Open Access Articles- Top Results for Body odor

Body odor

Body odor or body odour
Classification and external resources
ICD-10 L75.0
ICD-9 705.89
DiseasesDB 28886
eMedicine derm/597
NCI Body odor
Patient UK Body odor

Body odor or body odour or BO is present in animals (including humans), and its intensity can be influenced by many factors (behavioural patterns, survival strategies). Body odor has a strong genetic basis both in animals and humans, but it can be also strongly influenced by various diseases and psychological conditions. Body odor is considered an unpleasant odor among many human cultures.


In humans, the formation of body odors is mainly caused by skin glands excretions and bacterial activity.[1] Between the different types of skin glands, the human 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.[2] 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.[3]

The main components of human axillary odor are unsaturated or hydroxylated branched fatty acids with E-3M2H (E-3-methyl-2-hexenoic acid) and HMHA (3-hydroxy-3-methyl-hexanoic 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).[4] E-3M2H is bound and carried by two apocrine secretion odor-binding proteins, ASOB1 and ASOB2, to the skin surface.[5]

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. These smaller molecules smell, and give body odor its characteristic aroma.[6] 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,[7] which is also present in several strong cheese types.

Factors such as food, drink, and diseases can affect body odor.[3] An individual's body odor is also influenced by lifestyle, sex, genetics, and medication.


See also: Pheromone


In many animals, body odor plays an important survival function. Strong body odor can be a warning signal for predators to stay away, or it can be also a signal that the prey animal is unpalatable.[8] 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 of the predators, although they can be still killed and eaten by the birds of prey, who have very poor sense of smell.

Body odor is an important feature of animal morphology. It plays a different role in different animal species. For example, in some predator species, who use stalking as a means of hunt (for example big and small cats), the absence of body odor is highly important, and they spend plenty of time and energy to keep their body free of odor. For other predators, who use long running after the prey as a means of hunting (dogs, wolves), the absence of body odor is not so important, on the contrary, can play a role of warning signal. In most of the animals, body odor intensifies in the moment of stress and danger.


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.[3] Compared to other primates, humans have extensive axillary hair and have many odor producing sources, in particular many apocrine glands.[9] 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.[10]

Humans can olfactorily detect blood-related kin.[11] 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.[12] Babies can recognize their mothers by smell and mothers, fathers and other relatives can identify a baby by smell.[3]

Humans have few olfactory receptor cells compared to dogs and few functional olfactory receptor genes compared to rats. This is in part due 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.[9]

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. 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.[13] According to the researchers, this research suggests a possible role for human pheromones in the biological basis of sexual orientation.[14]


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.[3]

East Asians have fewer apocrine sweat glands compared to people of other descent, and the lack of these glands make East Asians less prone to body odor.[15][16] The reduction in body odor and sweating may be due to adaptation to colder climates by their ancient East Asian ancestors.[17] The ABCC11 gene is known to determine axillary body odor, but also the type of earwax.[4][17][18][19] Most of the world's population secrete the wet-type earwax, however, East Asians are genetically predisposed for the allele that codes the dry-type earwax, associated with a reduction in axillary body odor.[4][17][19] 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.[19][20] The non-functional ABCC11 allele is predominant amongst East Asians (80–95%), but very low in other ancestral groups (0–3%).[4] It affects apocrine sweat glands by reducing secretion of odorous molecules and its precursors.[4] 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.[4]

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.[4] It also results in 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).[4]

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.[19]


Body odor may be reduced or prevented or even aggravated by using deodorants, antiperspirants, disinfectants, underarm liners, triclosan, a medical device/procedure called miraDry [21] special soaps or foams with antiseptic plant extracts such as ribwort and liquorice, chlorophyllin ointments and sprays topically, and chlorophyllin supplements internally.[22] Although body odor is commonly associated with hygiene practices, its presentation can be affected by changes in diet as well as the other factors discussed above.[23]

Medical conditions

The condition can be known medically as bromhidrosis, apocrine bromhidrosis, osmidrosis, ozochrotia, fetid sweat, body smell, or malodorous sweating.[24][25]

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).[18] 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.[18]

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.

