Body odor

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Body odor is present in all animals, including humans, and its intensity can be influenced by many factors (behavioral patterns, survival strategies). Body odor has a strong genetic basis, but can also be strongly influenced by various diseases and physiological conditions. Though body odor has played an important role (and continues to do so in many life forms) in early humankind, it is generally considered to be an unpleasant odor amongst many human cultures.


In humans, the formation of body odors is caused by factors such as diet, gender, health, and medication, but the major contribution comes from bacterial activity on skin gland secretions.[1] Humans have three types of sweat glands; eccrine sweat glands, apocrine sweat glands and sebaceous glands. Eccrine sweat glands are present from birth, while the two latter become activated during puberty.[2] Among the different types of human skin glands, the body odor is primarily the result of the apocrine sweat glands, which secrete the majority of chemical compounds needed for the skin flora to metabolize it into odorant substances.[1] This happens mostly in the axillary (armpit) region, although the gland can also be found in the areola, anogenital region, and around the navel.[3] In humans, the armpit regions seem more important than the genital region for body odor which may be related to human bipedalism. The genital and armpit regions also contain springy hairs which help diffuse body odors.[4]

The main components of human axillary odor are unsaturated or hydroxylated branched fatty acids with E-3M2H (E-3-methylhex-2-enoic acid) and HMHA (3-hydroxy-3-methylhexanoic acid), sulfanylalkanols and particularly 3M3SH (3-methyl-3-sulfanylhexan-1-ol), and the odoriferous steroids androstenone (5α-androst-16-en-3-one) and androstenol (5α-androst-16-en-3α-ol).[5] E-3M2H is bound and carried by two apocrine secretion odor-binding proteins, ASOB1 and ASOB2, to the skin surface.[6]

Body odor is influenced by the actions of the skin flora, including members of Corynebacterium, which manufacture enzymes called lipases that break down the lipids in sweat to create smaller molecules like butyric acid. Greater bacteria populations of Corynebacterium jeikeium are for example found more in the armpits of men whereas greater population numbers of Staphylococcus haemolyticus are found in the armpits of women. This causes male armpits to give off of a rancid/cheese-like smell whereas female armpits give off a more fruity/onion-like smell.[7] Staphylococcus hominis is also known for producing thioalcohol compounds that contribute to odors.[8] These smaller molecules smell, and give body odor its characteristic aroma.[9] Propionic acid (propanoic acid) is present in many sweat samples. This acid is a breakdown product of some amino acids by propionibacteria, which thrive in the ducts of adolescent and adult sebaceous glands. Because propionic acid is chemically similar to acetic acid with similar characteristics including odor, body odors may be identified as having a vinegar-like smell by certain people.[citation needed] Isovaleric acid (3-methyl butanoic acid) is the other source of body odor as a result of actions of the bacteria Staphylococcus epidermidis,[10] which is also present in several strong cheese types.

Factors such as food, drink, and diseases can affect body odor.[4] An individual's body odor is also influenced by lifestyle, sex, genetics, and medication.[citation needed]



In many animals, body odor plays an important survival function. Strong body odor can be a warning signal for predators to stay away (such as porcupine stink), or it can also be a signal that the prey animal is unpalatable.[11] For example, some animals species, who feign death to survive (like opossums), in this state produce a strong body odor to deceive a predator that the prey animal has been dead for a long time and is already in the advanced stage of decomposing. Some animals with strong body odor are rarely attacked by most predators, although they can still be killed and eaten by birds of prey, which are tolerant of carrion odors.

