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Humans are evolutionarily adapted to caloric restriction resulting from

ecologically dictated dietary deprivation imposed during the Plio-Pleistocene
period

Article  in  Medical Hypotheses · February 2006

DOI: 10.1016/j.mehy.2005.11.013 · Source: PubMed

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Medical Hypotheses (2006) 66, 978–984

http://intl.elsevierhealth.com/journals/mehy

Humans are evolutionarily adapted to

caloric restriction resulting from
ecologically dictated dietary deprivation
imposed during the Plio–Pleistocene period
 n Amen-Ra
Nu *

Amenta Press Inc., P.O. Box 236, Damascus, MD 20872, USA

Received 29 October 2005; accepted 3 November 2005

Summary Humans are evolutionarily adapted to chronic undernutrition as a consequence of ecologically dictated
dietary restriction. Increased aridity, cooler temperatures and increased climatic oscillation effected an alteration
of the quantity and quality of vegetation upon which hominids depended for food during the Plio–Pleistocene
period. Hominids responded physiologically to climate-induced caloric curtailment in the same way organisms
respond to experimentally imposed caloric restriction: by reducing the rate and/or altering the manner in which
they metabolized fuel. Such metabolic alterations are mediated principally by the hypothalamus and it is herein
hypothesized that the human hypothalamus was subjected to substantial selective pressure, promoting an
energetically conservative hypometabolic state. Moreover, the most salient phenotypic characteristics typifying the
human species – long lifespan, low reproductive potential, lengthy development and high brain/bodyweight ratio –
are effectuated in organisms undergoing caloric restriction. These phenotypic/physiological characteristics – herein
termed the quadripartite complex – can be modulated by metabolic rate, which is, in turn, modulated by the
hypothalamus. An appreciable alteration in climate occurred between 2.0 and 1.5 million years ago, a juncture at
which one hominid lineage (Paranthropus) went extinct. Paranthropus was characterized by such external
adaptations as robust cranio-facial morphology and pronounced enamel deposition, indicative of subsistence on
tough, low-quality vegetal foods. Conversely, the Homo lineage responded to its marginal dietary repertoire through
internal means, centering on metabolic suppression. It is herein hypothesized that this adaptive metabolic
alteration, enacted in response to ecologically imposed caloric restriction, produced the defining morphologic
attributes of Homo and enabled the evolutionary success of the human species. Among the implications of this line
of thinking is that modern humans may be particularly sensitive to the deleterious effects of excess energy intake
and, concomitantly, particularly amenable to the ameliorative effects of caloric restriction.
c 2005 Elsevier Ltd. All rights reserved.

* Tel.: +1 240 899 6550.

E-mail address: AmentaPr@AmentaPress.com.


