The Project Gutenberg EBook of Some Medical Aspects of Old Age, by 
Humphry Davy Rolleston

This eBook is for the use of anyone anywhere in the United States and most
other parts of the world at no cost and with almost no restrictions
whatsoever.  You may copy it, give it away or re-use it under the terms of
the Project Gutenberg License included with this eBook or online at
www.gutenberg.org.  If you are not located in the United States, you'll have
to check the laws of the country where you are located before using this ebook.



Title: Some Medical Aspects of Old Age

Author: Humphry Davy Rolleston

Release Date: May 26, 2018 [EBook #57215]

Language: English

Character set encoding: UTF-8

*** START OF THIS PROJECT GUTENBERG EBOOK SOME MEDICAL ASPECTS OF OLD AGE ***




Produced by Turgut Dincer, Charlie Howard, and the Online
Distributed Proofreading Team at http://www.pgdp.net (This
file was produced from images generously made available
by The Internet Archive)









Transcriber’s Note: Italics are indicated by _underscores_; superscripts
are indicated by ^carets. Other Notes are at the end of this eBook.




SOME MEDICAL ASPECTS

OF OLD AGE




  MACMILLAN AND CO., LIMITED
  LONDON · BOMBAY · CALCUTTA · MADRAS
  MELBOURNE

  THE MACMILLAN COMPANY
  NEW YORK · BOSTON · CHICAGO
  DALLAS · SAN FRANCISCO

  THE MACMILLAN CO. OF CANADA, LTD.
  TORONTO




  SOME MEDICAL ASPECTS
  OF OLD AGE

  BEING THE LINACRE LECTURE, 1922,
  ST. JOHN’S COLLEGE, CAMBRIDGE

  BY

  SIR HUMPHRY ROLLESTON, K.C.B.
  M.D., D.C.L., LL.D.
  PRESIDENT OF THE ROYAL COLLEGE OF PHYSICIANS OF LONDON
  EMERITUS PHYSICIAN, ST. GEORGE’S HOSPITAL
  SOMETIME FELLOW OF ST. JOHN’S COLLEGE, CAMBRIDGE

  MACMILLAN AND CO., LIMITED
  ST. MARTIN’S STREET, LONDON
  1922




  COPYRIGHT

  PRINTED IN GREAT BRITAIN.




PREFACE


The material in this small volume was collected in connexion with
the Linacre Lecture at St. John’s College, Cambridge, and has been
somewhat expanded since its delivery on 6th May 1922. The introduction
is chiefly of local interest in connexion with the history of the
Linacre Lecture. Without attempting a complete account of old age and
its diseases I have passed in review some ancient and modern medical
aspects of this subject, but, except for incidental references, medical
treatment has not been considered.

For ready help, especially as regards the illustrations, my cordial
thanks are due to C. J. S. Thompson, Esq., M.B.E., of the Wellcome
Historical Museum, and for the index I am much indebted to H. M.
Barlow, Esq., Assistant Librarian of the Royal College of Physicians of
London.

            H. R.




CONTENTS


                                                                    PAGE
     I. INTRODUCTION                                                   1

    II. DURATION OF LIFE                                               9

   III. ONSET OF OLD AGE                                              26

    IV. FACTORS INFLUENCING LONGEVITY                                 32

     V. CAUSES OF SENESCENCE, WITH A NOTE ON SENESCENCE AND
            CARCINOMA                                                 62

    VI. NORMAL STRUCTURAL CHANGES IN OLD AGE                          90

   VII. THE PHYSIOLOGY OF OLD AGE                                    115

  VIII. THE DESCRIPTION OF OLD AGE IN THE TWELFTH CHAPTER OF
            ECCLESIASTES                                             129

    IX. DISTINCTION BETWEEN HEALTHY AND MORBID OLD AGE               135

     X. DISEASES IN AND OF OLD AGE                                   139

        INDEX                                                        157




ILLUSTRATIONS


  FIG.                                                         FACE PAGE
  1. William Heberden, M.D., F.R.S.                                    2

  2. Sir Thomas Watson, Bt., M.D., F.R.S.                              4

  3. Professor John Haviland, M.D., F.R.C.P.                           6

  4. Henry Jenkins, reputed to have lived 169 years                   20

  5. Thomas Parr, reputed to have lived 152 years                     22

  6. Katherine, Countess of Desmond, reputed to have lived 140
         years                                                        24

  7. Petratsch Zortan, in his reputed 185th year                      26

  8. Hungarian husband and wife, reputed to be 172 and 164 years old
         respectively                                                 36

  9. Sir Henry Pitman, M.D., F.R.C.P., a medical centenarian          52




I

INTRODUCTION


The Linacre Foundation dating from 1524 is the oldest medical
Lectureship in the University, for it was sixteen years later that the
Regius Professorship of Physic was established by Henry VIII. Formerly
this College Lectureship was held more or less indefinitely by Fellows
of the College, with two eminent exceptions, namely, Sir George Paget
and Dr. J. B. Bradbury; but in 1908 the Lectureship was made an annual
and open appointment, and until this year no member of the College has
held this office: I am therefore most deeply conscious of the high
honour that has been conferred upon me.

Though the statute that the Lecturer should explain Galen’s treatises
_De Sanitate Tuenda_ and _De Methodo Medendi_ as translated by Linacre,
or _De Elementis et Simplicibus_, has long lapsed, his first words
should be directed to the pious memory of the founder; but as in 1908
the late Sir William Osler[1] devoted the first of the new series
of Linacre Lectures to a sympathetic consideration of his brother
scholar-physician, it would be worse than unwise to attempt more than
the briefest reference.

[Illustration: FIG. 1.--William Heberden, M.D., F.R.S., in his 86th
year. Linacre Lecturer, 1734–38.

From an engraving by James Ward of a portrait painted by Sir William
Beechey, R.A.]

Thomas Linacre (1460–1524) was born at Canterbury of parents who have
eluded research, and his connexion with the old family that took
its name (Linacre = flax farmer) from a hamlet near Chesterfield
in Derbyshire was regarded by J. F. Payne as merely an assumption.
Believing that those devoted to learning should be free from the
obligations of the married state Linacre remained single, so that he
had no direct descendants; his will[2] contains references to his
brother, who had the same Christian name--Thomas--as himself, two
sisters Alice and Joan, two nieces Agnes and Margaret, and two cousins
Robert Wright of Chester and Richard Wright; but according to Payne[3]
the family history cannot be traced any further. I recently had a
faint hope that I had got on the track of collateral descendants,
but on enquiry it was courteously made clear that though the family
in question was descended from a Mrs. Linnecar, her connexion with T.
Linacre rested on tradition only and that no documentary evidence or
genealogical tree existed to justify any claim. It may be remembered
that Linacre was one of the earliest English students (_circa_ 1488),
more than a century before William Harvey, to study medicine and take
the doctorate at the ancient University of Padua, which celebrated its
seven-hundredth anniversary in May 1922. It is, next, natural to look
back to the first holder of this Lectureship, and to wonder what manner
of man he was and what he taught. To the Master of St. John’s College I
am indebted for the few details that are known of Christopher Jackson
(B.A. 1524–25, M.A. 1527), who was buried in the old Chapel on July
2, 1528, his death according to a brass erected to his memory in the
new antechapel being “e sudore britanico.”[4] Some of the Lecturers
were without a medical qualification, and of these Matthew Prior
(1664–1721), the poet and diplomatist, who was a “Medical Fellow”
for life and Linacre Lecturer from July 5, 1706, to July 7, 1710, was
the most famous. That he ever lectured is more than doubtful, but he
appears to have thought out reasons for not doing so: at any rate his
_Alma or the Progress of the Mind_ (written about 1715) contains in its
third canto the lines:

                how could I explain
  The various labyrinths of the brain!
  Surprise my readers whilst I tell them
  Of cerebrum and cerebellum!
  How could I play the commentator
  On dura and on pia mater!

Three of the Linacre Lecturers under the old dispensation stand out for
special remembrance on account of their influence on Medicine:

William Heberden the Elder (1710–1801), the author of the _Commentarii
de Morborum Historia et Curatione_, published posthumously (1802), held
office from 1734–38, and was described by Sir William Osler as the
“English Celsus.”[5]

[Illustration:

  FIG. 2.--Sir Thomas Watson, Bt., M.D., F.R.S. President of the
      Royal College of Physicians of London, 1862–67. Linacre
      Lecturer, 1822–26.

  From an engraving by George Cousins, R.A., of a portrait painted
      in 1867 by George Richmond. R.A., now in the Royal College of
      Physicians of London.
]

Sir Thomas Watson (1792–1882), whose _Lectures on Physic_ held its
place longer than any medical text-book of modern times and set an
example of style that still commands our admiration and imitation, was
Lecturer 1822–26, and in the first year of office was also a Proctor.
Subsequently (1862–67), he was President of the Royal College of
Physicians of London, the most magnificent of Linacre’s Foundations;
this appropriate association was shared by William Baronsdale (P.R.C.P.
1589–1600), by Thomas Gisborne, who was President on three separate
occasions (1791, 1794, 1796–1804) alternately with his senior Sir
George Baker, and by Sir Norman Moore of St. Catherine’s College
(P.R.C.P. 1918–22), who gave the Linacre Lecture under the new
regulations in 1913 on _The Physician in English History_.[6]

John Haviland (1785–1851), the only one of these three who remained
in Cambridge, and the only one who did not become a nonagenarian,
was Linacre Lecturer for two periods (1817–22, 1826–47), Sir Thomas
Watson intervening. As Professor of Anatomy (not human anatomy) from
1814–17 he delivered the first regular course of lectures on human
anatomy; and when he succeeded Sir Isaac Pennington (also Linacre
Lecturer, 1767–1816) as Regius Professor of Physic (1817–51) he was
the first to give courses in pathology and the practice of medicine,
thus rousing the post from the sleep of a sinecure, and to make the
medical examinations a real and rigid test instead of little more than
a farcical form consisting of a few _viva voce_ questions. Further,
had it not been for his influence and insistence the medical faculty
might have been abolished, and it was said[7] after his death that the
subsequent success of the medical school was due to his exertions. He
wrote little and perhaps for that reason his name is seldom mentioned
now, but if the work that has since been done by this medical school be
his monument he could hardly have a greater.

[Illustration:

  FIG. 3.--John Haviland, M.D., F.R.C.P. Professor of Anatomy
      1814–17, Regius Professor of Physic in the University of
      Cambridge, 1817–51; Linacre Lecturer, 1817–22 and 1826–47.

From a drawing done in 1851 by Wageman. For this I am indebted to H. A.
Haviland, M.B.]

The somewhat neglected subject of Old Age has a very pertinent
connexion with the most essential aim of medicine as a whole, namely,
the prevention of disease. For when the ideal of the prophylaxis
of infection and of other causes of morbid action is attained,
a healthy old age and physiological death without attendant
disabilities and horrors should be the common lot of man instead of
being somewhat exceptional in the case of the first and extremely
rare as regards the final act. The conditions favouring longevity and
_mens sana in corpore sano_ are those necessary to make the future of
the human race a happy and beneficent prospect instead of a problem
inspiring doubt if not pessimism; or in Descartes’ words, “we might be
free of an infinity of maladies both of body and mind, and even of the
infirmities of old age, if we had sufficient knowledges of their causes
and remedies.” But in addition to this broad ground of interest there
are reasons why a discussion of this subject has a special claim for
consideration in Cambridge. The objects of a University include the
preparation of its alumni for life in its fullest and best sense, and
from this point of view the permanent ornaments of the community ever
set an unobtrusive example of the way to deserve and enjoy a healthy,
happy, and useful old age, namely, activity of mind and body and
moderation in all things; such a life of 75 years (that of Professor
G. D. Liveing) in the University must be in your recollection as
described by the Public Orator as _tam honesta, tam utilis_. Further,
as in private duty bound, I cannot forget that Sir George Humphry,
to whom this great medical school owes so much, greatly interested
himself in the subject of old age and published the results of an
elaborate collective investigation. Lastly, it is desirable that the
problems of old age should be attacked by young and active minds in the
laboratories of the University and not left as a semi-personal field
of enquiry and observation to those whose “way of life is fall’n into
the sere, the yellow leaf,” and who hear old age’s stealthy footsteps
catching them up in the race; for in the past most of the writers on
geriatrics have written with at least some personal qualification
and interest, such as Cornaro, Sir John Sinclair, Sir Anthony
Carlisle, Charcot, Sir George Humphry, Sir Hermann Weber, R. Saundby,
Metchnikoff, Stanley Hall. As an exception, however, we may point to
Dr. John Smith,[8] who, in his thirty-fifth year, was the author of
_King Solomon’s Portraicture of Old Age_, which paraphrases in 266
pages the “six former” verses of the 12th Chapter of Ecclesiastes
containing 205 words.




II

DURATION OF LIFE


In the protozoa and some other lowly forms of animal life
multiplication by binary fission occurs indefinitely, so that one
organism is succeeded by two, and as there is no vestige of a corpse,
as Weissmann expressed it, the organism is immortal. Maupas’s[9]
investigations indicated that without occasional conjugation of two
individual protozoa and the resulting rejuvenation the organisms
undergo senile degeneration and die; but Woodruff[10] has shown
by observations extending over 13½ years that _Paramoecium_, and
so presumably infusoria in general, can multiply indefinitely in
favourable conditions without conjugation, though periodically an
internal reorganization (endomixis[11]) of the individual takes place.
It seems not improbable that endomixis provides the rejuvenation
otherwise resulting from conjugation. C. M. Child[12] brings forward
reasons for modification of the explanation that death is escaped
simply by division; he shows that in certain circumstances senescence
occurs in the protozoa as it does in the higher animals, but that death
is avoided by the rejuvenescence in each process of reproduction,
reconstitution occurring and new organs being formed in the place of
the old. In other words, all organisms from the protozoa to man undergo
senescence and die unless rejuvenescence intervenes; this compensation
holds good in the lower forms and death may never occur; but in the
higher forms rejuvenescence is so much restricted by the evolutionary
increase in the physiological stability of the protoplasmic substratum
and the resulting higher degree of individuation that senescence is
much more continuous and death is inevitable. It is the penalty for
high individuation, and is the result of conditions and processes that
have produced the complicated mechanism of the higher animals and man.
While holding out the faint hope that the advance of knowledge and of
experimental technique may make it possible at some future time to
bring about a greater rejuvenescence and retardation of senescence in
man and the higher animals, Child points out that the present condition
of their protoplasmic substratum is the result of millions of years of
evolutionary equilibration, and that this task must therefore be one of
extreme difficulty.

Modern biologists such as Driesch, E. Schultz, Child, Steinach, and
Julian S. Huxley, to the last of whom I am personally much in debt,
have indeed shown that experimentally the life cycle and growth,
which are so closely correlated, may be modified dramatically by
various methods. By starvation planarian flat worms become smaller
and their life cycle is reversed by the process variously called
dedifferentiation, reduction, or involution, whereby their structure
becomes simpler; similar retrogressive changes have been produced in
the social ascidians, _Clavellina and Perophora_ (J. S. Huxley[13]),
this process of dedifferentiation or reversible differentiation being
the primitive reaction of organisms to unfavourable circumstances. By
alternate feeding and starvation Child has kept planarian flat worms
at the same size while controls passed through nineteen generations,
thus showing that the life of cells is not a matter of time but of
metabolism. In the higher animals the conditions are of course more
complex on account of the self-regulating mechanisms, especially the
ductless glands. But by disturbing the endocrine balance experimental
biology has produced some remarkable results: by feeding white mice
with tethelin (a phospholipin obtained from the anterior lobe of the
pituitary) Robertson and Ray[14] found that epithelial proliferation
was accelerated, though increase in weight of the animals was retarded,
and that the duration of life was prolonged. Drummond and Cannan,[15]
however, failed to confirm these results, and feeding with the anterior
lobe of the pituitary has given rise to very contradictory reports;
acceleration (Clark, Robertson, Goetsch), retardation (Pearl, Wulzen),
and no effect (Gudernatsch, Lewis and Miller, Hoskins, Sisson and
Broyles[16]) have been described. Steinach’s rejuvenation of senile
rats by ligature of the vas deferens, which is followed by increase
in the interstitial cells of the testis and definite prolongation of
life, will be referred to later (_vide_ p. 76). The retardation of
growth due to a diet deficient in vitamins, first proved by Gowland
Hopkins[17] in 1912, may be maintained for long periods, but when the
diet is appropriately altered growth is resumed and proceeds to the
full standard (Osborne and Mendel[18]); it remains to be proved that
the total duration of life can thus be prolonged. Though every living
species of animal may in normal circumstances have its allotted span
of life, this is so subject to accidents and modifications by external
influences that the average duration of existence, especially in the
long-lived species, does not represent the natural term of years. Thus
the expectation of life at birth in England and Wales is 51·5 years
for males and 55·35 years for females, as contrasted with the ideal
physiological duration of life for 100 years. Violent death in one
form or another--traumatic or infective--is so much the rule that the
occurrence of natural death in the animal kingdom has been questioned,
just as de Candolle denied the natural death of trees and ascribed it
to injury or disease. Metchnikoff,[19] who paid special attention to
this question, described natural death in the Ephemerids, day-flies,
the imagines of which are incapable of feeding and after an hour or
two of “aerial life devoted to love” die, their ova falling into the
water; Sir Ray Lankester accepts the view that they are “wound up” for
a few hours only of life, but according to Child death is probably
due to starvation. In man natural death from old age--a physiological
ending--is very rare, much less frequent indeed than death certificates
and ordinary parlance would suggest; for in such cases there is very
commonly some latent disease, such as pneumonia, which just turns
the scale in the trembling balance. Montaigne warns us “what an idle
conceit it is to expect to die of a decay of strength, which is the
last of the effects of the extremest age, and to propose to ourselves
no shorter lease of life than that, considering that it is a kind of
death of all others the most rare and hardly ever seen.” While it must
be admitted that this still holds good, it is a stimulus to our efforts
to render it no longer true.

The length of days ascribed to Methuselah (969), Adam (930 or, if the
“conceit urged by learned men,” as Sir Thomas Browne[20] says, that
he was 50 or 60 years old when called into being be accepted, 980
years), Seth (912), has aroused attempts at explanation on the basis
of a difference in chronology. The suggestion that the “years” were
lunar and not solar, in other words containing 30 instead of 365 days,
was controverted at length by Eugenius Philalethes[21] (not Thomas,
twin of Henry Vaughan “the Silurist”) as too radical, for on this
interpretation some of the patriarchs would have become fathers of
children before they were ten years old. Long ago, Hensler, following
Justin, put forward the view that the year consisted of but three
months up to the time of Abraham, when it was extended to eight months
until the era of Joseph, after which it contained our full complement
of twelve months. This explanation was supported by Hufeland[22] on the
ground that some eastern nations still reckoned three months to the
year. Adopting this explanation Methuselah’s age would be cut down to
243 years.

The Psalmist’s threescore years and ten and its sorrowful extension to
fourscore are so often exceeded by human beings who appear normal that
the possibility of a far longer existence has often been raised. John
Sterne or Stearne (1624–69) who, though founder of the Irish College of
Physicians, was, according to Mahaffy,[23] more of a theologian than a
physician, believed that there was no reason why men should not live
as long as the patriarchs before the Flood; but he also argued that
these patriarchal ages must have been exceptional, for had all the
human beings between the Creation and the Flood, a period of more than
1400 years, lived to an average breeding age of 400 years and begun,
as did the patriarchs, to beget children at the rate of one male every
three years, the population of the earth could not have found standing
room on its surface; his colleague in Trinity College, Dublin, Miles
Symner, Professor of Mathematics, provided him with a calculation
showing that there would have been less than one cubic foot available
for each individual. This seems to be echoed in a slightly different
connexion by Weissmann’s conception of natural death as due to natural
selection and as an adaptation for the good of the species, the
degenerated organisms being no longer fertile or useful, an hypothesis
hardly necessary, as Metchnikoff points out, when degeneration which
is the prelude to dissolution has appeared. Roger Bacon[24] stating
that man, originally immortal and after the Fall able to live for a
thousand years, had his life gradually abbreviated by corruption of
his own making, believed that it should be possible by taking care as
to regimen to prolong life for a hundred or more years than the common
duration. Since the time of Aristotle the vital cycle has been thought
to be a multiple of the period of growth. Francis Lord Bacon considered
that animals in general should live eight times as long as they take
to come to maturity, and Hufeland,[25] adopting this principle, and
regarding 25 years as the termination of adolescence, concluded that
man’s natural span should be 200 years. Buffon took 14 years as the
age of puberty, and multiplying it by 7 decided that human life
should naturally be 100 years. Assuming that union of the epiphyses
of the long bones marked the time when growth was finally completed,
Flourens[26] calculated that throughout the animal kingdom life was
five times as long, and that as in man the epiphyses united at 20 or 21
years of age the span of human life should be 100 years.

More modern estimates of the duration of human life under ideal
conditions of protection against infection have been to the same
effect, thus conforming to the estimate of Cornaro,[27] who died
at that age, that a hundred years was “the time allowed to man by
God and nature.” Metchnikoff,[28] while admitting that there must
be variations, considered that man should live more than 100 years,
and Luciani fixed the physiological duration of life at 100 years.
Ebstein’s (1891) estimate of 70 years as the usual duration of life,
which is the age at which the maximum number of deaths occur when the
first few years of life are excluded, is different from the ideal
duration under the best physiological conditions and corresponds more
or less with B. W. Richardson’s rough rule that the individual’s
probable age at death can be arrived at by taking the average of the
ages of his parents and grandparents; in this procedure the important
factor of heredity is taken into account, and the disturbing part
played by accidents and infections in modifying the ideal expectation
of life is to some extent neutralized by taking the average of the six
lives.

Although 100 years may be regarded as the physiological life of man it
is rarely reached, and one of several reasons is that the physiological
requirements for this apparently exaggerated term of years are very
seldom provided. Sir Ray Lankester[29] suggested that just as giants in
stature are exceptional variations so centenarians should be regarded
in the same light, as giants in years instead of in inches. He meets
the obvious objection that whereas the parents of giants are of normal
height, longevity and centenarianism appear to run in families, by
doubting if the actual quality of potential long life is transmitted
and by ascribing family longevity to the inheritance of traditions
and habits favourable to long life. In this connexion it should be
remembered that many giants are pathological and due to acromegaly,
whereas unusual height, over six feet, certainly runs in families;
analogy therefore makes it reasonable to believe that length of
days, like length in inches, may run in families, although these two
approaches to giantism very seldom occur in the same individual.

[Illustration: FIG. 4.--Henry Jenkins, reputed to have lived 169 years
(1501–1670). Present at Battle of Flodden Field on September 9, 1513.]

The authenticity of persons alleged to be of great age rightly excites
critical examination, and some of the most famous examples, such as
Henry Jenkins (169), Thomas Parr (152¾), Katherine, Countess of Desmond
(145), as Sir George Cornewall Lewis and Mr. W. Thom showed, as well as
many of the 1712 centenarians in James Easton’s[30] list covering the
years A.D. 66 to 1799, cannot be regarded as established.[31] In the
same category we must place Petrasch Zorten (1537–1724), whose portrait
at the reputed age of 185 was reproduced by Sir John Sinclair.[32]
Old people take a natural pride in their age and tend to exaggerate
it; according to Mr. G. King[33] the excess in the census returns of
persons over 91 and the deficit in those between 85 and 90 years of
age could only be explained by the conclusion that the temptation to
overstate the age so as to appear among the nonagenarians had not been
resisted. The vast majority of centenarians are naturally among the
bulk of the population, namely, the poor, among whom natural selection
is provided with a correspondingly greater opportunity of finding those
“vigorous frames which promise a long life,” and in these circumstances
the means of checking the exact age may be less easy than in the case
of the well-to-do.

_Sex._--Females are more long-lived than males; the 1911 census
for England and Wales shows that after 10 years of age there are
more females than males living in all the quinquennial periods, the
proportion of females progressively increasing until at the age of
85 and upwards there are 645 females to 355 males in 1000 living at
that age group. Among centenarians also the ratio of the sexes is much
in favour of that popularly said to be the weaker. Out of the 691
reputed centenarian deaths registered in England and Wales during the
10 years 1910–19 inclusive, 504, or 73 per cent, were females, and
187, or 27 per cent, males. But during the same period in Ireland the
disproportion was much less: among the 945 reputed centenarian deaths
545, or 58 per cent, were females, and 400, or 42 per cent, males. It
has been said, though without sufficient statistical evidence, that
although the female sex is favourable to longevity extreme length of
days is attained only by males. The superior longevity of the female
sex, in spite of the risks attaching to child-birth, depends on several
factors, such as an existence less exposed to accident and infection,
a more temperate life, and in addition, so Sir George Humphry argued,
on a stronger inherent vitality, for during the first year of life when
there is no difference as regards the first two circumstances more
boys than girls succumb. The higher male death rate in the first year
of life, however, may be partly due to a mechanical cause, namely,
the large size of the male infant’s head, as a result of which the
numerical superiority of male infants born is reduced by the effects of
trauma. Another factor is, perhaps, that old women do not feel so old
as old men do, and that therefore auto-suggestion plays a less powerful
part with them.

[Illustration: FIG. 5.--Thomas Parr. Reputed to have lived 152 years
(1483–1635).

From a Print by Payne.]

The question must arise as to what is the object of the prolongation
of life after the reproductive function has waned as it does in
women--the more long-lived of the sexes--about half-way through the
physiological term of years. In some lower animals life terminates
very shortly after propagation of the species has been effected; but
this is not the rule, and the biological meaning of the continuation
of the life of individuals that but cumber the ground and may lead
a parasitic existence requires explanation, though educational
advantages and moral lessons may undeniably be provided by healthy
old age with its store of what a Cambridge man, now justly famous,
described in his rather rebellious youth as “that greatly over-rated
property experience.” It has been suggested by Sir Ray Lankester that
the inherent property resulting in longevity may be bound up as a
“correlated variation” with some other characteristic useful in the
struggle for existence and the perpetuation of the species. An obvious
possibility is that the long-lived have a higher fertility rate than
average mortals. Hufeland[34] argued that as very old people are nearly
always married more than once and generally at a very late period of
life “a certain abundance in the power of generation is favourable to
longevity.” There are few satisfactory data to determine the converse
proposition with which we are now concerned, namely, is longevity
accompanied by unusual fertility? As already mentioned, the great
majority of centenarians are found among the bulk of the population,
namely the poor, who are far more prolific than the well-to-do; but
this does not prove much, for the inverse correlation of fertility and
good social status is largely artificial and due to voluntary birth
control. Among the 824 persons between 80 and 100 years of age analysed
by Sir George Humphry[35] in 1889 there were 335 married men and 292
married women, and in each group the average number of children was
six, which is somewhat in excess of what is popularly supposed to be
the average size of a family; but the question of average fertility
is one on which Dr. Major Greenwood warns me that it is difficult to
give an unambiguous answer, for it all depends on whether completed
or incompleted fertilities are meant; thus in the 1911 census the
completed fertilities average 5·8 and the uncompleted 4·2. No value
could, he considers, be attached to the general figure obtained by
dividing the total number of children by the total number of couples
enumerated. Hence Sir George Humphry’s and other statistics are not
really comparable. While finding that longevity was equally shared by
the single and married women and by those who had children and by those
who were barren, Sir George Humphry stated that among those who had
children fertility was associated with longevity.

[Illustration: FIG. 6.--Katherine, Countess of Desmond. Died 1604 at
reputed age of 140.]




III

ONSET OF OLD AGE


The onset of old age varies in different countries, and, like the
development of puberty, is accelerated by the high temperature of
tropical countries. There is also considerable variation in families
and individuals of the same race and country; thus while one man may be
senile at 60 years of age another is vigorous both in mind and body at
80. The inconstancy of onset depends on the various factors that may
play a causal part; old age may be a physiological involution, but too
often is a pathological product. When the period of reproductive power
(maturity) wanes that of old age begins; in women this is marked by the
menopause, the age of 45 years being taken as the limit of fertility,
but before this even in the late thirties the spectre of fading
attractiveness may upset the matron and lead to the irregularities of
the “dangerous age.” For man there is no such index, and the change
is so insidious that most of us would expostulate at Stanley
Hall’s[36] statement that old age in men begins in the early forties
and sooner in women, or less than half-way through the physiological
lifetime of a hundred years. According to Dante 45 marks the
termination of youth, and it seems generally agreed that as a rule--and
every one is entitled to consider himself as the exception--

  The gay bloom of fifty passes quickly away
  And people get fat and infirm and all that.

