British Journal of Haematology - MedBlog

historical review
Thomas Addis of Edinburgh (1881–1949) and the coagulation
cascade: ‘for the greatest benefit done to practical medicine’
Derek Doyle
Retired Consultant in Palliative Medicine, Edinburgh, UK
Summary
Thomas Addis came of evangelical Scots stock; he was brought
up to care for others less fortunate than himself, to know what
he believed in and to defend it vigorously. Trained at the turn
of the 19th and 20th centuries in a Scotland still recovering
from wars and ecclesiastical schisms, yet producing record
numbers of missionaries and many social improvements, he
was a brilliant haematologist and innovative researcher.
Moving to Stanford his career continued to blossom as a
nephrologist whilst his concern for the less fortunate found
expression in his espousal of communist principles. Only in his
later years was he finally honoured for his many contributions
to medicine, science and social issues.
Keywords: Thomas Addis, coagulation cascade, Edinburgh,
Free Church of Scotland.
Thomas Addis (1881–1949) (Fig 1) was one of those rare men
for whom superlatives are appropriate. An Edinburgh pioneer
in the fields of haemophilia and coagulation and, after moving
to California, a famous nephrologist, he was a consummate
researcher, teacher and caring physician, a medical giant of the
20th century. This paper looks at his life and work in the
context of his remarkable family, the social and ecclesiastical
history of his times, his professional contemporaries and his
complex personality and character. He challenged and changed
current medical practice, sought to improve society and was,
towards the end of his eventful life, honoured and rewarded by
his peers, his pupils and his patients.
The coagulation cascade
The Coagulation Cascade seems a fitting description for the
complex sequence of events on which life itself can depend.
The rivalries and mutual criticisms of its researchers makes one
wonder if we should not speak rather of Coagulation Conflict!
Correspondence: Dr Derek Doyle, OBE, DSc, FRCSEd, FRCP (Lond.
and Edin.), FRCGP, 7 Kaimes Road, Edinburgh EH12 6JR, UK.
The clotting of the blood has always fascinated man
(Ratnoff, 1980). The Greek philosopher Plato speculated about
the process (Plato, 1892), believing that fibres in the blood
aided clotting as the blood cooled. Aristotle thought the fibres
were made of earth, were solid and that blood from which they
were removed did not clot (Aristotle, 1952). Malpighi (1686)
washed clotted blood and invited people ‘to enjoy the pretty
sight’ of the white fibres. Little more was learnt until the 1770s
when Hewson localised the source of the fibres to what he
termed the ‘coagulable lymph’, the liquid part of the blood we
now call plasma (Hewson, 1846). He was born in Hexham in
1739, became a surgeon partner of William Hunter and died at
age 34 as a result of an infection acquired in the dissecting
room.
Hewson showed that cooling blood slowed the clotting
process whilst other researchers showed that coagulation took
place most rapidly at body temperature. Hewson’s theory that
clotting took place when blood came into contact with air was
disproved by John Hunter, William’s brother, who demonstrated that it could happen in a vacuum (Hunter, 1817).
The name fibrin was first used by Chaptal (1797), who lived
and worked at the time of the French Revolution. He
postulated that the blood remained fluid because fibrin was
continually being removed, perhaps as a source of nutrition.
The next challenges were to define what effect temperature and
motion had on fibrin, how chemicals affected it and, more
importantly, where the fibrin came from.
Some suggested that fibrin was formed in rough areas in
blood vessel walls, a theory disproved by the German
pathologist Rudolph Virchow when he introduced a drop of
mercury into a blood vessel and produced coagulation
(Virchow, 1856). Others postulated that clotting was related
to motion and rest, a theory first disproved by Thackray (1819)
followed by many others who showed that clotting occurred
very slowly in a segment of vein between two ligatures. Wrote
Thackray, ‘the loss of motion is not in itself the cause of
coagulation’, a view supporting that of Hewsen: ‘rest of itself
does not in the least assist the coagulation of the blood’
(Hewson, 1846).
The first hints that fibrin might not be a constituent of
normal blood but be formed from, or as a result of, some other
substance came with the work of Babington (1830) and
E-mail: [email protected]
doi:10.1111/j.1365-2141.2005.05854.x
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Addis and coagulation
Fig 1. Thomas Addis (1881–1949). Reproduced with permission of
Lane Library, Stanford University, CA.
