Article
King George III and porphyria:
a clinical re-examination of the
historical evidence
History of Psychiatry
21(1) 3–19
© The Author(s) 2010
Reprints and permission: http://www.
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DOI: 10.1177/0957154X09102616
http://hpy.sagepub.com
Timothy J Peters
Institute of Archaeology and Antiquity, University of Birmingham
D Wilkinson
Institute of Education, University of London
Abstract
The diagnosis that George III suffered from acute porphyria has gained widespread acceptance, but re-examination
of the evidence suggests it is unlikely that he had porphyria.The porphyria diagnosis was advanced by Ida Macalpine
and Richard Hunter, whose clinical symptomatology and historical methodology were flawed.They highlighted
selected symptoms, while ignoring, dismissing or suppressing counter-evidence. Their claims about peripheral
neuropathy, cataracts, vocal hoarseness and abdominal pains are re-evaluated; and it is also demonstrated
that evidence of discoloured urine is exceedingly weak. Macalpine and Hunter believed that mental illnesses
were primarily caused by physical diseases, and their diagnosis of George III formed part of a wider agenda to
promote controversial views about past, contemporary and future methods in psychiatry.
Keywords
Acute porphyria, biological psychiatry, historiography, King George III, royal malady
The diagnosis that George III suffered from acute porphyria, an inherited metabolic disorder, was
first proposed in the 1960s by the psychiatrists Ida Macalpine and Richard Hunter, a mother-and-son
duo, who were keenly interested in the history of their profession. They had previously edited a
series of documents on the origins of psychiatry, and their controversial claim about George III
developed from this research (Macalpine and Hunter, 1963, 1966, 1968, 1969). Although their diagnosis was disputed, it gained significant support from experts such as Abraham Goldberg and Claude
Rimington (Goldberg, 1968; Macalpine, Hunter and Rimington, 1968). It has therefore become
commonplace for historians to portray the porphyria theory as more or less established fact (Black,
2006; Brooke, 1972; Christie, 1986; Hibbert, 1999; Thomas, 2002). Yet it can be demonstrated that
the porphyria diagnosis was based on weak foundations, bolstered by indiscriminate aggregation of
symptoms and suppression of contrary indicators. It appears very unlikely that the King was suffering from porphyria and therefore the causes of his ‘madness’ remain an unsolved mystery.
Corresponding author:
Timothy J Peters, Iron Lock Cottage, Beeston Brook, Tiverton, Tarporley, Cheshire CW6 9NH, UK.
Email: [email protected]
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History of Psychiatry 21(1)
In the autumn of 1788 George III became seriously ill and was unable to fulfil his royal duties.
Rumours were rife about his bizarre behaviour, and contemporaries found it difficult to distinguish
authentic information from wild speculation. The evidence available to historians, which includes
medical reports and private diaries, is more detailed and reliable. Sir George Baker, one of the royal
physicians, described the King as suffering from ‘an intire alienation of mind’.1 The Queen told a
confidential friend that the King’s eyes: ‘she could compare to nothing but black-current jelly, the
veins in his face were swelled, the sound of his voice dreadful; he often spoke till he was exhausted,
and the moment he could recover his breath began again, while the foam ran out of his mouth.’
(Harcourt, 1880–1905: IV, 21–2). Gradually, these extreme symptoms gave way to quieter irrationality and in due course the King was able to resume supervised meetings with his wife and daughters. In the spring of 1789, as mysteriously as they had arisen, the mental disturbances subsided and
then disappeared. Proceedings on legislation for a regency were abandoned, and George III returned
to public life. During the ensuing decade his mental health gave no serious cause for alarm.
Although he became unwell in 1801 and 1804, these briefer episodes were handled without creating another crisis. In 1810 George III became seriously deranged, and the following year a regency
was established that lasted until his death in 1820.
Macalpine and Hunter dogmatically asserted that the ‘madness’ of George III was a ‘classic
case’ of porphyria and that his mental derangement was a ‘toxic confusional state’ (Macalpine and
Hunter, 1968: 11–16; 1969: 35, 173). Considerable emphasis was given to the symptom of discoloured urine; Hunter, for example, stated in a radio broadcast that this provided ‘final proof’ (Hunter,
1966). Only a few instances of discoloured urine had been discovered, but this was attributed to
medical ignorance. They suggested that eighteenth-century doctors had no reason to notice
discoloured urine because porphyria and its symptoms were not identified until the twentieth century. Macalpine and Hunter also cited various other symptoms, claiming that these, by themselves,
would almost suffice as proof (Macalpine and Hunter, 1969: 174). The ensuing analysis therefore
examines the ancillary symptoms of muscular weakness, cataracts and vocal hoarseness (plus
some possible jaundice that was disregarded by Macalpine and Hunter) in order to culminate in a
re‑assessment of the crucial evidence for abdominal pain and discoloured urine.
Muscular weakness/peripheral neuropathy
Macalpine and Hunter (1968: 11; 1969: 172) claimed that the King’s illness ‘affected the peripheral nerves’, causing ‘painful weakness of the arms and legs, so that he could not hold a cup or a
pen, or walk and stand unaided’. On 17 Oct. 1788 George III told Baker that ‘of late he had been
much tormented in the night by a cramp in the muscles of his legs, and that he had suffered much
from the rheumatism, which affected all his limbs, and made him lame’.2 Fanny Burney also
recorded in early November that the King ‘grows so weak that he walks like a gouty man’
(D’Arblay, 1904–5: IV, 121). This was a peculiar sort of lameness, however, that did not affect his
ability to ride on horseback. George III wrote on 3 Nov. that he was ‘not in the least now fatigued
with riding, though he cannot yet stand long, and is fatigued if he walks’ (Stanhope, 1861–2: II,
App.v-vi). Macalpine and Hunter did not suppress this evidence, but simply ignored the obvious
point that alleged weakness in the hands and arms was inconsistent with holding reins while riding
at speed. Their suggestion that peripheral neuropathy made his hands so weak that he could not
hold a cup or a pen is false. ‘I saw him this night sit up and eat his posset, and afterwards take his
draught’, reported Robert Greville in early November; the King also played card-games and played
the flute, even drawing ‘plans of the house … with tolerable accuracy’ (Greville, 1788–9/1930: 81,
117). Therefore George III was able to manipulate riding-reins, feed himself, play games and
music, and perform feats of draughtsmanship.