[Illustration: FIG. 7.--Petratsch Zortan, a Hungarian. Reputed to have
lived from 1537 to 1724.]

It has from analogy of the female sex been rather fancifully suggested
that in man there occurs about the age of fifty a critical period
(_climacterium virile_) due to changes in the sex glands (Mendel[37])
or prostate (Rankin[38]); but of this there is no proof. It recalls
as a kind of echo the ancient conceptions of the grand climacterics
at 49 (a multiple of the number 7), 63 (7 × the magical number 9 of
the Arabians), and 81, and the description in 1807 by Professor B.
Waterhouse[39] of Cambridge, Mass., who in 1800 introduced Jennerian
vaccination into America, of a kind of male moulting between 43 and 50
and a worse one at 63, an idea expanded into the climacteric disease
imagined in 1813 by Sir Henry Holland.[40] There is indeed no doubt
that after an illness, and the so-called climacteric disease admittedly
seldom occurred without some previous factor such as an attack of gout,
a common cold, a bout of intemperance, recent marriage, or particularly
grief or bereavement, old age may come on apace. In some instances the
so-called climacteric disease was perhaps really chronic renal disease,
in others merely the prolonged or imperfect convalescence due to some
lingering infection after an acute illness, such as influenza; and,
as in the latter case recovery may occur, Holland’s contention that
recovery was an argument in favour of the existence of this climacteric
disease holds good only in distinguishing it from permanent senility,
which indeed was the objection that he was concerned to meet. The
conception of the climacteric disease is interesting historically only;
and it may be agreed that apart from accidents of environment the
progress of senescence in healthy men is gradual and uneventful.

So stealthy is the onset of senescence that commonly it is not
recognized by its victim and, though he may seldom mention it, every
man is firmly convinced that he not only looks but is at least ten
years less than the register would tell him. Though unconscious of the
change in himself he notes it with perhaps some self-congratulation
in his contemporaries. It is only if he tests himself, for example by
timing himself for a mile’s walk, that a healthy man of say 70 years
has it borne in on him that he is not what he was. The information that
he is old may be suddenly conveyed by overhearing the chance remarks
of others, by catching a reflection of his bent back in a mirror,
by tardy recovery from illness, or the advent of some disability,
such as hypertrophy of the prostate or dyspnoea on holiday exertion.
Perhaps the commonest warning is a feeling of fatigue. Sir Andrew
Clark regarded the onset of old age as the period when a man ceased
to adjust himself to his environment; but some persons never are
able to do this, and misfits are not necessarily old. Laurentius
divided old age beginning at 50 into the three stages of “the green
because it is accompanied with prudence, full of experience, and fit
to gouerne common weales,” the second at 70 years is “very cold and
drie,” and the last, without a specified age incidence, is that of
decrepitude corresponding to the famous description in the 12th chapter
of Ecclesiastes. A more modern and comforting division is that of
Lacassagne[41] of pre-senility, old age beginning at 60 or sometimes
70 in men, and in women 10 to 15 years earlier, advanced old age, and
lastly decrepitude. Nascher[42] speaks of a senile climacteric about
the latter part of the 7th or 8th decade--the transitional period
between old age and decrepitude--corresponding to the changes at
puberty and at the menopause.

_Precocious old age_ due to the effects of disease, especially syphilis
and acute infections, and to metabolic defects, which permanently
damage the cells of the body, has a special interest as it supports
Metchnikoff’s pathological view that old age as ordinarily seen is
a result of toxic injury (_vide_ p. 82). Hastings Gilford[43] has
specially investigated premature senility, and under the title progeria
has described a remarkable condition of premature senility combined
with, or secondary to, infantilism. This condition was independently
described in 1910 by Variot and Pironneau[44] as the senile type of
nanism. In such cases it would appear reasonable to ascribe these two
opposite conditions to the same toxic or other factor, the infantilism
depending more on damage to the ductless glands before development was
complete, and the senile changes to direct injury of the cells in the
body in general.




IV

FACTORS INFLUENCING LONGEVITY


The determining factors of long life may be broadly divided into
those included under heredity, environment, due functional activity,
and personal habits. It is impossible to separate these factors into
watertight compartments, for a certain amount of overlapping between
them is unavoidable.


HEREDITY

The influence of heredity has often been insisted upon and is perhaps
the most important factor in longevity. Out of 824 persons between 80
and 100 years of age analysed by Humphry, 406, or 49·4 per cent, came
of long-lived families. Numerous striking examples of such families
are on record, but a few only need be given. Roy[45] quotes the case
of Dr. Iverex, who died in 1700 at the age of 104, his father at 112,
his mother 107, and his grandfather 130 years, and gives four other
examples of three centenarians in the same family. Another remarkable
family group was that of Joseph Retas who died at Tarbes at the age
of 118 in 1888, and was the son of a man aged 111 years and had a
brother aged 114 years. Two centenarian twin sisters were recorded in a
village near Athlone[46]; centenarian sisters and brothers are not so
very exceptional. Sir Hermann Weber[47] recorded two families, in one
of which the average age of ten children was over 90 years and in the
other of eight children nearly 90 years.

A good stock may ensure long life in the face of adverse environment,
such as town life and alcoholism; thus Dr. John Brownlee[48] showed
statistically that while persons dying at the age of 51 in the average
environment would have, had they lived in the country, a mean life
of seven years longer, this difference was less at higher ages, and
remarks that a person who has the potentiality of living to the age
of 80 years has a force of life which is more or less independent of
environment. Sir George Savage[49] often noted that of two aged members
of the same family one was sober the other intemperate; and a good many
centenarians have taken alcohol in quantities that would be too much
for ordinary people.

Heredity is not an all-powerful factor, for an individual whose family
history is not remarkable for longevity may greatly prolong his life
by carefully correcting unfavourable hereditary tendencies. Thus the
late Sir Hermann Weber, who lived to the age of 95 as the result of
practising the maxims of his _Prolongation of Life_, mentions that his
mother died of cardiac failure before she was 60 and his father at 60
from cerebral haemorrhage, and he gives other instances of the same
happy result of wise management. Not unfrequently husband and wife both
live to an advanced age, no doubt often as the result of favourable
environment. A photograph of a married couple both 101 years old
appears as the frontispiece of Sir George Humphry’s book on _Old Age_,
and must of course be accepted; but the same cannot be said of the
frontispiece to volume ii. of Sir John Sinclair’s _Code of Health and
Longevity_ (1807), representing the Hungarian husband and wife, aged
respectively 172 and 164 years, who had been married 147 years.

It has been suggested that “cell-memory” by providing experience as to
the proper way to behave at the different periods of life has a bearing
on the coming of old age; Samuel Butler[50] argued that cells without
hereditary memory of past existence at, say, 75 years, would become
puzzled and so disordered as to die. Parkes Weber[51] has modified
this view by assuming a failure of the wish to live on the part of the
nerve cells of the brain, a want which might also be hereditary. The
possession by the cells of “the will to live” would be an important
factor in longevity and should be obtained by individual effort or in
other words be an acquired character, though the reverse conditions
such as physical mutilations,[52] often spoken of as acquired
characters, are known not to be inherited.

In different countries and in different individuals the cells of the
body may differ in the rate at which they live; they have, as Sir James
Paget[53] said, a different “time-rate”; in some the time-rate is
rapid, for example in the natives of hot climates where maturity comes
early and old age at a time that seems very premature by our standard;
in others the body, sometimes the mind, works slowly, is set at a more
leisurely rate and therefore takes longer to run its course. In some
persons this appears to be shown by a slow pulse, a characteristic that
may also be hereditary.

[Illustration:

  FIG. 8.--John Rovin and Sarah his wife, Hungarians, at their
      reputed ages of 172 and 164 years respectively; their married
      life lasted 147 years.
]

Of the hereditary factors most concerned in longevity the inherent
vitality of the central nervous system is the most essential;
physiological death in man and the higher animals is probably due to
failure of the cells of the brain, which do not multiply after birth
and are less capable of rejuvenescence than those of the other organs.
The integrity of the cardio-vascular system is also most important; in
Sir William Osler’s[54] words much depends “on the quality of arterial
tissue (vital rubber) which the individual has inherited.” According
to Sir Clifford Allbutt[55] there are two modes of hereditary
transmission of arteriosclerosis, the direct and the indirect; the
direct which he calls decrescent or primary, consisting in an original
frailty or toxic susceptibility which like other peculiarities may
run in families; and the indirect or hyperpietic, a secondary event
due not to inherent taint in the arterial walls but to metabolic
changes causing high arterial pressure; it is in such families with
hereditary high blood pressure that cerebral haemorrhage occurs in
one generation after another about the same age (65–70). In examining
people the discovery of a blood pressure low for their age often
justifies, in the absence of any pathological condition, the suggestion
that the family is long-lived. The frequency of cardiac hypertrophy
(43 per cent of Councilman’s cases), even though it be a pathological
condition, shows that its reserve power is good. Death among the aged
very commonly depends on some morbid change in the cardio-vascular
system; thus at the Royal Hospital, Chelsea, Majors R. J. C. Thompson
and R. E. Todd[56] found that among 169 deaths of pensioners with
an average age of 77·2 years the largest number 64, or 38 per cent,
were due to this cause; lesions of the respiratory system, pneumonia,
and bronchopneumonia, coming next with 41 deaths, or 24 per cent,
malignant disease being responsible for 22, or 13 per cent. The nervous
and circulatory systems are intimately correlated with each other,
disorder or disease of one, particularly of the cardio-vascular system,
exerting an evil influence on the other. In a negative manner weakness
of the digestive system may favour longevity by preventing the excesses
which vigorous individuals may for a time at any rate indulge in with
impunity; but as a rule the digestion of the long-lived is good.

The first-born is significantly handicapped, as Karl Pearson[57] has
shown, and more subject to tuberculosis, insanity, and criminality. But
out of 71 centenarians analysed by Sir George Humphry 17, or 24 per
cent, were firstlings, and 24 per cent of 824 persons between 80 and
100 were first-born. It must be remembered that first-born are more
numerous than any others, and some of the above were only children.
The most frequent position in the family among these 895 old people
analysed by Sir George Humphry was the third.


ENVIRONMENT

The influences included under the head of environment are numerous,
and this factor cannot be entirely separated from that of heredity,
for environment may favour and shape hereditary characteristics. The
subject of the harmony and the want of harmony existing between man and
his surroundings is so vast that it is possible to touch on a few only
of these aspects.

The average length of life varies in different countries; a temperate
or moderately cold climate is conducive to a slower development of
maturity and so to a longer life than tropical regions. The Balkans,
Greece, Scandinavia, the Pyrenees, California, and small islands are
considered favourable to longevity. A high elevation has been regarded
as an important factor, and the great age of the monks of Mount Athos
has been thus explained, though other influences, such as simplicity of
life, may well play a part. Switzerland, however, does not conform to
the view that a high elevation confers long life on its inhabitants.
From observations around Dijon Noirot[58] drew up a scale showing that
the elevation above the sea and length of life rose together. National
habits have a bearing, and this may help to explain the longevity of
the Jews, who follow the Mosaic laws of health, and why the French
appear to be more long-lived than the Germans. The long-continued
persecution and hard life that the Jews have undergone has led to the
survival of the fittest and a hereditary factor. The former simplicity
of the Russian peasants would also provide a reason for their reputed
longevity (one centenarian in every thousand). In Ireland, though
much depleted by migration of young adults, the absolute number of
centenarians is very high; in 1888 there were 208 such deaths, or 43
per million living; in the ten years 1911–20 inclusive there were
1030 centenarian deaths, or about 23 per million living; and the
Registrar-General, Sir William J. Thompson, kindly informs me that in
1921 there were 314 centenarians living in a population of 4,496,000,
or about 70 per million of the population. It seems probable that this
is the outcome of a simple life. In England and Wales the number of
centenarians is both relatively and absolutely less; in 1887 there
were said to be about 2 and the 1911 census returns showed 3·6 living
centenarians per million of the population; the return of the 1921
census is not yet available. In the ten completed years 1910–19 there
were 691 centenarian deaths, or an average of 69 annually among a
population averaging about 35 millions--about two per million living.
In California there are, according to Laurent,[59] 300 centenarians
in a population of three millions, or 100 per million, the extremely
favourable climatic conditions accounting for this high ratio. In the
same country there is a difference, much to the advantage of the rural
inhabitants, between the prospect of longevity in the towns and in the
sparsely populated districts. From their open-air life agricultural
labourers provide the largest percentage of long lives.

_Improved Conditions of Life._--There is good evidence that the average
expectation of life has improved in this country during the period that
increasing attention has been paid to sanitation. This is shown by the
tables of the Registrar-General. For most of the following information
I am indebted to Dr. T. H. C. Stevenson of the General Register
Office, Somerset House. In 1838–54 the expectation of males at birth
in England and Wales was 39·91 years, in 1901–10 the male and female
expectations at birth were 48·53 and 52·38 years respectively, and the
latest available expectations at birth (English Life, Table No. 8,
Supplement to the Seventy-fifth Annual Report of the Registrar-General,
Cd. 7512) are 51·6 for males and 55·35 years for females. But the
expectation is probably considerably more now, as the death rates
have fallen appreciably since 1910–12. The Prussian male expectation
of life at birth has increased from 35·38 years in 1867–77 to 46·43
in 1906–10;[60] and the Swedish[61] expectation of life at birth from
39·5 years in males and 43·6 years in females in 1816–40 to 54·5 and
57 years respectively in 1901–10. In North America[62] there has been
a fall in the death rate in every age group in 1920 as compared with
1910.

The increased expectation of life has been especially prominent in
early and adult life. Examination of the Registrar-General’s census
returns from 1851 to 1911 show that although there were more persons
per million living between the ages of 55 and 75 there were less above
the age of 75 at the end than at the beginning of this 60-years’
period. It has been suggested that the increased survival in the
earlier period of old age is due to the saving of life in infancy and
that, as these lives are not prolonged above the age of 75 or so, the
diminished proportion of persons living to become octogenarians is
explained (H. Weber).

_The influence of past diseases_ is perhaps most conveniently
considered in connexion with environment. As infection must necessarily
impair the vitality of the cells of the body, either temporarily or
permanently, it would be natural to expect that those who live to a
great age would show a remarkably clean bill of health. This is often
true. But it is at first sight rather disconcerting to find that nearly
half of the 824 persons between 80 and 100 years of age analysed by
Sir George Humphry had had severe illnesses at one time or another;
many of these, however, were acute infections. It is noticeable that
85 per cent were free from rheumatism in the hands (selected as a
convenient test in his collective investigation), which in the light
of present opinion that arthritis is the result of a focal infection
would appear to show that these old people are remarkably free from
chronic disease. Long-continued infection or intoxication would be a
far more potent factor than a transient illness in producing permanent
change in the cells. A short acute infection would cause changes in the
cells which might, like those of fatigue, be temporary and recoverable.
Saundby’s[63] dictum may be accepted as fairly accurate, exception
being made for peripheral mutilations, namely, that those only can
expect to live to extreme old age who at the age of 60 possess bodies
free from disease. But critical examination would no doubt show that
focal infections become increasingly frequent as the years go on;
this is particularly true as regards oral sepsis; after two years’
experience of 500 pensioners at the Royal Hospital, Chelsea, Thompson
and Todd have never seen a tooth in a healthy condition there. It is
noteworthy that dental disease seems to have become common with the
advent of civilization, as judged by examination of ancient skulls,
though the loss of teeth is an accompaniment of the bony changes in old
age, and very old people seldom have more than a few teeth left. On
the other hand, an acute illness is often the apparent starting-point
of old age; there may be a long and imperfect convalescence due to
persistence of infection, or deterioration may be due to auto- or
hetero-suggestion (_vide_ p. 48).

The influence of syphilis, whether congenital or acquired, is one of
the most important in the prevention of healthy longevity; it not
only directly disables and kills, especially in infancy and in the
fifth decade, but it damages the vitality of the cells thus producing
degeneration and premature senility, and favours secondary infections.

It is clear that for the preservation of health detection of disease
in the earliest stage is all-important, and that this can be attained
by periodic examination by a medical man; but obvious though this may
be, the average man waits to call in a doctor until he knows that he is
ill. Timely advice as to methods of life, food and drink, occupation,
or environment would often prevent disease and premature death. In 1913
the Life Extension Institute was founded in New York for such periodic
examination and report, and the Life Assurance Companies, finding that
persons so examined showed, at any rate for some years, a death rate
lower than that anticipated, gave it financial support.


FUNCTIONAL ACTIVITY

As is well known, disuse leads to atrophy, and biologically conditions
rendering an animal’s supply of food extremely easy and safe are
followed by atrophy of the parts no longer necessary in a state which
may thus come to border on parasitism; in an extreme degree this
result is shown in barnacles (degenerated crustaceans) and ascidians
(degenerated vertebrates). In man the cessation of an active life on
retirement to the country, described by Samuel Johnson as “a kind
of mental imprisonment,” or the sudden acquisition of wealth, often
exerts a most evil influence; for if the whole body is no longer kept
in a condition of functional activity, those parts allowed to remain
relatively idle begin to degenerate and atrophy; loss of function means
a diminished blood supply and nutrition, and so degenerative atrophy.
According to Laurentius “nothing hastens old age more than idleness.”
James Easton,[64] who collected 1712 records of centenarians, many of
them open to criticism, endorses Hufeland’s dictum that no idler has
ever attained to a remarkably great age; and Sir Thomas Browne’s[65]
quaint injunction “Dull not away thy days in sloathful supinity and the
tediousness of doing nothing” is old but true wisdom.

The axiom that disuse leads to atrophy applies perhaps even more to
mental activity, for resting and rusting of the brain slow the pace
of the whole body, whereas an alert mind can exist in an infirm body.
There is no doubt that occupation with a strong desire to live for
the accomplishment of a definite purpose exerts a most beneficial
influence, and there have not been wanting some, such as Karl Marx, who
have preached that old age is in great part a matter of will. Speaking
of the circle in which Madame du Deffand moved Lytton Strachey[66]
says “They refused to grow old; they almost refused to die. Time
himself seems to have joined their circle, to have been infected with
their politeness, and to have absolved them, to the furthest possible
point from the operation of his laws. Voltaire, d’Argental, Moncrif,
Hénault, Madame d’Egmont, Madame du Deffand herself all lived to be
well over eighty, with the full zest of their activities unimpaired.”
Want of this joy in life necessarily engenders carelessness and
neglect of personal hygiene, and loss of the power to react to the
environment. As the years advance and the younger generation come up,
the suggestion that “his day is done,” that he has had his innings,
and that it is time for him to step aside, is made to the senior not
only by his family and his juniors--hetero-suggestion--but by himself,
and he may then, after the modern fashion, get into the habit of
repeating mentally “I am getting older and older every day.” A slight
illness or incapacity may be magnified into a conviction that the
end is near, and as a result of the loss of self-reliance a state of
increasing invalidism is established and becomes progressive without
any other cause. Just as a fall, an exacerbation of rheumatic pain,
a slight operation or indisposition, necessitating rest in bed for a
short time, may be followed by a functional loss of power in the lower
extremities, so a more general suggestion of failing powers may lead
to mental deterioration. Thus too often a man’s last occupation is
to shorten his existence and make it miserable. Finot,[67] who rather
optimistically believes that man should be able to live 150 years,
regards this poisonous auto-suggestion as one of the factors that
prevent such an achievement. Observation of contemporaries suffering
from premature senile changes, due to pathological factors, may no
doubt stimulate this destructive form of auto-suggestion. There is
therefore a basis for the idea[68] attributed to the late Lord Rhondda
that old age was a transferable disease, and for his avoidance, as
far as possible, of the society of the aged on account of the risk of
contagion. Association with the young keeps one more or less of the
same age, very probably by suggestion to the unconscious, or in Oliver
Wendell Holmes’s words “While we’ve youth in our hearts we can never
grow old.” From experience at the Royal Hospital, Chelsea, where there
are 500 pensioners, Thompson and Todd[69] are convinced of the powerful
factor of lowered mentality due to loss of self-reliance, self-respect,
and the instinct of self-preservation in inducing premature senility,
and have been most successful in counteracting this by antidotal
suggestion conveyed by cheerful chaff and by the avoidance of
sympathetic condolence.

In addition to the _joie de vivre_ a happy disposition that thinketh no
evil, has no jealous suspicions, and is free from the tendency to worry
has an important influence in keeping the mind and body young. The
power of detachment from work and anxieties, as if the mind were fitted
with thought-tight compartments, is a valuable asset in maintaining
vitality unimpaired; this was a trait in Gladstone and Kitchener.

Professional men who retain their offices as in the Church, the Civil
Government, the Bar, tend to live longer than business men who retire
to leisured ease after a strenuous struggle. B. Yeo’s[70] analysis of
42 Bishops and Deans, 49 Judges, and 188 Peers, showed that in all
three classes the average duration of life was practically the same,
namely, 72 years. Among churchmen mention may be made of Cardinal de
Salis (110), Gregory IX. (100), Abbé Maignon (100), Martin Routh (100),
for 63 years President of Magdalen College, Oxford, thus surpassing
the more modern instance of Edward Atkinson, aged 96 years, for 59
of which he was Master of Clare, but not that of Laurence Chaderton
(1536–1640) who, after being Master of Christ’s College, Cambridge,
with great success for 38 years, survived for 18 years and became a
centenarian. There are some remarkable examples of artists retaining an
active life to a very advanced age, such as Titian, Giovanni Bellini,
Michael Angelo, Sidney Cooper. Politics often keep men busy and active
to an advanced age, and the names of Palmerston, Brougham, Lyndhurst,
the octogenarian premiers Gladstone and Clemenceau, Strathcona, Sir
Charles Tupper naturally come to one’s mind. In the legal profession
Chief Justices and Judges can retain their seats and so keep up their
vigour long past what is regarded in some walks of life as the retiring
age. Sir Edward Coke (82), Lord Mansfield (89), Lord Brampton (90),
Lord St. Leonards (93), and Lord Halsbury (97), are examples in point.
Within recent years there have been two octogenarian Lord Mayors of
London, Sir Thomas Crosby (in 1911), and Sir John James Baddeley
(1921); the first created a record by being the first medical man
to hold this office, and Sir John Baddeley celebrated his year of
Mayoralty by bringing out a beautiful historical account of Cripplegate.

[Illustration:

  FIG. 9.--Sir Henry Alfred Pitman (1808–1908), M.D., Camb.,
      F.R.C.P., Registrar of the Royal College of Physicians of
      London, 1858–1889.

From portrait in the Royal College of Physicians of London, painted in
1886 by W. W. Ouless, R.A.]

From the inevitable exposure to infection and worry the medical
fraternity is generally considered to rank low in the professions as
regards longevity, but it is easy to point to exceptions especially
among those whose mental vigour made them prominent in their own and
in one instance for all time. Hippocrates is variously stated to have
died at the ages of 85, 90, 104, or 106 years with the words “I leave
behind me two great physicians, temperance and frugality.”[71] I have
references to 43 medical centenarians for 18 of which, including the
record of W. G. Meade, physician at Tunbridge Wells and buried at Ware,
Herts, in November 1652, aged 148¾ years, I am indebted to my friend
Mr. R. R. James. The only one that I knew personally was Sir Henry
Pitman, for 31 years (1858–89) and until his 82nd year Registrar of the
Royal College of Physicians of London. Among the others Dr. de Bossy
of Paris may be mentioned as the son of a centenarian. From analysis
of 2113 eminent medical men Drinkwater[72] found that the average
age was 67 years, or considerably above the average age of the male
population over 21 years, which was estimated at 59 years, and that 627
or nearly a third of them all were between 71 and 80 years of age.

But the examples given of mental activity late in life, and they could
easily be multiplied,[73] are exceptions to the rule that the majority
of men begin to fail in their work between 60 and 70. This no doubt
is because most septuagenarians suffer in greater or less degree from
pathological old age. In the case of the healthy vigorous man enforced
retirement at the age of 65 or 70 is not to the advantage of either the
retiring victim or the community, for it restricts his opportunities
for production and useful activities guided by ripe experience. To
quote examples of epoch-making work done by men long past the age when
the majority have lost originality, initiative, and elasticity of mind:
Galileo, Newton, Charles Darwin, Sophocles, Voltaire, Molière, Goethe,
Michael Angelo, and Titian, made original and lasting contributions
to science, literature, and art long after fifty. Morgagni’s famous
_De Sedibus et Causis Morborum_, brought out when he was 80, and
the Commentaries of W. Heberden (aged 91), published posthumously,
represent the accumulation of many years and so cannot be fairly quoted
as examples of ability persisting into late life. Rules and regulations
must, however, be based on what is best for the majority and hence,
though the exceptions are prominent and regrettable, the age limit
of 65 to 70 must at present be accepted as generally advisable for
otherwise permanent appointments.

Although functional activity maintains the tissues in a state of
health, it is not an infallible panacea for the prolongation of life;
in the first place the danger of overwork and excessive fatigue must
be borne in mind. While the attractive suggestion that excessive
functional activity leading to extreme hypertrophy may exhaust the
vitality of the tissues and lead to atrophy, may not be borne out by
the examples quoted in its favour, such as the occupational neuroses
and atrophy of the upper arm muscles in hammermen and file-cutters,
there is some reason to retain a belief that this sequence of events
may occur, for example in dilatation of the extremely hypertrophied
hearts seen in long-continued high blood pressure, renal disease,
and valvular lesions;[74] but even here the possibility of other
degenerative changes, due to toxaemia, must be borne in mind. Further,
functional activity while keeping the cells of the body in a healthy
state depends on their structural integrity, and this in its turn is
the outcome of the modifications due to environment, and possibly of
the inborn lease of vitality. So that although an active life may
within limits prolong life, there are many instances in which, from
extrinsic pathological influences or inherent inadequacy, it fails to
do so, and a man becomes unequal to the demands of his position.


PERSONAL HABITS

All experience, medical and lay, such as is embodied in Cornaro’s
oft-quoted memoirs, Leonardus Lessius’s _Hygiasticon or the right
course of preserving life and health until extreme old age_ (1613),
George Cheyne’s _Essay of Health and Long Life_ (1724), Metchnikoff’s
orthobiosis, and the Arabian proverb of the ninth century, quoted by
Lacassagne,[75] that “the greatest dangers for an old man are a good
cook and a young wife,” is in agreement as to the immense importance of
strict moderation in indulging the appetites for the prolongation of
life. The life histories of centenarians show that they have usually
been small eaters, especially of meat. This is generally explained in
terms of minimizing toxaemia, and it has been said that “man does not
die, he kills himself” (Montaigne) and more graphically, if coarsely,
that “he digs his grave with his teeth.” In some lower forms of life,
such as the planarians (Child), partial starvation and the resulting
reduction lead to rejuvenescence and so to the inhibition of the onset
of senescence; hibernation has somewhat the same effect, though perhaps
this might be partly explained as merely starvation during prolonged
sleep. The question has often been raised whether partial starvation
in man has any such positive influence, and unprofessional “cures” on
these economical lines have not been unfashionable. It might indeed
be argued that the Allen treatment of diabetes, in which starvation
is followed by increased carbohydrate tolerance, depends on a certain
degree of rejuvenescence. Cures consisting in purgation may act by
partial starvation as well as by obviating toxaemia. After a period
of starvation a normal person may become heavier than before, and his
general health be improved. But in the present state of our knowledge
and in the light of the dangers of starvation the further investigation
in man of this problem is one that demands serious hesitation.

As to the bad influence of alcohol on longevity there can be no
reasonable doubt. Alcohol is a protoplasmic poison causing degenerative
changes in the cells and reducing the resistance to infection. A
collective investigation undertaken by Sir Isambard Owen[76] showed
that there were very few hard drinkers among the long-lived, and
Sir George Humphry concluded that the characteristics of the aged
included temperance; among 46 centenarians one, and among 73 men over
90 one confessed to taking too much occasionally, and out of 298 men
between 80 and 90 years of age 45, or 15 per cent, were classified
as taking much alcohol. That such exceptions occur is explicable by
great inherent vitality. It has been said that “wine is the milk of
old people,” but from his experience of the hygiene of the elderly Sir
Hermann Weber was not in sympathy with this view, and he pointed out
the weakness of the popular idea that the moderate enjoyment of alcohol
was harmless; for so-called moderate drinking is in reality often
immoderate indulgence for the individual, and most of us must have
recognized from observation that long-continued though moderate use
of alcohol is followed by premature deterioration. The proverb _vinum
lac veneris_ and the tendency that alcohol has to lead to incontinence
and so to venereal infection may be borne in mind in considering its
influence on longevity. As a medicine alcohol has its occasional use,
and though it may be a food it is an expensive one.

