Florida researchers find one in five college students may have misophonia – a hypersensitivity to sounds like lip smacking and pen clicking

Almost one in five college students is so sensitive to common, annoying sounds like lip smacking and pen clicking that they may have misophonia—a little-understood condition where people overreact to irritating noises. The results come from a University of South Florida study published in October 2014, where 483 students self-reported what sounds irritated them, and how they reacted. Among students who reported the strongest misophonia symptoms, more than half reported that their school and work lives suffered because of their discomfort and avoidance of triggering situations. While researchers have studied individual cases before, and even proposed diagnosis criteria for misophonia, this is the first study to estimate how widespread misophonia may be.

But do one in five people really have misophonia? Probably not. The authors point out that what they found among mostly white, female, middle-class college students is likely different from what they would find if they studied people who aren’t students at the University of South Florida. I also wonder how much the type of specific sounds varies between cultures. If the type does vary with culture, I would expect Americans to be more sensitive to loud eating noises, which are considered bad table manners.

Wu MS, Lewin AB, Murphy TK, & Storch EA (2014). Misophonia: incidence, phenomenology, and clinical correlates in an undergraduate student sample. Journal of clinical psychology, 70 (10), 994-1007 PMID: 24752915


What’s gnawing on Jane Austen’s hair?

An extreme close-up of one of Jane Austen's hairs, showing bits of skin (labeled 'S') and two different species of yeast ('M' and 'F').

An extreme close-up of one of Jane Austen’s hairs, showing bits of skin (labeled ‘S’) and two different species of yeast (‘M’ and ‘F’).

The years hadn’t been kind to the lonely lock of Jane Austen’s hair on display in a Hampshire museum. Light had bleached it to a straw color; only the shadowed underside remained its original brown. A few tiny flakes of skin still adhered, long after the legendary author had crumpled to dust. And the hair’s surface—visible only after vacuum coating it in a patina of carbon and metallic silver 2,000 times thinner than each hair itself, and then loading the coated hair into a Cambridge ‘Stereoscan Mk II’ scanning electron microscope*—was looking a little rough. To be more precise: a little gnawed.

So what was gnawing on Jane Austen’s hair nearly two centuries since it was detached from the dead author’s head?

In 1972, this wasn’t the most pressing question on the minds of the Jane Austen Society when they contacted Dr. J.A. Swift, a researcher in Middlesex, England. Concerned simply about the effects of display on the lock’s preservation, they asked him to examine a few hairs for signs of decay. But Dr. Swift saw more than some bleaching and dandruff: by using a powerful scanning electron microscope, he found what had been chewing on Austen’s hair.

The culprit? Yeast. But not the sort that ferments your beer and raises your bread: these were human scalp yeasts, which thrive on a diet of sweat and the waxy sebum that waterproofs our skin. Deprived of their food after Austen died and this lock of her hair was taken by her niece, Fanny Knight, the hungry yeast tried consuming the dead, flat scales of protein that make up human hair. But without a supply of their favorite sweaty food, they soon died themselves. Even now, their stringy, filamentous bodies remain tangled with the hair of their long-dead host.

A host who had unusually smooth, flat-surfaced hair—an indication that Austen’s hair must have been covered against the elements, and rarely combed in the last few years of her life. A state of hair which, Dr. Swift suggests, “might be consistent with an individual who placed little emphasis on the outward appearance of her hair.”

* The MkI was presumably in the shop.

Swift JA (1972). Scanning electron microscope study of Jane Austen’s hair. Nature, 238 (5360), 161-2 PMID: 4558459

Toxic levels of mercury contaminate 1 in 30 skin-lightening creams (and maybe not by accident)

Toxic levels of mercury contaminate about 1 out of 30 skin-lightening creams purchased in stores and online, according to an international team of researchers who measured mercury levels in more than 500 products worldwide. If you’re like me (pasty and with a family history of melanoma), then you may never have heard about these creams used by millions of women worldwide to smooth and lighten their skin color. When women apply these contaminated creams day after day, they are doing more than changing their skin: they are also dosing themselves with dangerous amounts of mercury that can damage their kidneys and poison their nervous systems.

Disturbingly, the most toxic creams may be best ones for lightening skin. The same traits that make mercury so deadly also make it great at disrupting the body’s ability to create melanin, which darkens our skin. This gives manufacturers a perverse incentive to ignore the FDA’s and European Union’s strict limits on mercury in cosmetics. Because the levels of mercury were so high in some products—up to 45,000 times the FDA’s limit, which is more than enough to sicken a large woman—the researchers accused manufacturers of deliberately adding the mercury to make their products more effective. And, unfortunately, more toxic.