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A diagnosis of peripheral neuropathy is also at variance with the physical exertions evident
during the manic phase of his illness. On 12 Nov., while lying in bed, ‘he had a violent struggle,
jerking very strongly with his arms and legs’. On the 25th he ‘gave one of the pages a smart slap
on the face’. Further violence was reported over the following days and the pages were ‘obliged
in the course of their painful duty to hold him in bed, and overpower his turbulence’. By the time
of his transfer from Windsor to Kew on 29 Nov. there was little sign of lameness: ‘on his arrival
he got out of the carriage … and then making a run he attempted to get into his appartments’.
Later that evening George III told Greville that ‘he was very strong and active, and in proof of this
he danced and hopped with more agility that I could have suspected’. That night he was ‘turbulent
and violent … pulled one of the pages by the hair and attempted to kick another’ (Greville,
1788–9/1930: 82, 104, 106, 112–14).
Violent outbursts were subsequently controlled by the use of a ‘straight waistcoat’, under a
system of management devised by Francis and John Willis. These new doctors, who arrived in early
December, were experienced at treating mental disorders. They believed that the King’s turbulence
had been exacerbated by the use of medicinal blisters that were supposed to draw ill humours from
the body. Despite their objections, this treatment was continued and by 16 Dec. the King was making ‘great complaints about – and signs of his legs hurting him exceedingly’. The following day
John Willis noted in his diary that ‘I told Dr Warren that the blisters were … greatly the occasion of
his Majesty’s restlessness’. Warren replied that ‘it was all trick in his Majesty’.3 Greville’s diary
entry on 19 Dec. lends some support to this cynical assessment. The King had apparently fooled the
Willises into thinking he could not rise from his chair, but becoming ‘angry with one of Dr Willis’s
men and taking his feet off the chair he walked up to him’. The attendant stated that the King ‘had
cheated them as he could walk very well’ (Greville, 1788–9/1930: 125).
The surviving evidence of the King’s ‘lameness’ does not match a diagnosis of peripheral
neuropathy. The porphyria expert Charles Dent pointed out that ‘if there is peripheral neuritis it
may take six to nine months for the patient to recover’. George III therefore recovered from ‘paralysis a little too quickly on occasions for this to have been porphyric neuritis’ (Dent, 1968a). The
King’s lameness was intermittent and probably not attributable to a single cause. Early symptoms
were ambiguous and unsustained; whereas later manifestations of pain and weakness in the legs
coincided with the excruciating discomfort of infected blisters. The King may also have exaggerated (or occasionally ‘shammed’) his lameness as the infections gradually healed.
It is not simply that Macalpine and Hunter made a doubtful diagnosis based on a partial reading of
the evidence, but they also disingenuously attempted to extend the duration of the alleged muscular
weakness. On 19 Jan. 1789 George III was allowed to take a walk in the grounds at Kew. Macalpine
and Hunter (1969: 77) claimed that ‘according to John Willis, the King had become progressively
weaker on the walk and had lain down when his legs would no longer carry him’. In fact this was
task-refusal, not neuropathic weakness. George III had been thwarted twice: firstly, he was refused
permission to walk into Richmond gardens; secondly, he was prevented from climbing the Pagoda,
even scuffling with his attendants in an abortive attempt to grab the key. This rebuff ‘offended’ the
King, who ‘now walked with difficulty: till at length he lay down upon the ground and would walk
no further’.4 When George III had been told ‘he must walk on’, he instead ‘sat down and afterwards
lay extended on the grass’ (Greville, 1788–9/1930: 179). Thereafter he was forcibly carried home on
the shoulders of his attendants. Macalpine and Hunter not only misrepresent this episode as muscular
weakness, but also omit to mention that the King had already walked at least a mile beforehand. The
following day George III walked in the garden for ‘an hour and 20 minutes’.5 Similar amounts of
exercise were taken over ensuing days, and these excursions were gradually extended: ‘he walked as
usual twice in the gardens, in all perhaps as is generally the case 4 hours’, noted Willis on 15 Feb.6
(Harcourt, 1880–1905: IV, 207–8). Symptoms of lameness can therefore be discounted in 1788–9.
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History of Psychiatry 21(1)
In 1804 the King had a swollen foot and became too weak to walk without a cane, but these
symptoms did not persist (Macalpine and Hunter, 1969: 131). The King was observed on the terrace at Windsor Castle in March 1811, walking with General Manners ‘holding him under the
arm’; he ‘stooped a little – looked thin – walked fast, talking continually’ (Simond, 1815: II, 115).
On 28 July 1812 it was reported that the King ‘has spoken of feeling weak upon his legs’. The doctors nevertheless explained this as ‘the natural effect of sitting so much without exercise’.7 On 23
Oct. 1812 the King ‘walked very lame and was annoyed in his feelings by a little superficial
inflammation and swelling on his foot’. This lameness disappeared after a few days. On the 26th
the doctors noted that ‘the skin of the foot [is] less red’, and the King walks with scarcely any
appearance of lameness’.8 These were intermittent ailments, probably attributable to infection,
inflammation, immobility or the process of ageing. The evidence does not support a diagnosis of
peripheral neuropathy, which is in any event a weak indicator of porphyria, occurring only in a
minority of cases and generally as a result of recurrent attacks. When it does occur it generally lasts
several months, even in patients in remission following an acute attack (Dean, 1971: 82–3;
Wikberg, Andersson and Lithner, 2000).
Cataracts
Macalpine and Hunter made a ludicrous attempt to link bilateral cataracts to porphyria: ‘it is known
that metabolic disorders such as porphyria predispose to cataract, and besides George III several of
George IV’s brothers and sisters were likewise afflicted’ (Macalpine and Hunter, 1969: 240). While
it is true that some metabolic disorders, such as diabetes mellitus, are associated with a high prevalence of cataract, there is absolutely no evidence of any connection with porphyria. Macalpine and
Hunter chose to ignore sound advice from Rimington on this matter; and it therefore beggars belief
that they should suggest that simply because porphyria is a metabolic disorder there was an automatic predisposition to cataract.9 George III was treated with emetics and purgatives that may
cause dehydration and malabsorption, which are risk factors for the development of cataract, as too
are the various topical medications he was given (Harding, 1991). The King became almost totally
blind, and surgery to remove his cataracts was considered but eventually rejected. The doctors
speculated that blindness might contribute towards continued madness; but, after examining other
cases, concluded that ‘deranged persons who are blind’ were not ‘more apt to become imbecile that
those who see’.10
Vocal hoarseness
Macalpine and Hunter (1968: 14) claimed that the King’s hoarseness was another indicator of a
‘textbook case’ of porphyria because ‘vocal paresis’ was a sign of ‘bulbar involvement’. A
moment’s reflection on the implications of this assertion reveals its absurdity. Extensive neurological involvement in the porphyric process would be necessary, with quadraparesis and cranial
nerve involvement. Post-mortem studies show extensive demyelination in such cases (Ebaugh
and Holt, 1963; Meyer, Schuurmans and Lindberg, 1998). In the eighteenth century such symptoms, if attributable to porphyria, would almost certainly be a prelude to death. Even with modern
and effective treatments, recovery may take at least a year (Dean, 1971; Lamon, Frykholm, Hess
and Tschudy, 1979). A more plausible suggestion may be offered: the King’s voice became hoarse
because he spoke for hours upon end. ‘He has talked away his voice’, noted Burney on 1 Nov.