Smoking among centenarians was specially investigated by Sir George
Humphry, who found that among 19 male centenarians 8 smoked much,
one a little, and 10 not at all; while out of 30 female centenarians
4 smoked much, 2 moderately or little, and 24 not at all. There is
no doubt that with advancing years there is commonly a relative loss
of tolerance for tobacco, so that unpleasant symptoms ranging from
cardiac extra-systoles, through abdominal pain, to tobacco angina,
may dictate discontinuance of the habit. But a large number of old
people have smoked in earlier life though subsequently non-smokers.
Personal tolerance to tobacco shows great variations, and there is no
doubt that well-marked symptoms may be caused by tobacco. But that
moderate smoking diminishes the chance of longevity has certainly not
been proved. Much discussion has taken place as to the relation between
smoking and arteriosclerosis; it is true that in animals nicotine in
considerably larger doses than can be absorbed by smokers, damages
the arteries, and Huchard and Lazarus were convinced that it caused
arteriosclerosis. Sir Clifford Allbutt,[77] after quoting the various
opinions, points out that if tobacco be a cause of arterial disease,
it acts very slowly, for at 45 years of age, after a quarter of a
century’s exposure, the smoker’s arteries are not distinguishable from
those of the abstainer’s; and he mentions the arteriosclerosis of
the ancient Egyptians and of women as incidents detracting from any
argument that tobacco is an important cause of arterial disease.

A large proportion of the centenarians and persons over 80 years of
age collected by Sir George Humphry obeyed the adage early to rise and
early to bed, and I well remember that he used to lay stress on the
factor of getting up directly one woke and so denying the flesh the
luxury of further sleep. Whether going to bed early and getting up
early is more than an index of a life otherwise spent in accordance
with the late Sir Andrew Clark’s “laws of physiological righteousness”
may be questioned.

_Bodily Conformation._--Long-lived people are usually spare, obesity
being rare, and, allowing for some shortening due to age, of a good
average height (Humphry). It is interesting in this connexion to quote
the conclusions arrived at by Robertson and Ray[78] from comparison of
groups of long-lived and short-lived white mice in similar conditions.
The long-lived were relatively stable, highly resistant to external
disturbing factors, displaying subnormal variability and a more or
less well-marked, but not invariable, tendency to early overgrowth
and relative paucity of tissue accretion in late life; while the
short-lived animals showed exactly the opposite features with a
tendency to rapid increase of tissue in late life.

The importance of a healthy life with plenty of fresh air, sunshine,
exercise, proper diet, and absence of worry hardly needs insistence.
Leonard Williams[79] has epigrammatically summed up the hygiene of old
age as “Fresh air, meagre fare, freedom from care.”




V

  THE CAUSES OF SENESCENCE AND GENERAL ATROPHY: LIMITED VITALITY
      OF CELLS--INFLUENCE OF THE ENDOCRINE GLANDS--METCHNIKOFF’S
      PATHOLOGICAL EXPLANATION

  SENESCENCE AND CARCINOMA


The causation of old age is so complex that it is not possible to
argue with any conviction that any one of the following explanations
exclusively solves the problem satisfactorily.


LIMITED VITALITY OF THE CELLS

To explain the atrophic processes normal to old age it has naturally
been assumed that the constituent cells are endowed with a certain
store of vitality for themselves and their descendants, and that
as this becomes exhausted the process of involution begins. This
conception of an inherent limit of life is probable from the analogy
of the existing limit of height and size, though in certain plants
and trees growth in size and length of days do not show a natural
limitation. The process of ageing of the cells is thus regarded as just
as much part of their development or life cycle as are their earlier
and progressive stages. The exception is that the reproductive cell
when it meets with its complement--the ovum with the spermatozoon--and
as it were with new blood, starts a fresh lease of life, and so in Sir
Edward Sharpey-Schafer’s[80] words “we can only be immortal through our
descendants.” That there is a more or less definite cycle during which
the cells multiply and after which they cease to do so receives support
from the anatomical and physiological changes in old age; thus the
ovary undergoes fibrotic atrophy and ceases to be actively functional
after the menopause. The atrophy or hypoplasia of the organs is due
to diminution of the proliferation of the constituent cells. This is
well shown in the lymphatic glands and spleen which are so active in
youth and atrophied in advanced life. Salimbeni and Gery[81] point out
that the hypoplasia in the woman aged 93 whom they minutely examined
was most prominent in the lymphatic tissues and the bone marrow which
have to supply the cells most constantly needed. Even in the lowest
forms of life senescence and death would occur in the absence of the
rejuvenescence associated with reproduction. In the complex congeries
of cells making up the higher animals and man this rejuvenescence does
not accompany reproduction, and the vitality of the constituent cells
diminishes until eventually atrophy and death supervene.

Many of the vital phenomena of cells may, as Martin Fischer,[82]
Lumière,[83] and others point out, be interpreted in terms of the
behaviour of simple hydrophilic colloids. Bechhold[84] has shown that,
like a simple colloidal jelly, the cells of the human body, which are
colloidal masses, lose their affinity for water progressively with age
and become less elastic; the water content of the fetus being 94 per
cent, as compared with 70 per cent at birth and 58 per cent in adult
life, thus recalling the old idea of the dryness of elderly bodies.
According to Marinesco[85] dehydration of the colloids in the cells is
an inherent progressive change in evolution and leads to senescence and
death. It has also been thought that as the result of differentiation
and metabolism the cell protoplasm may become overladen with products
inimical to its vitality, which it cannot, as can the protozoa, utilize
for rejuvenation, and which hinder metabolism. The micellae, or
aggregations of albumin constituting the colloids of the cells, alter
in structure and become more stable until the colloid state disappears
and the cell accordingly dies (Lumière, Danysz). Such changes must
obviously be greatly influenced, as H. Campbell[86] and others have
insisted, by their environment; the individual cells are in some degree
of material continuity by “protoplasmic bridges” which probably serve
not only for nutritional purposes but also for the transmission of
physiological impulses. It also appears that the life cycle of the
cell is determined not so much by time as by the interaction of the
tissues and the plasma. By cultivating connective tissue in the plasma
of chickens of different ages Carrel[87] showed that its growth was
more abundant in the plasma of younger chickens than in that of older
ones. Working on these lines Loeb and Northrop[88] concluded that the
duration of life was determined either by a substance leading to old
age or by the destruction of a substance which normally prevents old
age and natural death. More recently Carrel and Ebeling[89] found that
in these cultures of connective tissue the rate of multiplication of
fibroblasts and the duration of life _in vitro_ varied in inverse ratio
to the age of the animal from which the plasma was taken, and that
this depended on the presence of an inhibitory body in the plasma of
older animals. These experiments recall the practice centuries old of
transfusion of young persons’ blood into the old which, however, led to
disastrous results on account of a technique now known to be dangerous.
Whether with modern methods success will be obtained remains to be
proved, but probably repeated transfusions would be required. But to
return to the subject: Carrel, Champy, and Grandcourt have shown that,
with frequent washings to remove waste products, tissue cells can be
cultivated indefinitely for years _in vitro_, and in themselves have
an unlimited capacity for multiplication; it therefore appears that
the ageing of cells in the living organism is determined by extrinsic
factors in the plasma rather than by any inherent limitation in the
cells. In the ordinary conditions of life senescence of the cells
might be regarded as the result of increasing differentiation and,
possibly from accumulation of material which cannot be utilized for
rejuvenation, of diminished metabolic activity. In the physiological
life of gland cells, for example, the salivary glands and pancreas,
granules are manufactured and discharged, but the hypothetical material
which collects in elderly cells, of which pigment may possibly be an
example or the visible sign, remains in these cells and hampers their
functional activity. As atrophy of the functional cells and increase
of connective tissue are regarded as characteristic of senescence,
and a high proportion of cells as characteristic of embryonic life,
Robertson and Ray[90] suggest that the potential longevity of any
individual is determined by the relative velocities of anabolism in the
cells on the one hand, and in the fibrous tissue on the other hand. A
low rate of cellular anabolism increases the growth of the cells and
delays the increase of fibrous tissue; this they were able to effect
by feeding white mice with tethelin. The relations of the functionally
active cells and the connective tissues have also been investigated
by Nathan[91] and his collaborators, who bring forward experimental
evidence in favour of the modified view that while dense connective
tissue inhibits cellular proliferation, young loose connective tissue
favours the multiplication of cells in proportion as it approaches the
structure of the embryonic mesenchyma. Drew’s[92] observations on the
culture of tissues and tumours show that the stroma acts like embryonic
tissue in favouring growth.

To sum up: the cells of the complex organism depend for their duration
of life not so much on an inborn store of vitality as on metabolic
changes in the colloids which in their turn are modified or controlled
by extrinsic factors of various kinds.


RELATION OF THE ENDOCRINE GLANDS TO SENESCENCE

As the metabolic activities of the cells of the body generally are
markedly influenced by the secretions of the ductless glands, the
relations between these endocrine glands and senescence demand some
discussion.

The process of reproduction leads to rejuvenescence in the protozoa,
and it might therefore be imagined that in the higher animals continued
activity of the sexual glands would similarly exert a rejuvenating
influence on the remaining cells of the body. But the process of
specialization has gone so far in the cells of the higher animals
that the highly differentiated cells, especially of the nervous
system, cannot fairly be compared with the constituent molecules of a
unicellular organism. As sexual activity is the biological reason for
existence and as in vigorous men sexual power may last long beyond the
usual period, man being regarded as old as his sexual glands, it has
been widely imagined that the functional activity of the sex glands is
in some way a cause, rather than a manifestation, of the preservation
of bodily vigour, and conversely that failure and atrophy of the sexual
glands cause old age and senility. There is an attraction, though
not without the danger of fallacies, in interpreting the words of
older writers as prophetic anticipations of quite modern knowledge.
But with this caution in mind there is some ground for crediting
Hufeland[93] with some idea of the internal secretion of the sexual
glands: as long ago as the end of the eighteenth century he wrote “the
organs of generation have the power of secreting the finest and most
spiritual parts of our nourishment; but at the same time they are so
organised that these perfected and ennobled juices can again return
and be received into the blood. Like the brain, therefore, they belong
to those important organs which serve for bringing to perfection and
ennobling our organic matter and power, and even ourselves.”

Since 1889 when Brown-Séquard, at the age of 72 (6 years before his
death) put forward the idea that rejuvenation could be brought about
by the hypodermic injection of testicular emulsion, the view that old
age and senile changes are due to failure of the glands of internal
secretion has become popular. The thyroid (V. Horsley, Léopold-Lévi),
the testis and ovary, or most or all of the glands (pluriglandular
insufficiency) have been incriminated; Lorand,[94] indeed, regards old
age as a disease caused by degeneration of not one but several of the
endocrine glands, Biedl[95] expresses much the same view in referring
old age to a disturbance of the endocrine balance, and Berman[96] in a
recent semi-popular book states that old age is an exhaustion permanent
and irreparable of all the glands of internal secretion; like Lorand he
ascribes considerable importance to failure of the internal secretions
of the sexual glands. It is highly desirable to arrive at some
conclusion as to the relation between changes in the glands of internal
secretion and senescence, for in medical practice this conception
of cause and effect has been acted upon; various glandular extracts
have been employed to counteract and delay the disabilities that may
accompany advancing years and, though not so freely, operations, viz.,
ligature of the vas deferens and implantation of testicular grafts,
have been carried out.

    Lydston[97] implanted testes from boys recently dead into men
    with atrophied or destroyed testes and reported improvement.
    Stanley and Kelker[98] implanted 11 cases with testicular
    grafts obtained from executed criminals, and 5 cases with the
    testes of rams, obtaining improved general condition, though
    not claiming that life was prolonged. Stanley[99] injected by
    means of a large syringe strips of testes of rams, goats, or
    bears under the skin of the abdomen of more than 300 prisoners,
    and stated that conditions of neurasthenia and senility were
    relieved.

The stimulating effect of thyroid secretion on growth and metabolism,
shown both experimentally and clinically in the therapeutic triumphs
of thyroid treatment in myxoedema and hypothyroidism, seems to justify
the view that failure of thyroid function plays an important part in
reducing the capacity for multiplication and regeneration of cells.
Between the manifestations of hypothyroidism and those of old age there
are undoubtedly striking resemblances, such as the dry skin, the loss
of hair, the diminished mental and bodily energy, and the increased
amount of interstitial fibrous tissue. In some respects myxoedema and
cretinism imitate the senile state; myxoedema has indeed been described
as more than a simulation and as the best example of secondary senilism
(Hastings Gilford[100]); but this is a very different condition from
healthy old age which does not present the picture of complete loss
of thyroid function; old age therefore cannot be regarded as due to
athyroidism. Usually atrophy of the thyroid accompanies and corresponds
to that of the senescent body as a whole. No doubt pathological changes
may occur in the thyroid, especially in women, during advancing years,
and it is in such instances that thyroid feeding produces so much
improvement that it has revived in our day the hope of an elixir of
life and perpetual youth. It is not improbable that the administration
of thyroid gland extract may, by preventing high blood pressure, delay
or obviate the onset of arteriosclerosis, and so stave off senility
due to this cause, but this is pathological old age and not the
physiological involution.

In addition to the seminal tubules and ova, which provide their
external secretion, the testes and ovaries contain the interstitial
cells described by Bouin and Ancel[101] or, in Steinach’s phrase, “the
puberty gland”; the germ cells and the interstitial cells differ from
each other in structure, function, and reaction to external influences;
thus the germ cells though dominant are more susceptible to damage,
for example by ligature of the vas deferens, _x_-rays, alcoholism,
or pressure, as in the case of a cryptorchid. It is stated that when
the seminal tubules are active and prominent the interstitial cells
are scanty, and conversely that when the seminal tubules atrophy the
interstitial cells multiply; Lipschülz, Ottow, Wagner, and Bormann[102]
showed that hypertrophy of the interstitial cells as observed in
various experimental conditions depends on local factors in the testes
and has nothing to do with their internal secretion in relation to the
body as a whole. After ligature of the vas deferens in animals there
are, according to Steinach, Kuntz,[103] and others, two stages (1) the
seminal tubules atrophy while the interstitial cells multiply, and
(2) after some time the seminal tubules regenerate while a certain
amount of increase in the interstitial cells persists. Nathan[104]
ascribes the regeneration of the seminal tubes to the influence of the
interstitial cells, which he considers act like young connective tissue
by favouring growth. The interstitial cells of Leydig in the testis and
the interstitial or lutein cells of the ovary are generally regarded
as responsible by their lipoid internal secretion or hormone for the
secondary sex characteristics (Bouin and Ancel, K. Sand[105]), though
Blair Bell[106] and Sternberg[107] deny this. Sir Frederick Mott,[108]
who has extensively investigated the interstitial cells, especially in
connexion with dementia praecox and other forms of mental degeneration,
concludes that in fetal life they act as sex determinants, and that
later in life they are responsible for the sexual appetite. It has
been argued that atrophy of the interstitial cells is the cause of
senescence. Against this view is Sir Frederick Mott’s observation
that after birth the interstitial cells undergo progressive atrophy
and disappear, that they reappear and are in a state of functional
activity at puberty (a sequence of events described by Aron[109] as two
different interstitial glands), and that they are present in extreme
old age; Retterer[110] also described their presence in the testes of
men over 70 years of age. So far it might be concluded that changes
in old age, such as diminution in number and pigmentation, shown by
the interstitial cells, are not the cause but an accompaniment of
senescence.

Kenneth Walker’s[111] observation that the interstitial cells of the
testis show a gradual diminution in number from the age of about
30 years, might be quoted in favour of the contention that atrophy
of these cells plays a part in the production of senescence. In
addition there are the dramatic experiments on rats carried out by
Eugen Steinach,[112] who was formerly Professor of Physiology in
the German University of Prague and since 1912 has been Director of
the Physiological Section of the Experimental Biological Institute
at Vienna. He found that in apathetic senile rats with degenerative
changes in the thyroid, pituitary, and interstitial cells ligature
or section of one vas deferens causes atrophy of the seminal tubes
and active growth of the interstitial cells; the hormone thus
provided stimulates the thyroid, pituitary, and brain, and the rat
is rejuvenated, the sexual instincts and emotions become active, and
the rat may have offspring; when relapse into senility occurs, a
repetition of the operation on the other side brings about a further
rejuvenation; and later the same result is effected by grafting the
testes of a young rat. In this way life is definitely prolonged. This
procedure has been advocated in man with some success by Steinach;
Lichtenstern of Vienna, who has done 36 such operations and 21
implantations on account of senile changes, has not encountered any bad
results, but admits that he has not been uniformly successful, and that
the number of cases is not sufficient to justify a final conclusion.
From observation in Vienna Benjamin[113] estimated that the operation
was followed by no results at all in from 10 to 20 per cent of the
cases. Obviously a considerable time must elapse before any decision as
to prolongation of life can thus be assured.

    In the autumn of 1921 a man aged 70 was advertised to speak
    at the Albert Hall on “How I was made 20 years younger by the
    Method of Dr. Steinach of Vienna,” but he died on the morning
    of the day from pneumonia (Benjamin[113]), the necropsy not
    revealing, so it is said, any trace of an operation; the
    hypertrophy of the interstitial cells, however, may have been
    induced by the exposure of the testes to _x_-rays.

Steinach’s observations naturally aroused great interest and have
been repeated with discordant results by a number of investigators:
Simmonds[114] and Tiedje[115] have failed to confirm the occurrence
of the changes in the testes after vasectomy; and Romeis[116] and
Marinesco[117] have not obtained the striking clinical results
described by Steinach. Levy Lenz and Schmidt,[118] however, report
rejuvenation in 23 out of 24 cases of vasectomy, and Voronoff
encouraging results from implantation of chimpanzee’s testes into man.
But Marinesco compares Steinach’s published results with those of
Brown-Séquard.

It may be added that the operation of ligature of the vas deferens
which was performed some 25 years ago, before prostatectomy became
established, in order to cause atrophy of enlarged prostate, was not
noticed to be followed by rejuvenescence. Mr. C. Mansell-Moullin, who
published[119] a series of 14 such cases, has kindly informed me that
his patients did not show any evidence of such a change. Romeis has
also raised this objection to Steinach’s results which it has been
thought might be explained by suggestion (Freudenberg)--a view hardly
tenable in the light of the remarkable results described in animal
experiments.

The internal secretion of the ovary has never been isolated, and the
evidence of its existence rests on the results of removal. Castration
in men and in women does not bring on the phenomena of old age,
though this operation is followed by well-marked changes as regards
the secondary sex-characters, and, according to Voronoff, eunuchs
are short-lived. It may also be pointed out that the obesity so
common after castration is not a feature of “the lean and slippered
pantaloon.” Further, after the menopause the ovaries undergo fibrotic
atrophy, and it appears from Professor Turnbull’s observations (_vide_
p. 114) that the interstitial cells are very scanty or absent; further
observations are necessary as to the presence of interstitial cells in
senescent ovaries, but presuming that they are scanty it would follow,
on the hypothesis that the interstitial cells exert an influence
in preventing the onset of old age, that women should become old
much sooner than men in whom the interstitial cells are apparently
much more in evidence. It cannot of course be admitted that such a
difference in the sex incidence of old age exists. The improved health
and rejuvenation after _x_-ray treatment for metrorrhagia and uterine
fibromyomas at the climacteric or post-climacteric age have been
regarded by Steinach and Bordier as due to hypertrophy of the ovarian
interstitial cells following induced atrophy of the ova, but to accept
this there must be definite evidence that the interstitial cells are
increased in number. Harrower’s[120] dictum that the absence of a
hormone provided by the interstitial cells is responsible for premature
senility does not appear to be borne out by our present knowledge, but
a great deal of further work must be done before a final decision is
justified.

Testicular and ovarian extracts, often in combination with those of the
thyroid and pituitary, which are known to have a definite physiological
action, have been extensively used as a panacea. But is there any
undeniable evidence that the extracts of testis and ovary so far
employed have any effect apart from that of suggestion? According to
Frank[121] the available ovarian preparations are defatted and thus
deficient in the potent lipoid extracts; and very serious doubts as to
the activity of testicular extracts have been expressed by Professor
Cushny.

The possibility must be borne in mind that the use of thyroid and
other gland extracts that have a definite effect on metabolism is not
devoid of risk to cells that are gradually undergoing involution;
for, by stimulating metabolism unduly, the existing vitality may be
prematurely exhausted and, though for a time there is a gratifying show
of energy, it is but a flash in the pan that precedes a more rapid loss
of function. We are irresistibly reminded that “no man putteth new wine
into old bottles: else the new wine doth burst the bottles.”

At the present time it would be unwise to express a dogmatic opinion
about the relation of the endocrine glands to normal old age. That old
age is due to endocrine insufficiency or loss of balance cannot be
regarded as proved, and it is probably safer to regard changes, such
as atrophy, in the various glands of internal secretion as concomitant
with, rather than causal of, those in the senescent body.


METCHNIKOFF’S PATHOLOGICAL EXPLANATION

As an alternative to the belief that there is an inherent quantum
of vitality which may be harmfully or beneficially influenced by
environment and the wear and tear of life, it has been suggested that
the process of ageing depends solely on external factors and that
either there is no intrinsic limitation to the life of the organism or
that the possibility is entirely cast into the shade by predominance of
extrinsic influences. This doctrine is free from any tinge of fatalism
and has the advantage that it is a direct stimulus to efforts in the
direction of hygiene in all its forms; for as things are now old age
owes its discomforts to superadded and in most instances avoidable
complications. Élie Metchnikoff, as is well known, attributed the
senile accompaniments of advanced years to pathological and preventible
causes, namely toxaemia induced by alcohol, syphilis, and especially
by bacterial activity in the colon which in common with Barclay-Smith
and Arbuthnot Lane, he regarded as a harmful phylogenetic relic,
this point of view being expressed by the epigram “the longer the
colon the shorter is life.” He considered that the putrefactive
bacteria in the colon produce phenol, indol, skatol, and aromatic
bodies which cause degenerative changes in the cells of the body;
and that the more resistant macrophages, which do not attack healthy
tissues, absorb the damaged cells. He therefore employed means to
prevent excessive bacterial activity in the large intestine, and in
addition to care in diet so as to diminish the risk of introducing
bacteria into the alimentary canal, he advocated the destruction of
putrefactive bacteria in the colon by means of sour milk and cultures
of _Bacillus bulgaricus_, which form lactic acid and thus render the
contents of the bowel acid and unsuitable for the growth of the harmful
micro-organisms. Metchnikoff thoroughly practised his doctrine, but he
did not begin his regime until he was well over fifty, and, in spite of
several severe illnesses which had damaged his heart, he lived longer
than any of his family and passed the 70th milestone. His views on the
method of production of senility aroused great interest and criticism
not only from Marinesco,[122] Léri,[123] Sand, Laignel-Lavestine,
and Voisin, who disputed the reality of the macrophages devouring
the cells of the central nervous system, and Ribbert[124] who denied
the existence of such a physiological intoxication and ascribed old
age and death to the inevitable physico-chemical changes incident
to life, but also from Salimbeni and Gery,[125] working in the
Pasteur Institute, who while supporting most of his contentions did
not consider that they provided the whole explanation, _e.g._, the
involution of the ovaries at a fixed age was not thus accounted for.
The means Metchnikoff advised for the postponement of senility and
death were on much broader lines than the popular conception summed
up by “sour milk” might suggest, for he expounded the philosophy of
orthobiosis or a correct method of living.

That intestinal toxaemia due to stasis has a very important influence
in producing disease cannot be doubted, and Sir Arbuthnot Lane[126]
has brought this prominently to our notice; while clothing in modern
language the old ideas of the _primae viae_ he recalls to our memory
Abernethy’s[127] panacea for many ills of the flesh, namely a blue pill
at night followed by a mixture of gentian and senna in the morning.

Among his collaborators Mr. Ernest Clarke[128] has insisted on the
premature ageing of persons with intestinal stasis. From the analogy
of syphilis, alcoholism, and other intoxications, which may produce
degenerative changes simulating those found in old age, the hypothesis
of intestinal toxaemia gains a certain amount of support, and it may
not be so easy to exclude the agency of intestinal toxaemia as in the
case of syphilis and some intoxications. But intestinal toxaemia may,
as far as can be judged, be absent in healthy old age, and conversely
be present in early life without causing the phenomena of old age.
Further objections have been raised:--why should intestinal toxins be
harmless for 40 or 50 years and then exert such a serious influence?
why should women who are more subject than men to constipation be
more long-lived; and that in constipated persons the faeces, as shown
by Schmidt and Strasburger, contain fewer living bacteria than in
health.[129]

As applied to normal old age and death this hypothesis is pathological
and therefore has rather failed to interest those who are working at
the biological aspect. Perhaps the most that can be safely concluded
in balancing the pathological and biological arguments is that while
Metchnikoff’s view may be partially true it does not account for
all senile changes, and that normal old age or senescence cannot be
regarded as the result of toxins absorbed from the alimentary canal.


OLD AGE OF CELLS AND CARCINOMA

The relation between ageing of the cells on the one hand and the
development of carcinoma on the other hand is a subject of great
interest. According to Karl Pearson’s[130] statistical enquiry the
incidence of carcinoma reaches its maximum at the age of 46 years in
women and 56 years in men; Lazarus-Barlow[131] concluded that the
range of years over which cancer is likely to occur is practically the
same in the two sexes, namely 46 to 64, and that among 4659 cases of
malignant disease there were only 35, or 0·7 per cent, over 80 years
of age.[132] The cancer age, therefore, coincides with the waning of
maturity and the onset of old age; that carcinoma is rare in very
old persons is also shown by the occurrence of one case only among 71
centenarians collected by Sir George Humphry. Laurent[133] considered
that whereas longevity depends on a condition of vital equilibrium,
the development of cancer is due to a want of this equilibrium, to a
state of anarchy, and that the factors disposing to orderly vitality
are conducive to longevity and antagonistic to the development of new
growth. The reason why malignant growths are prone to appear with
the onset of old age has naturally been the subject of much debate.
According to Thiersch degeneration lessens the controlling influence
normally exerted by connective tissue on epithelium, the inherent
proliferative capacity of which then runs riot. Ribbert believed
that from loss of resistance or diminution of surface tension in the
connective tissues post-natal “rests” of epithelium were produced
as the result of irritation and that these displaced cells then
grew because there was no controlling opposition. Adami suggested a
reversion of the highly specialized epithelial cells to a simpler form
with powers of proliferation, the cumulative habit of growth taking
the place of the habit of work, and practically anticipated the more
modern view. According to Hastings Gilford[134] malignant disease is
a premature cell senility and the result of the partial reversion of
immature or adult cells to an embryonic or quasi-embryonic state.
From a study of senescence in dogs Goodpasture[135] concludes that
degenerative changes in the cells lead not only to death of some
cells but to dedifferentiation of others, which, becoming simpler in
structure and function, recover their juvenile power of growth in
varying degrees, and that hence metaplasia and tumour growths occur as
accidents of commencing old age. A little later Oertel[136] insisted
on his view that cancer is not an embryonic reversion or a specific
change in the cell but a phenomenon of senescence--a degenerative
proliferation depending upon disturbances in the nucleus plasma
relations, specifically upon the loss of nuclear chromosomes; from age
or degeneration the tumour cell loses the higher functional chromosomes
and retains the genetically older and more resistant ones controlling
reproduction and vegetative activities; thus there arises a race of
cells without the differentiation of undegenerated cells.

These various expressions of opinion would justify the conclusion that
with the onset of old age the degenerative processes in the cells lead
to the production of less specialized cells which have the compensating
property of more vigorous growth, and that in certain circumstances,
one of which is very probably a diminished power of resistance on the
part of the surrounding tissues and another, and very important one,
irritation in some form or another, riotous proliferation of the cells
invades the adjacent parts. That the conditions necessary are usually
local is strongly suggested by the appearance of the new growth at one
spot only and by the frequent absence of recurrence after free removal.
There may be a premature local senescence of the tissues, just as there
is premature old age of the body generally, and this would explain
the exceptional occurrence of malignant disease in early life or long
before the usual time.