0306-9877/$ - see front matter c 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.mehy.2005.11.013
Humans are evolutionarily adapted to caloric restriction
Introduction
The hominid fossil record bears witness to a
divergence of two adaptively distinct lineages
from a common stock of ancestral australopiths.
This divergence transpired in the late Pliocene
around 3–2 million years ago (Mya) and eventu-
ated in Paranthrop and Homo clades. It is con-
ceivable that the proximate cause of this
speciation event was a gradually changing climate
characterized by increased aridity and conse-
quent alteration of ecological/vegetational condi-
tions coincident with the intensification of
glaciation in northern latitudes that marked the
end of the early Pliocene warm period [1]. Paran-
thropus specimens exhibit pronounced mastica-
tory robusticity, an attribute ostensibly
indicative of subsistence on coarse vegetal items.
This adaptation likely enabled more efficient
exploitation of fibrous resources prevalent in arid
environs. Homo, the lineage that eventuated in
modern humans, possessed no prominent external
traits indicative of increased subsistence on
coarse vegetation. Some theorists have inter-
preted the apparent absence of adaptations to
a marginal dietary repertoire as an indication
that Homo was a generalist, efficiently exploiting
a wide variety of resources including meat. This
physically inconspicuous behavioral alteration
apparently proved superior to the distinctive die-
tary adaptations of Paranthropus as this lineage
went extinct 1.5 Mya, leaving Homo as the sole
representative of the hominid family. It is plausi-
ble that the demise of Paranthropus was due to
yet another substantial shift in climate ensuing
2.0–1.7 Mya, which was also characterized by
increased aridity [2]. Contrary to prevailing opin-
ion, Homo was most probably possessed of dis-
tinctive physiological attributes and I aver that
these traits were responsible for its survival
amidst the appreciably altered environmental/
ecological milieu of the Plio–Pleistocene. Such
attributes include pronounced encephalization,
pronounced longevity, altriciality (i.e. protracted
development, slow growth rate) and reduced
reproductive potential. Each of these traits, col-
lectively called the quadripartite complex, con-
ceivably contributed to the evolutionary success
of Homo under conditions of limited dietary prov-
isionment. Interestingly, this distinctive assem-
blage of attributes, which are accentuated in
humans, is consistently induced in organisms sub-
jected to chronic caloric restriction [3], suggest-
ing a common mechanistic basis. I postulate that
this mechanism is hypothalamic hypometabolism.
979
Experimentally imposed dietary
restriction vs. ecologically imposed
dietary restriction
Caloric restriction (CR) is the only intervention
found to consistently extend the lifespan of di-
verse animals ranging from yeast to rodents to
(putatively) primates [4]. Indeed, this experimen-
tal protocol has emerged as an indispensable mod-
el in the scientific investigation of aging. Since the
seminal study by McCay and colleagues [5] demon-
strated the efficacy of CR in promoting longevity,
investigators have earnestly endeavored to eluci-
date the mechanism(s) by which dietary depriva-
tion attenuates aging and augments longevity.
Though there is support for various interpretive
theories, there are convincing reasons for regard-
ing two – the metabolic theory and the neuro-
endocrine theory – as the most parsimonious from
an evolutionary perspective [6–9]. Briefly, the
metabolic theory posits the suppression of meta-
bolic rate and/or alteration of energy allocation
as the proximate mechanism by which CR exerts
its life-prolonging effect, whereas the neuro-
endocrine theory implicates alterations in the
elaboration of endocrine hormones. As the hypo-
thalamus exerts ultimate control over the elabo-
ration of endocrine hormones and modulates
metabolic rate, there is compelling conceptual
convergence of the metabolic and neuro-
endocrine theories.
It is estimated that in the Turkana basin of East
Africa, a region encompassing parts of Kenya and
Ethiopia, upwards of 80% of mammalian fauna
were replaced between 3.0 and 1.8 Mya [10]. This
period was characterized by considerable climatic
flux and likely exerted a substantial influence on
the hominid species inhabiting the region. It is
clear from the record of vegetational patterns,
moreover, that the food supply available to homi-
nids was appreciably affected. At this juncture
there is evidence of a gradual replacement of C3
vegetation (predominantly tropical) with C4 vege-
tation (predominantly savannah-like) throughout
East Africa [11]. Importantly, herbivorous species
inhabiting these environs during the Plio–Pleisto-
cene bear adaptations indicative of increased
aridity, suggesting subsistence on plant products
of a more marginal nutritional quality [12]. Under
such conditions hominids would have experienced
a decrement in their available food supply, the
severity of which is perhaps suggested by the
eventual extinction of Paranthropus. In short, it
seems that during the formative period of human
980
evolution, hominids were subjected to a sort of
ecologically imposed dietary restriction.
The quadripartite complex
