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Chapter 26
Health and Immortality
Ilia Stambler
Abstract Is maintaining good health potentially compatible with a significant
or radical life extension? Historically, these phenomena have often been seen as
conflicting. Their potential principal incompatibility has often been derived from
either health (functional capacity) or lifespan being understood as finite or limited
values. The various concepts of limitations to the lifespan or health quantity are
surveyed in this work in their historical development, with reference to several domi-
nant theories of aging and mortality. The incompleteness and ambiguities of the limi-
tation theories are demonstrated. Thus, even when proposing limits to the lifespan or
healthspan, these limits have often been seen, evenby the same authors, as flexible and
modifiable. The exact conditions under which lifespan and healthspan “limitations”
end and the “possibilities” of their enhancement begin have remained uncertain in the
absence of a reliable quantitative formal theory of aging and mortality. An alternative
“life-extensionist” view assumes the potential replenishment of any vital resources
expended, and thus presumes no inherent natural limitations to either the lifespan or
health quantity (functional capacity). The validity of either of those views may be
tested in the future with the development of new medical technologies and a better
theoretical understanding of health, aging and mortality.
Keywords Health ·Lifespan ·Healthspan ·Functional capacity ·Aging ·Theory
of mortality ·Compression of morbidity ·Longevity dividend ·Rejuvenation ·
Life-extensionists
I. Stambler (B
)
Research division, Vetek (Seniority) Association – the Movement for Longevity and Quality of
Life, Tel Aviv, Israel
e-mail: ilia.stambler@gmail.com
© Springer Nature Switzerland AG 2020
J. Sholl and S. Rattan (eds.), Explaining Health Across the Sciences, Healthy Ageing
and Longevity 12, https://doi.org/10.1007/978- 3-030- 52663-4_26
453
454 I. Stambler
26.1 Is Significant Life Extension Compatible with Good
Health?
This essay will consider the principal question of the compatibility of health and
immortality. Can good health coexist with immortality? Here “immortality” is under-
stood as a trope implying a significant or radical lifespan extension, or unlimited life
extension, insofar as literal “immortality” or the certainty of having lived an infinite
amount of time is logically unattainable. In contrast, there is no law of logic or nature
that precludes the possibility of a significant, radical or even indefinite life extension,
even though it is at present technically unattainable. It is in this latter sense of a theo-
retical possibility of radical life extension that the term “immortality” is used here.
Would this radical life extension be commensurable with good health or functional
capacity?
A long philosophical and literary tradition has assumed they would not be compat-
ible (Stambler 2014). Such assumptions were likely based on the common obser-
vation that long-lived people are usually unhealthy at the end of their lives and the
commonsensical, though somewhat a priori, conclusion has been that if the end-of-
life period is extended, the illnesses of that period will also be extended, and thus
good health cannot be concomitant with radical life extension.
The archetype for this line of thought has been the ancient Greek story of
Tithonus, the lover of Eos the Goddess of the Dawn, who obtained from her the gift
of immortality. Yet, in his flawed human nature, he forgot to ask for eternal youth,
thus the gift of immortality became a curse of eternal suffering. This story has been
persistent and highly influential in the history of ideas about life extension. It first
appeared in the Homeric Hymn to Aphrodite (c. 7th or 8th century BC), was reintro-
duced in Ovid’s Metamorphoses (8 AD) (Ovid 1994) and to the present it has been
invoked in almost every philosophical discussion of the consequences of extreme
longevity. Another resounding instance of this archetype occurs in Jonathan Swift’s
Gulliver’s Travels (1726) that features the immortal Struldbrugs eternally suffering
from mental and physical debility (Swift 1892). There are other instances, but the
general presumption remains that, insofar as the end-of-life period is commonly
associated with disease and suffering, the extension of life will also be associated
with disease and suffering, and thus extreme longevity would be incompatible with
good health. This view has entailed a principal opposition to the pursuit of extreme
longevity.
The incompatibility of health and extreme longevity has been commonly assumed
by opponents of life extension. Yet, intriguingly, the idea that health may be at odds
with longevity also appears in the works of staunch life extension advocates, though
with a more positive perspective for longevity. This can be seen in the writings of
the German prolongevity hygienist Christoph Wilhelm Hufeland (1762–1836), the
author of the term “macrobiotics” that has survived to the present. In Macrobiotics
or the Art of Prolonging Human Life (1796), Hufeland thus distinguished the art of
life extension from the general medical art, and suggested that longevity and absence
of diseases are not necessarily equivalent (Wilson 1867, pp. IX–X):
26 Health and Immortality 455
This art [of prolonging life], however, must not be confounded with the common art of
medicine or medical regimen; its object, means, and boundaries, are different. The object of
medical art is health; that of the macrobiotic, long life. The means employed in the medical
art are regulated according to the present state of the body and its variations; those of the
macrobiotic, by general principles. In the first it is sufficient if one is able to restore that
health which has been lost; but no person thinks of inquiring whether, by the means used for
that purpose, life, upon the whole, will be lengthened or shortened; and the latter is often the
case in many methods employed in medicine. The medical art must consider every disease
as an evil, which cannot be too soon expelled; the macrobiotic, on the other hand, shows
that many diseases may be the means of prolonging life. The medical art endeavors, by
corroborative and other remedies, to elevate mankind to the highest degree of strength and
physical perfection; while the macrobiotic proves that here even there is a maximum, and
that strengthening, carried too far, may tend to accelerate life, and consequently, to shorten
its duration. The practical part of medicine, therefore, in regard to the macrobiotic art, is to be
considered only as an auxiliary science which teaches us how to know diseases, the enemies
of life, and how to prevent and expel them; but which, however, must itself be subordinate
to the highest laws of the latter.
Indeed, the emphasis on the treatment of particular diseases may distinguish general
medical practice from the pursuit of life extension. The cure of a disease might
be more readily and immediately perceived, while the ascertainment of human life
extension may be a more lengthy and confounded process. Moreover, the possibility
of “radical life extension” can hardly become subject to empirical confirmation any
time soon. These might be some of the reasons that, until quite recently, the terms
“life extension” or “lifespan increase” or “longevity extension” have not been regu-
larly considered in biological or medical discourse. And critically for the present
discussion, life extension may not be seen as necessarily tantamount to good health.
26.2 The Limits to Life and the Limits to Health
Another well-established intellectual tradition dealing with the relation of health and
life extension has presumed a strict limit to the maximum lifespan and/or maximum
inherent health quantity necessary to sustain life. In a sense, this is an even more
pessimistic position than just presuming the incompatibility of life extension with
good health as adversely influencing each other, seen in the former examples (when
life extension is perceived to come at the expense of health, and vice versa). When
presupposing limits to life or health, health may be conducive to longevity. However,
insofar as health is a limited quantity, also longevity cannot be significantly extended,
and vice versa. This view essentially presupposes the incompatibility of life exten-
sion with the continuation of life itself, due to fundamental health- and life-limiting
mechanisms inherent in living beings, as paradoxical as this statement may sound. In
this view, insofar as some degree of health (understood here as functional capacity)
would be needed to continue life, this capacity simply could not be maintained for
an indefinitely prolonged time, due to an inherent limit to life prolongation and/or
an inherent limit to the functional capacity.