VI

NORMAL STRUCTURAL CHANGES IN OLD AGE


Physiological old age, namely a process of involution and atrophy
uncomplicated by superimposed pathological changes, is extremely
rare; pathological processes may initiate and hurry on a condition
imitating old age, and indeed the morbid changes found after death in
old people commonly show the lesions of past infections in addition
to those of physiological involution, and the longer life lasts the
greater the probability that changes due to disease will accumulate.
It is therefore difficult to determine accurately where physiological
involution ends and pathological lesions begin, and there has been much
confusion between physiological old age and pathological senility.
It must, on the other hand, be admitted that the ideal condition of
physiological involution without some definite evidence of superadded
pathological change hardly ever comes before us. In fact at the best
old age is almost always but relatively physiological, in other words,
as Metchnikoff wrote in 1903, there is at present, from the conditions
of inharmonious environment, no chance of a really physiological old
age and death for mankind. But the view that old age is invariably the
accumulated product of multiple injuries due to infection and poisons,
or that it is due to arteriosclerosis (Boerhaave, Haller, Demange) is
an entirely different proposition and does not fit in with biological
knowledge. While fully recognizing the difficulties an attempt may be
made to tabulate the natural changes accompanying and responsible for
old age, and to contrast them with the pathological changes commonly
complicating the normal structural involution of the human body.

The general atrophy of old age, as grossly shown by loss of weight,
does not proceed equally in all parts of the body. The supporting
fibrous tissues of the body and organs certainly atrophy less than
the nobler, because actively functional, cells of the organs; it is
difficult to estimate the atrophy of the fibrous tissues, for from
shrinkage of the parenchyma of organs and of muscles the fibrous
framework stands out in greater prominence. Some proliferation or
replacement fibrosis follows atrophy of the nobler tissues, and
pathologically infection may cause fibrosis. But that the fibrous
tissue does to some extent share in the general atrophy is rendered
probable on the analogy of the change in the allied tissue of bone
which undergoes rarefaction and thinning. The subcutaneous and
perivisceral stores of fat diminish out of proportion to the fibrous
supporting tissues around them. The place of the fat in the fat cells
may be taken by fluid--serous atrophy--or the cells may simply revert
to the condition of connective tissue cells. In passing it may be
pointed out that it is curious that with the diminished metabolism of
old age the stores of fat are not increased as they are in similar
circumstances in adult life; Is it due to a widespread atrophy of the
connective tissue cells that store fat? If so, an accumulation of fat
in the liver might be expected, but this is not so. Possibly it is the
result of deficient assimilation. The heart, as Councilman[137] has
shown, is on the whole better preserved than the other organs; but it
might well be argued that the existence of such a cardiac condition is
a determining factor in the attainment of advanced age.

_The skin_ is dry, thin, smooth, glossy from atrophy, inelastic like
parchment, and is wrinkled from degeneration and disappearance of the
elastic tissue, subcutaneous fat and muscular fibre. These changes
are most advanced on the face, especially the forehead, and backs
of the hands from exposure. The degeneration of the elastic fibres,
recently studied by Kissmeyer and With,[138] gives a characteristic
mesh-like appearance, depending on the rigid wrinkles, to the skin,
which takes a yellow tint. The ivory pallor and coldness are due to the
diminution in the capillaries; the skin may show areas of pigmentation
and leucodermia--changes described by Sir Lenthal Cheatle as due to
the wear and tear of life (biotripsy); in a woman aged 93 Salimbeni
and Gery described almost complete disappearance of the papillae
and of the collagen fibres. The pigmentation has been regarded as a
means of protection, for there is a relation between it and malignant
disease, the latter being prone to occur when pigmentation fails
(Pringle[139]). These atrophic changes are far commoner on the backs
than on the palms of the hands, and it is noteworthy that among
Cheatle’s[140] 200 collected cases of malignant disease of the hand
there was one only on the palm. The subcutaneous fat is diminished in
amount, which is regarded by Sir Arbuthnot Lane, though not with any
special reference to old age, as one of the many results of colonic
toxaemia. The yellow fat contains excess of cholesterol. There is
diminished secretion by the sweat and sebaceous glands, and from this
cause and the diminished vascularity there is less loss of heat to
correspond with the slower metabolism.

_Hair._--Greying or whitening of the hair occurs commonly in old age,
but not universally for some centenarians have retained the natural
colour of the hair; coarse jet-black hair is specially prone to whiten
early. The change in colour has been ascribed by Metchnikoff to the
action of phagocytes (chromophages) which invade the roots of the hairs
and carry off the pigment granules. Like the arcus senilis it may occur
quite early in life and without any other indication of age, and is
often hereditary; as the sage of Norwich wrote, “Hairs make fallible
Predictions, and many Temples early Gray have outlived the Psalmist’s
Period.”[141] Lord Bacon[142] indeed said, “Hasty gray hairs, without
baldness, is a token of long time; contrarily, if they be accompanied
by baldness.” But baldness is often due to seborrhoea and so only
secondarily connected with advanced age. In some rare instances the
hair already grey or white has been known to regain its normal colour;
the late Sir Charles Cameron[143] recorded this event in his own life
after an accident confining him to bed for some months in his eightieth
year, and refers to the hair of a man aged 90 years returning to
its original brown colour; cases were also reported by Graves.[144]
Velasquez de Tarente[145] recorded an abbess who after an illness which
promised to be fatal in her hundredth year had a crop of brown hair,
and, like Sir Charles Cameron, put on weight. Four other cases are
given by Sir John Sinclair[146] in persons aged 80, 104, 105, and 114
years. Baldness may be definitely due to thyroid insufficiency and not
to atrophy of the hair follicles and sebaceous glands.

    A pensioner aged 75, whom I saw with Major R. J. C. Thompson,
    in the Royal Hospital, Chelsea, with baldness and a grey
    beard, was given thyroid extract, as he was thought to
    have hypothyroidism; his general condition then improved
    wonderfully, and his scalp became covered with dark brown hair
    which had to be cut at intervals. Parkinsonian tremor was
    rather more obvious during the first six months that he was on
    thyroid treatment.

The hair of the body may become scanty and lose its tendency to curl.
Excessive growth of hair (hypertrichosis) in women after the menopause
is an indication of disordered endocrine balance (loss of ovarian
internal secretion?) and is only so far an accompaniment of age; it may
be seen in comparatively young women from various causes.

_The nails_ are often longitudinally ridged, brittle, hard, and
thickened; but onychogryphosis is rather the result of neglect or of
disease than solely of old age.

_The brain_ as a natural result of atrophy becomes lighter; Boyd’s[147]
tables show that the male brain is 3 oz., and the female brain 4
oz., lighter in persons over 80 years of age than in the decade 20 to
30. The convolutions, therefore, become separated and the amount of
cerebrospinal fluid greater. The atrophy is not uniform, being less
in the posterior third than in the anterior two-thirds. The nerve
cells become smaller, pigmented, and degenerate. The brain is said
by Cerlette to be affected by a process special to old age--miliary
necroses scattered over the cortex and associated with changes in the
small arteries which show remarkable knots; a condition which suggests
a pathological softening secondary to arteriosclerosis, especially
as the change does not come on constantly at a definite age period.
Cavities with thickened walls, possibly due to miliary haemorrhages,
or to softening around the vessels are also described. Metchnikoff’s
description of phagocytic destruction of the nerve cells by macrophages
has been seriously questioned and thought to be based on erroneous
observation, the glia cells being regarded as macrophages (Marinesco).

The spinal cord shows an increased number of amyloid bodies, some
diffuse sclerosis, often obliteration, by epithelial proliferation, of
the central canal, and atrophy with pigmentation of the nerve cells,
especially in the anterior cornua. The membranes may contain small
calcareous plaques.

_The arcus senilis_, due to infiltration with fats, especially
cholesterol and lipochrome, and to degeneration of elastic tissue at
the periphery of the cornea, is often associated with arteriosclerosis
(Monauni[148]). It is not a necessary accompaniment of age; among 321
persons over 80 years of age, it was absent in 114, or 35·5 per cent
(Humphry); and it is well known that like grey hair, it may occur
in those young in years. Nascher,[149] the author of _Geriatrics_,
had an arcus senilis as a schoolboy. Rigidity and flattening of the
crystalline lens lead to presbyopia, which may be premature and due to
toxaemia, among the causes of which Ernest Clarke[150] gives intestinal
toxaemia a high place. The power of accommodation is also impaired by
weakness of the ciliary muscle brought about in the same way.

_Skeleton._--The atrophy characteristic of senescence is well shown
in the fixed tissues of the bony skeleton. Though the bones do not
as a rule alter materially in size or shape, they do so markedly in
substance from rarefaction and absorption, the latter taking place
mainly from the inside of the bones and especially the cancellous
tissue, the medullary cavity and the Haversian canals becoming larger
(senile osteoporosis). Hence fractures near the joints, particularly
intracapsular fracture of the neck of the femur, are favoured. The
absorption of the alveolar border of the jaw is intimately connected
with the loss of the teeth, and brings the mental foramen to the top
of the edentulous mandible. The angle of the jaw at the junction of
the body and the ramus now opens out and comes to resemble that of an
infant. It is often stated that the angle of junction of the neck and
shaft of the femur becomes less, more of a right angle, but Humphry
regarded this as exceptional.

From muscular weakness the back becomes bent and as a result the
vertebrae become altered in shape. Ossification of the anterior common
spinous ligament--a change analogous to rheumatoid osteophytes around
the more movable joints--is an added and not uncommon change but, like
calcification of the costal and laryngeal cartilages, it is a morbid
process, and when advanced constitutes spondylitis deformans. The
intervertebral discs undergo some loss of elasticity and atrophy,
thus contributing to the loss of height. The cranial bones are usually
thinned, and the parietal bones may show symmetrical or nearly
symmetrical oval areas of excessive absorption of the outer and even of
the inner table, so that the epicranium and the dura mater may be in
contact. These areas which are close to the longitudinal fissure must
not in the case of ancient skulls be mistaken for examples of early
trephining. The bony sutures tend to become obliterated. Instead of
thinning and loss of weight the skull, especially the vault, may show
thickening and be heavier than normal--a change involving chiefly the
inner surface and ascribed by Sir George Humphry to shrinkage of the
brain.

Calcification of the costal and laryngeal cartilages, which have
a yellow tint from fatty change, is, like a similar change in the
arteries, pathological and not part of the process of senescence. Thus
among 10 recorded necropsies on centenarians the costal cartilages were
calcified in 2 only. Calcification of the costal cartilages interferes
with the respiratory movements and was regarded by Sir George Humphry,
who tested for it by estimating the elasticity perceived when gentle
pressure is exerted on the lower part of the sternum, as a bad omen
for the future.

_The teeth_ are usually, but not invariably, few in the aged, for care
or lack of it, the accumulated effect of long-continued mechanical
injuries, altered calcium metabolism, and diminished resistance to
infection will necessarily influence the amount of decay. Statistics,
especially Humphry’s, show that in extreme old age very few teeth are
present, and it is tempting to correlate the diminished provision for
mastication with the lessened need for food. Sir Isaac Newton, however,
at the age of 85 was said to have lost one tooth only. The numerous
reputed instances of a third dentition can be explained only by the
appearance of a previously buried tooth through the atrophying gums,
for a genuine third dentition would necessitate the presence of dental
germs which do not exist.

_The gastro-intestinal tract_ shows atrophy of the muscular coat and
its secreting glands, so that dilatation of the thin-walled, pale
stomach and colon occur on less provocation than in adult life and
digestion is impaired; from lack of mucous secretion combined with
loss of motor vigour constipation is common. It may be added that
hypertrophy of the prostate by interfering with peristalsis of the
colon has been thought to cause gerontal constipation (Hollis[151]).
The pancreas shows fibrotic atrophy and becomes smaller and harder.
From the loss of fat and muscular atrophy visceroptosis is not uncommon.

_The liver_ diminishes in size and weight by about one half; atrophy
of considerable areas may expose the vessels and ducts on the surface
of the organ. Boyd’s tables show a difference of 18 oz. between
the weights in persons in the decade 20–30 and in those over 80.
Microscopically atrophy of the lobules and of the cells in the
centres of the lobules have been described (Luciani[152]), but the
latter change is not constant, for in a woman of 93 Salimbeni and
Gery[153] definitely noted that the cells were not atrophied. That
such atrophy of the liver cells is pathological is perhaps supported
by D. Symmers’s[154] observation that in the pancreas of such cases
the islands of Langerhans may show moderate enlargement, as if to
compensate for failure of the glycogenic function of the liver.
Pigmentation of the cells by a lipochrome is excessive, and the name
brown atrophy has been applied to the condition which is seen in the
other viscera of the old.

_The lungs_ become smaller, lighter, and the elastic tissue
degenerates; this is atrophous emphysema, and the chest capacity
diminishes. Roussy and Leroux[155] found that these lungs commonly
show endarteritis obliterans and fibrosis, conditions which favour
infarction, infection, and the terminal bronchopneumonia to which the
aged are so prone.

_The voluntary muscles_, according to Durante,[156] contain many fibres
with large globules of fat; but Jewesbury and Topley,[157] who describe
coarse fat globules mingled with brown pigment in the immediate
neighbourhood of the muscle nuclei in 50 per cent of cases of various
kinds, and almost constantly in old subjects, regard this condition as
independent of true fatty degeneration, and are doubtful if it has any
pathological significance. Excessive fatty and fibrotic change is found
in cases of senile paraplegia without any lesion in the spinal cord or
brain.

_Heart._--Some difference of opinion exists as to the condition of
the heart; Parkes Weber[158] says that the only true senile change
is diminution in size and weight; this as it is worded is no doubt
correct; but pure atrophy is less rare in the heart than in most parts
of the senile body. Charcot[159] indeed stated that it does not atrophy
in old age, but preserves the dimensions of middle life. The heart may
even hypertrophy in old people; this is pathological; Councilman[160]
found it in 248, or 43 per cent, of 580 persons over 60 years of age,
and could not refer it to aortic or renal arteriosclerosis or to the
diminished capillary area in the skin; but the average blood pressure
158 systolic/88 diastolic of the cases with cardiac hypertrophy was
higher than that 130/78 of the others.

Fatty degeneration of the myocardium is very frequent; Charcot stated
that at the Salpêtrière it was almost constant in old women, but
according to Councilman there is no clear evidence that it produces
permanent injury or functional insufficiency; he noted some fibrosis
in 15 per cent of his cases. Atrophy of the epicardial fat--serous
atrophy--is common, and increase of the so-called lipochrome pigment in
the muscular fibres which become smaller and fewer--brown atrophy--is
frequent as it is in the other organs in old age.

Chronic valvulitis and subendocardial fibrosis are, like
arteriosclerosis, common morbid changes.

_Arteriosclerosis_, contrary to what has been stated by Huchard and
others, is not constant in a considerable degree in old people, and
therefore cannot, as Demange and others considered, be regarded as
the cause of the atrophic changes seen in old age. Arteriosclerosis
is due to several factors, namely, infection and intoxication of
various kinds and to damage caused by long-continued high arterial
blood pressure. The primary changes are degeneration and weakness,
however brought about, in the middle coat. Ophülz[161] has recently
discussed the question whether the degeneration is entirely or largely
a senile change; if it were so, the curve of the incidence of arterial
sclerosis would begin gradually about the age of 40 years, so as to
include premature cases, and rise slowly until the age of 55 years,
when there would be a sudden increase to 80 or 90 per cent, and at
the age of 70 it would be improbable that any one would be free from
well-marked arteriosclerosis. He found that the curve of incidence was
very different from this; beginning much earlier its rise is gradual
all the way without any sudden increase, and indeed seems, if anything,
to be retarded by old age. Old persons may have practically healthy
arteries, so, although arteriosclerosis may undoubtedly produce atrophy
and senile changes in the tissues and organs by diminishing the blood
supply, for example in the case of the red granular kidney, it cannot
be regarded as the causal factor in healthy old age.

The primary calcification of the middle coat, sometimes called
Mönckeberg’s sclerosis, which leads to the formation of regular
rings in the degenerated muscular media and the “pipe-stem” arteries
associated with senile gangrene, may be independent of, or combined
with, endarterial sclerosis. It follows fatty degeneration of the
media, which is the commonest form of medial degeneration in the aged,
and specially picks out the elastic fibres.[162] The femoral, tibial,
radial arteries and the aorta are most often affected. It is difficult
to estimate its incidence, but that it is not very common, at any rate
in a high degree, seems probable from the comparative infrequency of
its detection in _x_-ray examinations of the lower limbs in old people.
It would be natural to associate its occurrence with the rarefaction of
bone that goes on in advanced life, and so to consider it as in some
respects different from the secondary calcification in endarteritic
sclerosis; in answer to an enquiry Professor W. T. Councilman of
Harvard kindly wrote to me that he did not regard calcification as
characteristic of any particular type of arterial disease, lime salts
being in certain cases more easily deposited in any pre-existing
lesions. Klotz describes fatty and calcareous change in the middle
third of the media of the aorta as quite characteristic of senescence.

Cazalis’s famous aphorism “man is as old as his arteries” is true in
so far that the state of the arteries is a good index of the general
condition, for they are extremely prone to suffer as the result of
infection, toxaemia, and strain; strictly speaking, therefore, the
state of the arteries is not so much an index of the individual’s age
as of his adventures.

Phlebosclerosis, analogous to arteriosclerosis, is common, and
dilatation, often due to stagnation and lack of the normal _vis a
tergo_, of the veins is a familiar change in the aged.

The capillary area is diminished in the skin and elsewhere, but not
uncommonly there are dilated venules or angiomas on the skin; the
latter, commoner on the trunk and upper limbs and in men, were formerly
known as “de Morgan’s spots” and were thought to accompany cancer, but
the association is only due to a rough correspondence of their age
incidence.

_The blood_ of healthy octogenarians may not show any departure from
that of the earlier periods of life as regards the number of the reds
and the amount of haemoglobin (Hansen[163]), though some have described
a secondary anaemia. Thus in a female centenarian Macnaughton[164]
found slight secondary anaemia with a normal number of leucocytes,
the differential count showing a relative lymphocytosis. The red bone
marrow diminishes, its place being taken by fat cells.

_The lymphoid tissues_ undergo atrophy all over the body including the
leucoblastic bone marrow, but though it does not appear that the blood
shows any definite change in the leucocyte count it is tempting to
correlate the diminution of resistance to acute infections, such as
pneumonia and erysipelas, with the atrophy of the lymphoid tissue. The
alimentary canal often shows lymphoid atrophy in a high degree, but two
normal Peyer’s patches were present in a man reputed to be 106 years
old (G. Rolleston[165]).

_The spleen_, in common with the lymphoid tissues elsewhere, shows
atrophy, sometimes to an extreme degree, so that instead of the normal
weight of 7 oz. it weighs a few drams only. The capsule is thrown into
folds, and is somewhat opaque; from atrophy of the pulp and Malpighian
corpuscles the vessels and fibrous trabeculae become prominent. _The
thymus_, contrary to the general opinion that it undergoes involution
long before puberty, has been found by Hammar[166] to increase in size
up to puberty when involution begins, but proceeds so gradually that
even in old age it is functional.

The _thyroid_, unless there is cystic change, is smaller than
natural; thus out of 40 thyroid glands from individuals between the
ages of six months and 77 years the smallest was in a woman aged 77
(Hale-White[167]). In colour it is darkish brown and on section rather
dry. Dr. Donaldson, Lecturer on Pathology at St. George’s Hospital, has
specially examined 19 thyroid glands from patients between the ages of
57 and 93; of these five showed cystic change; they all showed increase
in the amount of fibrous tissue which was progressive with age, and in
the absence of cystic change the size of the vesicles and amount of
colloid material were diminished.

_The Parathyroids._--From examination of a number of specimens Dr.
Donaldson finds that in old people the parathyroids appear to be
free from retrogressive changes, but he cautiously requires further
experience before concluding that this is the rule.

The _adrenals_ show involutionary atrophy in common with the body as
a whole, but sometimes the cortex is enlarged from excess of lipoids,
usually associated with considerable atheroma, and may also show
adenomas. As the increase in size of the adrenals is cortical its
relation to high blood pressure, if any, is that of a remote result,
namely from arteriosclerosis, and not causal as has been suggested.
According to G. M. Findlay[168] the amount of lipochrome in the cells
of the adrenals increases with advancing years and is accompanied by
the appearance of melanin in their nuclei.

The _kidneys_ show definite atrophy, and Councilman,[169] who has
recently made a study of them in 580 persons over 60 years of age,
calls the condition chronic atrophic nephropathy. The fat in the renal
pelvis is more obvious than usual, the capsules are slightly thickened
and occasionally but by no means always adherent, the surface finely
rough and sometimes showing small cysts, but the large and irregular
depressions characteristic of a granular kidney are not common. There
are, however, areas of fibrosis, and the cortex and medulla are equally
atrophied. Microscopically some glomeruli are fibroid, others smaller
than natural. In three-fourths of his cases the renal vessels showed
arteriosclerosis due to primary atrophy of the media with compensatory
hypertrophy of the intima; but Councilman gives reasons for hesitation
in accepting the obvious conclusion that the senile kidney is the
result of the vascular change.

_The prostate_ shows some degrees of enlargement after the age of
fifty in the vast majority of men, but in only a percentage of
these are there symptoms referable to it. Kenneth Walker[170] finds
that the maximum size is reached at the age of 60 and that from then
onwards there is a slow diminution in size; among 340 men between
80 and 90 there were 11, or 3·2 per cent, and among 92 men between
90 and 100 one only with hypertrophy of the prostate (Humphry). The
causation of prostatic hypertrophy has been much discussed; that its
association with arteriosclerosis (Launois[171]) is anything more than
a coincidence, the two conditions being common in the later years of
life, seems improbable; Walker found the two associated in 10 per
cent, and he regards the change as part of a general enlargement
and thickening of the peri-urethral, sub-cervical, and sub-trigonal
glands, and, as the interstitial cells in the testes become fewer
and degenerated, he considers that the prostatic enlargement is
possibly a degeneration connected with a disturbance of the endocrine
balance. Nemenow[172] argued that prostatic enlargement was due to
proliferation of the interstitial cells following senile atrophy
of the seminal tubules of the testes, but K. Walker found that in
prostatic enlargement the interstitial cells are diminished rather than
increased in number. An interesting parallel has been drawn between
the involutionary changes in the mamma and the prostate, and it is
probable that the same underlying factor is at work in both (Walker,
Paul). Hertoghe[173] regarded some cases of prostatic hypertrophy as
due to senile dysthyroidism, and recently benefit has been reported
from thyroid medication and also from prostatic extract. Dr. Leonard
Williams has told me of cases, as yet unpublished, showing well-marked
relief of symptoms and diminution in the size of prostatic enlargement
after doses of thyroid extract (½ grain once) and colloidal iodine
(one dram three times) daily. The prostatic plexus of veins is often
enlarged and may contain phleboliths.

The _testes_ become smaller, softer, and commonly show some atrophy of
the tubules with disappearance of the epithelial lining and thickening
of the basement membrane; but the testes of old men may be free from
any such change and the spermatozoa in the vesiculae seminales may
be active. According to K. Walker the interstitial cells gradually
diminish in number from the age of 30, but they may be present in men
over 80, and Mott[174] remarks that their persistence may account for
an increased and perverted sexual appetite, due to stimulation of the
desire without the power to perform the sexual act.

The _penis_ becomes smaller, often retracted, the _glans_ harder, and
the _scrotum_ smaller.

The _ovaries_ become shrivelled and fibrotic; the ova disappear
or small cysts may form. It is difficult to find statements about
the presence or absence of interstitial cells in the senile ovary.
Professor Turnbull has kindly informed me that in old women an
occasional cell which might be, but is not certainly, an interstitial
cell is visible, and that if they are interstitial cells their number
must be small and their development poor.

The _uterus_ becomes small, its cavity round, and the cervical canal
may be obliterated. The _external genitals_ atrophy.

The _mamma_ in women shows involution changes and when excessive
(cystic disease) these may, as Paul[175] has pointed out, be compared
with prostatic enlargement in the male.




VII

PHYSIOLOGY OF OLD AGE


The basis of the physiology of old age is progressive diminution in
functional activity, which corresponds to the characteristic structural
atrophy of the organs and tissues. Thus the lowered functional activity
of its glands is manifest in the dry skin; according to Haneborg[176]
there is usually a fall in the percentage of hydrochloric acid in the
gastric juice, though Bell[177] disputes this. The lessened amount of
mucus from the intestine probably plays some part in the tendency to
constipation. Other evidences of lowered metabolic rate are seen in
the diminished efficiency of the acid-base equilibrium (MacNider[178])
and the increased degree of urea-nitrogen in the blood, as shown in
50 per cent of 41 persons between 70 and 88 years of age examined by
Rappleye.[179]

_Temperature._--Before the era of the clinical thermometer it was
supposed that the body temperature of the aged was below normal. This
belief was part of the ancient view that the cause of old age was
exhaustion by the natural heat of the radical moisture which, like lamp
oil, supported the innate heat and with the passage of years could not
be supplied as perfectly as before; as a result of this loss of radical
moisture the body was thought gradually to dry and cool.[180] But it is
now known that the internal temperature is almost constant at all ages,
and Charcot proved that the only real difference is that the axillary
is lower than the rectal reading; this is due to the diminished
vascularity of the skin and to the corresponding fall in the loss of
heat, which again may be correlated with the lower metabolic rate of
old age. Aub and Dubois’[181] observations on six men between 77 and
83 years of age, mainly with arteriosclerosis, granular kidney, and
emphysema, showed that the basal metabolism was 12 per cent below the
average for men between 20 and 50.

Blunting of sensibility to pain is a beneficent process, suggesting
that with the gradual process of involution and approach to a
physiological death the need for the warning normally conveyed by
symptoms is no longer needed. This is connected with the simultaneous
atrophy of the nervous tissues which look after the conduction,
perception, and reference of pain. The latency of disease, as shown by
an absence of the characteristic symptoms observed in earlier adult
life, is often remarkable in the aged. Thus death may occur suddenly
from extensive but entirely unsuspected pneumonia; the passage of
biliary or urinary calculi may be unaccompanied by the violent colic
of these events in ordinary cases, and extensive malignant disease may
exist without any definite localizing discomfort. This failure in the
power to react is also shown in fevers and infections (_vide_ p. 142).

Cutaneous sensation is little affected, and indeed the aged are very
sensitive to cold. Taste and smell are impaired, and presbyopia is due
to changes in the crystalline lens. The pupils are contracted and the
iris sluggish. From weakness of the orbicularis palpebrarum muscle
ectropion and epiphora may noticeably change the facial appearance.
With advancing years hearing commonly becomes less acute from various
causes, and after 60 there is a successive decrease in the number
of persons with normal hearing. According to Albert Gray[182] there
is probably a characteristic form of deafness for the higher notes
of Galton’s whistle in all old people, even when for all practical
purposes there is no obvious defect or tinnitus; this he regards as due
to progressive atrophy of the ligamentum spirale. Chronic progressive
labyrinthine deafness, due to atrophy of the auditory nerve and
fibrosis of the ductus cochleariae, is the most common condition in
persons over 60. Fixation of the stapes frequently causes deafness,
and the sequels of middle-ear disease accumulate with advancing years.
Gouty eczema of the external auditory meatus and collections of wax may
seriously interfere with hearing. Tinnitus in the elderly is commonly
associated with high blood pressure and arteriosclerosis.

_Appetite_ for food is sometimes capricious; old people may eat
excessively, possibly because the pleasures of the table are the only
ones to which they feel equal.

_Muscular movement_ is slow and somewhat uncertain, and the reflexes
are diminished except in the presence of sclerosis of the spinal cord.
According to Moebius the _knee-jerk_ is often absent in normal old
persons, but Sternberg, by employing methods of reinforcement not
available in Moebius’ time, found that it was invariably present even
in the tenth decade.

The _sleep_ of the aged is less continuous, and from interruptions
often appears to them to be much less than it really is. There is
often a tendency to irregularity, bad and good nights alternating. But
too much attention to disturbed sleep in the aged must be avoided, as
hypnotics are inadvisable, and it has been urged by Sir Hermann Weber
and others that too much sleep is more harmful than too little.