Body odor is an important feature of animal physiology. It plays a different role in different animal species. For example, in some predator species that hunt by stalking (such as big and small cats), the absence of body odor is important, and they spend plenty of time and energy to keep their body free of odor. For other predators, which use endurance running after the visually located prey as a hunting strategy (dogs, wolves), the absence of body odor is not critical. In most animals, body odor intensifies in moments of stress and danger.[12]


Sebaceous and apocrine glands become active at puberty. This, as well as many apocrine glands being close to the sex organs, points to a role related to mating.[4] Compared to other primates, humans have extensive axillary hair and have many odor producing sources, in particular many apocrine glands.[13] In women, the sense of olfaction is strongest around the time of ovulation, significantly stronger than during other phases of the menstrual cycle and also stronger than the sense in males.[14]

Humans can olfactorily detect blood-related kin.[15] Mothers can identify by body odor their biological children, but not their stepchildren. Preadolescent children can olfactorily detect their full siblings, but not half-siblings or step-siblings, and this might explain incest avoidance and the Westermarck effect.[16] Babies can recognize their mothers by smell while mothers, fathers, and other relatives can identify a baby by smell.[4]

Humans have few olfactory receptor cells compared to dogs and few functional olfactory receptor genes compared to rats. This is in part due to a reduction of the size of the snout in order to achieve depth perception as well as other changes related to bipedalism. However, it has been argued that humans may have larger brain areas associated with olfactory perception compared to other species.[13]

Studies have suggested that people might be using odor cues associated with the immune system to select mates. Using a brain-imaging technique, Swedish researchers have shown that homosexual and heterosexual males' brains respond in different ways to two odors that may be involved in sexual arousal, and that homosexual men respond in the same way as heterosexual women, though it could not be determined whether this was cause or effect. When the study was expanded to include lesbian women; the results were consistent with previous findings meaning that lesbian women were not as responsive to male-identified odors, while their response to female cues was similar to heterosexual males'.[17] According to the researchers, this research suggests a possible role for human pheromones in the biological basis of sexual orientation.[18]


World map of the distribution of the A allele of the single nucleotide polymorphism rs17822931 in the ABCC11 gene. The proportion of A alleles in each population is represented by the white area in each circle.

Body odor is largely influenced by major histocompatibility complex (MHC) molecules. These are genetically determined and play an important role in immunity of the organism. The vomeronasal organ contains cells sensitive to MHC molecules in a genotype-specific way.

Experiments on animals and volunteers have shown that potential sexual partners tend to be perceived more attractive if their MHC composition is substantially different. Married couples are more different regarding MHC genes than would be expected by chance. This behavior pattern promotes variability of the immune system of individuals in the population, thus making the population more robust against new diseases. Another reason may be to prevent inbreeding.[4]

The ABCC11 gene determines axillary body odor and the type of earwax.[5][19][20][21] The loss of a functional ABCC11 gene is caused by a 538G>A single-nucleotide polymorphism, resulting in a loss of body odor in people who are specifically homozygous for it.[21][22] Firstly, it affects apocrine sweat glands by reducing secretion of odorous molecules and its precursors.[5] The lack of ABCC11 function results in a decrease of the odorant compounds 3M2H, HMHA, and 3M3SH via a strongly reduced secretion of the precursor amino-acid conjugates 3M2H–Gln, HMHA–Gln, and Cys–Gly–(S) 3M3SH; and a decrease of the odoriferous steroids androstenone and androstenol, possibly due to the reduced levels and secretion of DHEAS and DHEA (possibly bacterial substrates for odoriferous steroids).[5] Secondly, it is also associated with a strongly reduced/atrophic size of apocrine sweat glands and a decreased protein (such as ASOB2) concentration in axillary sweat.[5]

The non-functional ABCC11 allele is predominant among East Asians (80–95%), but very low in other ancestral groups (0–3%).[5] Most of the world's population have the gene that codes for the wet-type earwax and normal body odor; however, East Asians are more likely to inherit the allele associated with the dry-type earwax and a reduction in body odor.[5][19][21] The hypothesized reduction in body odor may be due to adaptation to colder climates by their ancient Northeast Asian ancestors.[19]

However, research has observed that this allele is not solely responsible for ethnic differences in scent. A 2016 study analyzed differences across ethnicities in volatile organic compounds (VOCs), across racial groups and found that while they largely did not differ significantly qualitatively, they did differ quantitatively. Of the observed differences, they were found to vary with ethnic origin but not entirely with ABCC11 genotype.[23]

It has been noted that there is currently no evidence that sweat secretion glands nor sweat production varies across ethnicities.[24] One large study failed to find any significant differences across ethnicity in residual compounds on the skin, including those located in sweat.[25] If there were observed ethnic variants in skin odor, one would find sources to be much more likely in diet, hygiene, microbiome, and other environmental factors.[26][27][28]