Richardson (1858) who suggested that it might be formed
from a precursor called fibrinogen, first isolated from plasma by
de Commercy (Denis, 1858) and defined by Hammersten
(1911), its name being popularised by Virchow (1856). The
next challenge – to define the structure of fibrinogen and
identify what converted it to fibrin – was taken up by
Buchanan, professor of physiology at the University of
Glasgow (Buchanan, 1879–80), and Schmidt (1892) of Estonia
who identified the converting agent, calling it fibrin ferment,
later to be renamed thrombin. Realising that thrombin could
not exist in normal circulating blood he postulated that it too
must have a precursor during clotting, a substance that came
to be called prothrombin. The search began to learn more
about prothrombin.
In 1905 (the year Addis qualified) Paul Morawitz, then an
assistant physician in the Medical Clinic, Strasburg, described
what he called the extrinsic pathway of coagulation. There
were, he said, two stages in the process, the first where
thromboplastin from damaged tissue changed prothrombin
(which he believed originated in platelets) to thrombin and the
second where fibrinogen converted to fibrin, calcium being
needed only for the first stage (Morawitz, 1905). Woolridge, a
contentious assistant physician at Guy’s in London, with little
time for anyone who disagreed with him, asserted that blood
contained A-fibrinogen and B-fibrinogen, each composed of
protein and lecithin (Woolridge, 1893; Morawitz, 1905).
Howell, working in Baltimore, believed that thrombin came
directly from damaged tissues and white cells and, particularly
after the discovery of heparin, his views and those of Morawitz
diverged (Howell, 1935), Howell being convinced that clotting
depended on the overcoming of inhibitors, but that and the
discovery of the many ‘factors’ we know today were to be long
after Thomas Addis came on the scene for a few years.
Addis will be remembered in Edinburgh primarily for his work
on clotting time and haemophilia, work begun when he joined
the University Department of Physiology in the University of
Edinburgh after his house jobs.
It will be recalled that in 1906, the source of thromboplastin
and prothrombin was still hotly debated, there was no reliable
method of estimating coagulation time (Addis, 1908), no one
knew whether or not calcium salts had any part to play in
coagulation, haemophilia was a mystery (Addis, 1910a), no
one knew whether or not blood transfusion would help
haemophiliacs, none of today’s ‘factors’ had been identified
and blood groups were unknown [they were not even
mentioned in Crile’s textbook on transfusion (Crile, 1909)].
Addis addressed almost all of them (Addis, 1910a).
His MD thesis (Addis, 1908) was on normal human blood,
important because until then no consistently reliable method
of estimating coagulation time had existed. He modified a
somewhat cumbersome but reliable apparatus, first devised by
McGowan (working in the RCPEdin. laboratory), later trying
it out on patients in Gloucester and Bristol (Figs 2 and 3;
Addis, 1910a). In his own words ‘When a current of oil streams
against the edge of a drop of blood suspended in oil, a
continuous smooth flow of the corpuscles is induced, although
the drop as a whole does not rotate. Under the microscope this
flow will be seen to cease quite suddenly after a certain time
has elapsed. This is due to the occurrence of coagulation in the
drop. This method is a modification of Brodie and Russells’
method. Instead of intermittent jets of air at an unknown and
variable temperature, a continuous stream of oil at a known
and constant temperature is used. The end point also is
entirely different.’
He was able to demonstrate the influence of temperature
and dismiss any diurnal aspect of clotting. He showed that oral
calcium and citrate had no effect on clotting, contrary to what
Sir Almoth E. Wright had said (Wright, 1893), and Addis said
so in no uncertain terms, somewhat tactlessly. ‘By means of a
more accurate method than Sir A E Wright’s I have shown that
he was mistaken in his statement that soluble calcium salts and
citric acid are capable of altering the coagulation time of the
blood of people in health….’ Addis had been qualified less
than 3 years!
Not afraid to challenge accepted theory, Addis also showed
that plasma contained complement, in contrast to Gengou’s
theory that it derived from white cells (Addis, 1912). Further
controversy, this time acrimonious, erupted when he
addressed the Pathology Section of the British Medical
Association (BMA) in July 1910. After giving notice of what
he planned to say he claimed that the fault in haemophilic
blood lay in an inherited qualitative defect in the prothrombin.