Compared to our closest extant primate relatives,
humans have larger brains (both relatively and
absolutely), longer maximum lifespan, protracted
developmental trajectory and lower lifetime repro-
ductive potential. Considering the marginal eco-
dietary conditions under which the human lineage
evolved, it would be illuminative to derive theoret-
ically valid teleological explanations for these sali-
ent features of the human phenotype. That these
phenotypic features are interrelated is suggested
by their responsiveness to metabolic rate and the
dependence of metabolic rate, in turn, on energy
(calorie) allotment. We shall first consider the phe-
nomenon of altriciality or developmental depres-
sion because it likely facilitated induction of the
other three components of the quadripartite com-
plex and because it was undoubtedly the most
adaptive of the four.
The rate and extent to which mammalian organ-
isms develop is dictated, principally, by two endo-
crine hormones: thyroid hormone (TH) and
somatotropin (growth hormone, GH). Released by
the thyroid and pituitary glands, respectively,
these hormones not only induce tissue growth but
also elevate metabolism by increasing the influx
of nutrients into the cells of proliferating or grow-
ing tissue. Under conditions of chronic caloric
restriction, levels of these anabolic hormones are
substantially reduced and, as a result, animals sub-
jected to this restrictive regimen develop at a
slower rate than control animals fed ad libitum
[3]. The adaptive consequence of this effect is
clear: reducing the rate with which an organism
grows reduces the quantity (and, indeed, quality)
of food needed thereby. Developmental depression
would have enabled hominids to support their
young (and themselves) with less food. Further sup-
port for this line of reasoning is to be found in con-
sideration of lactation. Lactation – a task that
places high energetic demands on nursing females
– is governed by the hypothalamus. Two hormones
mediate hypothalamic control over lactation: thy-
rotropin releasing hormone (TRH) and prolactin
inhibiting hormone (PIH). These hormones, respec-
tively, prompt and inhibit pituitary release of pro-
lactin, the proximal mediator of breast milk
elaboration. In addition to causing ejection of
breast milk, prolactin causes the breast to augment
production of casein and lactalbumin, the principal
protein constituents of milk. Interestingly, human
Amen-Ra
breast milk has the lowest protein concentration
of any primate, a value of 7% in comparison to
the primate norm of 20% [13]. This would seem
to buttress the notion that humans are exquisitely
adapted to dietary deprivation. Moreover, it under-
scores the role of the hypothalamus as the agent
‘recruited’ by natural selection to buffer the ef-
fects of ecologically induced dietary restriction.
This adaptation – de-enrichment of human milk
– is ostensibly tied to developmental depression
(altriciality): Slowly growing infants can be sus-
tained on milk of a lower nutritional content. Con-
ceivably, reduction of milk protein enrichment
could have been effectuated by decreasing TRH
or, alternatively, by increasing PIH, though the lat-
ter mechanism is perhaps more plausible insofar as
the hypothalamus exerts mainly an inhibitory ef-
fect on prolactin secretion [14]. The phenomenon
of milk de-enrichment also calls into question the
prevailing notion that human evolution was tied
to or contingent upon provisioning of meat.
Clearly, the nutritional quality of milk – the sole
source of sustenance for the growing human infant
– should come to reflect a nutritional profile of
dietary enrichment rather than dietary deprecia-
tion if, indeed, meat consumption was a formative
factor in the evolution of the human species. Such
is not the case. Rather, the nutritional profile of
human breast milk suggests a perennial diet cen-
tered on low-calorie, plant food. Interestingly,
caloric restriction has been shown to result in de-
creased concentrations of circulating levels of pro-
lactin [15]. This further supports the adaptive role
played by the hypothalamus in mitigating ecologi-
cally imposed nutritional stress during human
evolution.
The maintenance of reproductive receptivity
and procreative power are energy-intensive imper-
atives. These imperatives are, however, superflu-
ous under conditions of caloric curtailment. It is
therefore not surprising that animals subjected to
caloric restriction are less fertile than free-fed
controls. Female animals release fewer eggs during
ovulation and have smaller litters while males elab-
orate less semen and produce fewer sperm under
conditions of chronic CR [16,17]. These effects
are mediated collectively by reductions in gonado-
tropins (i.e. luteinizing hormone, and follicle stim-
ulating hormone) and by reductions in sex
hormones (principally testosterone and estrogen).
Interestingly, both testosterone and estrogen are
known to increase whole body metabolic rate
markedly [14]. Thus, suppression of circulating
sex hormones in hominids would have been doubly
adaptive in that the likelihood of reproduction
would have been reduced and the rate with which
Humans are evolutionarily adapted to caloric restriction
limited energy resources were utilized would have
been curtailed considerably, augmenting the calo-