1788, ‘and is so hoarse it is painful to hear him’ (D’Arblay, 1904–5: IV, 121). Between 18 and 19 Nov.
the King ‘talked for nineteen hours without scarce any intermission’ (Greville, 1788–9/1930: 89–90).
There was a consistent pattern: hoarseness was consequent upon the physical exertion of incessant
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talking or occasionally from a ‘head cold’. To give just one later example, on 16 Jan. 1812 ‘the
King talked rapidly and violently for twenty five hours without intermission’.11
Faecal pallor and jaundice
Macalpine and Hunter sought symptoms indiscriminately, highlighting those that they believed to be
favourable, and ignoring counter-evidence or alternative explanations. For example, pale stools were
a recurrent feature of the King’s illness, being variously described as ‘straw-coloured’, ‘pale’, ‘white’,
‘slate colour’ or ‘ash color’d’.12 These signs were sometimes short-lived and at other times continued
for months at a time. Their significance is uncertain: faecal pallor may be due to hepatic, pancreatic
or intestinal disease; they may likewise be a response to medication. Macalpine clearly hoped that
there was a link with porphyria and consulted her collaborator Abraham Goldberg, who replied correctly in the negative.13 Pale stools are not a feature of porphyria, but they can be caused by biliary
obstruction caused by gallstones. Macalpine and Hunter avoided this explanation because it undermined their argument. They repeatedly denied that George III suffered from jaundice. On the other
hand, as they researched the King’s ancestors, they discovered that James I suffered recurrent episodes of jaundice. This resulted in an inconsistent strategy of denying that jaundice explained George
III’s symptoms, while suggesting that James I’s jaundice supported a diagnosis of porphyria. They
stated that ‘exacerbations’ of acute porphyria ‘are often accompanied by transient hyperbilirubinaemia
or even frank clinical jaundice’ (Macalpine and Hunter, 1968: 27). They cited an article by Claude
Rimington, one of their collaborators, on a single case report from 1941–3 of a patient with suggested
porphyria cutanea tarda. This is a quite different form of porphyria that is due to liver disease and is
not one of the acute porphyrias (Moore, McColl, Rimington and Goldberg, 1987: 179–99). The
patient was suffering from liver dysfunction: ‘an epidemic of acute hepatitis prevailed at the time
when our patient was experiencing attacks of jaundice’ (Gray, Rimington and Thomson, 1948: 126).
There is no support for the claim by Macalpine and Hunter that the acute porphyrias are accompanied
by jaundice. Their citation was either woefully ignorant or deliberately dishonest.
Abdominal pains
Macalpine and Hunter claimed that abdominal pains consistent with porphyria were a recurrent
feature of the King’s illness. In October 1788 Baker recorded that the King complained of ‘a very
acute pain in the pit of the stomach, shooting to the back and sides’. This does not sound like the
sort of deep persistent pains that are frequently a feature of porphyria. George III’s abdominal pains
seem to have been transient. Yet in order to create the impression that the King suffered from
chronic pain, Macalpine and Hunter (1969: 77) stated that, on 17 Jan. 1789, ‘for the first time in
many weeks the King had no abdominal discomfort’. The reference cited by Macalpine and Hunter
does not support the assertion made in the text. None of the sources records abdominal pains after
the initial attacks. Greville makes no mention of any complaints about abdominal pains during this
period. John Willis’s medical notes record numerous clinical features (such as the pain from the leg
blisters, the quality of the King’s stools, and sometimes the quantity of urine passed), but nothing
about persistent abdominal discomfort. The Willises disputed repeatedly with the other doctors
over the significance of symptoms such as the King’s pulse or his night-sweats. They argued
strongly that ‘fever’ underlay the mental disturbances. Warren conversely denied the existence of
‘fever’ and maintained that bodily health, combined with mental derangement, amounted to
untreatable insanity and permanent fatuity. It seems highly unlikely that the Willises would have
neglected to record complaints about chronic abdominal pains because these would have provided
useful ammunition against their medical adversaries.
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History of Psychiatry 21(1)
Diagnosis of the state of the King’s abdomen during January and February 1789 is further complicated because of repeated prescriptions of tartarized antimony, an emetic (to induce vomiting)
which was deemed ‘very quieting’ when ‘symptoms of irritability appear’. There is no evidence of
persistent abdominal pain in 1788–9 and there are only occasional and inconclusive references in
the later episodes of illness. Tartar emetic was again prescribed after the King became ‘very bilious
and unwell’ in February 1801; and there were transient reports of ‘undesirable pain in the abdomen’ on 26 November 1810; and ‘violent pain’ in his ‘stomach and back’ during March 1811
(Macalpine and Hunter, 1969: 76, 80, 111, 147, 156).
Discoloured urine
The significance of the King’s physical symptoms is the reverse of that proposed by Macalpine and
Hunter. They maintained that features such as peripheral neuropathy, cataracts, vocal hoarseness
and abdominal pains were sufficient on their own to suggest a diagnosis of porphyria, for which the
evidence of discoloured urine provided final proof. These other symptoms have been analysed
above in order to demonstrate that evidence was distorted by Macalpine and Hunter to create misleading impressions. Without strong evidence of ‘discoloured’ urine their diagnosis of porphyria
must therefore collapse.
Macalpine and Hunter initially claimed only four episodes of discoloured urine, but in their fulllength book this was increased to six: ‘the records of the royal physicians contain six instances in
which they describe his urine at the height of his attacks as “dark”, “bilious” or “bloody”, and even
noted on occasion that it left a bluish stain on the vessel after it had been poured away’ (Macalpine
and Hunter, 1969: 174). No footnote is provided to support these alleged additional occurrences in
the medical records.