The Swiss haematologist, Hermann Sahli of the eponymous
haemoglobulinometer (1856–1933), was in the audience and
disputed Addis’s claim, saying that, as he himself had proved,
washed corpuscles of haemophilic blood accelerated clotting
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Fig 2. Addis’s apparatus for estimating clotting time. P, large glass
bottle containing paraffin oil suspended from an upright, so that it can
be raised or lowered; Sc, scale on upright; p, flexible metal tubing
leading the oil from the glass bottle to the spiral (sp) contained within
the water vessel (V); t, metal tube continuous with the spiral and
emerging from the water tank at the level of the microscope stage; ch,
Bogg’s coagulometer chamber with thermometer (th) inserted into it;
r, reservoir into which the overflow of oil from the stage is received; w,
waste tube by which oil from r is removed; R, Schafer’s thermostat (gas
regulator); g, rubber tube from gas tap; g¢, rubber tube from thermostat to gas burner under the water vessel. Reproduced from Addis
(1908).
proving that the defect lay in the corpuscles. Addis retorted
that Sahli’s washing technique had obviously been inadequate!
(Addis, 1910b, 1911).
One cannot discuss the measurement of clotting time or the
mechanism of clotting without turning to haemophilia. It had
fascinated and puzzled observers for many years (Immerman,
1878). In 1819, a surgeon by the name of Ward suggested it
was due to a defect in the clotting mechanism (Wardrop,
1837). At the end of that century, George Hayem agreed with
that but, because there was no satisfactory method of
measuring clotting time, did not pursue the matter (Hayem,
1856). Koch (1905) of bacteriology fame regarded it as a
manifestation of scurvy whilst others saw it as a feature of
rheumatoid arthritis, excessive thinness of blood vessel walls,
and, because it only affected males, a form of vicarious
menstruation. By 1878 efforts were being made to devise a
reliable means of measuring clotting time, essential if haemo270
Fig 3. Addis’s apparatus for estimating clotting time (close-up view).
In addition to the parts identified in Fig 2: This gives a closer view of
the stage apparatus. The lid of the Bogg’s coagulometer (ch¢) has been
taken off, and the glass cone with its truncated apex, from which the
drop of blood hangs, is shown. Reproduced from Addis (1908).
philia was to be studied. Wright (1893) explained the
condition by saying the clotting time was abnormally high in
the condition; also in 1893 Manteufel (a student of Schmidt’s)
reported that tissue extracts (Schmidt’s ‘zymoplastic substance’) shortened the clotting time of haemophilic blood
(Manteuffel, 1893).
In 1910, on the day of King Edward VII’s funeral, Addis gave
the first ever transfusion of fresh anticoagulated blood to a
haemophiliac patient.
On another occasion he gave a patient 15 cm3 of 96-h-old
human serum and showed acceleration of clotting but found
that normal or antidiphtheritic horse serum older than
5 weeks, given i.v., had no measurable effect.
Three months later, following Weil’s use of 20 cm3 i.v.
antidiphtheritic horse serum in a 40-year-old about to have
surgery for an abscess and his subsequent recommendation
that it be used routinely for haemophiliacs pre-operatively,
Addis gave a patient 8 cm3 i.v. of human serum, accelerating
the clotting time but not as successfully as after blood
transfusion (Boulton, 2003).
Addis was familiar with phosphate, possibly because it had
been used in Edinburgh since the 1880s to anticoagulate blood
prior to transfusion and possibly because he had discussed it
with Cotteril (President of the Royal College of Surgeons of
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Edinburgh 1907–10) who, in the year Addis graduated, had
given him a career testimonial (Rabe & Solomon, 1920; Risak,
1935; Imperato & Dettori, 1958; Addis, 1910b).
Without doubt his seminal paper was that published early in
1911 when he was settling in at Stanford (Addis, 1910b). The
conclusions are worth quoting in full:
1 Fibrinogen is present in as large amount in haemophilia as
in normal blood. Haemophilic fibrinogen is as readily
coagulated by thrombin as normal fibrinogen.