rie conserving effects of low TH and GH noted pre-
viously. When viewed in terms of the ‘reproductive
quotient’ – that is, the ratio of reproductive life-
span to total lifespan – human females are far less
fecund than chimpanzees. Viewed differently, the
duration over which human females are reproduc-
tively receptive (relative to total lifespan) is re-
duced. If the reproductive range – the period
from menarche to menopause or cessation of ovu-
lation – of both chimpanzees and humans is
approximated to be 30 years and the maximum
lifespan of chimpanzees and humans is approxi-
mated to be 60 and 120 years, respectively,
then humans have experienced a 2-fold relative
reduction in their ‘reproductive quotient’. Though
this reduction is attributable in part to increased
absolute longevity (without concomitant augmen-
tation of reproductive longevity), negative selec-
tion cannot be ruled out, especially when
consideration is given to the fact that human fe-
males attain sexual maturity several years after
their simian counterparts, gestate their young for
a longer period and typically experience an abrupt
cessation of menstruation and ovulation by about
the fifth decade of life. I posit that comparisons
of reproductive potential between such socially
sophisticated species as humans and chimpanzees
are more practicable and tractable than reproduc-
tive rate or output as the former measure is likely
more indicative of underlying physiological factors
and less subject to complex situational variables.
The term reproductive quotient is therefore espe-
cially instructive as it expresses an estimation of
the length of time over which a given female is
reproductively receptive relative to its maximum
lifespan. It is in this respect that I maintain that
the lineage eventuating in humans experienced a
reduction in reproductive potential (reproductive
quotient) relative to extant apes and (inferentially)
to ancestral hominids. It is conceivable that natural
selection served to suppress human fertility (or
more precisely, reduce reproductive range relative
to lifespan) in the face of food scarcity, thereby
promoting the preservation of precious energy re-
serves. Indeed, it is estimated that energy expendi-
ture is 7% lower in women when the endometrium
is in a regressed (non-receptive) state [18]. Clearly,
the assumption of amenorreah (i.e. temporary ces-
sation of menstruation) in the face of protracted
energy deprivation can effectuate conservation of
copious amounts of energy and avert potential
parental investment in offspring likely to suffer
malnutrition and premature death due to food
scarcity.
981
The human brain is three times more massive
than the typical ape brain (1/2 kg) and twice as
massive as the first supposed member of the genus
Homo, H. habilis. The pronounced increase in the
size of the human brain warrants particular atten-
tion due to the considerable metabolic expense
of neural tissue, especially in light of the evidence
that the formative period of human evolution was
marked by food scarcity. The key to understanding
the evolutionary accommodation of human
encephalization may lie in the very nature of the
nervous system. Not only is the brain a privileged
organ, receiving a disproportionate allotment of
nutrients, it is also exceptionally sensitive to met-
abolic deficits. Due to their high metabolic rate and
limited capacity for anaerobic metabolism, neu-
rons depend on a constant, nearly invariant supply
of nutrients from the systemic circulation – an
abrupt cessation of nutrient delivery to the brain
results in unconsciousness within seconds. Another
indication of the brain’s special metabolic status is
the fact that it does not require insulin in order to
effectuate influx of glucose, as do non-neural tis-
sues. As a consequence, the brain is perpetually
provisioned with its full complement of glucose
while the rest of the body must ‘‘make do’’ with
the remainder. Even in diabetics with marginal
insulin production, glucose diffuses readily into
the brain [14]. Moreover, when the level of circu-
lating glucose is too sparse to meet the brain’s
needs, the body mobilizes its fat deposits, convert-
ing fatty acids into ketone bodies that are, in turn,
preponderantly metabolized by the brain, kidneys
and skeletal muscle. Thus, in the absence of appre-
ciable nutrient availability, the body is able to ex-
ploit its embedded energy reserves (fat) and
convert this vital resource into a form (ketone
bodies) utilizable by the nervous system to the
exclusion of other organ systems. Though the liver
plays a central role in the conversion of fatty acids
into brain-bound ketone bodies, these volatile mol-
ecules are also produced locally in the brain by
astrocytes [19]. This mechanism would seem to en-
sure adequate appropriation of ketone body inter-
mediates by the brain and, additionally, ensure
exclusive sequestration of ketone bodies within
the nervous system. There is, moreover, evidence
which suggests that ketone bodies, in addition to
serving as energy substrates for the brain, confer
protection to the brain from toxic insults [20]. In-
deed, a study by Leite and colleagues found that
brain-derived beta-hydroxy-butyrate (the most
abundant circulating ketone body) induces in-