These new claims prove to be unimpressive. One of them is casually advanced during an account
of the King’s illness in 1801. In February Charles Abbot ‘heard that the disorder was “turning to a
black jaundice” – which, since he was not jaundiced, meant that his urine was dark’ (Colchester,
1861: I.245; Macalpine and Hunter 1969: 116). This throwaway assertion is highly misleading.
Firstly, the evidence does not come from the records of the royal physicians. Charles Abbot was a
politician who only had access to rumours and second-hand reports. There is no way of establishing where Abbot got his information, and it is unreasonable to claim that it refers to urine.
Historically, jaundice has been subdivided into various ‘colours’, for example, yellow, blue, green,
red and indeed black. The terminology ‘black jaundice’ has sometimes been used in the past to
denote melaena or Weil’s disease. Yet it is highly doubtful that Abbot was making such a specific
diagnosis. It was the loose terminology of a layman that therefore provides no medical basis for
inferring discoloured urine.
The second additional instance of allegedly discoloured urine is buried in the midst of a convoluted passage about the state of the King’s health in December 1810. Second-hand gossip and
newspaper reports (which are notoriously unreliable) are combined with the brief quotation from a
doctor’s report to create the impression that this attack was ‘a return of his old abdominal trouble’.
According to Macalpine and Hunter (1969: 151), the King’s stools ‘varied from dark to pale’, and
‘sometimes their colour could not be “distinctly seen, the water being discoloured”’. This quotation has been traced to a report by the royal physician Sir Henry Halford on 30 Dec. The King ‘had
two motions in the night and one this morning, rather pale, but not distinctly seen the water being
discolour’d’. It is more plausible that frequent and therefore probably loose stools might have
contaminated the urine sample. Notwithstanding the claim that ‘discoloured’ urine occurred ‘sometimes’ during this period, there is no recorded repetition of this phenomenon. Also, Macalpine and
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Hunter (1968: 25) seem to have entertained doubts about whether this could really be counted as a
clear-cut example of porphyric urine, only deploying it initially as circumstantial evidence of ‘how
little importance’ the doctors ‘attached to urine’. The alleged increase in evidence from four to six
occurrences of discoloured urine is therefore illusory. Intriguingly, the same manuscript diary contains a report on 5 Feb. 1811 that the King passed ‘four stools in the night, one of a light green
colour, being tinged with iron’.14 Macalpine and Hunter do not cite this, nor is it diagnostic of
porphyria. It should remind us, however, that illness, medication and diet can have varied effects
on urine and faeces.
Analysis of the remaining four alleged instances of porphyric urine reveals that Macalpine and
Hunter manipulated their quotations from the source material, made a crucial factual error, and
ignored contradictory indicators or alternative explanations. This is how they cited the four alleged
instances of discoloured urine (Macalpine and Hunter, 1968, 15):
18 October 1788, Sir George Baker: “urine bilious” (Diary); 6 January 1811, Sir Henry Halford: “The
water is of a deeper colour – and leaves a pale blue ring upon the glass near the upper surface” (Willis
MSS), and 14 January 1812, “Bluish 8 and 9 [ounces]” (Royal Archives); and 26 August 1819, report of
Drs. Baillie and John Willis: “His Majesty has passed … bloody water … during the last 16 hours,” of
which “no tinge” remained the following day. (Queen’s Council Papers; Willis MSS)
It is instructive to examine these episodes in reverse chronological order. The evidence from 1819
of ‘bloody water’ can be explained in terms of the inherent likelihood of an eighty-year-old patient
suffering occasional bouts of blood in the urine:
Aug. 26 … His Majesty has passed some blood with his water during the last sixteen hours, but this
appearance has now in great measure subsided. It is not unusual for bloody water to be made by persons
advanced in life, and this symptom is generally of no importance. It will sometimes go off in a few hours
or days, and sometimes it will continue more or less for several weeks without doing any real injury to
the constitution – His Majesty slept three hours and a half without interruption last night and this morning
looked very well in the countenance … Aug. 27 … The urine is now quite free from any tinge of blood
and His Majesty appears to be quite well and comfortable.15
The first point to note is that the doctors did not simply describe ‘bloody water’, but also specifically stated that the King ‘passed some blood with his water’. Macalpine and Hunter omitted this
important detail, which weakens the case for porphyric urine. It is reasonable to accept at face
value that there was ‘blood’ in the urine. Macalpine wildly overstated her case in a private letter to
Dent: the ‘bloody water … can hardly be interpreted in any other way’.16 Yet, as the contemporary
doctors realized, such symptoms were unexceptional in an aged and infirm patient. George III died
only five months after this episode, aged 81 years. It is also interesting to note that other physical
features that characterize a porphyric attack did not accompany the urinary findings. Instead the
King is described as being ‘quite well and comfortable’.
The next example reveals a failure to transcribe accurately and cross-check sources thoroughly.
They claim that Sir Henry Halford’s diary in the Royal Archives contains a reference on 14 Jan.
1812 to ‘Bluish 8 and 9 [ounces]’. Significantly, they have added the supposed measurement of
volume in square brackets. Although blood-letting would often be described in term of ‘ounces’,
there is no basis for suggesting that urine might be so measured. It was not contemporary practice
minutely to measure the amount of urine. Comments were sometimes expressed in general terms,
such as a large or small quantity of urine. On one occasion in 1788 Dr Willis did record an
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History of Psychiatry 21(1)
estimated volume, but he did not use fluid ounces as his measurement. He noted on the morning of
18 Dec. that during the previous ten hours the King ‘has made 4 quarts of water’.17 Doubts that ‘8
& 9’ in Halford’s diary in January 1812 referred to fluid ounces of ‘bluish’ urine are confirmed by
the chain of events leading to the following discovery.