In old age the _mental condition_ varies in different individuals
according to their previous character and their present physical state.
Freedom from sexual and other perturbations often renders the minds of
old people calm, tolerant, less susceptible to disappointed ambition,
and philosophic when the part of spectator has been accepted in place
of that of actor in life’s drama. In what may be regarded as normal old
age psychical activity diminishes; not only do initiative, elasticity,
and originality fail, but new ideas and fresh lines of thought are
assimilated with difficulty; hence the old are commonly conservative
and _laudatores temporis acti_. Mental fatigue occurs more readily and
the power of concentration and attention is impaired so that the old
may appear deaf; the mind begins to show disintegration and a return to
the primitive condition in which each act demands individual care; it
has indeed been said that old age is nothing but progressive fatigue.
A less agile memory for names is commonly one of the early symptoms of
senescence, and long precedes the characteristic loss of memory for
recent events while that for the remote past remains, as if the nerve
cells were photographic plates which in course of time have all become
occupied with impressions. With commencing failure of memory there
is often a tendency to make the same remark or tell the same story
repeatedly, to mislay things, and unconsciously to become careless
about personal appearance and habits. As a kind of protest against the
inevitable there may, in the early stage of old age, be a tendency
to ape the young and to conceal the true age; thus a man may remove
the date of his birth from _Who’s Who_ and books of reference, and a
mother may delay the “coming-out” of her daughter. On the other hand,
at a later stage there may be the opposite desire to appear a wonderful
prodigy of senescence. The old are notoriously less subject to feel the
loss of relatives and friends by death; they become more self-centred;
this may be because retirement from active work switches their minds on
to their own feelings, and possibly in part depends on loss of touch
with the external world, resulting from failure of the sense organs.
This when exaggerated develops into selfish dependence and demands on
relatives. Senile vanity is not uncommon, and Eden Phillpotts[183]
remarks that all old people love to be in the centre of the stage, one
of the pathetic things in life being that they are seldom allowed to
be there. The ego-centric frame of mind may lead to hypochondriasis
with fads and meticulous attention to details of personal health and
to experiments in diet and patent medicines. Loss of control, due to
failure of the higher centres, engenders restlessness, garrulity,
emotional weakness, and peevishness. There may be considerable
variation in the moods, so that the deep depression of one day may
vanish the next, and irritability and apathy may alternate.

Regression, which closely corresponds to the “devolution” of Hughlings
Jackson, who argued that in disease the organism tends to retrace the
steps of its development, accounts for the phenomena of “the second
childhood.” Thus the old are prone to nervous apprehension, and liable
to suggestion and to hysteria which Rivers[184] defined as a protective
mechanism representing a recrudescence of the reaction to danger in an
early stage of animal development. Will power, like their gait, becomes
hesitant and uncertain. This devolutionary change progresses partially
and not universally; memory for personal names, as mentioned above, is
often the first to fail, because, like the mathematical faculty, it
has from the attendant difficulty a high place in the order of mental
processes; hence forgetfulness of personal names is a criterion of
psychical fatigue and neurasthenia (Dupuis[185]).

In old animals it is natural for the instinct of self-preservation to
fade, as is exemplified in the day-flies which in their larval stage
are well endowed with this property, and as their end draws near
animals seem to acquire an instinct for death comparable to that for
sleep. But in human beings, although they usually dislike old age,
there is generally what Matthew Arnold[186] called “a passionate,
absorbing, almost bloodthirsty clinging to life.” Metchnikoff specially
investigated this point and found hardly any instances in which death
was anticipated with the same feelings of pleasure as is sleep by the
weary. Considering the discomforts of many old people it is rather
remarkable how very seldom they endorse the words of the burial
service: “We give thee hearty thanks for that it hath pleased thee to
deliver this our brother out of the miseries of this sinful world.”
Various explanations have been offered for this want of harmony between
the mental and physical states of the old; it has been ascribed to
the idea of eternal punishment, and to the presence of pathological
conditions which bring on senility and death prematurely and thus
alter what should be the normal mental attitude of healthy old age.
In speaking of the usual fear of death in old people it should be
mentioned that shortly before death this commonly disappears and, as
G. E. Day,[187] R. W. Mackenna,[188] and Thompson and Todd point
out, the aged when seriously ill commonly regard death as a welcome
release; the famous William Hunter’s last words in his sixty-fifth year
expressed his sense of resignation: “If I had strength enough to hold a
pen, I would write how easy and pleasant a thing it is to die.”

_The Cardio-Vascular System._--The pulse rate is usually rather
increased in frequency as compared with that in adult life;
extra-systoles are so common in persons who appear otherwise normal
that they cannot be regarded as having any important significance.
Among Sir George Humphry’s collection of 824 persons over 80 years of
age one-fifth had an irregular or intermittent pulse.

Although, like arteriosclerosis, a well-marked high blood pressure
without evidence of renal disease, to which Sir Clifford Allbutt
has given the name of senile plethora or hyperpiesia, is common in
the decline of life, it is a pathological and not a physiological
change; and a distinction must be drawn between the gradually rising
blood pressure seen from birth onwards and an increase above that
normal to an arterio-vascular system that has been active for over
half a century. In the same way the venous pressure increases with
age (Hooker[189]). That a definitely high blood pressure in the
aged is pathological appears to be shown by observations quoted by
Councilman from the Peter Bent Brigham Hospital, Boston; among 94
patients (male and female) averaging 66 years of age, 44 per cent
with cardiac hypertrophy as shown by necropsy, had an average blood
pressure of 158 systolic / 88 diastolic, whereas the 56 per cent
without cardiac hypertrophy had an average blood pressure of 130/78.
In both series the differences between males and females were never
more than 7 mm. Hg. From observation of 102 Chelsea pensioners over 75
years of age Thompson and Todd found that the average blood pressure
was 145 systolic / 80 diastolic, estimations varying from 190/100 to
115/70, and that the average pulse pressure, or difference between
the systolic and diastolic pressures, was 67 mm. They came to the
conclusion that it was not possible to arrive at a normal blood
pressure for old people on account of the varying conditions of the
heart and arteries.[190]

The urine, in consequence of the lowered metabolism and general
atrophy, is somewhat diminished in quantity with a fall in the solids,
though the specific gravity remains about normal. The chlorides are
stated to be normal and the phosphates and urea to be diminished.
Slight glycosuria as a result of a low sugar tolerance (_vide_
Spence[191]) is not uncommon, especially in obesity. Prolonged
confinement to bed has been thought to be responsible for casts in
the urine. A trace of albumin is not rare; this may be due to various
factors, and in itself is not a cause for anxiety; but a well-marked
fall in the specific gravity is a sign of renal inadequacy which may be
preceded and anticipated by the discovery of nitrogen retention in the
blood.

_Sexual activity_ in man wanes generally speaking after 50, but there
are great variations in this respect, and sometimes there are periods
of considerable excitement in old men, often thought to be associated
with prostatic enlargement.

It would naturally be expected that _wounds_ and _fractures_ of bones
would heal more slowly in the old than in the young, and, according
to Carrel and Ebeling,[192] the cicatrization of human wounds varies
inversely, if accurately measured, with the age of the patient;
Humphry, however, found that, provided sloughing did not occur, wounds
and ulcers in the aged heal as quickly as in middle life, and that the
failure of union in intracapsular fracture of the neck of the femur is
due to want of apposition and not to the age of the patient.

In some respects the _reaction to drugs_ in the senescent body is
different from that in ordinary adult life. In old people absorption
from the alimentary canal is slow and this is particularly so with
gelatin-coated pills and drugs, such as cinchona, containing tannin,
which should therefore be avoided. The physiological response to drugs
is slower and more prolonged than in early life, so that for this
reason and from the frequency of constipation an accumulated action
is thought to be more likely to occur in the aged. It is sometimes
said that large doses are not borne well by the old and that morphine
is dangerous as it is in infants, but Nascher[193] states that if,
in order to obviate the paralysing effect of morphine on a weakened
respiratory centre, atropine is given before the morphine so that
their action can be timed to coincide, instead of giving them at the
same time when the effect of the atropine comes later, morphine can
be given in the same doses as in maturity. Purgatives may be required
in larger doses than in ordinary practice. According to Leonard
Williams[194] bromides are likely to produce mental confusion in old
people and if persisted in, even in ordinary doses, may be followed
by vascular thrombosis and permanent impairment of the intellectual
powers. Sedatives and hypnotics when necessary should be given in small
doses and discontinued as soon as possible; but they may be necessary
for restlessness which would otherwise seriously exhaust the failing
strength.




VIII

THE DESCRIPTION OF OLD AGE IN THE TWELFTH CHAPTER OF ECCLESIASTES


When first approaching the subject of old age every one must recall
the famous description in the first six verses of the twelfth chapter
of Ecclesiastes beginning “Remember now thy Creator in the days of
thy youth while the evil days come not, nor the years draw nigh when
thou shalt say I have no pleasure in them.” Formerly ascribed to King
Solomon (977 B.C.) the book of Ecclesiastes (in Hebrew Koheleth = the
preacher) has been shown by the higher criticism to date only from
the end of the third century B.C., and from internal evidence, namely
references to the brain, spinal cord, and other anatomical structures,
though expressed with poetic imagery, it may fairly be assumed that
a medical man was concerned with its construction. In his attractive
work, _A Gentle Cynic_,[195] the late Professor Morris Jastrow, jun.,
of Philadelphia explained that the book of Ecclesiastes as it appears
in the authorized version, consists of (i.) the original, cynical, but
good-natured _obiter dicta_ of the unknown dilettante who preferred
to veil his identity under the name of Koheleth, and (ii.) additions
and modifications made by various hands to render it more orthodox and
compatible with the tradition that it was written by Solomon; thus
the admonition “of making books there is no end and much study is a
weariness of the flesh” may very probably have been intended as a hint
that Koheleth’s views should not be taken too seriously. Following this
conception Jastrow reconstructed the text of the book of Ecclesiastes
to what he argued was its original form, and compared it with the more
modern writings of Omar Kháyyám and Heinrich Heine. As we all must have
speculated over the correct interpretation of the various metaphors in
this description of the last stage of life, the explanations offered
by others, such as Andreas Laurentius (1599),[196] Master Peter Lowe
(1612),[197] founder of the Faculty of Physicians and Surgeons of
Glasgow, Bishop J. Hall (1633),[198] John Smith (1665),[199] Richard
Mead (1775),[200] and Jastrow may be very briefly mentioned. The second
verse, “While the sun, or the light, or the moon, or the stars, be
not darkened, nor the clouds return after the rain,” is regarded by
Laurentius, Lowe, and Hall as referring to the ocular disabilities
of old age, whereas Smith and Mead consider that mental failure and
depression are meant. As regards the third verse, “In the day when
the keepers of the house (the hands) shall tremble, and the strong
men (the legs) shall bow themselves (become bent), and the grinders
(teeth) cease because they are few, and those that look out of the
windows (the eyes) be darkened,” there is general agreement, Lowe
specially designating cataract as meant in the last sentence. “And the
doors shall be shut in the streets,” is regarded as referring to the
mouth by Laurentius and Mead, and to the various orifices including
the results--constipation and dysuria--by Smith; “when the sound
of the grinding is low,” is considered by Jastrow to mean impaired
hearing, and by Smith as a lowered rate of metabolic processes, such
as assimilation, blood formation, and various secretions. “And he
shall rise up at the voice of the bird,” implies, according to Smith
and Mead, the early waking of the elderly; “and all the daughters of
music shall be brought low” signifies to Laurentius the failure of
voice, to Mead deafness, and to Smith all the organs concerned with
sounds, namely the lips, tongue, larynx, and the auditory apparatus.
“Also when they shall be afraid of that which is high, and fears shall
be in the way” is regarded by Smith as describing the general mental
attitude of anxiety for things both small and great and a bad head for
height, but a more modern commentator suggests that “afraid of that
which is high” refers to dyspnoea on climbing a hill. “And the almond
tree shall flourish” is by Laurentius, Hall, and Smith thought to
refer to the white hair or “churchyard flowers” of the old, but Mead
argued that loss of smell is meant. “And the grasshopper shall be a
burden” has been very variously interpreted: Hall is content to accept
the literal meaning that the least weight is a nuisance; Laurentius
and Lowe understand oedema of the legs; John Smith that the aged body
undergoes the reverse change of shrivelling, hardening, and angularity;
Mead suggests scrotal hernia, and Jastrow, as according to the Talmud
the grasshopper is a symbol for the male sexual organ, considers that
the sentence refers to the loss of sexual activity. In the sixth verse
the words “Or ever the silver cord be loosed,” refers, according to
Laurentius, Lowe, Mead, and Jastrow, to kyphosis, but Smith translates
them into paralysis of the spinal cord and nerves. “Or the golden bowl
be broken,” signifies cardiac failure to Laurentius and Lowe, but
cerebral haemorrhage to Smith, who thus explains the next line, “or the
pitcher (the veins) be broken at the fountain (the right ventricle),
or the wheel (the arterial circulation) broken at the cistern” (the
left ventricle), and therefore concludes that King Solomon was
perfectly acquainted with the circulation of the blood discovered by
William Harvey in 1616. “The pitcher” is regarded as the vena cava by
Laurentius, and as the urinary bladder by Mead and Jastrow; “the wheel
broken at the cistern” suggests the kidneys and bladder to Laurentius
and Lowe, cardiac failure to Mead, and intestinal and hepatic
insufficiency to Jastrow.




IX

DISTINCTION BETWEEN HEALTHY AND MORBID OLD AGE


In any individual instance the exact line which separates healthy
old age (senescence) from old age complicated by a morbid process,
_i.e._ by some factor other than the gradual atrophy and restriction
of functional activity, or senility, may be difficult or impossible to
draw. The dictum of Terence, Cicero, and Sanatorius that old age is a
disease probably still finds acceptance with many. It is indeed clear
that exposures to infections and poisons would produce changes more
easily in cells that are beginning to fail in vitality. Healthy old
age should be a normal process of involution with progressive atrophy
and loss of vitality, and free from any morbid change due to other
factors whether extrinsic, such as infection, or intrinsic and due to
abnormal metabolism. As the bodies of the aged usually show a number
of changes additional to those of normal involution, some of which,
such as arteriosclerosis, are so frequent that they have sometimes
been erroneously regarded as part or even the cause of old age, it
is essential to recognize and to try to draw a distinction between
physiological old age and senility from the effects of disease (_Senium
ex morbo_). But about the anatomy and physiology of normal old age much
remains to be learnt; more indeed is known about the pathology of the
aged, a subject which includes the damage done in the past, perhaps in
youth, and morbid processes starting during advanced life.

In attempting to decide when old age should be regarded as a disease
or merely as a process of involution or retrogression which naturally
follows the earlier and progressive stage (youth) of development, it
may be well to refer to the meaning of “disease” and “health.” Disease,
or want of ease, has been variously defined as evidence of imperfect
function, as discord, and as maladjustment between the individual
and his environment (Moon[201]), and Health as the indication of
perfect functional activity, as harmony between the individual and his
environment. In the different stages of life’s cycle there should be a
correspondence between the individual’s desires and his powers so that
there is harmonious co-ordination; this should hold good in normal old
age as it does in youth.

The frequent complaints of old people show that there is maladjustment
and disease, for if the decline of vitality were uniform throughout
the body the equilibrium would, though altered as a whole, still be
maintained, and there would no longer be a discordant desire for
activity, for which other parts of the body are, from a more advanced
state of atrophy or morbid change, unable. Thus it would appear that
the conscious disabilities of old age are not the necessary results of
a true physiological involution, and that the late Sir Andrew Clark’s
definition of Old Age as “the period at which a man ceases to adjust
himself to his environment” should be regarded as true of senility or
morbid old age but not of senescence or healthy old age.

The organs of the body do not all start to grow old at the same time or
progress at the same time. That such variations in involution may be
so exaggerated as to become morbid without any very obvious cause is
highly probable, but the latter event is clearly a departure from the
progress of normal old age. The precocious atrophy of some tissues or
organs may be ascribed to several factors, such as inherent weakness,
the effects of overstrain, though without producing gross changes, or
to the influence of a definite infection or intoxication in the past.
Thus deafness may be hereditary, senile paraplegia has been known to
occur in energetic walkers, and thyroid deficiency may be the outcome
of a past attack of enteric fever. These errors in the chronometry of
life, as Sir James Paget[202] termed the different ageing of organs,
cannot be regarded as a physiological process.




X

DISEASES IN AND OF OLD AGE


Strictly speaking, it cannot be said that there are any diseases
special to length of days, for premature senility shows the changes
and diseases usually correlated with ordinary old age. Inherent want
of vitality and the resulting degenerative atrophy, or Gowers’s
abiotrophy, may imitate the results of prolonged wear and tear of the
tissues, and thus it appears that Charcot’s[203] group of diseases
special to old age, namely senile marasmus, senile osteomalacia, senile
atrophy of the brain, senile heart weakness, and arteriosclerosis,
are not confined to senescence. Old age, however, is prone to the
incidence of diseases which are chiefly but not exclusively seen in
the evening of life, such as those due to the degenerative changes
resulting from the accumulated effect of past infections and from
metabolic disturbance. Thus arteriosclerosis, granular kidney, cardiac
failure, cerebral haemorrhage, emphysema, hepatic cirrhosis, prostatic
enlargement, and carcinoma commonly appear in the sixth decade. In a
series of five publications dealing with the diseases of the age of
fifty, which he calls the critical age, Leclercq[204] describes, in
addition to some of the above, gout and paragouty affections, obesity,
diabetes, cardio-aortic diseases, and albuminuria. Old age, moreover,
modifies the manifestations and course of infections, notably of
pneumonia and erysipelas. It would be unnecessary and from reasons of
space impossible to refer to all the diseases that may attack the aged,
but a few remarks will be made about some disorders that appear to call
for special notice.

Senescence has some nosological compensations; thus some acute
infections, such as measles, scarlet fever, enteric fever, and
diphtheria, are very rare, probably because immunity has gradually been
developed in the course of time; pneumonia and erysipelas, however,
are notable exceptions in being specially prone to occur in the aged.
Migraine usually becomes less troublesome or disappears with the march
of years. As mentioned on p. 86, malignant disease is comparatively
rare in very advanced age; lymphadenoma and leukaemia are rarer than
in early life; and as pathological, like normal, processes are slower,
carcinoma, especially of the breast, may become stationary.

_Diseases of the Skin._--From atrophy of the skin and its secretory
glands the skin is less resistant to infection and accordingly has been
thought to be more susceptible to parasitic attack, such as pityriasis
versicolor. The aged who are often less scrupulous in cleanliness
than their juniors are more prone to skin affections, such as eczema,
erythema, and erysipelas. The so-called senile prurigo is largely
due to the presence of lice. From the atrophic condition of the skin
the cutaneous nerves are more exposed, and this has been regarded
as playing a causal part in senile pruritus, which is an exception
to the general rule that sensory impressions are less prominent in
the aged than earlier in life. It may, like prurigo, be due to an
external cause, such as pediculi, or it may be metabolic in origin. In
almshouses and institutions for the aged epidemics of scratching may
develop from imitation of a genuine case of pruritus. Senile pruritus
is usually general and from its obstinate resistance to treatment may
be a terrible affliction. Sir Gilbert Blane (1749–1834) suffered from
it for the last 13 years of his life, and was obliged to take opium in
increasing quantities until his daily dose reached the equivalent of a
dram of the solid drug.

Erysipelas, like pneumonia, with which or with bronchopneumonia it may
be combined, is less obvious in its symptoms than in ordinary adult
life on account of the diminished power of reaction, as shown by the
slight degree of leucocytosis in the aged in erysipelas (Lamy) and
by its longer course. From want of resistance and arteriosclerosis,
especially Mönckeberg’s form with calcification of the media, senile
gangrene may follow slight accident or injury, such as occurs in
cutting the toe nails. Absorption from the gangrenous area may cause
toxic glycosuria, and such cases, when they come under observation
at this stage, are sometimes regarded as diabetic gangrene. It is
remarkable how well amputations for diabetic gangrene do; in July 1922
I saw with Professor F. H. Edgeworth a man with double amputation of
the legs perfectly healed, and in good health though the glycosuria
persisted.

Herpes zoster, though far from confined to advanced life, has in the
old the unfortunate tendency to leave persistent pain in its site.
Rodent ulcer, although sometimes seen comparatively early in life, is
specially common in advanced years. It often supervenes on the dry
yellow or brown spots (senile keratosis) seen on the face in persons
over 60 years of age.

_Vertigo_ is extremely common in later life and may be due to various
causes; the most frequent form is that of aural origin, such as
labyrinthine or nerve lesions and chronic changes in the middle ear.
Increased blood pressure and cerebral arteriosclerosis are frequently
responsible. Attacks of giddiness may occur in Stokes-Adams disease
or follow exertion in the aged, as if from cerebral anaemia; and
gastric disturbance may apparently also be a determining factor. In
rare instances epilepsy or migraine may be represented or initiated by
vertigo.

_Senile tremor_, rare under the age of 70, begins in the hands,
especially in that most used, and spreads to the neck and head, rarely
occurring in the lower limbs. It is a slow intention tremor, from 4
to 5 per second, and is distinguished by its relation to movement
from that of paralysis agitans which is continuous but diminished on
muscular contraction. The tremor of the jaw resembles that of munching
food; that of the lips is fine. It is compatible with good health.

_Paralysis agitans_, described by James Parkinson, surgeon and
palaeontologist, in 1817 as “the Shaking Palsy,” has now about a
century later been shown, largely as a result of S. A. K. Wilson’s
work, to be one of the forms of the extra-pyramidal symptom complex
and due to degenerative changes in the efferent motor system of the
globus pallidus system. Although juvenile forms occur and encephalitis
lethargica may show the Parkinsonian syndrome, paralysis agitans is
a disease of the early part of the later period of life, the great
majority of the cases beginning between 50 and 70 (Gowers[205]), after
which there is a small incidence only. It is twice as common in males
as in females. Though unfortunately, from the degenerative nature of
the lesion, incurable, it is a chronic disease; thus Maclachlan[206]
refers to a Chelsea pensioner aged 107 years in whom it was known to
have existed for 47 years.

Vascular lesions, haemorrhage or thrombosis, are the most important
factors in the production of grave nervous disease between the ages of
50 and 70; among 500 cases of cerebral haemorrhage 321, or 64 per cent,
and of 110 cases of cerebral thrombosis 67, or 61 per cent, occurred
in the sixth and seventh decades (Michell Clarke[207]). _Cerebral
haemorrhage_ increases with frequency from the fourth decade and the
largest number of cases occur between 50 and 60. From analysis of 154
cases at St. Bartholomew’s Hospital F. W. Andrewes[208] found that
the apparent maximum is in the middle of the sixth decade, but that
correction for the age distribution of the population shows that the
liability of the individual to this form of death increases steadily
up to old age. _Thrombosis of atheromatous vessels_ is an accident of
later incidence than cerebral haemorrhage, and thus contrasts with
hemiplegia due to syphilitic endarteritis which occurs about the prime
of life.

The physiological involution of the mind and accompanying organic
changes in the brain gradually shade off into senile dementia.
A regression to the mental state of childhood, which Dupré[209]
called puerilism, may occur in widely different conditions, such as
structural change of the brain, hysteria, and toxaemia. It may be acute
and be transient or come on slowly and be permanent. Just as an old man
may relapse into the speech and accent of his youth, so if he had a
hard pecuniary struggle in his early days may he become miserly in the
evening of his life.

_Senile dementia_ is an exaggeration of the mental changes occurring in
old age and due to further changes in the brain from vascular disease
or toxic influences. It varies much in its features; some patients
are maniacal, others depressed and melancholic, some feeble, some
delusional, and a few immoral. The senile mania may be mainly nocturnal
and was compared by Clouston[210] to the night delirium of a febrile
neurotic child; it may pass into dementia. Of the melancholic group in
which suicide may occur Clouston found that 30 per cent recovered.

_Senile paraplegia_ may be divided into four etiological groups: (1)
The functional dysbasias or pseudo-paraplegias described by Marie and
Léri,[211] which in general terms resemble those met with during adult
life, but the varieties are less distinct in the old. Quesnel[212]
recognizes three groups of functional disturbance of walking in old
people: (_a_) the slight and usually curable, (_b_) severe functional
disturbance depending essentially on the mental state of the patient,
and (_c_) the organo-functional in which a bony, articular, or nervous
lesion is present; thus confinement to bed for a fracture may cause
a functional paraplegia. (2) Spastic paraplegia due to sclerosis in
the lateral and posterior columns of the spinal cord; the influence
of arteriosclerosis, as advocated by Oppenheim, has been the subject
of some debate, and Lejonne and Lhermitte point out that the nervous
lesions are not necessarily perivascular and that there is a want of
proportion between the vascular and the nervous changes. (3) Paraplegia
of cerebral origin with descending degeneration in the cord and mental
deterioration. (4) Paraplegia from muscular fibrosis and contracture,
the central nervous system being intact.

From the presence of emphysema bronchitis is prone to occur in the old.
_Lobar pneumonia and bronchopneumonia._ Lobar pneumonia has always been
considered the great enemy of the aged; it is often latent, and may
be found after sudden death and in persons supposed to have died of
old age, because they were walking about or complained not at all or
only of trivial symptoms. In spite of Charcot’s[213] considered opinion
to the contrary, it is probable that pneumonia has been often used to
describe what was really bronchopneumonia. For Roussy and Leroux[214]
found that among 300 necropsies at the Hospice Paul Brousse there were
164 cases, or 55 per cent, of bronchopneumonia and only 4 cases, or 1·4
per cent, of lobar pneumonia. The bronchopneumonic areas are triangular
with the base towards the pleural surface, and indeed are infarcts, due
to pre-existing endarteritis obliterans which disposes to secondary
infection. In 110 out of the 164 cases of bronchopneumonia there was
arterial thrombosis, which was of older date than the infected areas of
infarction and bronchopneumonia.

_Senile tuberculosis_, contrary to what has sometimes been stated,
is fairly common though it is often latent; a patient with pulmonary
tuberculosis may have little or no cough, expectoration, fever, or
night sweats, and the physical signs, if present, may be regarded as
those of bronchitis and emphysema or bronchiectasis, unless the sputum
is available and examined for bacilli. Such unrecognized cases are an
obvious danger in institutions, and it may be added that hereditary
disposition plays a much less important part in the aged than in early
life. Senile tuberculosis, however, is usually either a persistence of
that infection or a recrudescence of quiescent infection, and is seldom
primary. The disease may be chronic or acute, and either local or
generalized.

The _senile heart_ has attracted much attention, and myocardial
degeneration and fibrosis due to past infections or to coronary
arteriosclerosis are extremely common. The myocardial change is of
great importance in reducing the reserve power of the heart, so that
cardiac failure is prone to supervene in acute infections, such as
influenzal pneumonia. Chronic valvulitis akin to and associated
with arteriosclerosis is common; the mitral valve is often affected
and incompetent, with a loud systolic murmur at the apex which is
displaced outwards; but the most characteristic lesion of advanced
years is pure aortic stenosis; this is commonly regarded as part of the
arteriosclerotic process in the aorta, but, as I have often noticed,
the aorta may be remarkably healthy and even thinner than usual in old
people with extensive calcification of the valves reducing the aortic
orifice to a chink; it has indeed been thought that such stenosis
of the aortic valves may protect the aorta from strain and so from
arteriosclerosis. Although involvement of the bundle of His giving rise
to the symptom complex of Stokes-Adams disease, and angina pectoris
may complicate aortic stenosis, the presence of this valvular defect
is compatible with remarkable prolongation of life. This may be due
to the more placid life of these old patients, as is suggested by Sir
Clifford Allbutt,[215] who regards aortic stenosis as more unfavourable
in persons under 55 years of age than in their elders.

_Aneurysm of the large arteries_ is rare in the aged, although
arteriosclerosis is common. Diffuse dilatation especially of the
arch of the aorta and of the common iliacs is not infrequent, and
occasionally latent saccular aneurysms are present. In rare instances
large abdominal aneurysms causing pain or remaining latent until
rupture occurs are reported. Among 112 abdominal aneurysms collected by
Nunneley[216] 15 were over 50 years of age; these figures included 32
from St. George’s Hospital, three of them being over 65 years of age.
Miliary aneurysms are of course extremely common in the subjects of
cerebral haemorrhage.

_Spasm_, especially of arteriosclerotic vessels, may be responsible for
attacks of giddiness or faintness, particularly on exertion, and there
may be some doubt whether such symptoms are the outcome of cerebral
anaemia or of cardiac insufficiency. Frequent transient attacks of
aphasia or paralysis, due to spasm of arteriosclerotic middle cerebral
arteries, may occur in patients with high blood pressure (Peabody,[217]
Osler[218]).