creased secretion of a brain growth factor with a
role in nerve cell proliferation [21]. Two hormones
in particular are crucial catalysts of ketogenesis:
982
cortisol and epinephrine. Cortisol is released from
the adrenal glands principally in response to food
deprivation (hypoglycemia). Ultimate control over
cortisol secretion is exerted by the hypothalamus,
however, through release of corticotropin releas-
ing hormone which, in turn, prompts pituitary
secretion of adreno-corticotropic hormone, there-
by eliciting release of cortisol by the adrenal
glands. Cortisol thereupon accelerates gluconeo-
genesis and facilitates avid conversion of fatty
acids into ketone bodies. The ketogenic compound
epinephrine is also secreted by the adrenal gland,
though the proximate cause of its release is direct
discharge of sympathetic nerves from the hypo-
thalamus in response to physical exertion (inten-
sive foraging for example). Theoretically, by
prompting increased secretion of the ketogenic
compounds cortisol and epinephrine, the hypothal-
amus could augment availability of ketone body
intermediates, thereby providing the brain with a
plentiful supply of nutrients (ketone bodies) during
bouts of malnourishment and by so doing provide
protection to the brain as well as molecular stimuli
for increased neural proliferation. This latter phe-
nomenon is particularly intriguing in light of the
teleological necessity of explaining human enceph-
alization amidst apparent nutritional marginaliza-
tion. Ketone-catalyzed neurogenesis is a plausible
hypothesis or at least a clarifying component of a
more comprehensive theoretical complex. Central
to this theoretical complex is the robust corpus of
research establishing the capacity of caloric
restriction to increase expression of the neurotro-
phic factors NGF, BDNF and GDNF and its capacity
to augment expression of neural chaperone pro-
teins which play a role in ensuring proper protein
conformation [22–25]. Quite tellingly, while there
is no experimental evidence that caloric enrich-
ment induces brain hyperplasia, there is compel-
ling evidence that caloric deprivation does so.
This calls into question theories of human brain
evolution that invoke dietary enrichment, hunting
and meat procurement to explain the augmenta-
tion of encephalization in hominids ancestral to hu-
mans [26]. Moreover, the importance of meat
acquisition in human evolution is questionable con-
sidering the circumstantial nature of the evidence
of early hominid hunting [27]. The juxtaposition
of hominid remains and those of putative prey
and the exhibition of alleged ‘‘cut marks’’ inflicted
by hominid hunters form the basis of much specula-
tion about the centrality of meat provisionment in
human evolution. A more conservative approach to
the issue of hunting in human evolution is to posit
that the practice did not commence until hominids
were in possession of lethal, lithic projectile weap-
Amen-Ra
ons that would have enabled them to accurately
hurl implements at animals from relatively safe dis-
tances. If such a ‘projectile postulate’ is consid-
ered, then human hunting conceivably coincided
with the emergence of the atlatl (spearthrower)
and bow and arrow a mere 20,000 years ago and,
accordingly, would have exerted no appreciable ef-
fect on human evolution [27]. Thus, whereas die-
tary enrichment, meat eating and the hunting
hypothesis have long been invoked to explain the
evolution of the human brain, the available molec-
ular evidence suggests that dietary deprivation can
appreciably augment neural accretion via en-
hanced expression of endogenous neurotrophic
agents and this impressive body of research may
provide the most parsimonious explanatory frame-
work for the evolutionary encephalization of the
human brain. Taken together, the elements of this
theoretical edifice are intriguing: Chronic caloric
deprivation imposed during the formative stages
of human evolution caused a radical shift in nutri-
ent allocation resulting in preferential provision-
ment and protection of the brain, an alteration
which ultimately accelerated encephalization.
Maximum human lifespan is more than twice
that of our nearest relative, the chimpanzee, with
maximal human longevity exceeding 120 years [28]
and captive chimpanzees (which are more longe-
vous than their wild counterparts) approaching 60
years. As to which physiological phenomenon facil-
itated this accretion in lifespan, it should be noted
that there exists a robust correlative relationship
between the lifespan of animals and the rapidity
with which they metabolize food – the longer the
lifespan the lower the metabolism of the animal
[29]. Though the underlying mechanism by which
metabolic rate modulates aging and longevity is
not altogether clear, there is theoretical support
for a free radical-mediated mechanism. That is,
because the generation of damaging free radicals
is ineluctably elicited upon ingestion of food, the
more calories an animal intakes and the more pre-
cipitous the combustion of consumed calories, the
more damage done to tissues and the more rapidly
aging ensues. Indeed, one of the means by which
caloric restriction is thought to augment longevity
is via suppression of metabolic rate, by reducing
the rapidity with which marginal meals are metab-