Private correspondence reveals that Macalpine and Hunter received help from Robin MackworthYoung, Assistant Keeper of the Royal Archives. Macalpine wrote gratefully on 18 Feb. 1965 that
‘your “bluish” reference is exciting’. She had previously asked for permission to consult the Royal
Archives, but this request was denied. Instead Macalpine managed to persuade Mackworth-Young
to undertake some research on her behalf. Macalpine was later supplied with photostats of relevant
items, but was denied direct access.18 She did cross-check with the Manners Sutton Papers to establish the King’s state of health, but failed to make an obvious connection to other medical records
in the Willis Papers. On 14 Jan. 1812 the following entry was made: ‘There were given to the King
between 8 & 9 o’clock Jalap. gr. iii, Antim. Tart. gr. i.’.19 This is a record of the timing of the administration of a prescription, comprising three grains of a purgative made from the jalap root, and one
grain an emetic of tartarized antimony. There is no doubt that this is identical in meaning to the
entry for the same date in the Halford diary in the Royal Archives, which reads ‘Between 8 & 9.
the K. had Jalap. gr. iii, Antim. Tart. gr. i.’.20 The only difference is that Halford did not bother to
write out the words ‘o’clock’. Wishful thinking seems to have led to a misreading of ‘Between’ as
‘Bluish’. A careful scrutiny of Halford’s diary for the period from 5 Oct. 1811 to 29 Jan. 1812
reveals that there are no other significant references to urine. The full and abbreviated reports of
the King’s physicians were also examined with the same result.
Historical research has therefore undermined a key claim of Macalpine and Hunter about
discoloured urine. It must also be noted that bluish urine is not in fact diagnostic of porphyria.
Porphyric urine is dark reddish-brown. Indeed, porphobilinogen itself is colourless and the porphyrins are excreted as colourless precursors. Only with time are the red-brown porphyrins
formed. A characteristic of porphyric attacks is that the urine darkens significantly after it has
been allowed to stand, particularly if exposed to light. Macalpine feebly suggested that the ‘bluish tinge’ was ‘an early colour change to purple, which after all is a mixture of blue and red’.21
This ruse conspicuously failed to convince the porphyria expert Charles Dent.
More recently, a somewhat contrived explanation for bluish urine has been offered by Arnold
(1996). He suggested that bacterial fermentation of the urine may have formed indigo blue from
indican, a normal metabolite formed from the amino acid tryptophan. This does not confirm the
diagnosis of porphyria. At most, this symptom would merely be consistent with the constipation
that frequently accompanies porphyric attacks.
One reason why Macalpine and Hunter were so excited about the phantom ‘bluish’ reference in
the Royal Archives was because it seemed to chime with another piece of evidence. On 6 Jan. 1811
Halford recorded that ‘the water is of a deeper colour – and leaves a pale blue ring upon the glass near
the upper surface’. Macalpine and Hunter (1969: 174) slightly misreport this as the urine having ‘left
a bluish stain on the vessel after it had been poured away’. What is actually described seems to have
been a coloured suspension, floating towards the surface of the urine. Various possibilities may
explain this phenomenon. Not enough research has been conducted into the precise nature of the
medical prescriptions given to George III. Some of these preparations would have been produced
using solvents other than water, such as ethanol. Perhaps, one of these medications directly contaminated the inspection vessel, or unabsorbed medicine may have been passed with the urine, which on
the other hand might have been cross-contaminated from the stools. These can only be surmises.
One possible candidate for creating such a symptom is extract of gentian. It would be tempting
(but probably erroneous) to think that this medicine would have shared the same bright blue
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pigment as the flowers of the same name. It would appear, however, that extract of gentian was
usually prepared from the roots. This was nevertheless a dark preparation that was prepared by
alcoholic extraction (Chevallier, 1996; Graves, 1934). The King commenced treatment that
included gentian only a few days before the report of the ‘pale blue ring upon the glass’.22 An alternative possibility, suggested by Brownstein (1997: 44), is that medication with aloes and senna,
emodin cathartics or possibly other drugs may have been responsible.
Macalpine was aware that there was a problem in reconciling blue urine with a diagnosis of
porphyria, but her correspondence with Dent on this matter appears shockingly dishonest. Dent
wrote privately on 10 Jan. 1966, making it clear that ‘I do not think you have proved he had a porphyria type disease’. Among various criticisms (such as the nature of paralytic complications, the
severity of the disease, and the role of modern synthetic drugs in triggering attacks), Dent focused
in particular on the urinary symptoms:
In severe attacks a change of colour of the urine becomes quite noticeable and I do not see how they could
have avoided mentioning this as a constant feature during each illness. I do not know what you mean by
the blue colour of the urine. I think this must have been indigo and have represented an unrelated finding.
I do not think your four references are adequate. Goodness knows what the disease was. The mental
symptoms being so non-specific would fit many other diseases as well as porphyria.23
Macalpine attempted to counter-attack by attributing sentiments to Dent that he did not hold: ‘I
suppose you would agree on the clinical evidence that the King suffered from a systemic disturbance affecting his peripheral and central nervous system’, insisting also that ‘the symptomatology
and clinical course of his illness are those of acute intermittent porphyria’. Dent was unconvinced
and duly replied in the negative.24 Dent also continued to believe that recurrent urinary symptoms
would not have gone unnoticed (Dent 1968a, 1968b). The following extracts from a contemporary
monograph suggest that his hunch was entirely reasonable. Dr William Perfect, owner of the principal private asylum in Kent, published case histories from the late 1770s to the early 1800s. He
included observations about his patients’ urine, such as ‘water was highly coloured’; ‘urine was
pale and limpid’; ‘urine concreted, copious, and white’; ‘copious sediment, mixed with fabulous
concretions’; ‘urine was sometimes pale and sometimes high coloured, and never deposited any
kind of sediment’; ‘urine was generally high coloured, and deposited a copious red sediment of the
nature of bran’ (Perfect, c.1809/1976: 2, 21, 42, 123, 132,183). If George III had suffered repeated
attacks of porphyria, it would have been more likely that discoloured urine was observed than
overlooked. Macalpine firmly maintained the opposite position:
We must have given the wrong impression of the nature of the medical records for you to assume that his
urine was regularly inspected and discolouration should therefore have been noted more often. In fact,
apart from a very few references to large amounts of pale urine, the four references to discoloured urine
are almost the only mention …
… Certainly I cannot think that the urine was ever allowed to stand.25
Macalpine should have been aware from the medical records that the urine must sometimes necessarily have been allowed to stand. Firstly, there was a regular system of rotation between nighttime and day-time physicians, including collective consultations to exchange information.
Secondly, there are occasional records of the amount of urine being passed during the night.
Unless we are to imagine that this was immediately inspected by candle- or lamp-light, it can only
have been examined in the morning, after standing for several hours. Macalpine also failed to
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History of Psychiatry 21(1)
mention that pale urine was reported during attacks. On 12 Mar. 1801 the King ‘made as he has
done for some nights a great deal of pale water’.26 Indeed, in the weeks prior to the single report
of the ‘pale blue ring’ on 6 Jan. 1811, there were six occasions when pale urine was reported: ‘has
made water frequently, in the last 24 hours, clear and palish’ (16 Nov. 1810); ‘water very pale’ (22
Nov.); ‘urine pale’ (26 Nov.); ‘water pale’ (1 Dec.); ‘three times at the water closet, but no motion
in the night – water pale’(2 Dec); ‘several times out of bed to make water, which was pale’ (1 Jan.
