In general, the term anosmia is used to refer to the inability to discriminate or detect qualitatively different olfactory sensations, or in simpler terms, an absence of one’s sense of or ability to smell [6, 19]. Related terms include partial or specific anosmia, which refer to deficient ability to detect a specific odorous stimulus or a limited class of odorous stimuli [6, 10, 19]. A fairly large number of specific anosmias have been identified [1, 10]. The terms hyposmia or microsmia have also been used to label instances of decreased sensitivity to odorous stimuli [19, 22].
As with most any trait or ability, individuals show variability in their capacity to smell . Some deficits in our olfactory sense are probably normal  and it is generally agreed that females report more acute sensitivity to odors than males [3, 12]. It is also reported that a likely majority of humans will experience measurable deficits in their olfactory sense as a function of aging . The ability to smell can be impaired or disrupted by a number of conditions, such as lesions to the brain, particularly of the orbitofrontal cortex area [11, 13]. Blows to and injuries of the head are often followed with deficits in olfaction as the olfactory nerve is easily lacerated . Severe sinus infections can result in total or partial anosmia, as can exposure to some chemicals [6, 8, 19]. An impaired ability to identify odors has been found co-occurring with disorders such as Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, Korsakoff’s psychosis, chronic alcoholism, HIV infection and schizophrenia [2, 7, 17, 18]. It is clear that the vast majority of anosmia cases are acquired deficits . The incidence rates of these olfactory deficits range from an estimated 1 to over 50% of the population under and over age 65, respectively ; other published reviews reported 67% of some population samples displaying measureable disruptions of the ability to smell, with slightly over 31% showing a complete loss of smell .
There is sparse information regarding any genetic or congenital basis for anosmia; the main genetic syndrome associated with anosmia is Kallman’s syndrome in which there is either a disruption of the requisite prenatal migration of neurons from the brain to olfactory structures and or insufficient or absent neuronal synapses in the olfactory structures and pathways . Kallman’s syndrome is a rare condition, with incidence rates found to range between 1 in 10,000 and 1 in over 80,000 persons .
The research connections between olfactory dysfunction and the putative effects of as yet to be identified human pheromones have been termed provocative  as well as disputed . Despite studies showing evidence of a physiological effect [15, 16, 20], there is little evidence for any actual changes in human behavior resulting from alleged pheromones ; although humans do possess most of the same structures involved in the actions of pheromones in other mammals , the human circuitry has sparse neurons, few if any neuronal connections to the brain and is likely more vestigial than functional [5, 7].