The Prevalence of Androstenone Anosmia

Abstract

It has been estimated that approximately 30% of the population is unable to detect the odor of androstenone. These estimates, however, were made using tests and criteria optimized for identifying detection. Such criteria favor Type II over Type I errors--that is, they are excellent at identifying true detectors at the cost of erroneously labeling some detectors as non-detectors. Because these criteria were used to identify non-detectors, it is possible that the rate of non-detection may have been overestimated. To test this we screened 55 subjects for non-detection employing previously used methods. This screen yielded nine putative non-detectors, a 16.3% putative non-detection rate. We then retested these putative non-detectors using a forced choice (yes-no) paradigm to obtain a precise measure of their sensitivity. We found that this group of putative non-detectors was significantly above chance at detecting androstenone (P < 0.001), despite very low self-confidence in their performance. Based on the results of the signal detection analysis in this sample, we estimate the rate of actual androstenone non-detection in young healthy adults is between 1.8 and 5.96%, which is significantly lower than previously estimated. This finding is significant considering the implications of specific anosmias on the understanding of odor discrimination.

Environmental Effects Exceed Genetic Effects on Perceived Intensity and Pleasantness of Several Odors: A Three-Population Twin Study

“…This supports the genetic contribution to the general hyposmia, as suggested recently by Pinto et al (2008). Genetic contribution to variation in detection thresholds (Wysocki and Beauchamp 1984;Gross-Isseroff et al 1992) and in experienced intensity and pleasantness (Keller et al 2007) has been demonstrated for androstenone, an odorant that shows relatively high prevalence of specific anosmia/ hyposmia (20-30%; Wysocki and Gilbert 1989; for a review see Bremner et al 2003), and thus large phenotypic variation. Significant genetic effects have also been found for the detection of isoamyl acetate, an odorant with no known specific anosmia (Gross-Isseroff et al 1992).…”

A preliminary investigation into a genetic basis for cis-3-hexen-1-ol odour perception: A genome-wide association approach

“…The latter can manifest as either enhanced sensitivity to an odorant (specific hyperosmia) or as a strongly reduced capacity to smell particular odorants. This diminished sensitivity, also known as specific anosmia, has been reported by several investigators and in connection with a range of odorants (e.g., Amoore, Venstrom, & Davis, 1968;Bremner, Mainland, Khan, & Sobel, 2003;Hirth, Abadanian, & Goedde, 1986;Kendal-Reed, Walker, Morgan, LaMacchio, & Lutz, 1998;Lison, Blondheim, & Melmed, 1980;Lunde, Skuterud, Nilsen, & Egelandsdal, 2008;Meilgaard, 1993;Pelosi & Pisanelli, 1981;Plotto, Barnes, & Goodner, 2006;Snyder, 1931), and recently the first reports confirming a genetic basis for differences in human olfactory phenotypes have emerged (Keller et al, 2007;Menashe et al, 2007). These reports extend previous work, notably twin studies by, for example, Finkel, Pedersen, and Larsson (2001), Segal, Topolski, Wilson, Brown, and Araki (1995), and Wysocki and Beauchamp (1984), indicating heritability in olfactory functioning.…”

Evaluation of various boar taint detection methods

“…The cooking odour of entire male pigs with boar taint may be evaluated more negatively by androstenone sensitive people (Furnols et al, 2003). Most cooks are female who are up to six times more sensitive to androstenone than men (Bremner et al, 2003). A cook is therefore more likely to detect boar taint than an average consumer.…”