1811).27 These reports coincided with severe attacks of mental disturbance. On 22 Nov. the King’s
‘conversation was loud, turbulent, and incoherent’, continuing ‘imprudent and a little irrelevant’
on the 28th. By 24 Dec. the King’s ‘pulse had risen to 120’ and ‘the whole frame is so much disturbed, as to make us consider him in some danger’. The crisis passed, but on the 30th his conversation was still ‘mixed with delusions’. On 1 Jan. 1811 he was reportedly ‘free from talking in the
night, but much occupied with arranging his bedclothes’.28 During this period the ‘straight waistcoat’ was also used.29
Macalpine and Hunter (1968:15) emphasized that their chosen urinary observations had been
made ‘during paroxysms when the excretion of porphyrins and porphobilin-like chromagens is
known to be greatest’. They cannot have it both ways. It is clear that during a serious attack of
mental disturbance in 1810–11 the King’s urine was carefully monitored and repeatedly noted as
being pale. These observations, moreover, were apparently recorded during daylight hours after
night-time urine had been allowed to stand. For Macalpine to have withheld such key data from her
private correspondence with Dent was reprehensible; the failure to include such details in their
published work amounted to sharp practice.
It has been demonstrated that three out of the four instances of discoloured urine can be safely
discounted. This leaves one further example to be considered. This was a transitory occurrence of
‘bilious’ urine during the early stages of the King’s illness in the autumn of 1788. On 17 Oct.
George III summoned Baker on account of ‘a spasmotic byleous attack, though much slighter than
in the month of June’.30 The King clearly regarded this as a recurrence of the physical illness that
had induced him to take the waters at Cheltenham during the summer. We can be reasonably sure
that the King did not exhibit signs of mental disturbance while at Cheltenham, nor was this aspect
of the ensuing illness immediately apparent in October. Here is Baker’s account from his diary:
Friday 17 Oct. 1788. Early this morning I received the King’s commands to attend him immediately at
Kew House. I found his Majesty sitting up in his bed, his body being bent forward. He complained of a
very acute pain in the pit of the stomach shooting to the back and sides, and making respiration difficult
and uneasy. This pain continued all the day, though in a less degree of acuteness towards the evening; but
it did not cease intirely until the bowels had been emptied …
Saturday 18 Oct. … This morning he had a slight degree of fever; but he had passed the night quietly
except when interrupted by the effect of his medicine. He now first complained of a pain in his left foot,
which on the upper part and one side was a little swollen, and slightly inflamed … Some yellowness in
the eyes and urine bilious …
Sunday 19 Oct. He complained of pain and tenderness in the left foot, the inflammation of which was
abated, but the swelling had increased. This day the right foot was likewise swollen and in pain without
apparent inflammation. The yellowness of the eyes disappeared and urine of natural colour …
There is no further mention of urinary symptoms. Abdominal pain reappeared in the early hours of
the 20th, but treatment ‘in a short time gave him relief’, with only some residual ‘soreness of the
whole belly’. On 21 Oct. there was ‘a return of the pain in the stomach; but it was only slight, and
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Peters and Wilkinson
ceased without the assistance of medicine, or application, except that of hot cloths’. Signs of mental derangement did not become manifest until 22 Oct., when the King was ‘in an agitation of
spirits nearly bordering on delirium’. George III recovered sufficiently to attend a levée at
St James’s on the 24th, returning afterwards to Windsor. The Queen was alarmed by the King’s
behaviour and therefore summoned Baker, who reported on 27 Oct.:
When I arrived the King was at the concert … During the whole music he talked continually, making
frequent and sudden transitions from one subject to another, but I observed no incoherence in what he
said, nor any mark of false perception … He was lame; complained of rheumatic pain, and weakness in
the knees, and was continually sitting and rising.
There was another period of respite over the next few days, during which time he visited a local
family and also had a meeting with the prime minister. George III also suffered some visual disturbances, becoming ‘near-sighted’ so that ‘whenever he attempted to read a mist floated before
his eyes’. He nevertheless regained enough physical strength to ride on horseback, even alarming
his attendants by ‘his very incautious manner of riding’. There was, however, an accompanying
deterioration in his mental state that culminated in ‘an intire alienation of mind’ on the evening of
3 Nov. The final entry in Baker’s diary on the 7th reported ‘the same alienation of mind’.31
Macalpine was aware that these urinary and abdominal symptoms were consistent with an
attack of obstructive jaundice. There was yellowness in the eyes and dark-coloured urine, accompanied by shooting abdominal pains. This is why Macalpine, in her correspondence with Dent,
stated: ‘Sir George Baker noted that it [the urine] was “bilious” because having diagnosed gallstones he was presumably looking for signs of jaundice’;32 and thus ‘biliary colic’ was dismissed
as a simple case of misdiagnosis (Macalpine and Hunter, 1968: 15). The fact remains, however,
that Baker did observe that the urine returned to its natural colour when the eyes lost their yellowness and the abdominal pains subsided. The disappearance of these symptoms was entirely
compatible with gallstones obstructing the bile duct having shifted (Peters and Sarkany, 2005).
Brownstein (1997: 44) has suggested another possibility: ‘three doses of physic were administered for abdominal pain. The cathartates from senna, aloes, etc. may darken urine’.
Macalpine was aware of the weakness of the evidence for discoloured urine, but nevertheless
made a desperate effort to convince Dent by arguing that:
If the case we reported had been that of a present day patient, to have found typically discoloured urine on one
occasion would have been sufficient to confirm the diagnosis. On how many other occasions the urine was
positive would be of interest for understanding the disease better but would not be essential for, or alter the
diagnosis for which one positive urine will do.33
This reveals her ignorance of the complexity of diagnosing porphyria from urine samples. The
present-day experience of the King’s College Hospital porphyria clinic is instructive. Approximately
a quarter of patients referred for investigation (often with urinary abnormalities including darkening) prove not to have porphyria when analysed with modern techniques (Marsden, Walsham and
Rees, 2007; Peters and Sarkany, 2005).
