Research
The Genetics of Body Odor: The ABCC11 Gene
A single, common change in one gene, ABCC11, helps determine how much underarm odor a person produces, and it does so together with a surprising partner trait: earwax type. The variant, a single-nucleotide polymorphism written 538G>A, was first identified as the determinant of wet versus dry earwax and later shown to govern the formation of underarm odor molecules as well. People with two copies of the A version (the A/A genotype) tend to have dry earwax and produce little underarm odor. This page summarizes the verified genetics: what the SNP does, how its frequency varies by ancestry, the biochemistry that links it to odor, and what population data say about real-world deodorant use.
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
538G>A
the single ABCC11 SNP (rs17822931, Gly180Arg) that determines both earwax type and axillary odor
Yoshiura 2006 (Nat Genet)
A/A
genotype = dry earwax and markedly less underarm odor; G carriers have wet earwax and typical odor
Yoshiura 2006; Martin 2010
East Asia
where the dry-earwax, low-odor A allele is very common; it is nearly absent in African populations
Yoshiura 2006
77.8%
of genetically low-odor (A/A) white Europeans still used deodorant: biology is not destiny
Rodriguez 2013 (ALSPAC, ~17,000)
One gene, one letter, two traits
In 2006, Yoshiura and colleagues reported in Nature Genetics that a single-nucleotide polymorphism in the ABCC11 gene, rs17822931, a G-to-A change at position 538 that swaps one amino acid (Gly180Arg), is the determinant of human earwax type. People with the G/G or G/A genotype have wet (sticky) earwax; people with the A/A genotype have dry (flaky) earwax. The authors called it "the first example of DNA polymorphism determining a visible genetic trait."
ABCC11 codes for a membrane transporter that moves molecules out of cells. The A version reduces that transporter's activity (the study showed A-allele cells had lower excretory activity). Because the same transporter operates in the apocrine glands of the underarm, the SNP affects far more than earwax; it also shapes how much odor precursor reaches the skin surface for bacteria to convert.
What each genotype means
Because the low-activity A allele is recessive, only people with two copies (A/A) show the dry-earwax, low-odor phenotype. A single G copy is enough to restore the wet-earwax, typical-odor phenotype.
| Genotype | Earwax type | Underarm odor tendency |
|---|---|---|
| G/G | Wet | Typical odor production |
| G/A | Wet | Typical odor production |
| A/A | Dry | Markedly reduced odor production |
Genotype-phenotype pairing from Yoshiura 2006 (earwax) and Martin 2010 (odor). Odor is a tendency, not an absolute; the skin microbiome and other genes also contribute.
Why the trait varies so much by ancestry
The A allele is not evenly distributed around the world. Yoshiura and colleagues found a clear geographic gradient: the dry-earwax A allele is very common in East Asian populations (such as Chinese and Korean groups), present at intermediate levels in European populations, and nearly absent in African populations. This makes rs17822931 one of the most differentiated common variants between human populations, and it is sometimes used as an ancestry-informative marker.
The practical consequence is that the proportion of people who are genetically low-odor differs sharply by ancestry: high in parts of East Asia, low in populations of African ancestry. This is a description of allele frequencies, not a value judgment: 'odor' here means the biochemical raw material for underarm smell, nothing more.
How the gene changes the smell
The link between the gene and the smell is biochemical. In the apocrine gland, odor compounds start out bound to carrier molecules as odorless conjugates. Martin and colleagues (2010) showed that the ABCC11 transporter is needed to move these odorless precursors into secretory vesicles and out to the skin surface, where bacteria cleave them into the volatile, smelly forms (such as the thioalcohol 3M3SH).
When someone carries two low-activity A alleles, much less precursor is transported to the skin, so the bacteria have far less raw material to work with, and much less odor is produced. Their study found A/A individuals had significantly lower levels of the characteristic underarm odorants than G carriers. In other words, the gene sets the supply of odor precursor; the skin bacteria (covered on our companion page) do the rest.
Genetics is not destiny: real-world behavior
Knowing your genotype does not fully predict what you do about odor. A large study using the ALSPAC cohort (Rodriguez 2013, ~17,000 individuals) found strong statistical evidence that deodorant use tracks ABCC11 genotype (P ≈ 3.7 × 10⁻²⁰): A/A homozygotes were roughly five-fold overrepresented among people who never or rarely use deodorant.