Research has indicated a strong association between people with axillary osmidrosis and the ABCC11-genotypes GG or GA at the SNP site (rs17822931) in comparison to the genotype AA.[21]


Body odor may be reduced or prevented or even aggravated by using deodorants, antiperspirants, disinfectants, underarm liners, triclosan, special soaps or foams with antiseptic plant extracts such as ribwort and liquorice, chlorophyllin ointments and sprays topically, and chlorophyllin supplements internally. Although body odor is commonly associated with hygiene practices, its presentation can be affected by changes in diet as well as the other factors.[29] Skin spectrophotometry analysis found that males who consumed more fruits and vegetables were significantly associated with more pleasant smelling sweat, which was described as "floral, fruity, sweet and medicinal qualities".[30]


As many as 90% of Americans and 92% of teenagers use antiperspirants or deodorants.[31][32] In 2014, the global market for deodorants was estimated at US$13.00 billion with a compound annual growth rate of 5.62% between 2015 and 2020.[33]

Medical conditions[edit]

The condition can be known medically as bromhidrosis, apocrine bromhidrosis, osmidrosis, ozochrotia, fetid sweat, body smell, or malodorous sweating.[34][35]

Osmidrosis or bromhidrosis is defined by a foul odor due to a water-rich environment that supports bacteria, which is caused by an abnormal increase in perspiration (hyperhidrosis).[20] This can be particularly strong when it happens in the axillary region (underarms). In this case, the condition may be referred to an axillary osmidrosis.[20]

Trimethylaminuria (TMAU), also known as fish odor syndrome or fish malodor syndrome, is a rare metabolic disorder where trimethylamine is released in the person's sweat, urine, and breath, giving off a strong fishy odor or strong body odor.[36]

See also[edit]


