In 2013, Dutch psychiatrists proposed that misophonia – a hypersensitivity to common, irritating noises like eating, loud breathing, and pen clicking – be classified as its own psychiatric disorder. After evaluating 42 Dutch patients with the disorder, the psychiatrists concluded that their symptoms didn’t fully match those of people with obsessive-compulsive disorder or autism spectrum disorder. By proposing that misophonia get its own criteria in the Diagnostic and Statistical Manual of Mental Disorders – a classification system used by doctors, lawmakers, and insurance companies – the psychiatrists have taken the first step towards helping doctors recognize misophonia patients, and towards pursuing research into the disorder’s cause and treatment. Despite the small number of test subjects, the psychiatrists were able to find consistent patterns. Most of the patients reported that their earliest memories of misophonia were of a profound disgust at hearing their families eat. But unlike with other phobias, this disgust quickly became uncontrollable anger – and the patients reported lashing out verbally (or even physically) at the person making the noise. However, the patients considered their overreaction unacceptable, and were stressed and uncomfortable at the prospect of hearing triggering noises and losing self-control. Many coped by avoiding socializing or wearing headphones to mask noises. But what is causing such a stressful reaction in the first place? The psychiatrists speculated that it may be caused by recurrent conditioning – basically, the patients developing the habit of disgust. They also suggested that misophonia may be part of a more general overreaction to many stimuli, like noises and certain sights. Despite these speculations, the psychiatrists cautioned that because our understanding is still limited, it’s difficult to hypothesize about misophonia’s cause.
Reference: Schröder A. & Damiaan Denys (2013). Misophonia: Diagnostic Criteria for a New Psychiatric Disorder, PLoS ONE, 8 (1) e54706. DOI: http://dx.doi.org/10.1371/journal.pone.0054706
Kids who snore are more likely to wet the bed than kids who don’t. Strangely enough, the reason may be their too-big tonsils, which can cause the snoring and sleep apnea affecting 1 in 10 kids. In 2013, Michigan scientists reported that removing the tonsils stopped bedwetting in 20 out of 46 kids, almost three times the number who would stop bedwetting on their own. But while removing the tonsils can stop bedwetting, it doesn’t always–and the difference between may lie in kids’ sleep patterns before the surgery.
These results surprised the scientists: like other researchers and doctors, they’d expected that the difference would be linked to different levels of the hormones controlling blood fluid levels. Instead, they found that the cured kids had had their sleep disturbed more often by their snoring or apnea before surgery. Their bodies also got less oxygen during sleep–which, along with their snoring and bedwetting, was relieved by the surgery. In contrast, the kids who weren’t cured had woken up more often before surgery. Other factors–such as ADHD or other medical issues not involving the tonsils–might lie behind these kids’ bedwetting.
Researchers have long suspected that the link between large tonsils, sleep problems, and bedwetting comes from the tonsils blocking kids’ throats, which changes the internal pressure in their chests. In response, heart cells release brain natriuretic peptide–a hormone which triggers the body to excrete more water and salt into the blood, increasing the urge to pee. Presumably, getting rid of the large tonsils would make kids’ chest pressure normal and reduce the amount of brain natriuretic peptide. The Michigan scientists caution that this suspected link may still be true, and that their preliminary study needs to be repeated with more kids.
Kovacevic L, Wolfe-Christensen C, Lu H, Toton M, Mirkovic J, Thottam PJ, Abdulhamid I, Madgy D, & Lakshmanan Y (2014). Why does adenotonsillectomy not correct enuresis in all children with sleep disordered breathing? The Journal of urology, 191 (5 Suppl), 1592-6 PMID: 24679871
A North American mink frog with an extra limb. Image from USGS.
The toxic cyanobacteria that clog ponds with thick, green muck may cause deformities in frogs, according to Czech scientists. Since the 1970s, more and more frogs around the world have been born with missing legs or deformed eyes. Scientists have suspected that the deformities may come from the frogs’ exposure as tadpoles to retinoic acids, a class of chemicals produced by toxic water bacteria. Using samples from Europe and the United States, the Czech scientists have identified three common types of cyanobacteria that secrete retinoic acids into water. Disturbingly, the scientists found that these bacteria-made retinoic acids caused laboratory fish to develop birth defects similar to those increasingly experienced by frogs in the natural environment.
Jonas A, Buranova V, Scholz S, Fetter E, Novakova K, Kohoutek J, & Hilscherova K (2014). Retinoid-like activity and teratogenic effects of cyanobacterial exudates. Aquatic toxicology (Amsterdam, Netherlands), 155, 283-90 PMID: 25103898