But the link was far from absolute. Among genetically low-odor (A/A) white Europeans, 77.8% still used deodorant regularly, while 4.7% of genetically typical-odor (G-carrying) individuals used none. Habit, culture, and social norms clearly matter as much as genotype. The takeaway is that a common gene variant meaningfully shifts odor biology, but it does not dictate personal-care behavior.
What this means in plain terms
Body odor has a real, well-mapped genetic component centered on one letter of one gene. The A/A genotype (common in East Asia, rare in Africa) pairs dry earwax with low underarm odor because the ABCC11 transporter delivers less odor precursor to the skin. Everyone else produces the usual precursor, which their skin bacteria turn into odor. None of this is a health problem in itself; it is normal human variation. Concerns about excessive or sudden changes in body odor are best raised with a clinician.
Methodology and limitations
This page draws on the primary discovery paper linking ABCC11 rs17822931 to earwax type (Yoshiura 2006, Nature Genetics), the biochemistry study establishing the gene's role in odor formation (Martin 2010, J Invest Dermatol), and a large population-cohort study of deodorant behavior by genotype (Rodriguez 2013, J Invest Dermatol). Each figure was traced to its source and confirmed on the source page.
Limitations: allele-frequency patterns are described qualitatively by broad ancestry group because precise percentages vary by the specific population sampled; we did not assert exact frequencies we could not confirm on a source page. Odor is a tendency set by genotype but modified by the skin microbiome and other genes, so A/A does not guarantee no odor and G carriage does not guarantee strong odor. The ALSPAC behavior figures come from one predominantly white European cohort. Nothing here is a diagnosis or medical advice.
Frequently asked questions
- Which gene controls body odor?
- ABCC11. A single SNP in it (rs17822931, written 538G>A) helps determine how much underarm odor precursor reaches the skin. It was first identified as the gene that sets earwax type (Yoshiura 2006).
- What is the ABCC11 A/A genotype?
- Having two copies of the A version of the SNP. A/A people tend to have dry earwax and produce markedly less underarm odor, because the ABCC11 transporter delivers less odor precursor to the skin (Yoshiura 2006; Martin 2010).
- Why is low body odor more common in East Asia?
- The low-odor A allele is very common in East Asian populations, present at intermediate levels in Europeans, and nearly absent in African populations, a well-documented geographic gradient (Yoshiura 2006).
- Does earwax type really predict body odor?
- They share a genetic cause. The same ABCC11 SNP sets both, so dry earwax (A/A) tends to accompany low odor, and wet earwax (G carriers) accompanies typical odor. It is a tendency, not a guarantee.
- If I have the low-odor gene, do I still need deodorant?
- That is a personal choice. In one large study most genetically low-odor people still used deodorant (77.8%), while a minority of typical-odor people used none, showing habit and culture matter alongside genetics (Rodriguez 2013).
- Does the gene make the smell directly?
- No. ABCC11 controls how much odorless precursor reaches the skin; skin bacteria then convert that precursor into the actual smell. The gene sets the supply, the microbiome does the chemistry.
Sources
Primary peer-reviewed studies and official sources first, then reviews and institutional framing (secondary).
- Yoshiura K, Kinoshita A, Ishida T, et al. A SNP in the ABCC11 gene is the determinant of human earwax type. Nat Genet. 2006;38(3):324–330. PubMed
- Martin A, Saathoff M, Kuhn F, Max H, Terstegen L, Natsch A. A functional ABCC11 allele is essential in the biochemical formation of human axillary odor. J Invest Dermatol. 2010;130(2):529–540. Full text
- Rodriguez S, Steer CD, Farrow A, Golding J, Day IN. Dependence of deodorant usage on ABCC11 genotype: scope for personalized genetics in personal hygiene. J Invest Dermatol. 2013;133(7):1760–1767. Full text
How to cite this page
Sweat Explained. The Genetics of Body Odor: The ABCC11 Gene. Published 2026-07-13; last reviewed 2026-07-13. Available at: https://sweatexplained.com/research/genetics-of-body-odor-abcc11
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.