olized [8,30]. CR seems to induce increased effi-
ciency of energy extraction and, ostensibly, lower
levels of radicals released per calorie consumed.
Considering the centrality of energy equilibration
in determining the physiological disposition of
organisms – rate of growth, rate of senescence,
extent of encephalization and reproductive poten-
tiality – it is plausible that the modulation of
Humans are evolutionarily adapted to caloric restriction
metabolism supervenes each component of the
quadripartite complex. Further, it is to be noted
that each component of the complex – altriciality,
longevity, lessened lifetime fertility, and pro-
nounced encephalization – are ultimately induc-
ible neuro-endocrinologically via alteration of
hypothalamic hormones: Physical maturation and
sexual maturation, which have undergone selective
suppression in the course of human evolution, are
modulated by growth hormone and thyroid hor-
mone in the case of the former and by steroidal
sex hormones and gonadotropins in the case of
the latter; longevity, which has been augmented
during the course of human evolution, is modulated
by metabolic rate and this physiological attribute
is, in turn, modulated by growth hormone, thyroid
hormone and sex hormones; finally, encephaliza-
tion has been increased dramatically over the
course of human evolution and this attribute was
effectuated by meticulous metabolic conserva-
tion/reallocation/preservation, a role reserved pri-
marily for the hormone cortisol (and, secondarily,
epinephrine). To reiterate, release of growth hor-
mone is controlled by the hypothalamic hormone
GHRH, release of thyroid hormone is controlled
by the hypothalamic hormone TRH, release of sex
hormones are elicited by release of gonadotropic
hormones and release of these gonadotropic hor-
mones is ultimately controlled by the hypothalamic
hormone GnRH and release of cortisol is controlled
by the hypothalamic hormone CRH. Thus, evolu-
tionary economization could conceivably have
been effectuated by merely modulating the meta-
bolic disposition of the hypothalamus, the body’s
chief homeostatic/regulatory organ. This econom-
ization gave early Homo a selective advantage over
sympatric hominids as members of this genus could
subsist on foods of lower nutritional quality and
consume less thereof.
If indeed humans are evolutionarily adapted to
caloric restriction, this may suggest that dietary
indulgence is particularly deleterious for our spe-
cies. Clearly, organisms exhibiting increased energy
efficiency have a heightened capacity for energy
storage and are able to accrete appreciable
amounts of adipose when food is abundant. Exces-
sive adiposity is associated with increased morbid-
ity and mortality in humans, promoting the
pathogenesis of myriad degenerative diseases
[31,32]. Interestingly, racial differences in mortal-
ity may contribute to an elucidation of the relation-
ship between metabolism and longevity. Caucasoid
Homo sapiens likely experienced an increase in
metabolic rate as an adaptation to the colder Eur-
asian climate, whereas Africoid humans remaining
on the African continent during the Pleistocene per-
983
iod would have experienced no compensatory met-
abolic elevation [33]. Thus, Blacks might be
expected to exhibit increased metabolic efficiency
relative to Caucasians as suggested by some studies
[34–36]. Under conditions of comparable calorie
consumption, therefore, Blacks may be expected
to accrete more body mass and exhibit increased
susceptibility to those conditions catalyzed or com-
plicated by obesity. Conversely, Blacks who do not
engage in excessive energy intake and avoid obesity
may benefit from heightened metabolic efficiency,
with a higher proportion attaining advanced ages
relative to Caucasians. Indeed, data from National
Vital Statistics Reports (since 1997 when such data
are available) exhibit a clearly discernible trend,
with Black nonagenarians and centenarians having
longer life expectancy relative to Whites and the
general US population [37]. While the statistical sig-
nificance of this apparent trend has yet to be estab-
lished, I posit that the phenomenon is stable,
significant and mediated by metabolic differences
between racial subgroups. Indirect support for this
view can be found in a seminal study on CR con-
ducted by Weindruch and colleagues which found
that among murine animals subjected to similar de-
grees of dietary restriction, the most metabolically
efficient subjects experienced more marked in-
creases in longevity [38]. This investigation ostensi-
bly implies that within a highly homogeneous
population of organisms, natural variations in met-
abolic efficiency exist and such differences are
determinants of longevity within the strain studied.
In accordance with the theoretical complex delin-
eated in this paper I hypothesize that Blacks have
a higher maximum lifespan potential that is facili-
tated by a higher energy efficiency relative to
Whites and that the shorter average lifespan of
Black Americans is attributable in large part to
the deleterious effects of overfeeding in organisms
adapted to conditions of caloric paucity.
Acknowledgment
This exposition was made possible in part by a gen-
erous gift form the Alicia & Enrique H. Vidal
Foundation.
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