456 I. Stambler
The latter line of thought arguably has the same conceptual basis as the former
one that posited the incompatibility of life extension with maintaining good health,
namely both presume health (functional capacity) to be a limited quantity. What
differs is the emphasis and the presumed temporal mode of distribution of that limited
quantity. In the former view, there would not be enough ‘health quantity’ to last, hence
life could only be extended with a diminished health. In the latter view, health would
only suffice for a limited time beyond which life prolongation would be impossible.
But in both ramifications, the presumption of inherent limits to health and life is
fundamental.
Yet crucially, at the same time, it has also been realized in the history of ideas about
health and life extension, even by the very same thinkers who proposed “limits” to
the lifespan and/or the life-sustaining health quantity, that these “limits” are rather
flexible and the duration of life and quantifies of health are quite modifiable. The
exact extent where the health and lifespan’s “inherent limitations” would end and
healthy life extension “possibilities” begin, has remained uncertain.
Thus, the founder of Gerontology Elie Metchnikoff posited in 1903 the inherent
disharmony of human nature that eventually leads to human demise (Metchnikoff
1961). Yet, he also maintained that under proper “orthobiotic” conditions, human
life can be extended to 150 years and beyond. Similarly, the American pioneer of
aging research Raymond Pearl argued that the dissonance of differentiated body
parts is inexorably engraved in human nature, and that the lifespan is an inherited
quantity that can only be manipulated to a very limited degree (Pearl 1922). And yet,
in Pearl’s experiments, the lifespan of Drosophila flies was extended significantly by
genetic selection, decreasing the population density, chemical stimulants, or else by
lowering the temperature of their environment and reducing their food supply, gener-
ally decreasing their “rate of living.” The German physiologist Max Rubner famously
posited a limited amount of metabolic activity for any species during their lifespan
(Rubner 1908). He found that most mammals, during their life course, consume about
the same amount of energy per kilogram body weight (approximately 200,000 kcal)
and die when the “life-energy” quota is spent. According to Rubner, for man the
value is outstandingly high (~725,000 kcal), but is a preordained quantity nonethe-
less. Intense metabolic activity was, in this view, fatal. Nonetheless, he also believed
in the possibility of life prolongation, according to his famous dictum that “the art
of prolonging life consists in learning not to shorten it” (Lautenbach 2010, p. 25).
The uncertainties regarding the “limits” to the human lifespan and health have
persisted for quite some time, with their discussion intensifying in the late 1970s—
early 1980s. Thus, Nathan Keyfitz (1913–2010) of Harvard upheld the so-called
“Taeuber Paradox” (named after Conrad Taeuber, 1906–1999, Chief of the Population
Division of the US Census Bureau who observed the phenomenon), which suggested
that aging organisms become generally frail, and therefore, if an aging person will not
die of one age-related disease, he will die of another. Consequently, even the entire
elimination of a major age-related disease, such as cancer, will not significantly
increase the general life-expectancy, as some new disease will come in its place.
As Keyfitz wrote: “A cure for cancer would only have the effect of giving people
the opportunity to die of heart disease.” This was a major motivation damper for
26 Health and Immortality 457
attempting to find cures against specific age-related diseases, and clearly posited the
incompatibility of life extension with absence of diseases (Keyfitz 1977). However,
in the same article, Keyfitz stated: “If cancer, heart disease, etc., are merely alternative
ways in which the aging of body cells makes itself manifest, then eradicating any
one of them may make little difference. The proper entity to attack is the process
of aging itself.” Elsewhere, Keyfitz further advocated for increasing research into
cellular senescence, as an underlying general cause of many age-related diseases,
rather than into any specific single disease. Such research would allow us “to break
through the barrier that now seems to be set at about 80 years” (Keyfitz 1978).
Further, the Stanford gerontologists James F. Fries and Lawrence M. Crapo,
in Vitality and Aging. Implications of the Rectangular Curve, posited that “the
maximum life span is fixed at about 100 years, and the median life span is fixed
at about 85 years” (Fries and Crapo 1981, p. 140). This “natural” lifespan is deter-
mined by “a steady decline in homeostasis and organ reserve in many vital systems”
(Fries and Crapo 1981, p. 136). This decline in organ reserves results in an exponen-
tial increase in the mortality rate with age (Fries and Crapo 1981, p. 37). The authors
predicted that a society will increasingly progress toward a “rectangular survival
curve” when health care measures will produce a “compression of morbidity.” This
basically implied that people will remain sufficiently healthy until the age of about 85
and then collapse and die rapidly, saving on national health care expenditures. This
scenario has been elaborated and disseminated (Fries 1980,1983) and has become
highly influential for the later concepts of “healthy aging.” The authors called such
a scenario “optimistic” and “a celebration of life.” Still, the authors believed that
“if we could understand the aging process at the cellular level and its underlying
molecular mechanisms, then we might be able to alter the information units in the
cells and thereby alter the life span” (Fries and Crapo 1981, p. 135, 139).
In contrast to Fries and Crapo’s ideal of the “compression of morbidity,” an
“expansion of morbidity” was often observed in conjunction with life extension, as for
example in the seminal work by the American psychiatrist and epidemiologist Ernest
M. Gruenberg, “The failures of success” (Gruenberg 1977). Despite the differences
of emphases, the main conclusions are similar in that limitations are assumed for the
extension of life and of health. Moreover, the extension of life by medical technology
is observed often to limit the sum total of population health. As Gruenberg noted, “The
goal of medical research work is to ‘diminish disease and enrich life’, but it produced
tools which prolong diseased, diminished lives and so increase the proportion of
people who have a disabling or chronic disease.” The recommendations from the
“expansion of morbidity” perception are also similar to those from the “compression
of morbidity” vision, namely the ensuing appeal to increase the portion of health
research and health care dedicated to prevention of chronic diseases. In this way, it
would be possible to achieve the extension of life concomitant with the extension of
health.
Further limits on the human lifespan—biological, technological, ethical and
economic—were proposed by J. Michael McGinnis, of the US Department of Health
and Human Services, in 1985. Yet, McGinnis concluded with “an essentially opti-
mistic perspective.” For example, regarding the limits imposed on life extension by
458 I. Stambler
the deficiencies of available technology, the pace of technological change was said
to be rapid and “the limits of today will become the opportunities of tomorrow”
(McGinnis 1985).