2 The amounts of thrombin developed in the complete
coagulation of the same quantities of haemophilic and
normal blood are equal. Haemophilic thrombin is as active
in coagulating fibrinogen as normal thrombin. The rate of
formation of haemophilic thrombin is slower than that of
normal thrombin. The degree of this retardation in
formation is proportional to the degree of delay in the
coagulation of the blood. The proximate cause of the delay
in coagulation is the slowness of the formation of haemophilic thrombin.
3 There is no appreciable difference between the antithrombin content of haemophilic and normal blood.
4 There is no substance in haemophilic blood, not present in
normal blood, which hinders the formation of thrombin.
5 There is no appreciable difference in the amount or activity
of calcium in haemophilic and normal blood.
6 Haemophilic thrombokinase, derived either from the
formed elements of the blood or from the tissue cells, is
as abundant and active as normal thrombokinase.
7 Prothrombin is present in as large amount in haemophilic
as in normal blood. There is a defect in haemophilic
prothrombin which reveals itself in the longer time it
requires for the change into thrombin, in the presence of
thrombokinase and calcium. This qualitative defect in the
prothrombin is the cause of the delay in coagulation of
haemophilic blood.
Boulton (F. Boulton, personal communication) is in no
doubt that Addis anticipated the standard clotting tests –
prothrombin time and partial thromboplastin time – and also
the tests for clotting inhibitors in plasma by double dilutions.
His study of Addis’s papers leads him to believe that Addis was
on the verge of assaying ‘antihaemophiliac’ activity in plasma.
Howell was able to show that Addis had been wrong in
believing that there is a defect in haemophilic prothrombin
(Howell, 1935; Bordet, 1921), 24 years later. It fell to those
who followed Addis and continued in haemophilia research,
well into the 20th century, to define the antihaemophilic factor
and its defects. By then Addis was making his mark as a
nephrologist (Quick, 1943; Quick et al, 1935; Risak, 1935;
Seegars, 1962).
Addis the nephrologist
What made Addis accept the 1910 invitation of Dr Ray
Lyman Wilbur, Dean of the newly established Medical School
in Stanford, to leave Edinburgh and work in California, not
in haematology but in nephrology? We know Lyman was
encouraged to invite him by Sir Clifford Allbutt, Regius
Professor of Physics at Cambridge, who had been at the
conference where Addis and Sahli had crossed swords. Did
Addis feel undervalued, his work not recognised, particularly
by Gulland and Goodall, both to become Professors of
Medicine and Presidents of the RCPEdin? In fact, Gulland
and Goodall (1911) said haemophilia was due to ‘an
inherited abnormality in the structure of the prothrombin
of the blood’ but persisted for the next 11 years in
recommending high doses of calcium and injections of
serum. Hutchison, writing from the London Hospital in
1912, quoted Addis but still recommended blood transfusion
(Hutchison, 1912).
Was Addis troubled by the war clouds gathering over
Europe or the crescendo of discontent in Russia? Were his
developing left wing views, so prominent later, making him
uncomfortable with Scotland’s poverty and social malaise? Did
he feel liberated from dogmatism and doctrinal ties now that
his grandfather, grandmother and mother had died? Had he
already met the American lady he was to marry in 1913?
Perhaps the reason for his move was simply his wanting to
exchange the old albeit historic building where he did his
research for a new and exciting one of almost unlimited
possibilities in a climate considerably more attractive that that
in which he had grown up, a chance to work in a new medical
school, well funded, dedicated to research and under the
charismatic leadership of Wilbur, with the possibility of being
offered a professorship? Whatever the reason, he went to
Stanford in spring 1911, his departure marked in the archives
of the Physicians laboratory by a brief hand written note – Tom
Addis left for California.
Surprisingly, in view of the importance of his research work
and the impact his findings made, Addis published only 10
papers when based in Edinburgh, but they were all within
6 years of qualifying, a feat seldom achieved or achievable
today. In the 30 plus years he worked in California (Fig 4), he
published no less than 131 papers (Anonymous, 1954) and one
outstanding book.
Most doctors will know of him because of the ‘Addis count’,
the ‘Addis formula’ or the ‘Addis–Shevky concentration test’.
