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


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