  1. ^ a b Lundström, Johan N.; Olsson, Mats J. (2010). "Functional Neuronal Processing of Human Body Odors". Pheromones. Academic Press. p. 4. ISBN 978-0-12-381516-3.
  2. ^ "The Biology of Body Odor". March 13, 2012. Retrieved April 3, 2018.
  3. ^ Turkington, Carol; Dover, Jeffrey S. (2007). The encyclopedia of skin and skin disorders (3rd ed.). New York: Facts on File. pp. 363. ISBN 978-0-8160-6403-8.
  4. ^ a b c d e Wedekind, Claus (2007). "Body Odours and Body Odour Preferences in Humans". Oxford Handbook of Evolutionary Psychology. doi:10.1093/oxfordhb/9780198568308.013.0022. ISBN 978-0-19-174365-8.
  5. ^ a b c d e f g Martin, Annette; Saathoff, Matthias; Kuhn, Fabian; Max, Heiner; Terstegen, Lara; Natsch, Andreas (2010). "A Functional ABCC11 Allele Is Essential in the Biochemical Formation of Human Axillary Odor". Journal of Investigative Dermatology. 130 (2): 529–540. doi:10.1038/jid.2009.254. PMID 19710689.
  6. ^ Zeng, C.; Spielman, A. I.; Vowels, B. R.; Leyden, J. J.; Biemann, K.; Preti, G. (June 25, 1996). "A human axillary odorant is carried by apolipoprotein D." Proceedings of the National Academy of Sciences. 93 (13): 6626–6630. Bibcode:1996PNAS...93.6626Z. doi:10.1073/pnas.93.13.6626. PMC 39076. PMID 8692868.
  7. ^ De microbemens by Remco Kort
  8. ^ "Bacterial genetic pathway involved in body odor production discovered" (Press release). Society for General Microbiology. March 30, 2015.
  9. ^ Buckman, Robert (2003). Human Wildlife: The Life That Lives On Us. Baltimore: The Johns Hopkins University Press. pp. 93-4
  10. ^ Ara, Katsutoshi; Hama, Masakatsu; Akiba, Syunichi; Koike, Kenzo; Okisaka, Koichi; Hagura, Toyoki; Kamiya, Tetsuro; Tomita, Fusao (April 1, 2006). "Foot odor due to microbial metabolism and its control". Canadian Journal of Microbiology. 52 (4): 357–364. CiteSeerX doi:10.1139/w05-130. PMID 16699586.
  11. ^ Ruxton, Graeme D.; Allen, William L.; Sherratt, Thomas N.; Speed, Michael P. Avoiding Attack: The Evolutionary Ecology of Crypsis, Aposematism, and Mimicry. Oxford University Press. ISBN 978-0-19-186849-8.[page needed]
  12. ^ Takahashi, Lorey K. (March 11, 2014). "Olfactory systems and neural circuits that modulate predator odor fear". Frontiers in Behavioral Neuroscience. 8: 72. doi:10.3389/fnbeh.2014.00072. PMC 3949219. PMID 24653685.
  13. ^ a b Roberts, S. Craig; Havlicek, Jan (2011). "Evolutionary psychology and perfume design". Applied Evolutionary Psychology. pp. 330–348. doi:10.1093/acprof:oso/9780199586073.003.0020. ISBN 978-0-19-958607-3.
  14. ^ Navarrete-Palacios, Evelia; Hudson, Robyn; Reyes-Guerrero, Gloria; Guevara-Guzmán, Rosalinda (July 2003). "Lower olfactory threshold during the ovulatory phase of the menstrual cycle". Biological Psychology. 63 (3): 269–279. doi:10.1016/s0301-0511(03)00076-0. PMID 12853171. S2CID 46065468.
  15. ^ Porter, Richard H.; Cernoch, Jennifer M.; Balogh, Rene D. (March 1985). "Odor signatures and kin recognition". Physiology & Behavior. 34 (3): 445–448. doi:10.1016/0031-9384(85)90210-0. PMID 4011726. S2CID 42316168.
  16. ^ Weisfeld, Glenn E; Czilli, Tiffany; Phillips, Krista A; Gall, James A; Lichtman, Cary M (July 2003). "Possible olfaction-based mechanisms in human kin recognition and inbreeding avoidance". Journal of Experimental Child Psychology. 85 (3): 279–295. doi:10.1016/s0022-0965(03)00061-4. PMID 12810039.
  17. ^ Berglund, H.; Lindstrom, P.; Savic, I. (May 16, 2006). "Brain response to putative pheromones in lesbian women". Proceedings of the National Academy of Sciences. 103 (21): 8269–8274. Bibcode:2006PNAS..103.8269B. doi:10.1073/pnas.0600331103. PMC 1570103. PMID 16705035.
  18. ^ Wade, Nicholas (May 9, 2005). "Gay Men Are Found to Have Different Scent of Attraction". The New York Times.