His work on nephritis (Bright’s Disease) was as innovative and
important as his work on haemophilia. He pioneered the
‘protein-poor-but-not-protein-free’ diet, no doubt in consultation with his dietician wife. His book Glomerular Nephritis:
Diagnosis and Treatment (Addis, 1948) gives a more complete
picture of the man, his research and his philosophy of life than
any paper such as this one could ever do.
After being naturalised he served as a Captain in the US
Army Medical Corps (1917–19) and as consultant to the
Surgeon General (1942–45). He and his wife had two
daughters, the elder one marrying David Karnowski, an
oncologist, and the younger studying with the Bolshoi Ballet
(F. Boulton, personal communication).
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Fig 4. Addis (complete with pipe) in his Stanford Laboratory.
Reproduced with permission of Lane Library, Stanford University,
California.
How can we describe him? Totally dedicated to his patients
and the highest standards of medical care and research, a selfassured and a formidable exponent and defender of his
theories who may sometimes have appeared arrogant but was
usually justified in his confidence; a man whose life reflected
the myriad influences of his childhood and background but
whose thinking and vision were ahead of his time (Peitzman,
1990).
What were these influences that made such a man?
The family of Thomas Addis
So profound were the influences of Addis’s family on him, his
life and work that we must go back many years before he was
born and see them in the context of a rapidly and dramatically
changing society, in that respect not unlike the days in which
we live today.
Addis’s paternal great grandfather, born of Methodist
parents in London, subsequently worked in Edinburgh as a
plumber, through the time of the French Revolution and
Napoleonic Wars. He may well have seen French prisoners-ofwar (PoW) being taken to Edinburgh Castle or the Bass Rock
in the Firth of Forth, both at that time prisons for PoW as well
as religious dissenters.
In 1814, his son Thomas, was born, the boy who was to
become a leading divine in the Free Church of Scotland as well
as grandfather of the central figure in this paper.
Young Thomas went to St Andrews University and Divinity
Hall, graduating and being ordained as a minister in 1841, a
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momentous time in the ecclesiastic history of Scotland. Many
felt that the national church – the Church of Scotland – was
too much influenced by the government and, in theory, by the
sovereign, its nominal head. In 1843, one-third of the ministers
of the Church of Scotland walked out of its General Assembly
and formed a new church – The Free Church of Scotland. The
young Rev. Thomas Addis was one of them, probably
influenced by Rev. Professor Thomas Chalmers, one of his
parishioners and the driving force behind the schism.
After this dramatic split in the church he returned to his
parishioners, a large number of whom elected to remain with
him as their young minister though now without a church
building, calling themselves Morningside Free Church of
Scotland. For a short time, they used Dr Chalmer’s house in
which to worship, filling rooms on the ground and first floors
while the minister preached standing on the stairs, in the
summer occasionally using a marquee in a nearby field. During
the 56 years of his ministry, Addis built no less than three
churches: one in the 1850s, one in the 1870s (the current
Baptist Church) and in 1892, when preparing to retire, a large
church, which, by 1965, had been converted into a theatre!
What was once The Free Church Schoolhouse was soon too
small for all the children and became the Brethren Meeting
Place, when the Free Church children moved to larger premises
(Smith, 1982). Awarded a Doctorate in Divinity towards the
end of his long ministry, he died in 1899.
In 1842, he had married Robina Stewart Thorburn, the
daughter of a Leith merchant and the half-niece of the Church
of Scotland minister there when Thomas was his assistant.
They had 12 children in the first 19 years of their marriage, ten
surviving into adulthood. However, the effects of his dominating personality were soon evident.
William, the first-born son became a Roman Catholic, then
an Unitarian and finally an Anglican priest. Robina, named
after her mother, married a minister of the Church of Scotland.
Charles (1861–1945) the youngest of the 12 children left
Edinburgh Academy at the age of 15, no longer able to endure
his father’s overbearing authoritarianism (often demonstrated
by his use of the cane). He worked in commerce before moving
into banking, learning Mandarin Chinese whilst in Shanghai,
and eventually becoming a Chairman of the Hong Kong
Shanghai Banking Corporation and a valuable trade envoy
between Britain and China at a difficult time in their relations.