The question of the “limits” to the human life span and life expectancy has
remained open to the present. Thus, at the turn of the twenty-first century, the geron-
tologists Stuart Jay Olshansky of the University of Illinois at Chicago and Bruce
Alfred Carnes of the University of Oklahoma, in The Quest for Immortality. Science
at the Frontiers of Aging (2001) suggested that “given the current state of medical
technology, life expectancy at birth will not rise above 85 years.” But the qualifica-
tion regarding “the current state of medical technology” seems to be crucial. “The
legitimate science of aging,” the authors maintained, “has already led to remarkable
extensions of life for many people. We can expect the hard work of researchers and
medical practitioners to add to that success in the future.” Thus, once again, a limit
to the lifespan is posited, but it was understood that it can be quite flexible and modi-
fiable. As the author admit, “The ongoing debate over limits to life expectancy is not
likely to be resolved any time soon” (Olshansky and Carnes 2001, p. 142, 149, 211,
219).
Later on, Olshansky and collaborators have developed those ideas and dissemi-
nated the notion of the “Longevity Dividend” based on the concept of “healthspan”
(healthy lifespan) extension, namely the aspiration to use medical technology to
increase the healthy life expectancy in the population, while keeping constant or
changing little the general life expectancy. Simply put, in this view, people are hoped,
so to paraphrase, ‘to die healthy’ or ‘live healthy until their death’ (or almost until
their death). The achievement of this visionary scenario is supposed to produce
massive savings (“dividends”) for the healthcare and welfare systems (Olshansky
et al. 2006; Olshansky 2019). The same vision is presupposed by the “Geroscience”
school of gerontology who perceive aging as the main “risk factor” for multiple age-
related diseases and hope that by intervening into the aging process it may be possible
to postpone the emergence of those diseases and increase the population’s healthy
life expectancy or healthy lifespan, but not necessarily the general life expectancy
or lifespan. Or, at the very least, the gains in healthy life expectancy are hoped to
exceed the gains in general life expectancy (Sierra and Kohanski 2017). In fact, this
view posits a limit to the human lifespan, but not to the healthspan (until it reaches
the value of the lifespan). It assumes the ability of biomedical technology to inter-
vene into human biology, but only to modify the “healthspan” up to that lifespan
limit. Thus, the uncertainties and ambiguities concerning the limits of life and health
extension have remained.
26.3 Theories of Mortality
Despite the ambiguity regarding the actual value of the “limits” of lifespan vs. “pos-
sibilities” of life and health extension, the existence of some limits to life extension
and/or health extension, and their potential incompatibility, were posited by the
26 Health and Immortality 459
majority of researchers of aging so far. But what is the precise law of this compati-
bility or incompatibility? Why is it, exactly, that life cannot be extended indefinitely
and health improved indefinitely, as assumed by the proponents of the lifespan or
health limitations? Or else, why should people “die healthy” as professed by the advo-
cates of the “compression of morbidity” scenario? Why would the “one-hoss shay”
metaphor often used in the “compression of morbidity” discussions (Holmes 1858;
Fries and Crapo 1981), where the “shay” (carriage) stands intact until it suddenly falls
apart in its entirety, be relevant for the human organism? Or why, in principle, can’t
people continue to live on healthily while their life is being extended, as maintained
by the observers of “expansion of morbidity”? These are fundamental theoretical
questions that could be answered by formal, mechanistic and mathematical theory-
based models of aging and mortality. Such quantitative theoretical models might be
able, in principle, also to account for or predict, in a formal and quantitative manner,
the actual values for the “limits” or “possibilities” for life and health extension. Yet,
there has been a traditional scarcity of such models. Indeed, any theory of aging may
be perceived as an explanation of the limit of life or health, or of the incompatibility
of life extension with health extension. Yet, formal, mathematical and mechanistic
explanations have been few. This may have been partly due to the paucity of rele-
vant data and partly due to the specifics of common training of biologists of aging
and gerontologists that placed less emphasis on formal mathematical modeling. Yet
some formal theories started to be developed, about 60 years ago, in the 1950s–1960s.
Since then, the formal mathematical theories of aging and mortality appear not to
have developed very strongly, but mainly reiterated the original premises.
The theories of mortality developed in the 1950s built on much earlier concepts,
such as Benjamin Gompertz’s law of an exponential increase in mortality rate with
age, posited in 1825, or Karl Pearson’s population mortality statistics of 1900. Yet,
they were more elaborate, quantitatively relating the rate of (molecular and cellular)
damage and loss to the rate of mortality. Several theories of mortality were formu-
lated between 1952 and 1960. Thus, according to the theory of Elaine Brody and
Gioacchino Failla, the “mortality rate is inversely proportional to the vitality.” In the
theory proposed by Henry Simms and Hardin Jones, death was attributed to “auto-
catalytic accumulation of damage and disease,” where “the lessening of vitality [is
regarded] as the accumulation of damage” and “the rate at which damage is incurred
is proportional to the damage that has already been acquired in the past.” George
Sacher’s theory stated that “death occurs when a displacement of the physiologic
state extends below a certain limiting value” (Mildvan and Strehler 1960).
Yet, perhaps the most developed and publicized theory of mortality was the theory
proposed by Bernard Strehler and Albert Mildvan or “the Strehler-Mildvan theory”
(Strehler and Mildvan 1960). It claimed that “the rate of death is assumed to be
proportional to the frequency of stresses which surpass the ability of a subsystem
to restore initial conditions” (Mildvan and Strehler 1960). The theory was based on
the Maxwell–Boltzmann distribution (originally formulated for the kinetic theory
of gases in the 1860s), where the linear decline of function of particular organs in
time was supposed to eventually lead to an exponential increase of risk for systemic
failure of homeostasis of multiple organ systems and hence an exponential increase
460 I. Stambler
of mortality rate. The loss of organ function or “organ functional reserve” was poten-
tially attributable to progressive loss of functioning organ and tissue units, such as
cells, or gradual impairment in the functional capacities of individual cells (Mildvan
and Strehler 1960; Strehler 1960a; Shock 1960a,b). This model formed the theo-
retical basis for the “compression of morbidity” concept (Fries and Crapo 1981;
Shock 1977). Recently, the Strehler-Mildvan theory was criticized for its presum-
ably uncertain statistical basis, and accordingly its positing of a limit to lifespan
extension was questioned (Tarkhov et al. 2017). Yet, to the best of my knowledge,
no equally comprehensive formal theory of mortality has yet been proposed.
Though these theories did not appear to refer to any specific goals of life extension,
they were designed for a thorough quantitative elucidation of the aging process,
deemed a necessary precondition for any actual intervention. Indeed, despite positing
a formal theory of lifespan limitation, Strehler was among the most active seekers of
life-prolonging means, mainly focusing on enzymatic mechanisms of DNA repair,
as he believed that an improved DNA repair system can protect the stability of
the human genes against mutations and thus radically increase the human lifespan
(Strehler 1960b; Kahn 1985).