Discussion
Macalpine and Hunter do not appear to have had any clinical experience in diagnosing or treating
porphyria. Certainly, they were heavily reliant on collaborators such a Rimington, whose own
research into so-called X‑porphyrin seems to have played a part in shifting their initial diagnosis
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History of Psychiatry 21(1)
from acute intermittent porphyria to variegate porphyria (Macalpine and Hunter, 1968: 21).
Rimington’s role in developing a new diagnostic test (which is no longer used) for variegate porphyria, together with some historical evidence about skin sensitivity, persuaded Macalpine and
Hunter to alter their diagnosis. Understandably, ‘to sceptics it looked like a sign of confusion and
uncertainty, seeming to weaken their argument’ (Dent, 1968a; Röhl, Warren and Hunt, 1999: 32).
To non-specialists this may appear to have been merely a shift from one recondite technical term
to another. One recent historian has argued that Macalpine and Hunter amended their diagnosis
from acute intermittent porphyria to ‘an alternative and even more severe form of the same illness,
variegate porphyria’ (Green, 2005: 230). In fact, variegate porphyria is, especially with respect to
mental and neurological disturbances, a milder form of porphyria (Dean, 1971; Hift and Meissner,
2005; Meissner, Hift and Corrigall, 2003; Millward, Kelly, Deacon, Senior and Peters, 2001;
Millward, Kelly, King and Peters, 2005). The change in diagnosis therefore not only weakened
their argument, but also affected subsequent genetic research. When Röhl and his colleagues examined bones removed from the grave of Princess Charlotte (a grand-daughter of Queen Victoria)
they concentrated their efforts on amplifying PPOX, the defective gene in variegate porphyria.
They were able to report a mutation, but being ‘unable to assess directly the effect of the mutation
in Charlotte’s PPOX gene on the activity of the protein, we cannot be completely certain that we
have identified a disease causing-mutation’ (Röhl et al., 1999: 266, 269). This cautious verdict is
entirely warranted. Indeed, this DNA analysis is inconsistent with current reported mutations in
variegate porphyria. It may well be the case that these are nothing more than intronic polymorphisms of no functional significance. Recent research indicates that mutations in the PPOX gene
for variegate porphyria are consistently found in the exonic DNA (Whatley, Mason, Elder, Woolf
and Badminton, 2007).
The significance of any evidence about the descendants of George III depends in great measure
upon the original assessment of the King’s symptoms. Quite simply, if George III did not have
porphyria in the first place, then tracing the condition in descendants is irrelevant. Likewise, a
recent investigation of levels of arsenic in a reputed hair-sample from George III may prove to have
been an ingenious (albeit unconvincing) irrelevance (Cox et al., 2005).
The symptoms manifested by George III, as detailed in the surviving historical evidence, do not
provide a sound basis for a diagnosis of porphyria. None of the observations of discoloured urine
survives critical scrutiny, and they are themselves numerically outweighed by observations of pale
urine during attacks. Discoloured urine would have remained a recurrent and persistent feature of
severe porphyric attacks. Other features such as abdominal pain and peripheral neuropathy would
also have been more persistent, and not such short-lived and otherwise explicable symptoms.
Acute porphyria is potentially a very serious disease. If porphyria-induced bulbar palsy had been
the true cause of the King’s hoarseness in 1788, then he would almost certainly have died. Yet, only
a month before his death, when aged 81 years, George III ‘talked for fifty-eight hours with scarcely
a moment’s intermission’ (Hibbert, 1999: 408). Such loquacity readily explains vocal hoarseness,
without any need for bulbar neurological involvement. Moreover, the King’s longevity testifies to
the robustness of his constitution and the unlikelihood that he suffered from porphyria.
Further research is currently underway in order to address some remaining questions. Why were
Macalpine and Hunter able to bring about a widespread acceptance of their theory? What were their
motives, and those of their supporters and detractors? What light, if any, may be shed on George III’s
mental symptoms by present-day psychiatric classifications (see Peters and Beveridge, 2010)?
Some provisional suggestions may be cautiously advanced. One reason that the porphyria diagnosis became the orthodox interpretation was because Macalpine and Hunter have, until now, enjoyed
a reputation for thoroughness and integrity. The eminent medical historian Roy Porter (1993: 168)
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Peters and Wilkinson
described them as ‘sticklers for scholarship’. They certainly trawled through a large amount of
material. The sheer quantity of records is intimidating: the Willis Papers relating to the King’s illness comprise 52 manuscript volumes and there are a further 40 volumes in the Manners Sutton
Papers, not to mention various other diaries and correspondence, both published and unpublished.
The daunting prospect of re-tracing the steps of Macalpine and Hunter appears to have deterred any
detailed challenge to the evidential basis of the porphyria diagnosis. Perhaps the fact that they were
joint researchers gave added credence to their claims. It remains somewhat surprising that no one
thought to conduct even a spot check. The reports of pale urine in 1811–12 might readily have been
discovered and thus the selective use of evidence would have been exposed from the outset. The
porphyria experts merely confined themselves to disputing symptoms instead of inspecting the
records. Historians, who should have been more curious about the archives, naïvely accepted that
porphyria had somehow solved the mystery of the ‘madness’ of George III.
Macalpine and Hunter (1969: 277–86) were driven by deep convictions about the nature of mental
illness, and the collective moral responsibility of the psychiatric profession. In some respects this
was commendable: they loathed the coercive methods of the Willises, whose ‘system of government
of the King by intimidation, coercion and restraint’ was little short of brainwashing:
A great deal of the trouble and violence that ensued was in direct response to the control and coercion
to which he was subjected and against which he rebelled. Unfortunately, the lesson that harsh treatment
makes violent patients and that violence is often a reaction of fear was not learned until the nineteenth
century. The Willises took it as a sign of irrationality and accordingly increased the sternness – not to say
cruelty – of their measures and medicines, so creating a vicious circle of reciprocal violence between
patient and keeper. (Macalpine and Hunter, 1969: 78)
This was not simply an impartial historical judgement; it was an integral feature of their views on a
range of twentieth-century psychiatric practices. By the time Macalpine and Hunter came to research
the ‘madness’ of George III, they had developed a low opinion of Freudian psychoanalysis and also
a revulsion towards treating mental illness by electroconvulsive therapy, psychosurgery or neuroleptic drugs. They believed that mental illnesses were primarily caused by physical diseases, most of
which were still waiting to be discovered. In their opinion, modern psychiatry was in some respects
as foolish and barbaric as old-fashioned mad-doctoring. With future scientific progress Freudian
ideas would seem as daft as Georgian notions of flying gout; electric-shock treatment would appear
comparable to brutal coercion by strait-jacket; and neuroleptic chemical coshes would look almost
as bizarre as the purgatives of the Willis era. Just as Francis Willis’s claims about curing George III
(with a combination of willpower, strait-jacket and emetics) had proved to be unfounded, so too
would cherished ideas and fashionable treatments of modern psychiatry be found erroneous.