But why would women use skin lighteners in the first place? I’d always assumed that prizing light skin was a legacy of Victorian colonialism and discrimination in the U.S. and Africa. But it turns out that China and India have long favored fair skin, thanks to its associations with being the pre-industrial equivalent of a wealthy person with an indoor desk job.  It’s easy to just dismiss women who use lightening creams as being vain—and the health risks they take as being deserved—but given the numerous social and career advantages afforded to attractive women, I think it would be equally possible to argue that they’re taking rational risks.

But I’m not going to argue for either vanity or rationality. Instead, I’m going to argue for giving the FDA and other countries’ enforcement agencies the means—and by means, I mean money—to better enforce their regulations. Because regardless of their motives—vanity, or logic—people deserve to be safe from exposure to one of the worst toxins out there.

Hamann C.R., Boonchai W., Wen L., Sakanashi E.N., Chu C.Y., Hamann K., Hamann C.P., Sinniah K. & Hamann D. (2013). Spectrometric analysis of mercury content in 549 skin-lightening products: is mercury toxicity a hidden global health hazard?, Journal of the American Academy of Dermatology, PMID: http://www.ncbi.nlm.nih.gov/pubmed/24321702

Can’t stand the sounds of chewing, loud breathing, or pen clicking? Dutch psychiatrists propose that may be the symptom of a new disorder

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

Getting your tonsils removed: A (sometimes) cure for bedwetting

ResearchBlogging.orgKids 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

Toxic bacteria: a possible cause of frog deformities

A North American mink frog with an extra limb.  Image from USGS.

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

Did Jane Austen die from (a) Addison’s disease, (b) cancer, or (c) disseminated bovine tuberculosis?

Jane Austen, writer extraordinaire, died in July 1817 at the age of 41.  Amazingly for her time, she had survived childhood and–by remaining a spinster–avoided childbirth, which killed off four of her sisters-in-law.  But despite this early good luck, good health ultimately eluded her.  In the February before she died, she wrote to her niece with characteristic dry humor (and loooooong sentences) that:

CassandraAusten-JaneAusten(c_1810)_hires“I certainly have not been well for many weeks, and about a week ago I was very poorly, I have had a good deal of fever at times and indifferent nights, but am considerably better now and recovering my looks a little, which have been bad enough, black and white and every wrong colour.  I must not depend upon ever being blooming again.  Sickness is a dangerous indulgence at my time of life.”

Sadly, this ‘dangerous indulgence’ would kill her later that year.  Jane Austen died in the company of her beloved sister Cassandra, who went on to grieve and, unfortunately, destroy many of Jane’s letters which could have given clues about her illness.  But the paucity of evidence hasn’t stopped researchers from speculating over the years: what killed Jane Austen?

Addison’s disease

“…black and white and every wrong colour.”

Addison’s disease–a rare disorder arising from malfunctioning or damaged adrenal glands–was first proposed as the culprit by British doctor Zachary Cope in 1964.  Austen had many of its symptoms: progressive weakness; stomach troubles; and even the discolored skin, which she fretted about to her niece.  Austen also lived in an era when Addison’s disease was more common, because tuberculosis–which was rampant in 19th century England–can destroy the adrenal glands.

Hodgkin’s lymphoma

“I have had a cold and weakness in one of my eyes for some days, which makes writing neither very pleasant nor very profitable.”

But Cope’s proposal soon had competition: F.A. Bevan pointed out that Addison’s disease could not explain Austen’s frequent fevers or back pain.  Instead, he diagnosed the dead author with Hodgkin’s lymphoma, a cancer affecting the lymph system.  In 2005, Annette Upfal built an even stronger case for Hodgkin’s lymphoma.  Pointing to Austen’s face pain–possibly a consequence of nerve damage from a shingles infection–Upfal concluded that the author had suffered from immune deficiency.  This deficiency could have been caused by tuberculosis but was more likely, in Upfal’s opinion, to be caused by Hodgkin’s.

Disseminated bovine tuberculosis

“I will not boast of my handwriting; neither that nor my face have yet recovered their proper beauty.”

If not Addison’s or Hodgkin’s, what was the culprit?  In 2009, K.G. White proposed that only tuberculosis caught from contaminated milk could explain all of Austen’s symptoms.  In particular, she pointed out that Addison’s patients often suffer from mental confusion–a symptom that would have made the legendary author much less legendary.  Disseminated tuberculosis would be more likely than Hodgkin’s to have caused Austen’s joint problems.  However, White concluded that, without an autopsy, it’s impossible to completely determine what killed Austen.

While it’s fascinating to speculate on what ‘dangerous indulgence’ killed Jane Austen, it’s a relief to know that even when ill, the extraordinary author was able to write that, “My head was always clear, and I had scarcely any pain.”

Cope’s original article:
COPE Z (1964). JANE AUSTEN’S LAST ILLNESS. British medical journal, 2 (5402), 182-3 PMID: 14150900