For this he was made a knight commander of St Michael and St
George (KCMG) and a Fellow in Chinese studies at Oxford. He
married Eba (Elizabeth) McIsaac in 1894 when he was 33. The
first of their 15 children was another Thomas, born in 1895.
Yet another son of the divine was Thomas Chalmers Addis
Jr, his middle name honouring the Rev. Dr Thomas Chalmers.
Thomas Addis Jr was to be the father of our ‘hero’, Thomas.
He too never went on to university but, at the time of his son
Tom’s birth, was ‘a clerk 1st class’ in the Solicitor’s Department of the Inland Revenue eventually earning £1000 p.a. He
had a ‘Damascus Road conversion’ during Evangelistic Missions to Edinburgh in the 1870s. Like his son, he married an
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Fig 5. George Watson’s College, Edinburgh, shortly before Addis studied there. Reproduced with permission of George Watson’s College.
American lady, Cornelia Beers Campbell, daughter of a New
Orleans cotton merchant who, after the Civil War moved his
family to Hobroken in New Jersey. She died in 1901 aged 56 of
carcinoma of stomach.
Though his father, uncle and cousins attended The Edinburgh Academy, Tom Addis the 3rd, the focus of our
attention, went to George Watson’s College (Fig 5), at that
time adjacent to the Royal Infirmary of Edinburgh, beside the
Medical School. Watson’s, originally called a ‘hospital school’
had been founded in 1724 by the first accountant of the newly
created Bank of Scotland.
When his grandfather died in 1899, his grandmother in 1900
and his mother in 1901, Tom was preparing to study medicine.
In 1905 Thomas graduated as a Bachelor of Medicine (MB),
Bachelor of Surgery (ChB), to be followed in 1908 with his
Edinburgh Doctor of Medicine (MD) (with merit and a £50
prize) and becoming a Member of the Royal College of
Physicians (MRCP) Edinburgh. Between 1908 and 1910 he was
a Carnegie Fellow enabling him to visit and work in Berlin and
with Morawitz in Heidelberg (who allowed him to transfuse
his patients) as well as taking his new equipment for trials on
patients back to Gloucester where he had worked after
qualifying and to Bristol.
The life and times of Thomas Addis
What influenced the life and work of Thomas Addis?
The most important must have been the disciplined, deeply
religious lives of his grandparents and parents. Like all
members of this evangelical church they would have regarded
the Bible as the literal word of God and been skilled and
eloquent in the defence of all they believed and lived for, as
Thomas was to be with those who challenged his research. He
would have attended Sunday school and at least two church
services every Sunday and family prayers every night of the
week. The principles of total abstinence from alcohol, celibacy
before marriage, restrained language and respectful behaviour
at all times as well as practical concern for the less privileged
would have been inculcated in him from an early age.
The Presbyterian work ethic and social consciousness
dominated Scots life and society. Holidays were almost
unknown. Boys were taught that personal discipline, academic
diligence and the service of God and their fellow men were
Christian virtues. It is, therefore, not surprising that as a
student Tom worked in the slums and squalid lodging houses
of Edinburgh’s Grassmarket and in the Edinburgh Medical
Missionary Society’s (EMMS) Dispensary, a charity largely
staffed by volunteer medical students providing care to
thousands and, at the same time, preparing generations of
future medical missionaries.
Addis grew up when Scotland was sending abroad more
missionaries per capita than any other country, a result of
the evangelicalism sweeping the country, culminating in the
influential Edinburgh Missionary Conference 1910, yet it was
a time when the home church was torn apart by schisms and
fundamentalism, the country was either recovering from or
preparing for a war and British politics were in the
doldrums.
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Fig 6. Edinburgh’s Bedlam behind all that is left of the old City Wall, a drawing by an unknown artist in 1778. From Smith (1982).
The Addis family, and all who lived in the 19th century must
have been affected in one way or another by its six wars, the
Highland Clearances and the end of the slave trade in Britain
and its colonies, both, radically changing the economics of
Scotland and the quality of life of many of its people. It is little
wonder that so many emigrated.