Macalpine and Hunter (1969: 363) were therefore psychologically predisposed to favour a diagnosis of porphyria because it supported their personal agenda: ‘the royal malady may perhaps – as
in 1788 – serve psychiatry by indicating the direction of its future progress’. A former colleague
recalled that Hunter ‘generally elaborated his views … that most psychiatric treatment was empirical
without established rational basis, that patients often tended to recover spontaneously if left alone
and sympathetically handled during their illness’.34 Roy Porter also recognized that their interpretation of George III’s illness was ‘overtly polemical’ and driven by their ‘faith in the organic basis
of most psychiatric disorder’ (Porter, 1993: 170). They sought to clear ‘the House of Hanover of
“an hereditary taint of madness”’ (Macalpine and Hunter, 1968: 16). While no modern psychiatrist
would seek to rehabilitate the explanations offered by Isaac Ray in the mid-nineteenth century,
nor those of Manfred Guttmacher from the mid-twentieth, it may well be worth reconsidering
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History of Psychiatry 21(1)
Shale Brownstein’s more recent interpretation: George III’s ‘unipolar mania of late onset is a syndrome in this instance complicated by the toxicity of quinine, antimony, and purgatives’
(Brownstein, 1997: 38; Guttmacher, 1941; Ray, 1855).
The suggestion that a diagnosis of porphyria would somehow counteract the supposed stigma of
mental illness seemed a little outmoded even in 1966. Dent asked Macalpine: ‘why you were so
anxious to remove the “taint” of mental disease from the Royal Family? Our psychiatrists are always
telling us that mental disease should be considered exactly like any other disease and under no
circumstances should be thought any sort of disgrace’. Macalpine replied that ‘we should have put
“taint” in quotes in order to avoid the impression … we considered mental illness a disgrace’.35 It
was duly amended for their reprinted pamphlet. Yet there was no underlying change in point of view.
Macalpine and Hunter remained convinced that they had struck a blow for humanity and justice
against errors, both contemporary and historical, in the theory and practice of psychiatry. This not
only clouded their judgement as amateur historians, but also gave rise to unwarranted fears in many
patients subsequently diagnosed with porphyria, who understandably dreaded the prospect of extreme
mental symptoms, as suffered by George III. Yet ‘schizophrenia, bipolar disorder, and depression
are no more common in the acute porphyrias than in a control population’; the only exception is
‘anxiety disorder’, though ‘the basis of the association of chronic anxiety with porphyria is unclear’.
It is, however, only too apparent that ‘false claims about the madness of George III being due to
porphyria are frequently distressing to our patients, who constantly need reassurance on these issues’
(Patience, Blackwood, McColl and Moore, 1994; Peters and Sarkany, 2005: 275).
George III was most unlikely to have suffered from acute porphyria, and his extreme mental
symptoms are uncharacteristic of people who do have this condition, especially nowadays when
potential triggers can be avoided and the severity of attacks reduced by appropriate treatment. The
‘madness’ of George III should therefore hold no fear for porphyria sufferers.
Acknowledgements
We thank Her Majesty the Queen for gracious permission to examine medical records in the Royal Archives, and
Miss Pamela Clark, Registrar, for her assistance and advice. We are grateful for help from staff at the British
Library, Cambridge University Library, Lambeth Palace Library, the Leicestershire, Leicester and Rutland
Record Office, the National Archives, the Royal College of Physicians of London, and the Wellcome Library.
Dr Geoffrey Dean provided insights and encouragement, and we also thank Dr Hector Maclean for suggestions
concerning the King’s cataracts. The financial support of the Stone Foundation is gratefully acknowledged.
Notes
1
2
3
4
5
6
7
8
9
10
11
Baker Papers, 5 Nov. 1788.
Baker Papers, 17 Oct. 1788.
Willis Papers, Add. 41691, ff.6–11.
Willis Papers, Add. 41691, f.104.
Willis Papers, Add. 41691, f.107.
Willis Papers, Add. 41691, f.147.
Willis Papers, Add. 41702, f.47.
Willis Papers, Add. 41703, ff.45–8.
Hunter Papers, Rimington to Macalpine, 13 Dec. 1966.
Manners Sutton Papers, 2107, ff.71–2; Willis Papers, Add. 41736, f.9.
Manners Sutton Papers, 2111, f.32; 2121, ff.181, 185; 2127, f.51; 2128, ff.101, 109; Willis Papers, Add.
41700, ff.30.
12 Manners Sutton Papers, 2110, f.154; Willis Papers, Add. 41696, ff.55–6, 82, 85, 90.
13 Hunter Papers, 4 Mar. 1965.
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Peters and Wilkinson
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
Willis Papers, Add. 54202, f.18.
Willis Papers, Add. 41731, ff.24–5.
Hunter Papers, 24 Jan. 1966.
Willis Papers, Add. 41691, f.11.
Hunter Papers, Mackworth-Young to Macalpine, 18 Feb., 9, 15 Mar. 1965.
Willis Papers, Add. 41700, f.27.
Halford Papers, Add. Geo 15/874, 14 Jan. 1812.
Hunter Papers, Macalpine to Dent, 24 Jan. 1966.
Willis Papers, Add. 41696, f.72.
Hunter Papers, Dent to Macalpine, 10 Jan. 1966.
Hunter Papers, Macalpine to Dent, 15 Jan.; Dent to Macalpine, 18 Jan. 1966.
Hunter Papers, Macalpine to Dent, 15 Jan. 1966.
Willis Papers, Add. 41692, f.75.
Willis Papers, Add. 41696, ff.25, 31, 35, 40–1, 71, 72.
Willis Papers, Add. 41696, ff.31, 37, 62, 69, 71.
Willis Papers, Add. 41696, f.40.
Baker Papers, MS 92/17 unfoliated.
Ibid.
Hunter Papers, 15 Jan. 1966.
Hunter Papers, Macalpine to Dent, 24 Jan. 1966.
Greenberg Papers, GC/218, f.2.
Hunter Papers, Dent to Macalpine 18 Jan.; Macalpine to Dent 24 Jan. 1966.
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