In yet another line of theory-building, since the 1950s to the present, there have
been ongoing efforts to create theoretical constructs that relate the aging process
and mortality with an increase of physical entropy (disorderliness or chaos) of living
systems (Hirsch 1955; Quastler 1958; Hershey and Lee 1994; Krut’ko et al. 2018).
Considering the second law of thermodynamics that posits the inevitable increase of
entropy and the ultimate thermodynamic death of any closed system, an ostensible
analogy with the aging process and dying of living organisms intuitively appealed
to biologists (Hayflick 2007). Such an analogy suggested the sense of fatality, of
inevitable destructibility of living beings, or a limit to their existence. Notably, such
entropy-related descriptions of aging and dying have often been qualitative, without
concrete quantitative predictions, providing no tangible estimates as to the actual
terms of mortality or values of morbidity, and hence the immediate application of
such constructs for any practical medical, clinical or demographic purposes has
been minimal. Moreover, it has been generally established since the seminal work
of Erwin Schrödinger What is Life? (first published in 1944) that the notion of
a closed system, and accordingly the inevitable increase of physical entropy and
thermodynamic equilibrium (death), is not strictly applicable to living systems.
Schrödinger explained biological equilibrium in terms of order and organization,
as a low entropy (high order) system maintaining its orderliness by increasing the
disorder of the environment (Schrödinger 1996). Implicitly, such “entropy para-
sitism” (in Schrödinger’s words, “feeding on negative entropy”) seemed to present
no inherent physical constraints to its maintenance, and thus, theoretically could be
sustained indefinitely. Thus, this class of theoretical constructs, relating entropy with
aging and mortality, also presents a strong ambiguity regarding the inevitability of
limits vs. possibilities of life and health extension.
Furthermore, a series of limiting models emerged from the “reliability theories”
of aging, longevity and mortality (Koltover 2018). For example, one of such theories
proposed that “even those systems that are entirely composed of non-aging elements
26 Health and Immortality 461
(with a constant failure rate) will nevertheless deteriorate (fail more often) with age,
if these systems are redundant in irreplaceable elements” (Gavrilov and Gavrilova
2001). Despite this premise of inevitability of aging and demise, the theory still
had explicit positive propositions for the possibility of practical life extension: “It
also follows from this model that even small progress in optimizing the processes
of ontogenesis and increasing the numbers of initially functional elements (j) can
potentially result in a remarkable fall in mortality and a significant improvement in
lifespan” (Gavrilov and Gavrilova 2001).
Another version of biological reliability theory suggested that in a given system
there exist tradeoffs between robustness (duration) and performance (function),
which might provide another way of conceptualizing and justifying the incompat-
ibility of life extension and healthy function and a proposition of a limit for either
(Kitano 2007; Cohen 2016). The tradeoff between robustness and performance has
a strong relation to yet another set of explanations for the potential incompatibility
of life extension and health extension, namely the incompatibility of constancy and
change.
26.4 Life Extension Implies Constancy, Health Implies
Change: Are They Compatible?
Another persistent line of arguments against the compatibility of prolongation of
life with prolonged maintenance of health has been predicated on the notion of the
inherent mutability of healthy life. Health has been associated with the ability to
change, to adapt and respond to changing circumstances. In contrast, life extension
has entailed the maintenance of certain core components of life unchangeable or
with minimal change (Stambler 2017a). Thus, there appears to be an opposition of
functions.
On a continuum between the desire for absolute change and the desire for absolute
constancy, the proponents of life extension would seem to stand closer to the pole
of constancy. Indeed, without some notion of constancy, the concept of life exten-
sion, even of survival, would be meaningless. Consider such cases as the atoms of
a decomposing human body merging with the Universe, or human life being trans-
formed into the life of grave worms, as for example discussed by Jean Finot in The
Philosophy of Long Life (Finot 1909). Many boundaries are “transcended” in such
“transformations,” but one can hardly speak of “life extension.” If extinction is deter-
mined by “a critical rate of long-term environmental change beyond which extinction
is certain” (Burger and Lynch 1995)—notice, any change—then proponents of life
extension would wish to be as far from this rate of change as possible. Or else, they
would wish to design the technological armor that would make us impervious to such
changes. Without work invested in maintaining constancy, spontaneous deteriorative
change may be expected. Thus, the proponents of life extension might engage the
rhetoric of progressive change, but not just any change for change’s sake, but only
462 I. Stambler
such change that would serve to perpetuate some existing structure. In the words
of the protagonist of Giuseppe Tomasi di Lampedusa’s The Leopard, “If we want
things to stay as they are, things will have to change” (Tomasi di Lampedusa 1960).
And in the words of Lewis Carroll, “it takes all the running you can do, to keep in
the same place” (Carroll 1871). In this sense, the pursuit of life extension may be a
fundamentally “conservative” or “conservationist” enterprise (Stambler 2010).
In contrast, the proponents of maximum health might be more likely to advocate
substantial change, as would be required for growth and adaptation. This opposition
may have not only psychological or semantic underpinnings, but may have biological
or evolutionary roots. In several recent theories of aging, a deficit of species vari-
ability has been linked with the possibility of non-aging and/or radical life extension.
In these theories, an absence of aging would impair variation and thus reduce the
species evolvability and adaptability. For example, an ideal DNA repair mechanism
would make mutability impossible (all mutations would be immediately corrected).
And without mutability, there would be no diversity and no evolution. Any new
threat (e.g. a new infection) could then wipe out the entire stagnant population.
(Still, improved immunity and DNA repair may be assumed to provide improved
defense against a greater range of pathogens and environmental threats, such as radi-
ation, temperature changes and toxins, including bio-toxins, hence the ambiguity
regarding “limits” vs. “possibilities” remain.) A recent evolutionary model argued
almost precisely to the effect of incompatibility of change with radical life extension:
“when the system is completely stable, no mutation going on and no changing condi-
tions for worse, … it is to be expected that a population that shows senescence will be
driven to extinction.” However, “When conditions change, a senescent species can
drive immortal competitors to extinction.” The author concludes: “We age because
the world changes” (Martins 2011). Several other contemporary researchers have
pondered a return to August Weismann’s theory of evolutionary programmed aging,
proposing a direct evolutionary selection for senescence. A major suggested reason
for such a selection is that an absence of senescence would diminish the species’
variability and diversity, hence impair its adaptability and evolvability (Goldsmith
2004; Mitteldorf 2004; Skulachev 1997).
In cognate terms, it was further suggested that complexity and variability (a proxy
for adaptation) might be associated with youth and good health, whereas simplicity
and homogeneity (a proxy for stability) may be seen as a sign of aging and disease
(Lipsitz and Goldberger 1992; Blokh and Stambler 2017b).
