A polymorphism of the ability to smell urinary metabolites of asparagus.

Abstract

Summary and conclusionsThe urinary excretion of (an) odorous substance(s) after eating asparagus is not an inborn error of metabolism as has been supposed. The detection of the odour constitutes a specific smell hypersensitivity. Those who could smell the odour in their own urine could all smell it in the urine of anyone who had eaten asparagus, whether or not that person was able to smell it himself. Thresholds for detecting the odour appeared to be bimodal in distribution, with 10% of 307 subjects tested able to smell it at high dilutions, suggesting a genetically determined specific hypersensitivity. IntroductionThe urinary excretion of pungent odorous substance(s) after

Asparagus, Urinary Odor, and 1,2-Dithiolane-4-Carboxylic Acid

“…However, a metabolic causation is supported by an anecdotal report that a non-excretor (homozygous) may become an excretor during pregnancy, the unborn child presumed to be an excretor (heterozygous), as should be the father (McKusick 1983); I have also received communication from a primigravadi recounting this unusual experience. To obfuscate matters further, there are also suggestions that a specific anosmia to this odor exists, with some individuals not being able to detect it (Hoffenberg 1983;Lison, Blondheim, and Melmed 1980). A current paper has confirmed both of these phenomena and concludes that "individual differences exist in both odorant production and odor perception" (Pelchat et al 2011, p. 9).…”

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.…”

Stalking the asparagus trail

“…A small minority of about 10 percent constituted the minor peak on the dilute side of the antimode suggesting that the ability to detect a urinary odor after asparagus ingestion is a genetic trait. 5 These findings favor the smell-detection aspect of the asparagus-urine story. This latter paper is the only report in which smellers were subdivided into smellers and hypersensitive smellers.…”

“…The smellers (i.e., hypersensitive smellers) in the study conducted by Lison, Blondheim, and Melmed were able to detect the asparagus-induced odor in the urine of both stinkers and non-stinkers. 5 In this study of 307 subjects for smell hypersensitivity, a consistent bimodial distribution curve was obtained for the threshold level of the detection of the urinary asparagus odor. A small minority of about 10 percent constituted the minor peak on the dilute side of the antimode suggesting that the ability to detect a urinary odor after asparagus ingestion is a genetic trait.…”