Research
Bromhidrosis (Body Odor Disorder): Research Overview
Bromhidrosis is the clinical term for abnormal or excessive body odor, most often from the underarms. In its apocrine form, lipid-rich apocrine secretions are themselves odorless but become malodorous when skin bacteria break them down. In one large survey of Chinese higher-education students, 7.5% reported axillary apocrine bromhidrosis, and genetic studies tie the condition tightly to the "wet" earwax variant of the ABCC11 gene, present in about 99% of osmidrosis patients versus roughly 35% of the general population. This page compiles the verified prevalence, genetic, and treatment-outcome figures. It is general education, not a diagnosis.
By the Sweat Explained Editorial Team · Published 2026-07-13 · Last reviewed 2026-07-13 · Educational information, not medical advice.
Key statistics at a glance
7.5%
prevalence of axillary apocrine bromhidrosis among surveyed Chinese higher-education students (194/2,571)
Zhang 2023 survey
98.7%
of axillary osmidrosis patients carried the ABCC11 wet-type (GG/GA) genotype, vs 35.4% of controls
Nakano 2009
68.0%
of bromhidrosis cases reported a positive family history (132/194)
Zhang 2023 survey
60.3%
of bromhidrosis cases had wet (sticky) earwax (117/194)
Zhang 2023 survey
What bromhidrosis is
Bromhidrosis (also written bromidrosis, and closely overlapping with the term "osmidrosis") is excessive or abnormal body odor produced when skin bacteria and yeasts decompose gland secretions and cellular debris. The apocrine form is the one most associated with underarm odor: apocrine secretions are lipid-rich, initially sterile and odorless, and become odoriferous only after bacteria on the skin surface convert them into volatile acids. A separate eccrine form arises when bacteria degrade keratin softened by watery eccrine sweat, and can be influenced by foods such as garlic, onion, and curry.
Apocrine glands become active after puberty, which is why apocrine bromhidrosis typically begins in the teenage years. Because the odor depends on the interaction between gland secretions and skin microbes, it sits at the intersection of glandular activity and the skin microbiome rather than being a sweating disorder alone.
Onset clusters around puberty
In the Chinese survey of 2,571 students, most people who reported axillary apocrine bromhidrosis dated its onset to early adolescence, consistent with apocrine glands switching on after puberty. The chart shows the age-of-onset distribution among the 194 affected respondents.
| Group | Value |
|---|---|
| Under 10 yrs | 12.37% |
| 11–15 yrs | 53.09% |
| 15–20 yrs | 26.82% |
| 21–25 yrs | 7.22% |
Source: Zhang L, et al., Front Med (Lausanne) 2023;10:1232744. Chart is an original rendering of the cited data.
How common is it?
The best single prevalence figure comes from a 2023 cross-sectional survey of 2,571 Chinese higher-education students (conducted September–December 2021), which found axillary apocrine bromhidrosis in 7.5% (194/2,571). Rates were broadly similar by sex: 8.4% of men (84/1,005) and 7.0% of women (110/1,566). This is a self-reported, single-country student sample, so it should be read as an estimate within that population rather than a global rate.
That population matters. Apocrine bromhidrosis is closely tied to the ABCC11 gene, and the frequency of the odor-associated variant differs substantially between ancestries. A prevalence measured in a Chinese cohort will not necessarily transfer to populations with a very different distribution of that gene, so no single worldwide percentage is well established.
The ABCC11 "wet earwax" link
Apocrine odor and earwax type are governed by the same gene. A single change in ABCC11 (the SNP rs17822931) determines whether earwax is wet or dry; the same "wet" allele is associated with more active odor-producing apocrine secretion. In a Japanese genotyping study, nearly every axillary osmidrosis patient carried at least one copy of the wet-type G allele.
| Group | Wet-type (GG or GA) genotype | Notes |
|---|---|---|
| Axillary osmidrosis patients (n=79) | 98.7% (78/79) | Only 1 patient had the dry-type AA genotype |
| General population controls (n=161) | 35.4% (57/161) | Baseline wet-type frequency in this sample |
Difference significant at p < 1.1 × 10⁻²⁴ (Fisher's exact test). The wet allele appears necessary for strong apocrine odor, but carrying it does not guarantee bromhidrosis; 35% of unaffected controls also had it. Association is not the same as an individual diagnosis.
Family history and heritability
Because a single common gene drives so much of the trait, bromhidrosis clusters in families. In the survey, 68.0% of affected respondents (132/194) reported a positive family history, and 60.3% (117/194) had wet, sticky earwax, the outward marker of the same ABCC11 variant. These figures line up with a largely inherited, autosomal-influenced trait rather than a purely acquired one.