Notably, virtually all the researchers of aging under consideration, even those
proposing limitations to lifespan or healthspan, seem to be in favor of finding
at least some modest aging-ameliorating and life and health-extending means for
humans, suggesting that through a better understanding of the mechanisms of aging,
including evolutionary mechanisms, tradeoffs and thresholds, factors affecting health
and longevity can be identified and manipulated for people’s benefit.
26 Health and Immortality 463
26.5 Killing for Health
As seen in the previous examples, the propositions of limits to lifespan and healthspan
have been commonly accompanied by various ambiguities and caveats, where the
“limitations” would seem not really limiting, and the possibilities of life and health
extension emerged quite tangible. This appears to be the prevalent position of many
researchers of aging. Yet, in some authors, the supposition of a limit to lifespan
and/or healthspan was relentless. In their view, the limits are “written in stone” and
any attempts to modify them to any noticeable degree are futile and even in some
sense immoral. This view of the truly insurmountable limit to human life and/or
health, and of the incompatibility of health maintenance with life extension, has
often yielded some rather appalling practical implications and recommendations. A
common practical consequence has been the implicit or even explicit suggestion of
the desirability of death and abandoning health care for older people, when their “life
quality” (health) is below some acceptable limits.
There are quite a few famous examples of this attitude. In 1905, the renowned
Canadian physician William Osler (1849–1919) spoke of the “uselessness of men
above sixty years of age” (Osler 1905). The essays of the “humanistic” British
philosopher and mathematician Bertrand Russell (1872–1970) from the 1930s–1940s
provide another stark example. Thus, in his essay “On Euthanasia” (1934), Russell
suggested killing people in extremely ill health, such as in cases of “hydrophobia,”
“pneumonic plague,” “congenital idiocy” and other cases which “cannot be useful
to society.” Also “criminals condemned to long terms ought to have the option of
euthanasia” (Russell 1975a). Russell was consistent and logical, hence, according to
him, the prolongation of life was undesirable both for the very sick and the very old.
Thus, in “The Menace of Old Age” (1931) he was greatly worried by the prospect that
“every increase in medical skill is bound to make the world more and more conserva-
tive.” Hence, he proposed “to prevent all researches calculated to prolong the life of
the very old” (Russell 1975b). And in “How to grow old” (1944), he maintained that
“in an old man … the fear of death is somewhat abject and ignoble” (Russell 1956). In
a less blatant form, the Australian immunologist, the Nobel Laureate in medicine of
1960 and the author of the “intrinsic mutagenesis” theory of aging, Frank Macfarlane
Burnet (1899–1985) “doubt[ed] very much whether anything worthwhile would be
gained by extending the human life span beyond its present bracket of 70–100 years—
and that if we wanted this extension of life, I am deeply sceptical about our chance of
ever achieving it.” And furthermore, “death in the old should be accepted as some-
thing always inevitable and sometimes as positively desirable” (Burnet 1974, p. 63,
66).
These are not just theoretical attitudes. Under certain circumstances, they may well
translate into practice, specifically denying care for extremely ill elderly patients, as
“useless” and “hopeless.” Thus, as early as 1666, the British physician Dr. John
Smith urged (Freeman 1938):
Let none give over their patients when they come overburdened with the infirmities of Age,
as though they were altogether incapable of having any good done unto them. Those that
464 I. Stambler
are negligent toward their Ancient Friends, are very near of kin to those inhuman Barbarians
and Americans, who both kill and devour them.
This basic neglect of care may have come true in some of the severe cases of “ageism”
or discrimination based on age in healthcare (Ehni 2014; Wyman et al. 2018).
Alternatively, the valorization of “health” (understood as the maximization and
optimization of function) over “life extension” (or the “mere” continuation of life)
may well take the form of devising medical treatments that may invigorate (“reju-
venate”) the person for the short term, with a semblance of “good health,” yet in
fact shortening the older persons’ life, essentially killing them “for health.” This
possibility was vividly envisioned by Aldous Huxley, in Brave New World (1932).
In Brave New World, biotechnology is used by the society first and foremost for
pleasure, and not for the prolongation of life or intellectual growth. The residents of
the “New World” undergo “death conditioning” to inculcate the idea that death is
a natural, good and pleasant event: “Death conditioning begins at eighteen months.
Every tot spends two mornings a week in a Hospital for the Dying. All the best toys
are kept there, and they get chocolate cream on death days. They learn to take dying
as a matter of course” (Huxley 1965, p. 125). Those who prolong their days and
become old are the savages who live at the Reservation. The “civilized” ones are
simply not allowed to age and to live long, but die young and healthy at the age of
sixty (Huxley 1965, p. 84):
That’s because we don’t allow them to be like that [growing old]. We preserve them from
diseases. We keep their internal secretions artificially balanced at a youthful equilibrium.
We don’t permit their magnesium-calcium ratio to fall below what it was at thirty. We give
them transfusion of young blood. We keep their metabolism permanently stimulated. So, of
course, they don’t look like that. Partly, he added, because most of them die long before they
reach this old creature’s age. Youth almost unimpaired till sixty, and then, crack! the end.
It is unclear from the text why the balancing of the metabolism would lead to a
pre-determined early demise, but the passage seems to imply that this is due to an
excessive and permanent stimulation. Thus, Brave New World appears to reduce to
absurdity the common assumption of the incompatibility of life extension and good
health and shows its possible “logical” and “practical” conclusion: killing by keeping
good health.
Will our “Developed World” follow this “Brave New World” scenario via
designing “anti-aging,” “rejuvenating” and “bio-hacking” treatments that may
momentarily improve function (“health”) but disregard possible long-term adverse
effects and earlier death?
This is a possibility a founder of prolongevity hygiene, Christoph Wilhelm Hufe-
land warned against. According to Hufeland’s views (to express them in somewhat
more modern terms), any treatment of old age should consider the aging organism
and the aging process as a whole. Any attempt to artificially strengthen some faculty,
at the disregard of the general sensitivity and available resources of the entire aging
system, can further advance the disarray and bring about death sooner. The ultimate
goal is not “rejuvenation” for the sake of “rejuvenation,” but “macrobiotics”—the
26 Health and Immortality 465
prolongation of life. And paradoxically, “rejuvenation” or an immediate improve-
ment of function or health, can become an enemy of life prolongation. In Hufeland’s
own words, as stated in his Macrobiotics or the Art of Prolonging Human Life,Part3
“Means which prolong life,” Chap. 18 “Old Age. Proper Treatment of It” (translated
in Wilson 1867, p. 292):
Old age, though the natural consequence of living, and the commencement of death, can
itself, on the other hand, be a means for prolonging our existence. It does not, however,
increase the power to live, but it retards its being exhausted; and one may thus affirm, that a
man in the last period of life, at the time when his powers are lessened, would, were he not
old, finish his career sooner.
