<unk>  has an autosomal recessive pattern of inheritance. Most cases of<unk>  appear to be inherited in an autosomal recessive pattern, which means two copies of the gene in each cell are altered. The parents of an individual with an autosomal recessive disorder are both carriers of one copy of the altered gene. Carriers may have mild symptoms of<unk>  or experience temporary episodes of fish-like body odor. Mutations in the FMO3 gene, which is found on the long arm of chromosome 1, cause<unk> . The FMO3 gene makes an enzyme that breaks down nitrogen-containing compounds from the diet, including trimethylamine. These compounds are produced by bacteria in the intestine as they digest proteins from eggs, meat, soy, and other foods. Normally, the FMO3 enzyme converts fishy-smelling trimethylamine into trimethylamine N-oxide which has no odor. If the enzyme is missing or its activity is reduced because of a mutation in the FMO3 gene, trimethylamine is not broken down and instead builds up in the body. As the compound is released in a person's sweat, urine, and breath, it causes the strong odor characteristic of<unk> . Researchers believe that stress and diet also play a role in triggering symptoms. There are more than 40 known mutations associated with<unk> . Loss-of-function mutations, nonsense mutations, and missense mutations are three of the most common. Nonsense and missense mutations cause the most severe phenotypes. Although FMO3 mutations account for most known cases of<unk> , some cases are caused by other factors. A fish-like body odor could result from an excess of certain proteins in the diet or from an increase in bacteria in the digestive system. A few cases of the disorder have been identified in adults with liver damage caused by hepatitis. In 2007 the evolution of the FMO3 gene was studied, including the evolution of some mutations associated with<unk> .
Trimethylaminuria
Pentosuria
Iminoglycinuria
Orotic aciduria
Xanthinuria
Cystinuria
Hawkinsinuria
Sialuria