Blame your Bad Breath on This Gene – SELENBP1
It’s a mortifying problem for millions. Bad breath, or halitosis, is one of the great unmentionables, despite the fact that it affects a huge number of people. Eating garlic and a lax teeth-brushing routine aren’t the only causes of bad breath. Researchers at the University of California Davis have now identified a gene mutation they say could be a root cause for that kind of bad breath.
Solutions to date offer only temporary relief. Even scrupulously skipping onions and garlic, swishing mouthwash after every meal, and brushing and flossing one’s teeth until they gleam like pearls will probably not sweeten a case of stubbornly stinky breath.
But recent evidence from international research however, found a protein called “SELENBP1” and suggests that mutations in its parent gene might make the body produce stinky bad-breath molecules.
“It’s important to identify the cause of persistent halitosis, and differentiate that cause from relatively benign causes (e.g., gum disease) and the more morbid causes such as liver cirrhosis,” said Professor Kent Lloyd, director of the Mouse Biology Program at UC Davis.
About 3 percent of the population has chronic bad breath with no apparent cause.
The recent
research carried out in the Netherlands at Radboud University, and with collaborators across Europe, discovered that sulfur-based compounds are common in the breath of those whose halitosis runs in the family, according to the UC Davis researchers.Some bacteria can break down sulfur compounds. After scrutinizing bacterial genes, the Radboud University scientists identified a gene for a methanethiol oxidase (MTO), an enzyme that resembles a human enzyme, selenium-binding protein 1 (SELENBP1), which has been associated with several cancers.
Observations revealed that maybe SELENBP1 produces an enzyme responsible for breaking odorous molecules down. “The function of SELENBP1 might possibly be keeping the breath methanethiol concentration low,” the scientists write in the paper, “thus enabling the human nose to detect foul smells from environmental volatile sulfur compounds” instead of the human’s own foul breath.
Like the bacterial MTO, SELENBP1 converts methanethiol to hydrogen peroxide (H2O2), formaldehyde, and hydrogen sulfide (H2S). This activity, one not previously known to exist in humans, is reduced if the gene for SELENBP1 is impaired, for example, by mutations.
Such mutations do in fact occur, the Radboud University scientists and their colleagues at other universities reported.
Due to these mutations, the patients had high levels of methanethiol and dimethyl sulfide in their blood. When the blood reached the patient’s lungs, the unpleasant smell came out when they exhaled.
Similarly, mice with a genetic knockout of the mouse equivalent of SELENBP1 had low levels of the protein and high levels of methanethiol and other volatile sulfur compounds in their blood.
“While we didn’t put our noses up to the mice’s mouths, we did measure high amounts of some of these odor-forming chemicals in their blood, matching precisely what was found in the patients,” said Kent Lloyd.
So far, there is no evidence that the patients with chronic halitosis who participated in the study are at increased risk for cancer. Nevertheless, since the presence of sulfur-containing metabolites has been linked to some cancers, the researchers plan to investigate the matter further.
In the future, the work could lead to new treatments for bad breath and might identify cancer drug targets.