This position, which appears to be somewhat paradoxical, is confirmed by the following
explanation.
Man, during the period of old age, has a much smaller provision of vital power, and a much
less capacity for restoration. If he lived with the same activity and vigor as before, this
provision would be much sooner exhausted, and death would soon be the consequence. Now
the character of age lessens the natural irritability and sensibility of the body, by which the
effects of internal as well as external irritation, and consequently the exertion and wasting of
the powers, are also lessened; and, on this account, as consumption is less, he can with such
a stock of powers hold out much longer. The decrease in the intensity of the vital processes,
as age increases, prolongs therefore vital duration.
This is a lesson by Hufeland that may be well heeded by some contemporary reduc-
tionist “anti-aging” attempts who seek immediate health improvement in the elderly
without consideration of long-term effects and actual effects on the person’s life
duration (Le Couteur and Simpson 2011). It should also be well heard by radical
advocates of “healthspan” improvement and “healthy longevity dividend” who, in
extreme cases, may despise “mere” life extension per se as useless, if it is not accom-
panied by high functional performance. If taken to extreme, in a “Brave New World”
scenario, this attitude may result in some forms of “killing for good health.”
26.6 “And Yet It Moves”. The Denial of Lifespan
and Healthspan Limitations and the Possibility
of Radical Life Extension (or Biological Immortality)
Beside the schools of thought that posited relentless and inexorable limitations to
the human lifespan and/or healthspan, or limitations that are rather flexible, but still
finite, there has existed a school of thought that denied the necessary existence of
such limitations altogether. In this school of thought, theoretically no material limits
are inherent in the duration of life of organisms, as well as in the possibility of the
development of their functional capacities (health).
According to the proponents of this vision, it is theoretically possible to produce
changes in the organisms’ inner biological structure and/or environmental conditions,
thanks to improvements in biomedical technology, which may dramatically modify
any existing limitations on life and health imposed by the present conditions. Of
466 I. Stambler
course, it has been realized, even by the most optimistic advocates of human life
extension (often termed “life-extensionists”), that there are currently clear practical
limits and constraints in our ability to increase the human lifespan with the current
medical technological means (Stambler 2014). The life-extensionists simply do not
reconcile with those limits; they desire and strive to overcome them by improving
biomedical technology.
The assertion of limits on life and health presupposes the existence of some
limited life-sustaining material resource or reserve, a sort of nourishing substrate for
the “vital force” of a restricted amount that is being exhausted during the life course
and cannot be replenished, thus creating the limit. This putative irreplaceable material
resource could be the telomere length, the extant stem cell populations, maximum
DNA repair capacity, or some mysterious limited “adaptation energy” hypothesized
by the founder of stress physiology Hans Selye. Yet, the fundamental characteristic of
the life-extensionist worldview is that it strongly asserts the possibility to replenish
any material resources necessary for life, and thus modify any restrictive limits.
This view is quite ancient. It was, for example, expressed by the renowned Jewish
philosopher and physician Maimonides (1135–1204, Rabbi Mosheh ben Maimon)
who stated: “For us Jews, there is no predetermined end point of life. The living
being exists as long as replenishment is provided [for that amount of] its substantive
moisture [i.e. bodily humors] that dissolves” (Rosner 1998). This proactive view has
persisted and intensified to our time (Stambler 2014). Hans Selye, even though he
believed that “as far as we know, our reserve of adaptation energy is an inherited finite
amount,” nonetheless admitted the possibility of its replenishment, and thus life and
health extension. As he wrote: “If [the adaptation energy] amount is unchangeable,
we may learn more about how to conserve it. If it can be transmitted, we may explore
means of extracting the carrier of this vital energy—for instance, from the tissues of
young animals—and trying to transmit it to the old and aging” (Selye 1956, pp. 276,
303–304). The same proactive principle could be applied for any type of limiting
material resources.
Despite the well-recognized current practical limitations, the life-extensionists
have strongly asserted that, on the basic theoretical level, there is no law in nature that
sets a strict insurmountable limit to the lifespan or functional capacity of the human
organism. Regarding the presumed incompatibility of significant life extension with
optimal health, or the frequent fear of increasing “life quantity” at the expense of
“life quality,” the life extensionists denied any natural limitations to those values
and asserted the human ability to intervene and enhance them. This position was
well stated at the Galileo Symposium in 1964 by the Nobel Prize winning physicist
Richard Phillips Feynman (Feynman 1999, p. 100):
There is nothing in biology yet found that indicates the inevitability of death. This suggests
to me that it is not at all inevitable, and that it is only a matter of time before the biologists
discover what it is that is causing us the trouble and that that terrible universal disease or
temporariness of the human’s body will be cured.
Among the sources of hope, the life-extensionists have often cited the existence of
non-aging, slowly aging, and even “potentially immortal” life-forms and the constant
26 Health and Immortality 467
evolutionary adaptations of the lifespan even for the humans, according to particular
changing environmental and genetic conditions. There may be contingent limitations
due to the inner biological structure and external environment, but these are not
“limits” in the principal physical sense (like “nothing can travel faster than the speed
of light”). The existing practical limits to the human lifespan and functional capacity,
due to internal disorder, adverse environment and imperfect medical capabilities, are
“rules that can be broken.”
Some authors opposed the premises of limitation theories on specific points. An
intense debate over the limits to life and health expectancy took place in the 1980s.
Thus, the view proposed by Nathan Keyfitz about the intrinsic limit to aging health
and life-expectancy was disputed by Arthur Schatzkin of the US National Insti-
tute of Cancer. Schatzkin suggested that a single health care measure can improve
the outcome for several age-related diseases and the elimination of several risk
factors can have a cumulative effect, leading to a significant life extension (Schatzkin
1980). Several authors disputed Fries and Crapo’s conclusions about the compres-
sion of morbidity and argued that an approximation of a perfect “rectangular survival
curve” will not be possible, and health care measures can produce an extension of
life expectancy far beyond the 85-year “limit” (Schneider and Brody 1983). Later
on, additional evidence was presented about the existence of the “compression of
morbidity” and “rectangularization of survival” (temporal concentration of deaths)
trends, agreeing with the limitation theories (Faria 2015; Stallard 2016). Yet, these
trends were also debated (Crimmins and Beltrán-Sánchez 2011). Moreover, recently
a strong critique of the Strehler-Mildvan theory of mortality (lifespan limit) emerged
(Tarkhov et al. 2017) explicitly aiming to encourage the search for anti-aging and
life-extending therapies.