It is worth being precise about what "genetic" means here: the ABCC11 variant strongly raises the likelihood of odor-producing apocrine secretion, but skin bacteria, hygiene, hair, and clothing all shape whether and how much odor is actually noticeable day to day.
Treatment-outcome signals
Management options described in clinical references range from conservative measures (antibacterial washes, hair removal, prompt changing of sweaty clothing, and topical antibiotics such as clindamycin or erythromycin) to procedures including botulinum toxin, energy-based devices, and surgery, with results that vary by method and patient. Deodorants mask odor while aluminum-salt antiperspirants are designed to reduce underarm wetness; neither is endorsed here, and product choice is an individual decision.
Outcome data from the survey is limited but suggestive: among the 38 respondents who had received treatment, 73.7% reported a moderate-to-good response and 26.3% a poor response. This is self-reported, mixes different treatments together, and comes from a small subgroup, so it indicates only that many, but not all, people improve with treatment. Persistent or distressing body odor is worth discussing with a clinician, who can rule out other causes and review options.
Methodology and limitations
Prevalence, family-history, age-of-onset, and treatment-response figures are from a 2023 cross-sectional questionnaire survey of 2,571 Chinese higher-education students (Zhang L, et al., Front Med). The ABCC11 genotype figures are from a case-control genotyping study (Nakano M, et al., BMC Genetics 2009). The clinical definition and treatment overview draw on a professional dermatology reference (MSD Manual). Each figure was traced to its source page and confirmed.
Limitations: the prevalence and outcome data are self-reported and come from a single-country student sample, so they may not generalize to other ages or populations, particularly because the underlying ABCC11 variant frequency differs by ancestry. The genotype association shows that the wet-type allele is near-universal among osmidrosis patients, but roughly a third of unaffected controls carry it too, so genotype predicts susceptibility, not a diagnosis. Nothing here is medical advice.
Frequently asked questions
- How common is bromhidrosis?
- In a 2023 survey of 2,571 Chinese higher-education students, 7.5% reported axillary apocrine bromhidrosis (8.4% of men, 7.0% of women). That is a single-population self-reported estimate; a well-established global rate does not exist because the underlying gene varies by ancestry.
- Is bromhidrosis genetic?
- Largely, yes. It is tightly linked to the ABCC11 gene: 98.7% of axillary osmidrosis patients carried the wet-type genotype versus 35.4% of controls (Nakano 2009), and 68% of affected survey respondents reported a family history. Bacteria and hygiene still influence how much odor is noticeable.
- What does earwax have to do with body odor?
- The same ABCC11 variant determines both. People with the wet, sticky earwax type carry the allele associated with odor-producing apocrine secretion; those with dry, flaky earwax usually do not. In the survey, 60% of bromhidrosis cases had wet earwax.
- When does apocrine bromhidrosis start?
- Usually around puberty, when apocrine glands become active. In the survey, about 53% of cases dated onset to ages 11–15 and roughly 27% to ages 15–20.
- Can it be treated?
- Options range from antibacterial hygiene measures and topical antibiotics to botulinum toxin, energy-based devices, and surgery, with variable results. In the survey's small treated subgroup, about 74% reported a moderate-to-good response. Persistent or distressing odor is worth discussing with a clinician.
- Does carrying the wet-type gene mean I will have body odor?
- No. The wet-type allele appears necessary for strong apocrine odor, but it is not sufficient; about 35% of unaffected people in the control group carried it. Genotype indicates susceptibility, not a diagnosis.
Sources
Primary peer-reviewed studies and official sources first, then reviews and institutional framing (secondary).
- Zhang L, et al. Epidemiological analysis of axillary apocrine bromhidrosis in China: a survey from Chinese higher education students. Front Med (Lausanne). 2023;10:1232744. doi:10.3389/fmed.2023.1232744. Prevalence 7.5% (194/2,571). Full text
- Nakano M, Miwa N, Hirano A, Yoshiura K, Niikawa N. A strong association of axillary osmidrosis with the wet earwax type determined by genotyping of the ABCC11 gene. BMC Genet. 2009;10:42. PMID: 19650936. 98.7% of patients vs 35.4% of controls with the wet-type genotype. Full text
- Merck Manual (MSD Manual) Professional Version. Bromhidrosis. Dermatologic Disorders: Sweating Disorders. Clinical definition and management overview. (secondary) MSD Manual
How to cite this page
Sweat Explained. Bromhidrosis (Body Odor Disorder): Research Overview. Published 2026-07-13; last reviewed 2026-07-13. Available at: https://sweatexplained.com/research/bromhidrosis-prevalence-and-research
Please cite the original studies for the underlying figures. Journalists are welcome to link to this page; the charts are original renderings of the cited data.