaluation of inflammatory cytokines in mouse cutaneous melanoma experimental model, as markers of disease evolution. Moreover, to test our experimental model, we have used low doses of dacarbazine (DTIC). C57 BL/6J mouse of both sexes were subjected to experimental cutaneous melanoma and treated with low doses of DTIC. Clinical parameters and serum cytokines were followed during tumor evolution and during DTIC therapy. Cytokine/chemokine pattern was assessed using xMAP technology and the following molecules were quantified: interleukins (IL)-1-beta, IL-6, IL-10, IL-12 (p70), interferon (IFN)-gamma, granulocyte macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor (TNF)-alpha, macrophage inflammatory protein (MIP)-1alpha, monocyte chemoattractant protein (MCP-1), and keratinocyte-derived chemokine (KC). Significant differences were found between normal females and males mice, female mice having a statistically higher serum concentration of IL-1-beta compared to male mice, while males have a significantly higher concentration of MIP-1-alpha. During melanoma evolution in the female group, IL-1-beta, MIP-1-alpha, and KC circulatory levels were found 10-fold increased, while other cytokines doubled their values. In the male mice group, only circulatory KC increased 4 times, while IL-1-beta and TNF-alpha doubled their circulatory values. Various serum cytokines correlated with the disease evolution in cutaneous melanoma mouse model.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29318162 · DOI · PMC5727748
There is No Consensus on Biological Sex [4]
Abstract reading summary — source excerpts
- Opening excerpt
- There is ongoing scientific and societal discourse on the definition of biological sex.
- Closing excerpt
- Most importantly, regardless of scientific debates, no biological definition of sex should be used to dictate human rights.
- 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 (125 words)
There is ongoing scientific and societal discourse on the definition of biological sex. At this critical moment when misinformation about sex is being applied to policy globally, scientific clarification is valuable. Here, we evaluate the primary approaches to defining sex and synthesise the active discourse to conclude that there is no current consensus on a definition of sex that is free of assumptions and limitations. While there is no current consensus, we do not advocate for a single definition and contend that a lack of unanimity is not inherently problematic. No matter what definitional choices are used, we provide actionable recommendations to improve accuracy when describing sex. Most importantly, regardless of scientific debates, no biological definition of sex should be used to dictate human rights.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41786319 · DOI · PMC12962796
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 Female gender as a risk factor for torsades de pointes associated with cardiovascular drugs [5]
- Research article Sex hormones and hypertension [6]
- Research article Why sex and recombination? [7]
- Research article Renin angiotensin system and gender differences in the cardiovascular system [8]
- Research article Gender, sex hormones and autonomic nervous control of the cardiovascular system [9]
- Research article Rodent sex differences in emotional and related behavior [10]
References
- Helgason AR, Adolfsson J, Dickman P, Fredrikson M, Arver S, Steineck G. Waning sexual function--the most important disease-specific distress for patients with prostate cancer. . 1996. PMID 8645589 · DOI · PMC2074472
- Hörandl E, Speijer D. How oxygen gave rise to eukaryotic sex. . 2018. PMID 29436502 · DOI · PMC5829205
- Surcel M, Constantin C, Caruntu C, Zurac S, Neagu M. Inflammatory Cytokine Pattern Is Sex-Dependent in Mouse Cutaneous Melanoma Experimental Model. . 2017. PMID 29318162 · DOI · PMC5727748
- Eppley MG, Lee A, Dellinger R, Swank A. There is No Consensus on Biological Sex. . 2026. PMID 41786319 · DOI · PMC12962796
- Makkar RR, Fromm BS, Steinman RT, Meissner MD, Lehmann MH. Female gender as a risk factor for torsades de pointes associated with cardiovascular drugs. JAMA. 1993. PMID 8230644 · DOI
- Dubey RK, Oparil S, Imthurn B, Jackson EK. Sex hormones and hypertension. Cardiovasc Res. 2002. PMID 11861040 · DOI
- Barton NH, Charlesworth B. Why sex and recombination?. Science. 1998. PMID 9748151 · DOI
- Fischer M, Baessler A, Schunkert H. Renin angiotensin system and gender differences in the cardiovascular system. Cardiovasc Res. 2002. PMID 11861038 · DOI
- Dart AM, Du XJ, Kingwell BA. Gender, sex hormones and autonomic nervous control of the cardiovascular system. Cardiovasc Res. 2002. PMID 11861039 · DOI
- Archer J. Rodent sex differences in emotional and related behavior. Behav Biol. 1975. PMID 1100044 · DOI
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.