_Varicosity_ either localized, like aneurysms, or throughout the length
of veins, are common, especially in the lower limbs of women who have
borne children and done much standing; this condition disposes to
varicose ulcers in the lower third of the leg, and to acute phlebitis.
As pointed out by Trousseau, who was an illustration of his own dictum,
venous thrombosis may occur in the course of intra-abdominal malignant
disease.

Though _dyspepsia_ of adult life often diminishes or passes away in
the more tranquil conditions of old age, it is common; Fenwick[219]
estimated that it occurred in 21 per cent of the population over the
age of 65. Oral sepsis may be responsible for chronic gastritis and
much debility in the old. _Constipation_ often comes on after 60
and is mainly due to atonic dilatation and failure of peristalsis
in the colon, though diminished secretion of mucus may play a part.
Prostatic enlargement has been thought to interfere with peristalsis
(Hollis[220]), and in women large fibromyomas of the uterus may have
this effect. Gerontal constipation is usually more troublesome in women
than in men. Faecal accumulation in the rectum is a frequent cause,
especially in bed-ridden subjects, of what they describe as diarrhoea,
the real significance of which may be easily overlooked unless digital
examination of the rectum is undertaken. The pecten band of fibrous
tissue arising in the submucosa of the pecten, inside the external
sphincter, narrows the anal orifice and so prevents complete evacuation
of the rectum and diminishes the size of the faeces which are generally
voided in short pieces. It is usually, but not always, associated with
internal piles and due to the attendant congestion. W. E. Miles,[221]
who described the pecten band, tells me that it may be regarded as a
pathological development of advancing years, and that he has found
that it may so reduce the anal orifice in the elderly that it is with
difficulty the little finger can be introduced. Pruritus ani, due to
piles and local congestion, is not uncommon in the aged.

_Piles_ are common in the aged and are related to the frequency of
constipation. Like other diseases, they do not give rise to discomfort
so soon or so forcibly as in younger persons. From muscular atrophy
hernia, umbilical in both sexes, in men inguinal and in women femoral,
is prone to occur.

_Gallstones_ are more frequent in advanced life, especially in women,
than at other times of life, gallstones being found after death in
about a third of persons over 70 years of age, though, as mentioned
elsewhere, biliary colic is comparatively rare in old age.

The _urinary bladder_ in cases of prostatic enlargement shows
hypertrophy succeeded by dilatation, fasciculation, and sacculation in
response to the obstruction to micturition and degeneration of the
muscular fibres. The ureters in similar circumstances become dilated,
and the incidence of cystitis and pyelonephritis is thus favoured.

_Arthritic Affections._--Although gout is due to a defect in protein
metabolism analogous to diabetes mellitus as regards carbohydrate
metabolism and to obesity as a manifestation of disordered metabolism
of fat, reference to this disease may be made here. Heredity has a
potent influence on the incidence of the disease particularly in early
life, but acquired gout is essentially a disease of the latter part
of life or the early stage of old age when degeneration is beginning.
The first attack may not occur until old age, and is then usually
mild in character, and, in Sir William Roberts’s[222] words, appears
almost as if it were an incidence of senescence. How far the various
conditions spoken of as irregular gout, goutiness, or paragouty
diseases, which are so numerous as to recall Murchison’s lithaemia,
should be regarded as gouty is uncertain, but that they depend on
disordered protein metabolism is highly probable. The connexion of
gout with infection, as urged by Llewellyn,[223] has a bearing on
the fibrositis and Dupuytren’s contraction often regarded as gouty
phenomena. Dupuytren’s contraction of the palmar fascia, which has been
thought in some instances to be secondary to arteriosclerosis of the
medulla oblongata (Jardini[224]), often accompanies the fibrous pads
on the interphalangeal joints of the fingers described by Garrod[225]
and Hale-White.[226] The tendency of focal infections, especially
oral sepsis, to become more frequent with advancing years also has a
distinct bearing on the occurrence of chronic infective arthritis of
various forms. The most characteristic is morbus coxae senilis which is
not uncommonly associated with Heberden’s nodi digitorum, and sometimes
with Morrant Baker’s cysts due to distension of synovial bursae
with fluid; it may be confused with sciatica. Heberden’s nodes are
unimportant and commonly free from attendant symptoms.

Spondylitis deformans with ankylosis of the articulations and
ossification of the ligaments of the spine, in some cases further
complicated by an extension of the process to the proximal joints of
the limbs (rhizomelic spondylitis), may occur in the aged though also
earlier in life.

_Osteitis deformans_ or Paget’s disease of bone begins as a rule in the
later half of life, the average age being 50 years. Lannelonge[227] and
Fournier[228] argued that it is a lesion due to congenital syphilis;
but although luetic periostitis and osteitis may imitate it, there is
no convincing evidence in favour of their contention.




FOOTNOTES


[1] _Thomas Linacre_, Linacre Lecture, 1908, St. John’s College,
Cambridge, by William Osler, M.D., F.R.S., Cambridge University Press,
1908.

[2] _Life of Thomas Linacre_, by John Noble Johnson, M.D., p. 344, 1835.

[3] _De Temperamentis_, _Galeni Pergamensis_, etc. (translated by
Thomas Linacre), by J. F. Payne, p. 5, Cambridge, 1881.

[4] The fourth of the five epidemics of the remarkable disease the
English Sweating Sickness between 1486 and 1551 occurred in 1528–1529,
and is regarded by Dr. F. G. Crookshank as influenza [_Proc. Roy. Soc.
Med._, 1922, xv. (Sect. Hist. Med.) 27].

[5] The portrait of Heberden in his 86th year was painted by Sir
William Beechey, R.A., who when he got to Windsor found he had
forgotten his canvas and sent for a shirt on which he painted the
picture, now in the dining-room of the Master’s Lodge, St. John’s
College, Cambridge; there are two copies in the possession of the
Heberden family, and one in the Censors’ room of the Royal College
of Physicians. For some of this information I am indebted to Mr.
W. B. Heberden and to Mr. W. Fleming, Bedell of the Royal College of
Physicians of London.

[6] The Cambridge University Press, 1913.

[7] _Vide Gentleman’s Magazine_, 1851, N.S., xxxv. part i. 205.

[8] Γηροκομία βασιλική or _The Pourtract of Old Age wherein is
contained a Sacred Anatomy, both of Soul and Body, and a Perfect
Account of the Infirmities of Age Incident to them Both_, by John
Smith, M.D., London, 1665.

[9] Maupas, _Arch. de zool. expér._, 1899.

[10] Woodruff, L. L., _Proc. Nat. Acad. Sc._, Washington, D.C., 1921,
vii. 43.

[11] Woodruff and Erdmann, _Proc. Soc. Exper. Zool._, N.Y., 1913–14,
xi. 73.

[12] Child, C. M., _Senescence and Rejuvenescence_, p. 310, Chicago,
1915.

[13] Huxley, J. S., _Journ. Microscop. Sc._, 1921, lxv. 643.

[14] Robertson, T. B., and Ray, L. A., _Journ. Chem. Biol._, 1919,
xxxvii. 455.

[15] Drummond and Cannan, _Biochem. Journ._, Cambridge, 1922, xvi. 53.

[16] Sisson and Broyles, _Johns Hopkins Hosp. Bull._, Baltimore, 1921,
xxxii. 22.

[17] Hopkins, G., _Journ. Physiol._, Cambridge, 1912, xliv. 425.

[18] Osborne, T. B., and Mendel, L. B., _Journ. Biol. Chem._, 1915,
xxiii. 439.

[19] Metchnikoff, _The Nature of Man_, English translation, 1903, p.
272.

[20] Browne, T., _Pseudodoxia Epidemica_, p. 396, 6th edition, 1672.

[21] Eugenius Philalethes, junior, F.R.S., _Long Livers: A curious
History of such Persons of both sexes who have liv’d several Ages, and
Grown Young again_, 1722, p. 27.

[22] Hufeland, C. W., _The Art of Prolonging Life_, vol. i. p. 121,
English translation, 1797.

[23] Mahaffy, J. P., _John Stearne_, An Address at the Bicentenary of
the Medical School of Trinity College, Dublin, July 1912.

[24] Bacon, R., _The Cure of Old Age and Preservation of Youth_, p. 63,
1683. Translated by R. Browne.

[25] Hufeland, C. W., _Art of Prolonging Life_, 1797, vol. i. p. 176.

[26] Flourens, _De la longévité humaine ou de la quantité de vie sur la
globe_, 1856.

[27] Cornaro, L., _Discourses on a Sober and Temperate Life_, p. 101,
English translation, 1779, London.

[28] Metchnikoff, _The Nature of Man_, p. 278.

[29] Lankester, E. Ray, _The Advancement of Science_, p. 237, 1890,
London.

[30] Easton, J., _Human Longevity_, 1799, Salisbury.

[31] The _Observer_ of March 26, 1922, contained a note on the
discovery of a tombstone in the graveyard of Lamas Street Welsh
Congregational Chapel, Carmarthen, recording the death on Nov. 14,
1831, of Ann David, aged 181 years.

[32] Sinclair, J., _The Code of Health and Longevity_, Frontispiece to
vol. i., account in vol. ii. p. 274, 1807.

[33] King, G., _Census of England and Wales_, 1911, vol. vii. p. xlvi.

[34] Hufeland, C. W., _The Art of Prolonging Life_, 1797, vol. i. p.
168.

[35] Humphry, G. M., _Old Age_, p. 126, 1889, Cambridge.

[36] Hall, G. Stanley, _Senescence: The Last Half of Life_, 1922,
London and New York.

[37] Mendel, K., _Neurol. Centralbl._, 1910, xxix. 1124.

[38] Rankin, G., _Brit. Med. Journ._, 1919, i. 63.

[39] Waterhouse, B., Letter to Sir John Sinclair in the latter’s _Code
of Health and Longevity_, 1807, i. 33.

[40] Holland, H., _Med. Trans. Coll. Phys._, London, 1813, iv. 316.

[41] Lacassagne, A., _L’Homme vers la fin de sa vie_, p. 7, 1919, Lyon.

[42] Nascher, I. L., _Geriatrics: The Diseases of Old Age and their
Treatment_, p. 18, London, 1919.

[43] Gilford, Hastings, _Med.-Chir. Trans._, London, 1897, lxxx. 17.
_Disorders of Post-natal Growth and Development_, 1911.

[44] Variot et Pironneau, _Bull. Soc. pédiat. de Paris_, 1910, xii. 307.

[45] Roy, D., _Thèse de Paris_, No. 110, 1910.

[46] _Lancet_, 1889, ii. 349.

[47] Weber, Hermann, _On Longevity and Means for the Prolongation of
Life_, 1919, 5th edition, by F. P. Weber, London.

[48] Brownlee, J., _The Use of Death Rates as a Measure of Hygienic
Conditions_, p. 51. Special Report Series No. 60. Medical Research
Council, 1922.

[49] Savage, G., _Memorial to Sir William Osler_, vol. i. p. 247, 1919,
New York.

[50] Butler, S., _Evolution, Old and New_, p. 380, 1911.

[51] Weber, F. P., _Med. Press_, London, 1920, N.S., cix. 271.

[52] Compare Fischer, Martin H., _The Unpopular Review_, 1919, ix. 323.

[53] Paget, J., “Errors in the Chronometry of Life,” in _Studies of Old
Case Books_, p. 92, 1891, London.

[54] Osler and McCrae, _The Principles and Practice of Medicine_, p.
834, 1920, New York and London.

[55] Clifford Allbutt, _Diseases of the Arteries including Angina
Pectoris_, vol. i. pp. 164–7, 1915, London.

[56] _Lancet_, 1922, i. 874.

[57] _On the Handicapping of the First-Born_, Eugenics Lecture Series,
x., 1914.

[58] Noirot, L., _L’Art de vivre longtemps_, p. 195, 1868, Dijon.

[59] Laurent, O., _Bull. Acad. de méd._, Paris, 1919, lxxxi. 835.

[60] _Annuaire internationale de statistique_, Part II., Europe,
Movement of the Population, Table 12, pp. 180–81.

[61] _Statistiska Meddelanden_, Ser. A., Band I. 1 _Dödlighets-
och Lifslangdstabeller for Åren 1816–1910 af Kungl. Statistiska
Centralbyrån_, Stockholm, 1912, p. 28. (For this reference I am
indebted to Dr. Major Greenwood.)

[62] _Public Health Reports_, Treasury Department, Washington, 1922,
xxxvii. 487.

[63] Saundby, R., _Old Age, Its Care and Treatment_, p. 21, 1913,
London.

[64] Easton, J., _Human Longevity_, p. xxvi, Salisbury, 1799.

[65] Browne, T., _Christian Morals_, Part I. Section XXXIII.

[66] Strachey, L., _Books and Characters_, p. 83, London, 1922.

[67] Finot, J., _Rev. mondiale_, Paris, 1922, xxxiii. 387.

[68] _The Mirrors of Downing Street_, by a Gentleman with a Duster, p.
165, 1920.

[69] Thompson, R. J. C., and Todd, R. E., _Lancet_, 1922, i. 874.

[70] Yeo, B., _XIX. Century_, 1883, xxiii. 390.

[71] _Vide_ F. Adams, _Genuine Works of Hippocrates_, Sydenham Society,
vol. i. p. 10, 1849.

[72] Drinkwater, H., _Practitioner_, London, 1914, xciii. 844.

[73] For a consideration of this subject see Sir Hermann Weber’s _Means
for the Prolongation of Life_, and Dr. Lapthorn Smith’s book _How to be
Useful and Happy from 60 to 90_, London, 1922.

[74] Compare Allbutt, C., _St. George’s Hosp. Rep._, 1870, v. 43, and
C. Hilton Fagge, _Principles and Practice of Medicine_, 1886, vol. ii.
p. 22, London.

[75] Lacassagne, A., _L’Homme vers la fin de sa vie_, p. 44, Lyon, 1919.

[76] Owen, I., _Brit. Med. Journ._, 1888, i. 1312.

[77] Allbutt, C., _Diseases of Arteries, including Angina Pectoris_,
vol. i. p. 250, 1915, London.

[78] Robertson, T. B., and Ray, L. A., _Journ. Biol. Chem._, 1920,
xlii. 71.

[79] Williams, L., _Minor Ailments_, p. 319, 1920, London.

[80] Sharpey-Schafer, E. A., Presidential Address, Brit. Assoc., 1912,
_Brit. Med. Journ._, 1912, ii. 589.

[81] Salimbeni et Gery, _Ann. Inst. Pasteur_, Paris, 1912, xxvi. 577.

[82] Fischer, M. H., _Oedema and Nephritis_, 1921, New York.

[83] Lumière, A., _Rôle des colloïdes chez les êtres vivants_, 1921,
Paris.

[84] Bechhold, H., _Die Kolloide in Biologie und Medizin_, Dresden,
1912.

[85] Marinesco, G., _Études histologiques sur le mécanisme de la
sénilité_, 1904; also _Presse méd._, Paris, 1922, xxx. 309.

[86] Campbell, H., _Treatment_, London, p. 153, 1909.

[87] Carrel, A., _Journ. Exper. Med._, Baltimore, 1913, xviii. 287.

[88] Loeb and Northrop, _Journ. Biol. Chem._, 1917, xxxii. 103.

[89] Carrel, A., and Ebeling, A. H., _Journ. Exper. Med._, Baltimore,
1921, xxxiv. 599.

[90] Robertson, T. B., and Ray, L. A., _Journ. Biol. Chem._, 1920,
xlii. 71.

[91] Nathan, _Ann. de méd._, Paris, 1922, xi. 59.

[92] Drew, _Brit. Journ. Exper. Path._, London, 1922, iii. 20.

[93] Hufeland, C. W., _The Art of Prolonging Life_, 1797, vol. i. p.
227.

[94] Lorand, A., _Old Age Deferred_, pp. 51, 114, Philadelphia, 1921.

[95] Biedl, A., _Endocrinology_, Los Angeles, 1921, v. 523.

[96] Berman, L., _The Glands Regulating Personality_, p. 260, The
Macmillan Co., 1921, New York.

[97] Lydston, G. F., _Journ. Amer. Med. Assoc._, Chicago, 1919, lxxii.
396.

[98] Stanley and Kelker, _Journ. Amer. Med. Assoc._, Chicago, 1920,
lxxiv. 1501.

[99] Stanley, _Endocrinology_, Los Angeles, 1921, v. 708.

[100] Gilford, H., _The Disorders of Post-natal Growth and
Development_, p. 643, 1911, London.

[101] Bouin et Ancel, _Compt. rend. Acad. Sc._, Paris, 1903, cxxxvii.
1289, 1904, cxxxviii. 110.

[102] Lipschülz, Ottow, Wagner, and Bormann, _Proc. Roy. Soc._ Lond.,
1922, ser. B, xciii. 132.

[103] Kuntz, A., _Endocrinology_, Los Angeles, 1921, v. 190.

[104] Nathan, _Presse méd._, Paris, 1922, xxx. 237.

[105] Sand, K., _Journ. de physiol. et de path. gén._, Paris, 1921,
xix. 525.

[106] Blair Bell, _The Sex Complex_, p. 28, 1920.

[107] Sternberg, _Berl. klin. Wehnschr._, 1921, lviii. 556.

[108] Mott, F. W., _Brit. Med. Journ._, 1919, ii. 658; _Proc. Roy. Soc.
Med._, 1922, xv. (Sect. Psychiat.), 1–30.

[109] Aron, _Compt. rend. Soc. biol._, Paris, 1921, lxxxv. 107.

[110] Retterer, E., _Compt. rend. Soc. biol._, Paris, 1919, lxxxii. 423.

[111] Walker, K., _Brit. Med. Journ._, 1922, i. 297.

[112] Steinach, E., _Verjüngung durch experimentelle Neubelebung der
alternden Puberstätsdrüsen_, J. Springer, Berlin, 1920.

[113] Benjamin, H., _New York Med. Journ._, 1921, cxiv. 687.

[114] Simmonds (quoted by Marinesco), _Deutsche path. Ges._, Jena, 1921.

[115] Tiedje, H., _Deutsche med. Wehnschr._, 1921, xlvii. 35.

[116] Romeis, B., _München. med. Wehnschr._, 1920, lxvii. 600, 1821.

[117] Marinesco, _Presse méd._, Paris, 1922, xxx. 309.

[118] Lenz, L., und Schmidt, P., _Deutsche med. Wehnschr._, 1921,
xlvii. 327.

[119] Moullin, C. W. M., _Enlargement of the Prostate_, p. 194, 3rd
edition, 1904.

[120] Harrower, _Practical Hormone Therapy_, p. 344, 1914.

[121] Frank, _Journ. Amer. Med. Assoc._, Chicago, 1922, lxxviii. 181.

[122] Marinesco, _Études histologiques sur le mécanisme de la
sénilité_, 1904.

[123] Léri, _Le cerveau sénile_, 1906.

[124] Ribbert, H., _Der Tod aus Alterswäche_, Bonn, 1908.

[125] Salimbeni et Gery, _Ann. Inst. Pasteur_, Paris, 1912, xxvi. 577.

[126] Lane, W. A., _The Operative Treatment of Intestinal Stasis_,
1918, London.

[127] Abernethy, J., _The Constitutional Origin and Treatment of Local
Diseases_, 1811.

[128] Clarke, E., in _The Operative Treatment of Intestinal Stasis_, p.
246, London.

[129] Vide Saundby, _Old Age, its Care and Treatment_, pp. 5, 28,
London, 1913.

[130] Pearson, K., _Arch. Middlesex Hosp._, 1902, ii. 127.

[131] Lazarus-Barlow, W. S., _Ibid._, 1905, v. 43.

[132] On analysis of the Registrar-General’s returns for England and
Wales (1901–1909) C. Singer (_Quart. Journ. Med._, Oxford, 1911–12, v.
33), found that the incidence curves of carcinoma of the lip, face, and
breast were exceptional in rising up to the highest age recorded (90).

[133] Laurent, O., _Bull. Acad. de méd._, Paris, 1919, lxxxi. 835.

[134] Gilford, H., _The Disorders of Post-natal Growth and
Development_, 1911, London; and _Brit. Med. Journ._, 1913, ii. 1617.

[135] Goodpasture, E. W., _Journ. Med. Research_, Boston, 1918,
xxxviii. 127.

[136] Oertel, H., _Ibid._, 485.

[137] Councilman, W. T., _Contributions to Medical and Biological
Research_, dedicated to Sir William Osler, 1919, vol. ii. p. 918, New
York.

[138] Kissmeyer and With, _Brit. Journ. Dermat. and Syph._, London,
1922, xxxiv. 175.

[139] Pringle, J. J., _System of Medicine_ (Allbutt and Rolleston),
1911, ix. 549, London.

[140] Cheatle, G. L., _West London Med.-Chir. Journ._, 1921, xxvi. 154.

[141] _Letter to a Friend_, in Greenhill’s edition of _Religio Medici_,
p. 135, Macmillan, 1898.

[142] Bacon, F., _The History of Life and Death_.

[143] _Autobiography of Sir Charles Cameron_, p. 137, 1920.

[144] Graves, R. J., _Dublin Quart. Journ. Med. Sc._, 1847, N.S., iii.
339.

[145] Quoted by D. Roy, _Thèse de Paris_, No. 110, 1910.

[146] Sinclair, J., _Code of Health and Longevity_, 1807, i. 68.

[147] Boyd, R., _Phil. Trans. Roy. Soc._, 1861, cli. 241.

[148] Monauni, _Arch. d’opth._, 1921, xxxviii. 180.

[149] Nascher, I. L., _Geriatrics_, p. 36, 2nd edition, 1919, London.

[150] Clarke, Ernest, in _Operative Treatment of Intestinal Stasis_, by
W. A. Lane, p. 245, 1918, London.

[151] Hollis, W. A., _Brit. Med. Journ._, 1916, i. 677.

[152] Luciani, _Text-book of Physiology_, English translation, vol. v.
p. 302, London.

[153] Salimbeni et Gery, _Ann. Inst. Pasteur_, Paris, 1912, xxvi. 577.

[154] Symmers, D., _Arch. Int. Med._, Chicago, 1909, iii. 270.

[155] Roussy, G., et Leroux, R., _Ann. de méd._, Paris, 1921, ix. 161.

[156] Durante, _Manuel d’histologie pathologique_ (Cornil et Ranvier),
1902, ii.

[157] Jewesbury and Topley, _Journ. Path. and Bacteriol._, 1913, xviii.
432.

[158] Weber, F. P., _System of Medicine_ (Allbutt and Rolleston), 1905,
i. 185, London.

[159] Charcot, J. M., _Clinical Lectures on Senile and Chronic
Diseases_, p. 28, New Sydenham Soc., 1881.

[160] _Loc. cit._

[161] Ophülz, W., _Stanford Univ. Publications, Med. Sciences_, 1921,
vol. i. Part I. p. 31.

[162] Turnbull, H. M., _Quart. Journ. Med._, Oxford, 1913–14, viii. 201.

[163] Hansen, K. M., _Ugsek. f. Laeger_, Copenhagen, 1919, lxxxi. 1281.

[164] Macnaughton, F. G., _Brit. Med. Journ._, 1922, ii. 14.

[165] Rolleston, G., _Brit. and For. Med.-Chir. Rev._, 1863, xxxi. 505.

[166] Hammar, A., _Endocrinology_, Los Angeles, 1921, v. 543.

[167] Hale-White, W., _Med.-Chir. Trans._, 1888, lxxi. 181.

[168] Findlay, G. M., _Journ. Path. and Bacteriol._, Cambridge, 1920,
xxiii. 482.

[169] Councilman, W. T., _Contributions to Medical and Biological
Research_, Dedicated to Sir William Osler, 1919, vol. ii. p. 919, New
York.

[170] Walker, K., _Brit. Med. Journ._, 1922, i. 297.

[171] Launois, “Appareil urinaire des vieillards,” _Thèse de Paris_,
1885.

[172] Nemenow, M., _Ztschr. f. Urol._, Berl. und Leipz., 1921, xv. 45.

[173] Hertoghe, “L’Hypothyroidie bénigne chronique,” _Bull. Acad. roy.
de Belg._, 1899.

[174] Mott, F. W., _Brit. Med. Journ._, 1919, ii. 658.

[175] Paul, F. T., _Lancet_, 1910, ii. 294.

[176] Haneborg, _Acta Medica Scandinavica_, 1921, Supplement I. p. 117.

[177] Bell, _Lancet_, 1922, i. 715.

[178] MacNider, _Science_, 1917, xlvi. 643.

[179] Rappleye, _Boston Med. and Surg. Journ._, 1918, clxxviii. 191.

[180] _A Discourse Of The Preservation Of The Sight: Of Melancholic
Diseases: Of Rheums and Of Old Age_, composed by M. Andreas Laurentius,
Ordinarie Phisition to the King and Publike Professor of Phisicke
in the Universitie of Montpelier. Translated out of the French into
English according to the last Edition by Richard Surphlet, Practitioner
in Phisicke, p. 170, London, 1599.

[181] Aub and Dubois, _Arch. Int. Med._, Chicago, 1917, xix. 823.

[182] Gray, A. A., _Diseases of the Ear_, p. 335, 1910.

[183] _The Gray Room_, p. 261, 1922.

[184] Rivers, W. H. R., _Instinct and the Unconscious_, p. 148, 2nd
edition, Cambridge University Press, 1922.

[185] Dupuis, _Journ. de psychol._, Paris, 1921, xviii. 481.

[186] Arnold, M., _Essays in Criticism_, Preface, p. x. 1886.

[187] Day, G. E., _Domestic Management and Diseases of Advanced Life_,
p. 5, 1849, London.

[188] _The Adventure of Death_, p. 63, 1916, London.

[189] Hooker, D. R., _Amer. Journ. Physiol._, 1916, xl. 43.

[190] Thompson, R. J. C., and Todd, R. E., _Lancet_, 1922, ii. 503.

[191] Spence, J. C., _Quart. Journ. Med._, Oxford, 1920–21, xiv. 314.

[192] Carrel and Ebeling, _Journ. Exper. Med._, Baltimore, 1921, xxxiv.
599.

[193] Nascher, I. L., _Geriatrics_, p. 60, London, 1919.

[194] Williams, L., _Minor Ailments_, p. 332, 1920.

[195] _The Gentle Cynic, being a Translation of the Book of Koheleth,
commonly known as Ecclesiastes, stripped of later Additions, also its
Origin, Growth and Interpretation_, by Morris Jastrow, junior, 1919,
J. B. Lippincott Co.

[196] Laurentius, A., _A Discourse of the Preservation of the Sight; of
the Melancholic Diseases; of the Rheums; and of Old Age_, translated
out of French into English by Richard Surphlet, 1599.

[197] Lowe, P., _The Whole Course of Chirurgerie_, 1612.

[198] Hall, J., _Paraphrase upon the Hard Texts of the Whole Divine
Scripture_, 1633.

[199] _Loc. cit._, _vide_ p. 8.

[200] Mead, R., _Medica Sacra_, translated from the Latin by Thomas
Stark, 1775.

[201] Moon, R. O., _The Relation of Medicine to Philosophy_, p. 217,
1909, London.

[202] Paget, J., _Studies from Old Case Books_, p. 93, 1891, London.

[203] Charcot, J. M., _Clinical Lectures on Senile and Chronic
Diseases_, New Sydenham Society, 1881, p. 33.

[204] Leclercq, A., _Les maladies de la cinquantaine_, 5 vols., 1922,
Paris.

[205] Gowers, W. R., _System of Medicine_ (Allbutt and Rolleston),
1910, viii. 473, London.

[206] Maclachlan, D., _A Practical Treatise on the Diseases and
Infirmities of Advanced Life_, p. 213, London, 1868.

[207] Clarke, J. M., _Brit. Med. Journ._, 1915, ii. 665.

[208] Andrewes, F. W., _St. Barth. Hosp. Rep._, London, 1912, xlviii. 9.

[209] Dupré, E., _Nouv. iconograph. Salpêt._, Paris, 1905, xviii. 88.

[210] Clouston, T., _System of Medicine_ (Allbutt and Rolleston),
London, 1910, viii. 935.

[211] Marie, P., et Léri, _Séméiologie nerveuse, Traité de médecine_
(Gilbert et Thoinot), p. 450.

[212] Quesnel, M., _Thèse de Paris_, 1920, No. 258.

[213] Charcot, J. M., _Clinical Lectures on Senile and Chronic
Diseases_, New Sydenham Society, 1881, p. 239.