Yet, many life-extensionists resist the imposition of a limit on life and health not
on any specific technical grounds, but on the sheer postulate of the human ability
to employ natural processes to achieve benefits for humanity. Their greatest source
of hope is the rapid development of therapeutic means for health improvement and
life extension. The primary proofs of feasibility are based on the successful cases
of health improvement and life extension experimentally achieved in animal models
and emerging human studies, and the development of new intervention techniques,
based on the ever-better elucidation of the mechanisms of aging (Stambler 2017b).
There are now clear proofs of practical technological feasibility of interventions into
aging processes and healthspan and lifespan modification. These feasibility proofs for
aging modification and health and lifespan intervention are a part of the more general
and very encouraging trend of the rapid development of biomedical technologies.
The fact of progress in scientific, technological and medical capabilities is difficult
to deny. Though, of course, this progress is not a given, and may be brought to
naught in the absence of persistent human effort, ingenuity and investment. Yet, the
present progress gives encouragement and hope for overcoming the present practical
limitations of both the lifespan and healthspan, for extending life concomitantly
with the extension of good health, for keeping intellectual, physical and spiritual
capabilities without expecting a rigidly set end point. This is the profoundly optimistic
vision of health and life promoted by the life-extensionist school of thought.
468 I. Stambler
The truth or error of each school of thought will be shown in time, with fateful
impacts on the lives of every one of us, within our yet limited lifespan and healthspan.
References
Blokh D, Stambler I (2017) The application of information theory for the research of aging and
aging-related diseases. Prog Neurobiol 157:158–173
Burger R, Lynch M (1995) Evolution and extinction in a changing environment: a quantitative-
genetic analysis. Evolution 49(1):151–163
Burnet FM (1974) The biology of aging. Auckland University Press, Auckland NZ
Carroll L (1871) Through the looking-glass. Macmillan, London. Reprinted in Project Gutenberg.
https://www.gutenberg.org/files/12/12-h/12-h.htm. Accessed 1 Jan 2020
Cohen AA (2016) Complex systems dynamics in aging: new evidence, continuing questions.
Biogerontology 17:205–220
Crimmins EM, Beltrán-Sánchez H (2011) Mortality and morbidity trends: is there compression of
morbidity? J Gerontol B Psychol Sci Soc Sci 66B(1):75–86
Ehni H-J (2014) Ageism. In: Ten Have H (ed) Encyclopedia of global bioethics. Springer
International Publishing, Basel
Faria MA (2015) Longevity and compression of morbidity from a neuroscience perspective: do we
have a duty to die by a certain age? Surg Neurol Int 6:49
Feynman RP (1999) What is and what should be the role of scientific culture in modern society,
presented at the Galileo symposium in Florence, Italy, in 1964. In: The pleasure of finding things
out: the best short works of Richard P. Feynman. Perseus Books, New York, p 100
Finot J (1909) The philosophy of long life. Roberts H (transl). John Lane Company, London (first
published in French in 1900)
Freeman JT (1938) The history of geriatrics. Ann Med Hist 10:324–33. Quotes: John Smith, MD,
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, being a paraphrase upon the six
former verses of the 12. chapter of Ecclesiastes, J. Macock, London, 1666
Fries JF (1980) Aging, natural death, and the compression of morbidity. N Engl J Med 303:130–135
Fries JF, Crapo LM (1981) Vitality and aging. Implications of the rectangular curve. W.H. Freeman
and Co., New York
Fries JF (1983) The compression of morbidity. Milbank Q 61(3):397–419
Gavrilov LA, Gavrilova NS (2001) The reliability theory of aging and longevity. J Theor Biol
213:527–545
Goldsmith TC (2004) Aging as an evolved characteristic—Weismann’s theory reconsidered. Med
Hypotheses 62(2):304–308
Gruenberg EM (1977) The failures of success. Milbank Q 55(1):3–24
Hayflick L (2007) Entropy explains aging, genetic determinism explains longevity, and undefined
terminology explains misunderstanding both. PLoS Genet 3(12):e220
Hershey D, Lee WE III (1994) Entropy as a biological marker in human aging. In: Balin AK (ed)
Practical handbook of human biologic age determination. CRC Press, Boca Raton Florida, pp
233–264
Hirsch S (1955) Senescence, entropy, and cybernetics: a clarification of basic concepts in geron-
tological research. In: The 3rd congress of the international association of gerontology. London.
1954. Old age in the modern world. E&S Livingstone Ltd., London, pp 622–627
Holmes OW (1858) The deacon’s masterpiece or, the wonderful “one-hoss shay”: a logical story.
Quoted In: Fries JF, Crapo LM (1981) Vitality and aging: implications of the rectangular curve.
W.H. Freeman and Co., New York
26 Health and Immortality 469
Huxley A (1965) Brave new world and brave new world revisited. Harper Perennial, New York
(first published in 1932)
Kahn C (1985) Beyond the helix: DNA and the quest for longevity. Times Books, New York
Keyfitz N (1977) What difference would it make if cancer were eradicated? An examination of the
Taeuber paradox. Demography 14(4):411–418
Keyfitz N (1978) Improving life expectancy: an uphill road ahead. Am J Public Health 68:954–956
Kitano H (2007) Towards a theory of biological robustness. Mol Syst Biol 3:137
Koltover VK (2018) Mathematical theory of reliability and aging: a little bit of history and the state
of art. Gerontol Geriatric Stud 2(4):181–182
Krut’ko VN, Dontsov VI, Khalyavkin AV, Markova AM (2018) Natural aging as a sequential
poly-systemic syndrome. Front Biosci 23:909–920
Lautenbach E (2010) Medizin zitate lexikon (Medical citations lexicon). Iudicium, München
Le Couteur DG, Simpson SJ (2011) Adaptive senectitude: the prolongevity effects of aging. J
Gerontol A Biol Sci Med Sci 66(2):179–182
Lipsitz LA, Goldberger AL (1992) Loss of ‘complexity’ and aging: potential applications of fractals
and chaos theory to senescence. JAMA 267:1806–1809
Martins ACR (2011) Change and aging: senescence as an adaptation. PLoS ONE 6(9):e24328
McGinnis JM (1985) The limits of prevention. Public Health Rep 100:255–260
Metchnikoff II (1961) Etudy o prirode cheloveka (Etudes on the nature of man). Izdatelstvo
Academii Nauk SSSR (The USSR Academy of Sciences Press), Moscow (first published in
1903)
Mildvan AS, Strehler BL (1960) A critique of theories of mortality. In: Strehler BL, Ebert JD,
Glass HB, Shock NW (eds) The biology of aging: a symposium held at Gatlinburg, Tennessee,
May 1–3, 1957, under the sponsorship of the American Institute of Biological Sciences and with
support of the National Science Foundation. Waverly Press, Baltimore, pp 216–235
Mitteldorf J (2004) Ageing selected for its own sake. Evol Ecol Res 6:937–953
Olshansky SJ, Carnes BF (2001) The quest for immortality: science at the frontiers of aging. W.W.