Addis must have been aware that even the laboratory where
he worked was steeped in history. In 1887 the Royal College of
Physicians of Edinburgh decided to have its own laboratory for
the use of Fellows and Members for their clinical work and
research. No fees were to be charged. In 1888 they decided
against using the Poorhouse and ‘Edinburgh Bedlam’ (Fig 6),
built for ‘pauper lunatics’ (Smith, 1982), where the poet
Ferguson had died in squalor in 1774 aged 24, considering it
too large for their needs, preferring a small property nearer the
old Royal Infirmary. The college set aside £1000 p.a. for
running costs and paid the Superintendent £650 p.a. By 1895 it
realised it needed a larger property and bought the old Bedlam
for £7350 (Ritchie, 1953). In 1903 it came under the wing of
the Carnegie Trust. Addis produced two papers whilst working
there and Gulland and Goodall their paper on Leukaemia and
Chloroma (Gulland & Goodall, 1911), as was Goodall’s paper
on Haemophilia.
Addis would have known that some of his laboratory
buildings had been built on what had been the part of
Greyfriars’ Churchyard, where 1200 protesting Covenanters
had once been incarcerated for their objection to the reintroduction of episcopacy, most to die of exposure, disease or
hanging. Scotland had long been a place where men spoke out
for what they believed to be right.
A man of his time, Addis was clearly serious, disciplined,
quietly religious and wedded to his work. Nevertheless, Scot
that he was, in America he is said to have never lost his accent,
loved his pipe and his golf and, often found that he had
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insufficient money to pay his tram fare or round of drinks.
What would his grandfather and his parents have said about
that or his love of ballroom dancing?
Finale
He was showered with honours in the United States, including
being the first Visiting Fellow of the Long Island College of
Medicine, Brooklyn, membership of the Association of
American Physicians, the National Academy of Sciences, the
American Society for Clinical Investigation, a diplomat of the
American Board of Internal Medicine and from 1930, a Fellow
of the American College of Physicians. In the following year he
delivered the fourth course of lectures under the William
Sydney Thayer and Susan Read Thayer Lectureship in Clinical
Medicine in the School of Hygiene and Public Health, John
Hopkins University School of Medicine, Baltimore (Fig 7).
Interestingly his few obituaries are, for the most part brief,
factually accurate but terse (Bloomfield, 1950; Anonymous,
1954). We might wish to have heard more of his attitude to
money, his reluctance to charge fees or accept as a patient
anyone who discussed money with him or to have learnt more
of his care and concern for disadvantaged Chinese patients (so
like his uncle Sir Charles and cousin Sir John Mansfield Addis)
and others with whom he remained in touch for many years.
One such was Linus Pauling, the double Nobel Laureate, who
admired him and nominated him as the first doctor to be
elected to the National Academy of Sciences.
Do his obituaries reflect the times in which they were
written – 1949 and 1950? Addis and his wife never joined the
communist party but undoubtedly had strong left wing views
and Addis both lectured and wrote on the benefits of
communism (F. Boulton, personal communication). Several
reports attest to how some policemen who had reason to be
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grateful to him for his care forewarned him when a raid was to
be made on a Communist Party meeting. McCarthyism was
already casting its ugly shadow across America.
How has he been remembered in Edinburgh? Certainly not
by plaques or busts. The laboratories where he did his original
research have all but disappeared and in 2003 a new Royal
Infirmary was opened, the fourth to bear its name.
In 1942 the Royal College of Physicians of Edinburgh
honoured Addis, a medical giant of the 20th century, with
one of its most prestigious awards – The Cullen Prize – ‘for
the greatest benefit done to Practical Medicine’ – commemorating a giant of the 18th century, William Cullen (Fig 8).
Addis is the only Member of the College (as distinct from a
Fellow) and the only non-President ever to have been so
honoured. A few years later Addis was elected a Fellow of the
College.
Acknowledgements
Fig 7. Addis a few years before his retirement from Stanford. Reproduced with permission of Lane Library Stanford University, California.
This paper could not have been written without the
generous help of Dr Frank Boulton, the authority on Tom
Addis. To him and the relatives of Dr Addis I extend my
thanks. I also thank the librarians of the Royal College of
Physicians of Edinburgh, The National Library of Scotland
and Edinburgh City Libraries, the archivists of George
Watson’s College, The College of the Free Church of
Scotland, The Edinburgh Academy, the Church of Scotland
and the EMMS.
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