[214] Roussy, G., et Leroux, R., _Ann. de méd._, Paris, 1921, ix. 161.

[215] Allbutt, Clifford, _System of Medicine_ (Allbutt and Rolleston)
London, 1909, vi. 455.

[216] Nunneley, F. P., _Aneurysm of the Abdominal Aorta_, p. 8, London,
1906.

[217] Peabody, _Trans. Assoc. Amer. Phys._, Washington, 1891, vi. 170.

[218] Osler, W., _Journ. Canad. Med. Assoc._, 1911, N.S., i. 919.

[219] Fenwick, W. S., _Lancet_, 1909, ii. 1346.

[220] Hollis, W. A., _Brit. Med. Journ._, 1916, i. 677.

[221] Miles, W. E., _Surg., Gyn., and Obstet._, 1919, xix. 497.

[222] Roberts, W., _System of Medicine_ (Allbutt and Rolleston), 1907,
iii. 124, London.

[223] Llewellyn, L. J., _Gout_, 1920, London.

[224] Jardini, _Nouv. iconograph. Salpêtr._, Paris, 1906, xix. 553.

[225] Garrod, A. E., _Brit. Med. Journ._, 1904, ii. 8.

[226] Hale-White, W., _Quart. Journ. Med._, Oxford, 1907–1908, i. 47.

[227] Lannelonge, _Bull. Acad. de méd._, Paris, 1903, 3^e sér., xlix.
299.

[228] Fournier, _Ibid._, 1903, 3^e sér., xlix. 522.




INDEX


  Abernethy, J., 84

  Abiotrophy, 139

  Acquired characters, 35, 75, 79

  Activity. _See_ Functional; Muscular

  Adam, age of, 14

  Adami, J. G., 87

  Adolescence, termination of period of, 17

  Adrenals, 110

  Age, the “critical,” 140
    the “dangerous,” 26
    exaggeration of, by elderly people, 20, 21

  Albuminuria, 126

  Alcohol, abuse of, 57
    action of, on the tissues, 57
    influence on longevity, 33, 34, 57

  Alimentary canal, lymphoid atrophy of, 109

  Allbutt, Clifford, 37, 55, 59, 150

  Allen treatment of diabetes, 56

  Amputation, for diabetic gangrene, 142

  Anabolism, cellular, 67

  Anaemia, secondary, 108

  Anal orifice, narrowing of, 152

  Anatomical changes, 60, 63, 90–114

  Andrewes, F. W., 145

  Aneurysms, 150, 151

  Angiomas, 108

  Animal life, duration of, 17, 18
    experimental modification of life cycle and growth of, 11
    natural death in, 13, 14
    rejuvenation and senescence in, 9–11

  Aortic stenosis, 149

  Aphasia, transient attacks of, 151

  Appetite, 56, 118

  Arcus senilis, 98

  Arnold, M., 123

  Aron, 75

  Arteries, degenerative changes in, 97, 105–107
    “pipe-stem,” 106

  Arteriosclerosis, 97, 105–107, 149
    age incidence of, 105, 140
    causes of, 105, 142
    hereditary transmission of, 37
    influence of smoking on, 59
    prostatic hypertrophy and, 112
    spasm associated with, 151
    thyroid prevention of, 73

  Arthritic affections, 154

  Arthritis, chronic infective, 155

  Atheroma. _See_ Arteriosclerosis

  Athyroidism, 73

  Atkinson, Edward, nonagenarian, 51

  Atrophy--
    brown, 103, 105
    cardiac, 104, 140, 149
    degenerative, 46
    general, 62, 91, 139
      causes of, 137, 138
    genital, 114
    lymphoid, 108
    muscular, 103
    of auditory nerve, 118
    of skin and secretory glands, 141
    of thymus, 109
    precocious, 138
    renal, 111
    splenic, 109
    testicular, 113

  Atropine, 127, 128

  Aub and Dubois, 116

  Auditory nerve, atrophy of, 118

  Auto-suggestion, 48


  Bacon, Francis, 17, 95

  Bacon, Roger, 17

  Baddeley, J. J., 51

  Baldness, 95
    causes of, 96
    thyroid extract in, 96

  Barclay-Smith, E., 82

  Baronsdale, W., 5

  Bell, B., 75

  Bell, J. R., 115

  Benjamin, H., 77

  Berman, L., 71

  Biedl, A., 71

  Biochemistry of old age, 64–68

  Biological aspect of old age, 10, 11, 23, 63

  Biotripsy, 93

  Birth, expectation of life at, 13, 41, 42

  Birth control, 24

  Bladder, 133, 153

  Blane, G., 142

  Blood, condition of, 108, 115
    increase of urea-nitrogen in, 115

  Blood pressure, 125
    and heredity, 37
    high, 55, 124
    longevity in relation to, 37
    senile, 104, 124, 125

  Blood supply, diminished, 106

  Blood transfusion, 66

  Bodily vigour, sex gland activity as manifestation of, 69

  Body, cells of. _See_ Cells
    conformation of, 60
    fibrous framework of, 92
    structural changes in, 90
    temperature of, 116
    water content at birth and adult life, 64

  Boerhaave, 91

  Bone marrow, atrophy of, 108

  Bones, injuries to, healing of, 126, 127
    Paget’s disease of, 156
    rarefaction and absorption of, 99
      arterial degeneration with, 107

  Bony changes, 98, 99

  Bouin and Ancel, 73

  Brain, changes in, 96, 146
    degeneration of cells of, 97
    organic changes in, 145
    senile atrophy of, 139
    shrinkage of, 100
    weight of, 97

  Brain cells, activity of, influence on longevity, 35, 36

  Brampton, Lord, nonagenarian, 51

  Bromides, intolerance to, 128

  Bronchiectasis, simulating tuberculosis, 149

  Bronchitis, disposition to, 147
    simulating tuberculosis, 149

  Bronchopneumonia, 148
    and pneumonia, confusion between, 148
    tendency to, 103

  Brown atrophy, 103, 105

  Brown-Séquard, 70

  Browne, T., 14, 47, 95

  Brownlee, J., 33

  Buffon, 17

  Butler, Samuel, 35


  Calcification, of arteries, 106–107
    of cartilage, 100

  Calendar, length of, in the patriarchal era, 15

  California, centenarians in, 41

  Cambridge University, influence of John Haviland on the study
          of medicine, 6

  Cameron, C., 95

  Campbell, H., 65

  Cancer. _See_ Carcinoma

  Carcinoma, 141
    age and sex incidence of, 86, 140
    and senescence, 86–89
    rarity of, in extreme old age, 87

  Cardio-vascular system, 36–38, 103–108, 124, 133, 149

  Carlisle, Anthony, 8

  Carrel, A., 65, 66, 127

  Cartilages, calcification of, 100

  Castration, phenomena of old age and, 79
    secondary sex-characters following, 79

  Cazalis, 107

  Cell-memory, 35
    longevity in relation to, 35

  Cells, 62
    activity of, relation to connective tissues, 68, 88, 89, 92
    ageing of, 67, 88
      carcinoma in relation to, 86–89
      causes and significance of, 67
      senility in relation to, 86, 88
    changes in, infections causing, 43, 44
    changes in old age, 64
    colloidal changes in, 64, 68
    cultivation of, 66
    degeneration of, 62, 92, 135
      intestinal bacteria causing, 82, 83
    infections and intoxications producing changes in, 44
    life cycle of, 63, 65, 88, 89
      factors influencing, 65
      on what dependent, 68
      thyroid deficiency influencing, 72
    limited vitality of, 62
      sequels of, 64
    products inimical to life of, 65
    senile changes due to injury to, 30, 31, 67
    time-rate of, 36
    vital phenomena of, 63, 88, 89

  Census returns, 41, 43

  Centenarianism, 19
    heredity in relation to, 19

  Centenarians, 20, 33, 34
    age exaggeration by, 20, 21
    among Churchmen, 50
    among doctors, 52
    among professional men, 50
    census returns of, 20, 21
    family incidence of, 32, 33
    in California, statistics, 41
    in England and Wales, statistics, 40, 41
    in Ireland, statistics, 40
    medical, 52
    personal habits of, 56, 57
    rarity of cancer among, 87
    sex statistics of, 21, 22
    smoking among, 58
    statistics of, 21, 24
      deaths among, 21, 22, 41

  Cerebral arteries, changes in, 97

  Cerebral degeneration, 97

  Cerebral haemorrhage, 145
    age incidence of, 145

  Cerebral thrombosis, 145

  Chaderton, Laurence, centenarian, 51

  Charcot, J. M., 8, 104, 116, 139, 148

  Cheatle, G. L., 93

  Chest capacity, diminished, 103

  Cheyne, G., 55

  Child, C. M., 10, 14, 56

  “Childhood, second,” 122, 145

  Chromophages, 94

  Chromosomes, 88

  Churchmen, centenarians among, 50

  Cicero, 135

  Circulatory system, 38

  Clark, Andrew, 29, 60, 137

  Clarke, E., 85, 98

  Clarke, J. M., 145

  Climacteric, ancient conceptions of, 27
    senile, 30

  Climacteric disease, 28

  Climate, influence on longevity, 26, 39

  Coke, Sir Edward, octogenarian, 51

  Colloidal dehydration, leading to old age, 64, 65

  Colon, destruction of putrefactive bacteria in, 83

  Constipation, 101, 152
    age incidence of, 152
    gerontal, 102
    tendency to, 115

  Cornaro, on the duration of life, 18
    writer on old age, 8

  Costal cartilage, calcification of, 100

  Councilman, W. T., 37, 92, 104, 107, 111, 125

  Cranial bones, changes in, 100

  Crosby, T., 51

  Cushny, A. R., 81

  Cutaneous sensation, 117

  Cystitis, 154


  Darwin, C., 53

  Deafness, causes of, 118
    senile, 118

  Death, causes of, 13, 38
    mental attitude to, 123
    natural, 13, 14, 16, 91
      from old age, 14, 91
      in animal kingdom, 13, 14
      probable cause of, 36
      Weissmann’s conception of, 9, 16
    phenomenon of, 9, 10
    sudden, causes of, 117
      latent pneumonia causing, 148

  Death-rate, in various countries, 42
    sex incidence, 22

  Deaths, among centenarians, 41

  Decrepitude, 30

  Delirium, 146

  Delusions, 146

  Demange, 91, 105

  Dementia, senile, causes of, 146
    onset of, 145
    varied features of, 146

  “de Morgan’s Spots,” 108

  Dental decay, 101
    an accompaniment of old age, 44, 45

  Dentition, third, explanation of, 101

  Depression, senile, 146

  de Salis, Cardinal, centenarian, 50

  Descartes, 7

  Desmond, Countess of, centenarian, 20

  Devolution, course of, 122

  Diabetic gangrene, 142

  Diet, restricted, influence of, 56

  Digestion, impairment of, 101

  Digestive system, 38

  Disabilities of old age, 90–114, 137

  Disease, associated with old age, 30, 44, 139
    chronic, freedom from, in old age, 44
    definition of, 136
    influence of, on longevity, 43
    latency of, 117
    old age as a, 49, 136

  Doctors, duration of life of, 52, 53
    centenarian, 52

  Donaldson, R., 110

  Drew, A., 68

  Drinkwater, H., 52

  Drugs, reaction to, 127–128
    reaction to, during senescence, 127

  Dryness of elderly bodies, 64

  Ductus cochleariae, fibrosis of, 118

  Dupuytren’s contraction, 155

  Dysbasia, functional, 146

  Dyspepsia, frequency of, 152


  Early rising, 59, 60

  Ears, disorders of, 143

  Easton, J., 20, 47

  Ebstein, 18

  Eccentricities of old age, 120, 121

  Ecclesiastes, interpretation of, 129

  Eczema, 118, 141

  Emphysema, 147, 149

  Endarteritis obliterans, 103

  Endocrine glands, in relation to old age, 12, 68–81

  Endomixis, 9

  Environment, influence on longevity, 33, 34, 39–46, 55

  Erysipelas, 141
    disposition to, 140
    senile, course of, 142

  Erythema, 141

  Eunuchs, duration of life of, 79

  Expectation of life, 13, 41
    in various countries, 42

  Extra-systoles, 124

  Eyes, senile disorders of, 117


  Facial appearance, 93
    changes in, 93
      causes of, 118

  Fads, 121

  Faintness, 151

  Fat, reduction of, 92
    subcutaneous, disappearance of, 94

  Fatigue, excessive, danger of, 54
    physical and mental, 119, 120
    psychical, 122

  Fatty degeneration of arteries, 106
    of heart, 104
    of muscles, 103

  Femur, fracture of, 99, 127

  Fertility, age limit of, in women, 26
    average, estimation of, 24
    old age in relation to, 23, 24, 26
    social conditions influencing, 24

  Fibrosis, 91, 92

  Fibrositis, 155

  Fibrous tissues, atrophy of, 91

  Finot, J., 49

  First-born, handicapping of, 38
    longevity in relation to, 38

  Flourens, on the duration of life, 18

  Food, excess of, 56

  Fractures, delay in healing of, 126, 127
    tendency to, 99

  France, longevity in, 40

  Functional activity, danger of excess of, 54
    influencing longevity, 46, 55
    progressive diminution in, 115, 119, 135


  Gait, disordered, 122, 147

  Galileo, 53

  Gallstones, 153

  Gangrene, diabetic, 142
    senile, 142
      pipe-stem arteries with, 106

  Garrod, A. E., 155

  Gastric juice, composition, changes in, 115
    lack of, 101

  Gastro-intestinal tract, changes in, 101

  Generation. _See_ Reproductive power

  Generative organs, internal secretion of, 70, 73–80

  Genitals, external, atrophy of, 114

  Giantism, 19, 20

  Giddiness, 143
    causes of, 151

  Gilford, H., 30, 72, 88

  Gisborne, Thomas, Linacre lecturer, 5

  Gland activity, functional, diminution of, 115
    senility in relation to, 69

  Gland atrophy, 109, 110

  Gland cells, life cycle of, 67

  Gland secretions, influencing activity of body cells, 68, 69

  Gland, endocrine, metabolism stimulated by, 81
    rejuvenescence in, in relation to, 12, 73–80

  Gland, endocrine, theory of old age, 70, 71, 72

  Gland, endocrine, therapy during old age, 71
    of prostatic enlargement, 113
    rejuvenescence in relation to, 12, 73–80
    _See also_ Endocrine, Pituitary, etc.

  Glycosuria, 126
    toxic, cause of, 142

  Goethe, 53

  Goodpasture, E. W., 88

  Gout, 154
    acquired, age incidence of, 154

  Gowers, W. R., 139, 144

  Graves, R. J., 95

  Gray, A. A., 118

  Greenwood, Major, 24

  Gregory IX., centenarian, 50

  Growth, 60
    experimental modification of, 11
    influence of endocrine gland therapy on, 12, 72, 80
    retardation by vitamine deficiency, 13


  Habits, influencing longevity, 55

  Haemoglobin, 108

  Haemorrhage, 144
    cerebral, 145

  Hair, changes in colour of, 94
    excessive growth of, 96
    of the body, loss of, 96

  Hale-White, W., 109, 155

  Hall, Bishop, 131

  Hall, Stanley, 8, 27

  Haller, 91

  Halsbury, Lord, nonagenarian, 51

  Hands, appearance of, 93
    atrophic changes in, 94
    senile tremor of, 143

  Harrower, 80

  Haviland, John, influence on the Cambridge medical school, 6
    Regius Professor of Physic, 6
    Linacre lecturer, 5

  Head, senile tremor of, 143

  Health, definition of, 136

  Hearing, impairment of, 118

  Heart, atrophy of, 104
    condition of, 92, 103, 104
    diseases of, 149
    failure, 149
      age incidence of, 140
    hypertrophy of, 55, 104
      and blood pressure, 104
      longevity in relation to, 37
    senile changes in, 104, 139, 149

  Heberden, W. (the elder), 4, 54

  Heberden’s nodes, 155

  Height, cause of loss of, 100

  Hereditary tendencies, correction of, 34

  Heredity, firstlings in relation to, 38
    influence on longevity, 19, 32–39

  Hernia, tendency to, 153

  Herpes zoster, 142

  Hertoghe, 113

  Hetero-suggestion, 48

  High altitudes, influence on longevity, 39

  Hippocrates, age of, 52

  Holland, Henry, 28

  Holmes, O. W., 49

  Hopkins, G., 13

  Hot climates, influence of, on senescence, 26, 36, 39

  Huchard, 59, 105

  Hufeland, C. W., 17, 23, 70

  Humphry, G. M., 8, 22, 32, 34, 39, 43, 58, 60, 87, 98–100, 112, 124

  Hunter, W., 124

  Huxley, J. S., 11

  Hygiene of old age, 55–61

  Hyperpiesia, 37, 124

  Hypertrichosis, following the menopause, 96

  Hypnotics, 128

  Hypochondriasis, 121

  Hypoplasia, 63, 64

  Hypothyroidism, in relation to old age, 72


  Idleness, inimical to old age, 46, 47

  Individuation, phenomenon of, 10

  Infant mortality, sex incidence and causes, 22

  Infantilism, premature senility with, 31

  Infections, 140
    cell changes due to, 43, 44
    disposition to cardiac failure during, 149
    focal, tendency to, 155
    gout in relation to, 154

  Insomnia, 119

  Interstitial cells, 73–81

  Intestinal stasis, as cause of premature old age, 82, 85

  Intoxications, cause of senescence, 82
    influence on body cells, 44, 55

  Invalidism, auto- and hetero-suggestion producing, 48

  Ireland, centenarians in, 40

  Iris, sluggish, 117

  Iverex, Dr., centenarian, 32


  Jackson, Christopher, 3

  Jackson, Hughlings, 122

  James, R. R., 52

  Jastrow, M., 130

  Jaw, changes in shape of, 99
    tremor of, 144

  Jenkins, Henry, centenarian, 20

  Jews, longevity of, 40

  Johnson, S., 46

  Joints, fractures of, disposition to, 99


  Keratosis, senile, 143

  Kidneys, 126
    degenerative changes in, 111
    granular, age incidence of, 140

  King, G., 20

  Klotz, O., 107

  Knee-jerk, 119

  Koheleth, 139

  Kuntz, A., 74


  Labyrinthine deafness, 118

  Labyrinthine vertigo, 143

  Lacassagne, A., 30, 55

  Lane, W. Arbuthnot, 84

  Lankester, E. Ray, 14, 19, 23

  Laryngeal cartilage, calcification of, 100

  Laurent, O., 41, 87

  Laurentius, Andreas, 29, 46, 116, 131

  Lazarus, 59

  Lazarus-Barlow, W. S., 86

  Leclercq, A., 140

  Léri, 83, 146

  Leroux, 103, 148

  Lessius, Leonardus, 55

  Leucocyte count, 108, 109

  Leucodermia, 93

  Leukaemia, 141

  Leydig, interstitial cells of, 73–81

  Lichtenstern, 77

  Life, animal and human, duration of, 17, 18
    chronometry of, 138
    climacterics of, 27, 30
    duration of, 9
      among professional men, 50–53
      chemical theory of, 66
      early theories of, 17
      estimation of, 18
      _in vitro_, 66
      various writers on, 17, 18
      variation in different countries, 39
      modern theories of, 18
    expectation of, at birth, 13, 41
    prolongation of, experimental, 12, 13, 77
      following cessation of reproductive function, 23
      _See also_ Longevity

  Life cycle, experimental modification of, 11

  Ligament, spinous, ossification of, 99

  Ligamentum spirale, atrophy of, 118

  Linacre, Thomas, 2
    family history of, 2, 3

  Linacre Lectures, 3–6

  Linacre Lectureship, 1

  Lips, tremor of, 144

  Lipschülz, 74

  Liveing, G. D., 7

  Liver, atrophy of lobules and cells of, 102
    changes in size and weight of, 102
    cirrhosis of, 140

  Llewellyn, L. J., 154

  Longevity, alcohol influencing, 57
    among professional men, 50, 53
    auto- and hetero-suggestion influencing, 48, 49
    “cell-memory” in relation to, 35
    climatic conditions influencing, 39, 41
    conditions favouring, 7, 33
    diseases inimical to, 45
    endocrine atrophy in relation to, 68–81
    environment influencing, 33, 34, 39–46, 55
    factors influencing, 32
    fertility in relation to, 23, 24
    functional activity influencing, 46, 55
    hereditary aspects of, 19, 32–39
    idleness inimical to, 47, 48
    in the medical profession, 52
    influence of past diseases on, 43
    influence of blood pressure on, 37
    influence of brain cells on, 36
    integrity of cardio-vascular system necessary to, 36
    of nations, compared, 39, 40
    of the patriarchs, 15, 16
    personal habits influencing, 55
    potential, on what determined, 67
    sex incidence of, 21, 22
    smoking in relation to, 58
    syphilis preventing, 45
    vitality of central nervous system essential to, 36
    _See also_ Old Age; Senescence

  Lorand, A., 70

  Lowe, Peter, 131

  Luciani, 18, 102

  Lungs, changes in, 103
    diseases of, 147, 148

  Lydston, G. F., 71

  Lymphadenoma, 141

  Lymphoid tissues, atrophy of, 63, 108


  Maclachlan, D., 144

  Maignon, Abbé, centenarian, 50

  Malignant disease, 87, 141
    cell senility in relation to, 88

  Mammae, involution changes in, 114

  Mania, senile, 145, 146

  Mansell-Moullin, C. W., 78

  Mansfield, Lord, octogenarian, 51

  Marasmus, senile, 139

  Marie, P., 146

  Marinesco, 64, 78, 83, 97

  Marx, K., 47

  Mead, Richard, 131

  Medical men, centenarians among, 52
    duration of life of, 52, 53

  Melancholia, senile, 146

  Memory, impairment and loss of, 120, 122

  Menopause, onset of old age at the, 26
    ovarian changes at, 63, 79

  Mental activity, influence on old age, 47, 48, 50, 54
    unimpaired, in advanced age, examples of, 50, 51, 53

  Mental deterioration, 49, 119, 122, 145, 146
    causes of, 47, 48, 49
    onset of, 53

  Mental fatigue, tendency to, 120

  Mental state, 119, 122, 123
    and the physical, want of harmony between, 123
    influence of, 48–50

  Metabolism, disordered, 115, 116, 117, 154
    gland therapy stimulating, 72, 81

  Metchnikoff, E., 8, 13, 18, 82–86, 91, 97, 123

  Methuselah, 14

  Michael Angelo, mental activity at advanced age, 53

  Micturition, disorders of, 153

  Middle ear lesions, 143

  Migraine, 140

  Miles, W. E., 153

  Mind, 121
    and body, in old age, 47, 50
    disintegration of, 120
    disorders of, 122, 145, 146
    _See also_ Mental

  Molière, 53

  Mönckeberg’s sclerosis, 106
    causes of, 142

  Montaigne, 14, 56

  Moon, R. O., 136

  Moore, Norman, 5

  Morbus coxae senilis, 155

  Morphine, 127, 128

  Mott, F. W., on functions of cells of testes and ovaries, 75

  Muscles, voluntary, changes in, 103

  Muscular activity, danger of excess of, 54
    impaired, 99, 119, 135

  Muscular atrophy, 99, 119, 135
    among workmen, 54

  Myocardium, degeneration of, 104, 149

  Myxoedema, as secondary senilism, 72


  Nails, condition and appearance of, 96

  Nanism, senile type of, 31

  Nascher, I. L., 30, 98, 127

  Nathan, 68, 74

  National habits, influence on longevity, 40

  Natural death. _See_ Death

  Neck, senile tremor of, 143

  Nemenow, 112

  Nephropathy, chronic atrophic, 111

  Nerves, cutaneous exposure of, 141

  Nervous apprehension, tendency to, 122

  Nervous disease, 145

  Nervous system, 38
    vitality of, hereditary factor in longevity, 36

  Neurasthenia, 122

  New growths, rarity of, 87, 89

  Newton, Isaac, 53

  Nicotine, effects of, 59

  Nunneley, F. P., 151


  Obesity, 60

  Occupational neuroses, 54

  Octogenarians, among active professional men, 51
    census statistics of, 21

  Oertel, H., 88

  Old age, acceleration of, factors favouring, 26
    anatomical and physiological changes in, 63
    as a disease, 47, 136
    attainment of, on what dependent, 6, 7, 10
    biochemistry of, 64–68
    biological aspect of, 10, 11, 23
    bodily conformation in, 60
    causes of, 62–89
    cell changes leading to, 64, 65
    “cell-memory” in relation to, 35
    comparative freedom from chronic disease in, 44
    death during, common causes of, 38
    disabilities of, 137
    disease in relation to, 44
    diseases associated with, 93–114, 139–156
    fertility rate in relation to, 23, 24, 26
    glandular, endocrine, theory of, 70, 71, 81
    healthy and morbid, distinction between, 135
    hereditary aspects of, 32–39
    hygiene of, 55–61
    infantilism and, 31
    mental activity during, 50, 54
      examples of, 50, 51, 53
    natural death from, 14
    on what dependent, 10
    onset of, 26
      signs of, 29
    pathological, 30, 82, 90
      of septuagenarians, 53
    physiological, 26, 90, 135
    physiological and pathological confusion between, 90
      factors in, 26
    physiology of, 115
    premature, 30
      hot climates favouring, 26, 36
      intestinal stasis as a cause of, 85
      mental causes of, 48, 49
    production of, Metchnikoff’s theory, 83
    rarity of natural death from, 14, 91
    sex incidence of, 21, 22
    stages of, 29
    vitality of body cells in, 62–68
    writers on, 8, 15, 16
    _See also_ Senescence; Longevity

  Onychogryphosis, 96

  Ophülz, W., 105

  Oral sepsis, 44, 155

  Orthobiosis, 55, 84

  Osler, W., 2, 36, 151

  Osteitis deformans, 156

  Osteomalacia, senile, 139

  Osteoporosis, senile, 99

  Ovarian extract, rejuvenescence in relation to, 80

  Ovaries, activity and function of cells of, 73, 74
    degenerative changes in, 114
    fibrotic atrophy of, 63
      following menopause, 79
    in relation to senescence, 75
    internal secretion of, evidence of existence of, 79
    senile, 114

  Over-eating, 56, 118

  Overwork, danger of, 54

  Owen, I., 57


  Paget, James, 36, 138

  Paget’s disease of bone, 156

  Pain, blunting of sensibility to, 117

  Pallor, 93

  Pancreas, fibrotic atrophy of, 102

  Paralysis agitans, 144
    age and sex incidence of, 144
    causes of, 144
    senile tremor compared with, 143

  Paraplegia, senile, 138, 146
    causes of, 146, 147
    varieties of, 147

  Parathyroids, 110

  Parietal bones, changes in, 100

  Parkinsonian syndrome, 144

  Parr, Thomas, centenarian, 20

  Pathological old age, 53, 82, 90

  Patriarchal ages, length of the calendar during, 16

  Patriarchs, explanation of reputed old age of, 15, 16

  Pearson, K., 38, 86

  Pecten band, 152, 153

  Penis, changes in, 114

  Pennington, Isaac, 6

  Peristalsis, failure of, 152

  Philalethes, Eugenius, on old age, 15

  Phlebitis, 151

  Phlebosclerosis, 107

  Physical and mental states, want of harmony between, 123

  Physiological life of man, 19

  Physiological old age, 90
    and morbid senility, distinction between, 135–138

  Physiology of old age, 115–128

  Pigmentation, cellular, 103
    cutaneous, 93

  Piles, 153

  Pitman, Henry, medical centenarian, 52

  Pituitary extract, influence on weight and growth, 12
    rejuvenescence in relation to, 12, 80

  Pityriasis versicolor, 141

  Planarian flat worms, experimental modification of life cycle and
          growth of, 11

  Plasma, vital phenomena of, 65–67, 88

  Plethora, senile, 124

  Pneumonia, 147, 148
    disposition to, 140
    sudden death from, 117

  Premature senility, 30
    causes of, 48
    hot climates predisposing to, 26, 36
    syphilis producing, 45

  Presbyopia, 117

  Pringle, J. J., 94

  Prior, Matthew, 3

  Professional men, age of retirement of, 54
    longevity of, 50–54

  Progeria, 30

  Prostate gland, 27
    _climacterium virile_ due to changes in, 27
    hypertrophy of, 101, 112
      age incidence of, 140
      cause of, 112
      cell changes in, 112, 113
      glandular therapy of, 113
      vesical disorders due to, 153
    senile changes in, 111