See also


  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. ^ Turkington, Carol; Dover, Jeffrey S. (2007). The encyclopedia of skin and skin disorders (3rd ed.). New York: Facts on File. p. 363. ISBN 978-0-8160-6403-8. 
  3. ^ a b c d e The Oxford Handbook of Evolutionary Psychology, Edited by Robin Dunbar and Louise Barret, Oxford University Press, 2007, Chapter 22 Body odours and body odour preferences in humans by Claus Wedekind
  4. ^ a b c d e f g h 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. 
  5. ^ Zeng, C.; Spielman, A. I.; Vowels, B. R.; Leyden, J. J.; Biemann, K.; Preti, G. (25 June 1996). "A human axillary odorant is carried by apolipoprotein D.". Proceedings of the National Academy of Sciences 93 (13): 6626–6630. PMC 39076. PMID 8692868. doi:10.1073/pnas.93.13.6626. 
  6. ^ Buckman, Robert (2003). Human Wildlife: The Life That Lives On Us. Baltimore: The Johns Hopkins University Press. pp. 93-4
  7. ^ Ara K; Hama M; Akiba S et al. (2006). "Foot odor due to microbial metabolism and its control". Can. J. Microbiol. 52 (4): 357–64. PMID 16699586. doi:10.1139/w05-130. 
  8. ^ Ruxton, Graeme D., Thomas N. Sherratt, and Michael P. Speed. 2004. Avoiding attack. The evolutionary ecology of crypsis, warning signals, and mimicry. Oxford University Press
  9. ^ a b S. Craig Roberts and Jan Havlicek. "Evolutionary psychology and perfume design". In Roberts, S. C. (2011). Roberts, S. Craig, ed. "Applied Evolutionary Psychology". Oxford University Press. ISBN 9780199586073. doi:10.1093/acprof:oso/9780199586073.001.0001.  edit
  10. ^ Navarrete-Palacios E, Hudson R, Reyes-Guerrero G, Guevara-Guzmán R (July 2003). "Lower olfactory threshold during the ovulatory phase of the menstrual cycle". Biological Psychology 63 (3): 269–79. PMID 12853171. doi:10.1016/S0301-0511(03)00076-0. 
  11. ^ Porter RH, Cernoch JM, Balogh RD (1985). "Odor signatures and kin recognition". Physiol Behav 34 (3): 445–8. PMID 4011726. doi:10.1016/0031-9384(85)90210-0. 
  12. ^ Weisfeld GE, Czilli T, Phillips KA, Gall JA, Lichtman CM (July 2003). "Possible olfaction-based mechanisms in human kin recognition and inbreeding avoidance.". Journal of experimental child psychology 85 (3): 279–95. PMID 12810039. doi:10.1016/S0022-0965(03)00061-4. 
  13. ^ Savic, I."Brain response to putative pheromones in lesbian women." PNAS, May 16, 2006
  14. ^ Wade, N. "Homosexual Men are found to have Different Scent of Attraction." NY Times, May 9, 2005
  15. ^ Sherrow, Victoria (2001). For appearance' sake: The historical encyclopedia of good looks, beauty, and grooming. Phoenix: Oryx Press. p. 58. ISBN 978-1-57356-204-1. 
  16. ^ Stoddart, D. Michael (1990). The scented ape: The biology and culture of human odour. Cambridge: Cambridge University Press. pp. 60–61. ISBN 0-521-37511-8. 
  17. ^ a b c Yoshiura K; Kinoshita A; Ishida T et al. (2006). "A SNP in the ABCC11 gene is the determinant of human earwax type". Nat. Genet. 38 (3): 324–30. PMID 16444273. doi:10.1038/ng1733. 
  18. ^ a b c Kanlayavattanakul, M.; Lourith, N. (1 August 2011). "Body malodours and their topical treatment agents". International Journal of Cosmetic Science 33 (4): 298–311. PMID 21401651. doi:10.1111/j.1468-2494.2011.00649.x. 
  19. ^ 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. 
  20. ^ Preti, George; Leyden, James J (2010). "Genetic Influences on Human Body Odor: From Genes to the Axillae". Journal of Investigative Dermatology 130 (2): 344–346. PMID 20081888. doi:10.1038/jid.2009.396. 
  21. ^
  22. ^ "Chlorophyll and Chlorophyllin". Retrieved 2010-01-29. 
  23. ^ "Learn How to Fight Body Odor". Retrieved 2007-07-05. 
  24. ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. p. 779. ISBN 0-7216-2921-0.
  25. ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. p. 707. ISBN 0-07-138076-0.

External links

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