  19. ^ a b c Yoshiura, Koh-ichiro; Kinoshita, Akira; Ishida, Takafumi; Ninokata, Aya; Ishikawa, Toshihisa; Kaname, Tadashi; Bannai, Makoto; Tokunaga, Katsushi; Sonoda, Shunro; Komaki, Ryoichi; Ihara, Makoto; Saenko, Vladimir A; Alipov, Gabit K; Sekine, Ichiro; Komatsu, Kazuki; Takahashi, Haruo; Nakashima, Mitsuko; Sosonkina, Nadiya; Mapendano, Christophe K; Ghadami, Mohsen; Nomura, Masayo; Liang, De-Sheng; Miwa, Nobutomo; Kim, Dae-Kwang; Garidkhuu, Ariuntuul; Natsume, Nagato; Ohta, Tohru; Tomita, Hiroaki; Kaneko, Akira; Kikuchi, Mihoko; Russomando, Graciela; Hirayama, Kenji; Ishibashi, Minaka; Takahashi, Aya; Saitou, Naruya; Murray, Jeffery C; Saito, Susumu; Nakamura, Yusuke; Niikawa, Norio (March 2006). "A SNP in the ABCC11 gene is the determinant of human earwax type". Nature Genetics. 38 (3): 324–330. doi:10.1038/ng1733. PMID 16444273. S2CID 3201966.
  20. ^ a b c Kanlayavattanakul, M.; Lourith, N. (August 1, 2011). "Body malodours and their topical treatment agents". International Journal of Cosmetic Science. 33 (4): 298–311. doi:10.1111/j.1468-2494.2011.00649.x. PMID 21401651.
  21. ^ a b c d Nakano, Motoi; Miwa, Nobutomo; Hirano, Akiyoshi; Yoshiura, Koh-ichiro; Niikawa, Norio (2009). "A strong association of axillary osmidrosis with the wet earwax type determined by genotyping of the ABCC11 gene". BMC Genetics. 10 (1): 42. doi:10.1186/1471-2156-10-42. PMC 2731057. PMID 19650936.
  22. ^ Preti, George; Leyden, James J. (February 2010). "Genetic Influences on Human Body Odor: From Genes to the Axillae". Journal of Investigative Dermatology. 130 (2): 344–346. doi:10.1038/jid.2009.396. PMID 20081888.
  23. ^ Prokop-Prigge, Katharine A.; Greene, Kathryn; Varallo, Lauren; Wysocki, Charles J.; Preti, George (January 2016). "The Effect of Ethnicity on Human Axillary Odorant Production". Journal of Chemical Ecology. 42 (1): 33–39. doi:10.1007/s10886-015-0657-8. PMC 4724538. PMID 26634572.
  24. ^ Taylor, Susan C. (February 2002). "Skin of color: Biology, structure, function, and implications for dermatologic disease". Journal of the American Academy of Dermatology. 46 (2): S41–S62. doi:10.1067/mjd.2002.120790. PMID 11807469.
  25. ^ Shetage, Satyajit S; Traynor, Matthew J; Brown, Marc B; Raji, Mahad; Graham-Kalio, Diepiriye; Chilcott, Robert P (2014). "Effect of ethnicity, gender and age on the amount and composition of residual skin surface components derived from sebum, sweat and epidermal lipids". Skin Research and Technology. 20 (1): 97–107. doi:10.1111/srt.12091. PMC 4285158. PMID 23865719.
  26. ^ Tullett, William (July 2, 2016). "Grease and Sweat: Race and Smell in Eighteenth-Century English Culture". Cultural and Social History. 13 (3): 307–322. doi:10.1080/14780038.2016.1202008. S2CID 147837009.
  27. ^ Prokop-Prigge, Katharine A.; Greene, Kathryn; Varallo, Lauren; Wysocki, Charles J.; Preti, George (January 2016). "The Effect of Ethnicity on Human Axillary Odorant Production". Journal of Chemical Ecology. 42 (1): 33–39. doi:10.1007/s10886-015-0657-8. PMC 4724538. PMID 26634572.
  28. ^ Li, Min; Budding, Andries E.; van der Lugt‐Degen, Malieka; Du‐Thumm, Laurence; Vandeven, Mark; Fan, Aixing (June 13, 2019). "The influence of age, gender and race/ethnicity on the composition of the human axillary microbiome". International Journal of Cosmetic Science. 41 (4): 371–377. doi:10.1111/ics.12549. PMID 31190339.
  29. ^ "Learn How to Fight Body Odor". Retrieved July 5, 2007.
  30. ^ "Diet quality and the attractiveness of male body odor". Evolution and Human Behavior. 38 (1): 136–143. January 1, 2017. doi:10.1016/j.evolhumbehav.2016.08.002. ISSN 1090-5138.
  31. ^ Pomeroy, Ross (August 10, 2014). "Antiperspirants Alter Your Armpit Bacteria and Could Actually Make You Smell Worse". RealClearScience.
  32. ^ Considine, Austin (January 17, 2013). "Genetically, Some of Us Never Have Body Odor, But We Still Think We're Smelly". Vice.
  33. ^ "Global Deodorants Market is Expected to Reach USD 17.55 Billion by 2020". Retrieved July 29, 2016.
  34. ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. p. 779. ISBN 0-7216-2921-0.
  35. ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. p. 707. ISBN 0-07-138076-0.
  36. ^ "Body Odor: Causes, Prevention, Treatments". Medical News Today. Retrieved March 4, 2017.

External links[edit]

External resources