  Protoplasm, products inimical to vitality of, 65
    vital phenomena of, 64, 65, 88

  Protozoa, rejuvenation and senescence in, 9–11

  Prurigo, senile, 141

  Pruritus, senile, 141, 142

  Pseudo-paraplegia, 146

  Psychical activity, diminished, 119

  Psychical fatigue, 122

  Puberty, functional activity of cells of testes and ovaries at, 75
    period of, 17

  “Puberty gland,” 73

  Puerilism, 122, 145

  Pulmonary changes, 103, 147

  Pulmonary tuberculosis, 148

  Pulse-pressure, 125

  Pulse-rate, 124

  Pupils, contraction of, 117

  Purgatives, 128

  Pyelonephritis, 154


  Quinquagenarians, diseases of, 140, 145, 156


  Rectum, faecal accumulation in, 152

  Reflexes, 119

  Regression, 122

  Rejuvenescence, 10
    associated with reproduction, 9, 10, 64
    attainment of old age dependent upon, 9, 10
    experimental production of, 76, 77
    following vasectomy, 78
    gland extracts in production of, 12, 73, 80, 81
    in animal life, 9, 10
    power of reproduction favouring, 23, 24, 69
    restricted diet in relation to, 56
    testicular grafts producing, 77

  Renal inadequacy, 126

  Reproductive power, favouring rejuvenescence, 23, 24, 69
    waning of, onset of old age following, 26
    prolongation of life after waning of, 23

  Retas, Joseph, centenarian, 33

  Rheumatism, in old age, 44

  Rhizomelic spondylitis, 155

  Rhondda, Lord, 49

  Richardson, B. W., on the duration of life, 18

  Rivers, W. H. R., 122

  Roberts, W., 154

  Robertson and Ray, 12, 60

  Rodent ulcer, 143

  Roussy, G., 103, 148

  Routh, Martin, centenarian, 50

  Roy, D., 32, 95

  Russian peasants, longevity of, 40


  Salimbeni and Gery, 63, 84, 93, 102

  Sand, K., 75

  Saundby, R., 8, 44, 85

  Savage, G., 34

  Sclerosis, arterial, 105–107
    Mönckeberg’s, 106, 142
    spinal, 97

  Scrotum, 114

  “Second childhood,” 122, 145

  Sedatives, 128

  Self-preservation, instinct of, 122

  Self-reliance, loss of, 48, 49

  Seminal tubules, activity and function of, 74
    atrophy of, 74, 112, 113
      prostatic enlargement following, 112
    regeneration of, 74

  Senescence, 136
    castration not a disposing factor to, 79
    causes of, 62–89
      Metchnikoff’s theory, 82, 83
      pathological, 82
      toxaemic, 82
    cell changes during, 62–68
      in ovaries and testes, 75, 76
    colloidal dehydration leading to, 64, 65
    diseases associated with, 139
    endocrine glands in relation to, 68–81
    healthy and morbid, distinction between, 135
    nosological compensations of, 140
    progress of, 135
    rarity of carcinoma in, 87
    rejuvenescence necessary to, 10
    thyroid deficiency in relation to, 72
    _See also_ Longevity; Old age

  Senile climacteric, 30

  Senile type of nanism, 31

  Senility, 136

  _Senium ex morbo_, 136

  Sense organs, impairment and failure of, 117–121

  Sensibility to pain, blunting of, 117

  Septuagenarians, nervous disease among, 145
    pathological old age of, 53

  Sex characters, secondary, cause of, 75
    following castration, 79

  Sex glands, changes in, _climacterium virile_ due to, 27
    internal secretion of, 70

  Sex incidence of old age, 21, 22

  Sexagenarians, diseases common to, 140
    nervous disease among, 145

  Sexual activity, as manifestation of bodily vigour, 69, 70
    duration of, 69
    leading to rejuvenescence, 69
    waning of, 126

  Sexual appetite, on what dependent, 75
    perverted, 114

  Sexual atrophy, as cause of old age and senility, 69–71

  Shaking palsy, 144

  Sharpey-Schafer, E. A., 63

  Sight, impairment of, 117

  Sinclair, John, 8, 20, 35

  Singer, C., 86

  Skeleton, changes in, 98

  Skin, 93, 115
    diseases of, 141
      disposition to, 141
    dry, 115
    venules and angiomas on, 108

  Skull, 100

  Sleep, diminished, 119
    over-indulgence in, 60

  Smell, impairment of sense of, 117

  Smith, John, 8, 131

  Smith, Lapthorn, 53

  Smoking, influence on longevity, 58–59

  Sophocles, mental activity at advanced age, 53

  Sour milk, destruction of intestinal bacteria by, 83

  Spasm of arteriosclerotic vessels, 151

  Spastic paraplegia, 147

  Spinal cord, degenerative changes in, 97, 147

  Spleen, atrophy of, 63, 109

  Spondylitis, rhizomelic, 155

  Spondylitis deformans, 99, 155

  Stapes, fixation of, 118

  Starvation, influencing the onset of senescence, 56, 57

  Starvation treatment, 56, 57

  Steinach, E., 11, 77, 78

  Sterne, John, on the attainment of old age, 16

  Stevenson, T. H. C., 41

  Strachey, L., 47

  Structural changes of the body, 90

  Symmers, D., 102

  Syphilis, influence on longevity, 45


  Taste, impairment of, 117

  Teeth, decay of, 44, 101
    loss of, 44, 45, 99, 101
      causes of, 101

  Temperance, a characteristic of centenarians, 57

  Temperature, and longevity, 26
    of body, 116

  Testes, atrophy of, 113
    cells of, activity and function of, 73, 74
      in relation to senescence, 75
    changes in, following vasectomy, 77, 78
    internal secretion of, 69–72, 74
    prostatic atrophy in relation to, 112

  Testicular extract, rejuvenescence in relation to, 80

  Testicular grafts, rejuvenation by, 71, 72, 77
    results of experiments, 76, 79

  Thompson, R. J. C., 37, 44, 49, 96, 125

  Thompson, W. J., 40

  Thrombosis, 144
    age incidence of, 145
    cerebral, 145
    venous, 151

  Thymus, atrophy of, 109

  Thyroid deficiency, 138
    baldness resulting from, 96
    effect on activity of body cells, 72
    prostatic enlargement in relation to, 113

  Thyroid extract, rejuvenescence in relation to, 80
    for prostatic enlargement, 113

  Thyroid gland, degenerative changes in, 109, 110

  Tinnitus, 118

  Tissues, connective, relation of cellular activity to, 68, 88, 89, 92

  Titian, 53

  Tobacco, and arteriosclerosis, 59
    influence on longevity, 58
    symptoms due to, 59

  Todd, R. E., 37, 44, 49, 125

  Toxaemia, as a cause of senescence, 82, 86
    degenerative changes due to, 44, 55, 56, 86
    intestinal, as cause of senescence, 82, 85
    over-eating causing, 56

  Transfusion, 66

  Tremor, senile, 143

  Tropical life, influence on longevity, 26, 36, 39

  Trousseau, 151

  Tuberculosis, senile, 148

  Tumours, 86, 141

  Turnbull, H. M., 106, 114


  Ulcer, rodent, 143

  Urea-nitrogen in the blood, 115

  Urinary bladder, hypertrophy of, 153

  Urine, condition of, 126

  Uterine changes, 114


  Valvulitis, chronic, 149, 150

  Vanity, senile, 120, 121

  Variation, correlated, 23

  Varicosity, 151

  Vascular lesions, 144

  Vasectomy, changes due to, 74
    changes in testes following, 77, 78
    effect on sexual activity, 76
    rejuvenescence following, 71, 78

  Veins, changes in, 108

  Venous thrombosis, 151

  Vertebrae, changes in shape of, 99

  Vertigo, causes of, 143

  Visceral degeneration, 102, 103

  Visceroptosis, 102

  Vitality, danger of excess of, 54
    loss of, 115, 119, 135
    waning of, 139

  Vitamins, influence on growth, 13

  Voltaire, mental activity at advanced age, 53

  Voronoff, testicular grafting by, 78


  Walker, Kenneth, on changes in the testes, 112
    on prostatic enlargement, 112, 113

  Walking, functional disturbances in, 147

  Waterhouse, B., on the onset of old age, 27

  Watson, Thomas, Linacre Lecturer, 5

  Weber, Hermann, 8, 34, 43, 57, 119

  Weber, Parkes, 35, 104

  Weissmann, 9, 16

  “Will to live,” 35, 47

  Will power, failure of, 122

  Williams, Leonard, 61, 113, 128

  Wilson, S. A. K., 144

  Wounds, healing of, 126

  Wrinkles, cause of, 93


  Yeo, B., 50


  Zorten, Petrasch, centenarian, 20


THE END


_Printed in Great Britain by_ R. & R. CLARK, LIMITED, _Edinburgh_.




By SIR HUMPHRY ROLLESTON, K.C.B., M.D.

DISEASES OF THE LIVER, GALL-BLADDER AND BILE-DUCTS

Second Edition. Illustrated. 8vo.

31s. 6d. net.


_LANCET._--“An admirable work of reference in every sense. It presents
all the information obtainable from a very wide experience and an
encyclopaedic acquaintance with the literature of the subject in a
practical, interesting, and readily available manner.... We feel
confident that it will long remain the standard work of reference upon
the subjects of which it treats.”

_BRITISH MEDICAL JOURNAL._--“This is the most considerable work on
diseases of the liver which has appeared since the classical treatise
of Murchison. It fully deserves to take a high place among modern
text-books, and we heartily congratulate Dr. Rolleston on his success.”

_EDINBURGH MEDICAL JOURNAL._--“This compendious treatise is a veritable
mine of information on diseases of the liver and biliary passages.
No aspect of the subject, however small, seems to have escaped the
author’s notice, and his elaborate descriptions of the pathology and
clinical signs of liver disease, drawn from his own large experience
and an exceptional acquaintance with the literature, render the book
invaluable for study and for reference.... Dr. Rolleston’s book is
unquestionably a standard authority, and is a model of what a treatise
on a single department of medicine ought to be.”


A SYSTEM OF MEDICINE

BY MANY WRITERS

Medium 8vo. Second Edition.

EDITED BY

THE RIGHT HON. SIR T. CLIFFORD ALLBUTT, K.C.B., F.R.S.

AND

SIR HUMPHRY ROLLESTON, K.C.B., M.D.


Vol. I. Prolegomena and Infectious Diseases. 31s. 6d. net.

Vol. II. Part I. Infectious Diseases (continued), Intoxications. 31s.
6d. net. Part II. Tropical Diseases and Animal Parasites. 31s. 6d. net.

Vol. III. Certain General Diseases, Diseases of the Stomach. 31s. 6d.
net.

Vol. IV. Part I. Diseases of the Liver, Pancreas, and Ductless Glands.
31s. 6d. net. Part II. Diseases of the Nose, Pharynx, Larynx, Trachea,
and Ear. 31s. 6d. net.

Vol. V. Diseases of the Respiratory System, Disorders of the Blood.
31s. 6d. net.

Vol. VI. Diseases of the Heart and Blood-Vessels. 31s. 6d. net.

Vol. VII. Diseases of the Muscles, the Tropho-neuroses, Diseases of the
Nerves, Vertebral Column, and Spinal Cord. 31s. 6d. net.

Vol. VIII. Diseases of the Brain and Mental Diseases. 31s. 6d. net.

Vol. IX. Diseases of the Skin. General Index. 31s. 6d. net.


LONDON: MACMILLAN AND CO., LTD.




Transcriber’s Notes


Punctuation and spelling were made consistent when a predominant
preference was found in this book; otherwise they were not changed.

Simple typographical errors were corrected; occasional unbalanced
quotation marks retained.

Ambiguous hyphens at the ends of lines were retained; occurrences of
inconsistent hyphenation have not been changed.

In Chapter VI, the word “The”, followed by the italicized name of an
organ, sometimes was italicized and sometimes was not. This possible
inconsistency has not been changed here.

Footnotes, originally at the bottoms of pages, have been collected and
placed just before the Index.

Index not checked for proper alphabetization or correct page references.

Page 3: “e sudore britanico” was printed with a macron above the “n”
(n̄).

Fig. 1: “Sir William Beechey” was printed as “Beeching”, but the name
appears correctly in Footnote 5, originally on page 4.





End of the Project Gutenberg EBook of Some Medical Aspects of Old Age, by 
Humphry Davy Rolleston

*** END OF THIS PROJECT GUTENBERG EBOOK SOME MEDICAL ASPECTS OF OLD AGE ***

***** This file should be named 57215-0.txt or 57215-0.zip *****
This and all associated files of various formats will be found in:
        http://www.gutenberg.org/5/7/2/1/57215/

Produced by Turgut Dincer, Charlie Howard, and the Online
Distributed Proofreading Team at http://www.pgdp.net (This
file was produced from images generously made available
by The Internet Archive)


Updated editions will replace the previous one--the old editions will
be renamed.

Creating the works from print editions not protected by U.S. copyright
law means that no one owns a United States copyright in these works,
so the Foundation (and you!) can copy and distribute it in the United
States without permission and without paying copyright
royalties. Special rules, set forth in the General Terms of Use part
of this license, apply to copying and distributing Project
Gutenberg-tm electronic works to protect the PROJECT GUTENBERG-tm
concept and trademark. Project Gutenberg is a registered trademark,
and may not be used if you charge for the eBooks, unless you receive
specific permission. If you do not charge anything for copies of this
eBook, complying with the rules is very easy. You may use this eBook
for nearly any purpose such as creation of derivative works, reports,
performances and research. They may be modified and printed and given
away--you may do practically ANYTHING in the United States with eBooks
not protected by U.S. copyright law. Redistribution is subject to the
trademark license, especially commercial redistribution.

START: FULL LICENSE

THE FULL PROJECT GUTENBERG LICENSE
PLEASE READ THIS BEFORE YOU DISTRIBUTE OR USE THIS WORK

To protect the Project Gutenberg-tm mission of promoting the free
distribution of electronic works, by using or distributing this work
(or any other work associated in any way with the phrase "Project
Gutenberg"), you agree to comply with all the terms of the Full
Project Gutenberg-tm License available with this file or online at
www.gutenberg.org/license.

Section 1. General Terms of Use and Redistributing Project
Gutenberg-tm electronic works

1.A. By reading or using any part of this Project Gutenberg-tm
electronic work, you indicate that you have read, understand, agree to
and accept all the terms of this license and intellectual property
(trademark/copyright) agreement. If you do not agree to abide by all
the terms of this agreement, you must cease using and return or
destroy all copies of Project Gutenberg-tm electronic works in your
possession. If you paid a fee for obtaining a copy of or access to a
Project Gutenberg-tm electronic work and you do not agree to be bound
by the terms of this agreement, you may obtain a refund from the
person or entity to whom you paid the fee as set forth in paragraph
1.E.8.

1.B. "Project Gutenberg" is a registered trademark. It may only be
used on or associated in any way with an electronic work by people who
agree to be bound by the terms of this agreement. There are a few
things that you can do with most Project Gutenberg-tm electronic works
even without complying with the full terms of this agreement. See
paragraph 1.C below. There are a lot of things you can do with Project
Gutenberg-tm electronic works if you follow the terms of this
agreement and help preserve free future access to Project Gutenberg-tm
electronic works. See paragraph 1.E below.

1.C. The Project Gutenberg Literary Archive Foundation ("the
Foundation" or PGLAF), owns a compilation copyright in the collection
of Project Gutenberg-tm electronic works. Nearly all the individual
works in the collection are in the public domain in the United
States. If an individual work is unprotected by copyright law in the
United States and you are located in the United States, we do not
claim a right to prevent you from copying, distributing, performing,
displaying or creating derivative works based on the work as long as
all references to Project Gutenberg are removed. Of course, we hope
that you will support the Project Gutenberg-tm mission of promoting
free access to electronic works by freely sharing Project Gutenberg-tm
works in compliance with the terms of this agreement for keeping the
Project Gutenberg-tm name associated with the work. You can easily
comply with the terms of this agreement by keeping this work in the
same format with its attached full Project Gutenberg-tm License when
you share it without charge with others.

1.D. The copyright laws of the place where you are located also govern
what you can do with this work. Copyright laws in most countries are
in a constant state of change. If you are outside the United States,
check the laws of your country in addition to the terms of this
agreement before downloading, copying, displaying, performing,
distributing or creating derivative works based on this work or any
other Project Gutenberg-tm work. The Foundation makes no
representations concerning the copyright status of any work in any
country outside the United States.

1.E. Unless you have removed all references to Project Gutenberg:

1.E.1. The following sentence, with active links to, or other
immediate access to, the full Project Gutenberg-tm License must appear
prominently whenever any copy of a Project Gutenberg-tm work (any work
on which the phrase "Project Gutenberg" appears, or with which the
phrase "Project Gutenberg" is associated) is accessed, displayed,
performed, viewed, copied or distributed:

  This eBook is for the use of anyone anywhere in the United States and
  most other parts of the world at no cost and with almost no
  restrictions whatsoever. You may copy it, give it away or re-use it
  under the terms of the Project Gutenberg License included with this
  eBook or online at www.gutenberg.org. If you are not located in the
  United States, you'll have to check the laws of the country where you
  are located before using this ebook.

1.E.2. If an individual Project Gutenberg-tm electronic work is
derived from texts not protected by U.S. copyright law (does not
contain a notice indicating that it is posted with permission of the
copyright holder), the work can be copied and distributed to anyone in
the United States without paying any fees or charges. If you are
redistributing or providing access to a work with the phrase "Project
Gutenberg" associated with or appearing on the work, you must comply
either with the requirements of paragraphs 1.E.1 through 1.E.7 or
obtain permission for the use of the work and the Project Gutenberg-tm
trademark as set forth in paragraphs 1.E.8 or 1.E.9.

1.E.3. If an individual Project Gutenberg-tm electronic work is posted
with the permission of the copyright holder, your use and distribution
must comply with both paragraphs 1.E.1 through 1.E.7 and any
additional terms imposed by the copyright holder. Additional terms
will be linked to the Project Gutenberg-tm License for all works
posted with the permission of the copyright holder found at the
beginning of this work.

1.E.4. Do not unlink or detach or remove the full Project Gutenberg-tm
License terms from this work, or any files containing a part of this
work or any other work associated with Project Gutenberg-tm.

1.E.5. Do not copy, display, perform, distribute or redistribute this
electronic work, or any part of this electronic work, without
prominently displaying the sentence set forth in paragraph 1.E.1 with
active links or immediate access to the full terms of the Project
Gutenberg-tm License.

1.E.6. You may convert to and distribute this work in any binary,
compressed, marked up, nonproprietary or proprietary form, including
any word processing or hypertext form. However, if you provide access
to or distribute copies of a Project Gutenberg-tm work in a format
other than "Plain Vanilla ASCII" or other format used in the official
version posted on the official Project Gutenberg-tm web site
(www.gutenberg.org), you must, at no additional cost, fee or expense
to the user, provide a copy, a means of exporting a copy, or a means
of obtaining a copy upon request, of the work in its original "Plain
Vanilla ASCII" or other form. Any alternate format must include the
full Project Gutenberg-tm License as specified in paragraph 1.E.1.

1.E.7. Do not charge a fee for access to, viewing, displaying,
performing, copying or distributing any Project Gutenberg-tm works
unless you comply with paragraph 1.E.8 or 1.E.9.

1.E.8. You may charge a reasonable fee for copies of or providing
access to or distributing Project Gutenberg-tm electronic works
provided that

* You pay a royalty fee of 20% of the gross profits you derive from
  the use of Project Gutenberg-tm works calculated using the method
  you already use to calculate your applicable taxes. The fee is owed
  to the owner of the Project Gutenberg-tm trademark, but he has
  agreed to donate royalties under this paragraph to the Project
  Gutenberg Literary Archive Foundation. Royalty payments must be paid
  within 60 days following each date on which you prepare (or are
  legally required to prepare) your periodic tax returns. Royalty
  payments should be clearly marked as such and sent to the Project
  Gutenberg Literary Archive Foundation at the address specified in
  Section 4, "Information about donations to the Project Gutenberg
  Literary Archive Foundation."

* You provide a full refund of any money paid by a user who notifies
  you in writing (or by e-mail) within 30 days of receipt that s/he
  does not agree to the terms of the full Project Gutenberg-tm
  License. You must require such a user to return or destroy all
  copies of the works possessed in a physical medium and discontinue
  all use of and all access to other copies of Project Gutenberg-tm
  works.

* You provide, in accordance with paragraph 1.F.3, a full refund of
  any money paid for a work or a replacement copy, if a defect in the
  electronic work is discovered and reported to you within 90 days of
  receipt of the work.

* You comply with all other terms of this agreement for free
  distribution of Project Gutenberg-tm works.

1.E.9. If you wish to charge a fee or distribute a Project
Gutenberg-tm electronic work or group of works on different terms than
are set forth in this agreement, you must obtain permission in writing
from both the Project Gutenberg Literary Archive Foundation and The
Project Gutenberg Trademark LLC, the owner of the Project Gutenberg-tm
trademark. Contact the Foundation as set forth in Section 3 below.

1.F.

1.F.1. Project Gutenberg volunteers and employees expend considerable
effort to identify, do copyright research on, transcribe and proofread
works not protected by U.S. copyright law in creating the Project
Gutenberg-tm collection. Despite these efforts, Project Gutenberg-tm
electronic works, and the medium on which they may be stored, may
contain "Defects," such as, but not limited to, incomplete, inaccurate
or corrupt data, transcription errors, a copyright or other
intellectual property infringement, a defective or damaged disk or
other medium, a computer virus, or computer codes that damage or
cannot be read by your equipment.

1.F.2. LIMITED WARRANTY, DISCLAIMER OF DAMAGES - Except for the "Right
of Replacement or Refund" described in paragraph 1.F.3, the Project
Gutenberg Literary Archive Foundation, the owner of the Project
Gutenberg-tm trademark, and any other party distributing a Project
Gutenberg-tm electronic work under this agreement, disclaim all
liability to you for damages, costs and expenses, including legal
fees. YOU AGREE THAT YOU HAVE NO REMEDIES FOR NEGLIGENCE, STRICT
LIABILITY, BREACH OF WARRANTY OR BREACH OF CONTRACT EXCEPT THOSE
PROVIDED IN PARAGRAPH 1.F.3. YOU AGREE THAT THE FOUNDATION, THE
TRADEMARK OWNER, AND ANY DISTRIBUTOR UNDER THIS AGREEMENT WILL NOT BE
LIABLE TO YOU FOR ACTUAL, DIRECT, INDIRECT, CONSEQUENTIAL, PUNITIVE OR
INCIDENTAL DAMAGES EVEN IF YOU GIVE NOTICE OF THE POSSIBILITY OF SUCH
DAMAGE.

1.F.3. LIMITED RIGHT OF REPLACEMENT OR REFUND - If you discover a
defect in this electronic work within 90 days of receiving it, you can
receive a refund of the money (if any) you paid for it by sending a
written explanation to the person you received the work from. If you
received the work on a physical medium, you must return the medium
with your written explanation. The person or entity that provided you
with the defective work may elect to provide a replacement copy in
lieu of a refund. If you received the work electronically, the person
or entity providing it to you may choose to give you a second
opportunity to receive the work electronically in lieu of a refund. If
the second copy is also defective, you may demand a refund in writing
without further opportunities to fix the problem.

1.F.4. Except for the limited right of replacement or refund set forth
in paragraph 1.F.3, this work is provided to you 'AS-IS', WITH NO
OTHER WARRANTIES OF ANY KIND, EXPRESS OR IMPLIED, INCLUDING BUT NOT
LIMITED TO WARRANTIES OF MERCHANTABILITY OR FITNESS FOR ANY PURPOSE.

1.F.5. Some states do not allow disclaimers of certain implied
warranties or the exclusion or limitation of certain types of
damages. If any disclaimer or limitation set forth in this agreement
violates the law of the state applicable to this agreement, the
agreement shall be interpreted to make the maximum disclaimer or
limitation permitted by the applicable state law. The invalidity or
unenforceability of any provision of this agreement shall not void the
remaining provisions.

1.F.6. INDEMNITY - You agree to indemnify and hold the Foundation, the
trademark owner, any agent or employee of the Foundation, anyone
providing copies of Project Gutenberg-tm electronic works in
accordance with this agreement, and any volunteers associated with the
production, promotion and distribution of Project Gutenberg-tm
electronic works, harmless from all liability, costs and expenses,
including legal fees, that arise directly or indirectly from any of
the following which you do or cause to occur: (a) distribution of this
or any Project Gutenberg-tm work, (b) alteration, modification, or
additions or deletions to any Project Gutenberg-tm work, and (c) any
Defect you cause.

Section 2. Information about the Mission of Project Gutenberg-tm

Project Gutenberg-tm is synonymous with the free distribution of
electronic works in formats readable by the widest variety of
computers including obsolete, old, middle-aged and new computers. It
exists because of the efforts of hundreds of volunteers and donations
from people in all walks of life.

Volunteers and financial support to provide volunteers with the
assistance they need are critical to reaching Project Gutenberg-tm's
goals and ensuring that the Project Gutenberg-tm collection will
remain freely available for generations to come. In 2001, the Project
Gutenberg Literary Archive Foundation was created to provide a secure
and permanent future for Project Gutenberg-tm and future
generations. To learn more about the Project Gutenberg Literary
Archive Foundation and how your efforts and donations can help, see
Sections 3 and 4 and the Foundation information page at
www.gutenberg.org Section 3. Information about the Project Gutenberg
Literary Archive Foundation

The Project Gutenberg Literary Archive Foundation is a non profit
501(c)(3) educational corporation organized under the laws of the
state of Mississippi and granted tax exempt status by the Internal
Revenue Service. The Foundation's EIN or federal tax identification
number is 64-6221541. Contributions to the Project Gutenberg Literary
Archive Foundation are tax deductible to the full extent permitted by
U.S. federal laws and your state's laws.

The Foundation's principal office is in Fairbanks, Alaska, with the
mailing address: PO Box 750175, Fairbanks, AK 99775, but its
volunteers and employees are scattered throughout numerous
locations. Its business office is located at 809 North 1500 West, Salt
Lake City, UT 84116, (801) 596-1887. Email contact links and up to
date contact information can be found at the Foundation's web site and
official page at www.gutenberg.org/contact

For additional contact information:

    Dr. Gregory B. Newby
    Chief Executive and Director
    gbnewby@pglaf.org

Section 4. Information about Donations to the Project Gutenberg
Literary Archive Foundation

Project Gutenberg-tm depends upon and cannot survive without wide
spread public support and donations to carry out its mission of
increasing the number of public domain and licensed works that can be
freely distributed in machine readable form accessible by the widest
array of equipment including outdated equipment. Many small donations
($1 to $5,000) are particularly important to maintaining tax exempt
status with the IRS.

The Foundation is committed to complying with the laws regulating
charities and charitable donations in all 50 states of the United
States. Compliance requirements are not uniform and it takes a
considerable effort, much paperwork and many fees to meet and keep up
with these requirements. We do not solicit donations in locations
where we have not received written confirmation of compliance. To SEND
DONATIONS or determine the status of compliance for any particular
state visit www.gutenberg.org/donate

While we cannot and do not solicit contributions from states where we
have not met the solicitation requirements, we know of no prohibition
against accepting unsolicited donations from donors in such states who
approach us with offers to donate.

International donations are gratefully accepted, but we cannot make
any statements concerning tax treatment of donations received from
outside the United States. U.S. laws alone swamp our small staff.

Please check the Project Gutenberg Web pages for current donation
methods and addresses. Donations are accepted in a number of other
ways including checks, online payments and credit card donations. To
donate, please visit: www.gutenberg.org/donate

Section 5. General Information About Project Gutenberg-tm electronic works.

Professor Michael S. Hart was the originator of the Project
Gutenberg-tm concept of a library of electronic works that could be
freely shared with anyone. For forty years, he produced and
distributed Project Gutenberg-tm eBooks with only a loose network of
volunteer support.

Project Gutenberg-tm eBooks are often created from several printed
editions, all of which are confirmed as not protected by copyright in
the U.S. unless a copyright notice is included. Thus, we do not
necessarily keep eBooks in compliance with any particular paper
edition.

Most people start at our Web site which has the main PG search
facility: www.gutenberg.org

This Web site includes information about Project Gutenberg-tm,
including how to make donations to the Project Gutenberg Literary
Archive Foundation, how to help produce our new eBooks, and how to
subscribe to our email newsletter to hear about new eBooks.