Norton and Co., New York
Olshansky SJ, Perry D, Miller RA, Butler RN (2006) In pursuit of the longevity dividend: what
should we be doing to prepare for the unprecedented aging of humanity? Scientist 20(3):28–36
Olshansky SJ (2019) Longevity dividend. In: Dupre M, Gu D (eds) Encyclopedia of gerontology
and population aging. Springer, Berlin
Osler W (1905) Farewell address on leaving the Johns Hopkins University. Scientific American
3:25. Reproduced in full. In: Hall S (1922) Senescence, the last half of life. D. Appleton and
Company, New York, p 22
Ovid (1994) The metamorphoses. Slavitt D (transl). The Johns Hopkins University Press, Baltimore
Pearl R (1922) The biology of death. Philadelphia, J.B, Lippincott Company
Quastler H (1958) The domain of information theory in biology. In: Yockey HP (ed) Symposium
on information theory in biology, Gatlinburg, Tennessee, October 29–31, 1956. Pergamon Press,
New York, pp 187–196
Rosner F (1998) Moses Maimonides’ responsum on longevity. In: Rosner F (ed) The medicallegacy
of Moses Maimonides. Ktav, Hoboken New Jersey, pp 246–258
Rubner (1908) Das problem der lebensdauer und seine beziehungen zu wachstum und ernährung
(The problem of life-duration and its relations to growth and nutrition). Oldenbourg, München
Russell B (1956) How to grow old. In: Bertrand Russell, portraits from memory: and other essays.
Simon and Schuster, New York, pp 50–53 (written in 1944)
Russell B (1975a) The menace of old age. In: Bertrand Russell, mortals and others, American essays
1931–1935. Routledge Classics, London, pp 18–20 (written in 1931)
Russell B (1975b) On euthanasia. In: Bertrand Russell, mortals and others, American essays 1931–
1935. Routledge Classics, London, pp 267–268 (written in 1934)
Schatzkin A (1980) How long can we live? A more optimistic view of potential gains in life
expectancy. Am J Public Health 70:1199–1200
470 I. Stambler
Schneider EL, Brody JA (1983) Aging, natural death and the compression of morbidity: another
view. N Engl J Med 309:854–856
Schrödinger E (1996) What is life? Cambridge University Press, Cambridge (first published in
1944)
Selye H (1956) The stress of life. McGraw-Hill, New York
Shock NW (1960a) Discussion session II. Mortality and measurement of aging. In: Strehler BL,
Ebert JD, Glass HB, Shock NW (eds) The biology of aging: a symposium held at Gatlinburg,
Tennessee,May 1–3, 1957, under the sponsorship of the American Institute of Biological Sciences
and with support of the National Science Foundation. Waverly Press, Baltimore, pp 22–23
Shock NW (1960b) Age changes in physiological functions in the total animal: the role of tissue
loss. In: Strehler BL, Ebert JD, Glass HB, Shock NW (eds) The biology of aging: a symposium
held at Gatlinburg, Tennessee, May 1–3, 1957, under the sponsorship of the American Institute
of Biological Sciences and with support of the National Science Foundation. Waverly Press,
Baltimore, pp 258–264
Shock NW (1977) System integration. In: Finch CE, Hayflick L (eds) Handbook of the biology of
aging. Van Nostrand Reinhold Company, New York, pp 639–665
Sierra F, Kohanski R (2017) Geroscience and the trans-NIH geroscience interest group, GSIG.
GeroScience 39:1–5
Skulachev VP (1997) Aging is a specific biological function rather than the result of a disorder
in complex living systems: biochemical evidence in support of Weismann’s hypothesis.
Biochemistry (Moscow) 62(11):1191–1195
Stallard E (2016) Compression of morbidity and mortality: new perspectives. N Am Actuar J
20(4):341–354
Stambler I (2010) Life extension—a conservative enterprise? Some fin-de-siècle and early
twentieth-century precursors of transhumanism. J Evol Tech 21:13–26
Stambler I (2014) A history of life-extensionism in the twentieth century. Longevity history, Rishon
Lezion. https://www.longevityhistory.com/. Accessed 1 Jan 2020
Stambler I (2017a) Life-extensionism as a pursuit of constancy. In: Longevity promotion: multi-
disciplinary perspectives. Longevity history, Rishon Lezion. https://www.longevityhistory.com/.
Accessed 1 Jan 2020
Stambler I (2017b) Human life extension: opportunities, challenges, and implications for public
health policy. In: Vaiserman A (ed) Anti-aging drugs: from basic research to clinical practice.
Royal Society of Chemistry, London, pp 537–564
Strehler BL, Mildvan AS (1960) General theory of mortality and aging. Science 132:14–21
Strehler BL (1960a) Fluctuating energy demands as determinants of the death process (A parsimo-
nious theory of the Gompertz function). In: Strehler BL, Ebert JD, Glass HB, Shock NW (eds)
The biology of aging: a symposium held at Gatlinburg, Tennessee, May 1–3, 1957, under the
sponsorship of the American Institute of Biological Sciences and with support of the National
Science Foundation. Waverly Press, Baltimore, pp 309–314
Strehler BL (1960b) Discussion session IX. Methodology, information theory, design and approach.
In: Strehler BL, Ebert JD, Glass HB, Shock NW (eds) The biology of aging: a symposium
held at Gatlinburg, Tennessee, May 1–3, 1957, under the sponsorship of the American Institute
of Biological Sciences and with support of the National Science Foundation. Waverly Press,
Baltimore, pp 93–94
Swift J (1892) Gulliver’s travels into several remote nations of the world. Part III: A voyage to
Laputa, Balnibarbi, Luggnagg, Glubbdubdrib, and Japan. Chapter X (first published in 1726–7).
George Bell and sons, London. Reprinted in Project Gutenberg. https://www.gutenberg.org/files/
829/829-h/829-h.htm. Accessed 1 Jan 2020
Tarkhov AE, Menshikov LI, Fedichev PO (2017) Strehler-Mildvan correlation is a degenerate
manifold of Gompertz fit. J Theor Biol 416:180–189
Tomasi di Lampedusa G (1960) The leopard. Colquhoun A (transl). Pantheon Books, New York
26 Health and Immortality 471
Wilson E (ed) (1867) Hufeland’s art of prolonging life. Lindsay and Blakiston, Philadelphia (origi-
nally C.W. Hufeland, Makrobiotik; oder, Die Kunst das menschliche Leben zu verlängern, Jena,
1796)
Wyman MF, Shiovitz-Ezra S, Bengel J (2018) Ageism in the health care system: providers,
patients, and systems. In: Ayalon L, Tesch-Römer C (eds) Contemporary perspectives on ageism.
International perspectives on aging, vol 19. Springer, Cham
