After dark: the evolutionary ecology of human sleep

Full text

Evolutionary
Medicine
and Health
NEW
PERSPECTIVES
Edited
by
Wenda R. Trevathan
New Mexico State University
E. O. Smith
Emory University
James J. McKenna
University
of
Notre Dame
New York Oxford
OXFORD
UNIVERSITY
PRESS
2008
CHAPTER
16
After Dark
The Evolutionary Ecology
of
Human Sleep
Carol
M.
Worthman
Until relatively recently, studies
of
the sleep
of
human adults
or
infants
ignored the human adaptive context and circumstances within which human
sleep evolved. Perhaps a consequence
of
this is that medically trained sleep
researchers missed opportunities to understand the kinds
of
environmental
pressures and needs for which both contemporary adult and infant sleep
architecture and arousal patterns were originally designed. Worthman's
chapter provides a novel and innovative analysis
of
what various forms
of
human sleep are good and not good for and what factors best explain conun-
drums such as the apparent human inability to prevent sleep restriction
alongside and in relationship to the ubiquity
of
insomnia in modern life. The
need in the past and present for nighttime vigilance is one
of
the more impor-
tant aspects
of
her discussion. She also examines the dissociation between
objective measures
of
sleep (quantitative data) and what people subjec-
tively report (i.e., how people describe a "good"
or
"adequate" nights sleep).
Further, she notes that sleep researchers worry about Westerners sleeping
less when, according to epidemiological studies, death is more likely for
someone that sleeps more, rather than less. Similar to other anthropologists
who study sleep from an evolutionary point
of
view and have challenged the
Western cultural notion that infants should sleep alone, or that necessarily
uninterrupted early consolidated sleep is "good"
or
safe for babies, Worthman
flips around conventional understandings
of
how and why adult sleep
responds to local conditions as
it
does and what it all means for human
health. Her contribution illustrates what evolutionary medicine seems to do
quite well, i.e., not mistaking adaptation for pathology in the same way that
it forces a more careful distinction between defense and defect. Worthman's
broad ecological analysis includes new considerations
of
the evolutionary
origins and contexts
of
sleep. Her functional explanations expose instances
in which cultural ideologies are mistaken for more empirically based,
species-wide science. For example, she answers the question
of
why adults
291

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EVOLUTIONARY MEDICINE
AND
HEALTH
might sleep less than research suggests is ideal. What a surprise
it
is to learn
that one possible answer is that
we
are not supposed to!
Is
it possible that
there may
be
better things to
do
with our time than sleep, activities that more
effectively promote our mental and physical health at that particular time?
Worthman suggests that this might well
be
one answer to why Westerners
sleep as they do! Perhaps this is good news for students, who never seem to
find time to get enough sleep.
INTRODUCTION
Why do we sleep? Remarkably,
we
still don't know (Rechtschaffen, 1998). What we do
know
is
that sleep is as essential to life
as
oxygen
or
food: sleep disruption erodes psy-
chobehavioral performance and alters bodily function, and complete sleep deprivation
can lead to death nearly as swiftly as does starvation (Roth, 2004).
The
gap in knowledge
about the essential biological functions
of
sleep limits the efforts
of
sleep scientists and
clinicians to explain and identify treatments for sleep disorders, advise patients on best
sleep practices, and suggest public health guidelines for prevention
of
sleep problems.
In
the absence
of
a complete account
of
sleep function, a more broadly grounded under-
standing
of
the sources and sequelae
of
sleep problems might help, nevertheless, to
address some
of
these concerns. This possibility will
be
explored in light
of
expanding
knowledge about the physiology and phenomenology
of
sleep along with evolutionary
and comparative ethnographic analysis.
The
stakes for understanding sleep are rising as globalization inadvertently trans-
forms sleep practices around the world. Virtually universal introduction
of
schooling and
new forms
of
labor over the last 50 years have regimented daily schedules in new ways,
while the spread
of
electricity and media has altered capacity, options, and demands for
activity around the clock. Such spectacular technological and sociological transforma-
tions have attracted both credit and blame for sleep restriction and sleep-related prob-
lems, including accidents, psychiatric disorders, insomnias, obstructive sleep disorders,
and chronic physical diseases. The effects
on
sleep from striking structural and techno-
logical sources have tended to eclipse other more subtle ones, including changes in the
conditions under which people sleep. Adoption
of
modern forms
of
housing, beds and
bedding, and climate control alter the ecology
of
sleep, as does erosion
of
cosleeping
practices with increased secure space, changing notions
of
childhood and human devel-
opment, and the rise
of
the postmodern family. This essay will consider how the newly
configured material, social. and psychological contexts
of
sleep may exert
not
only direct
effects
on
sleep behaviors and related health problems. but also indirect ones through
interactions with lifestyle-defining macrosocietal shifts in technology, labor, and social
structure.
Another, larger question colors
the
struggle to understand linkages between changing
sleep habits and health. Sleep habits are highly plastic, shifting to meet the demands
of
cir-
cumstance and motivation
in
ways that sleep researchers argue can be deeply injurious
(Bounet &Arand, 1995; Dawson & Reid, 1997; Harrison & Horne, 2000; Landrigan et
aI.,
2004).
Why
such plasticity?
If
sleep is so important, strong countervailing pressures should
Chapter
16:
Evolutionary Ecology of Sleep
restrict the human capacity to adjust sleep behaviors in ways that adversely affect health.
A broader comparative and evolutionary view suggests some answers to
this
question, and
furthermore suggests why, when, and how disturbed
or
curtailed sleep becomes problem-
atic. Specifically, the present analysis identifies situations that provoke sleep restriction and
discovers the role
of
stress and stress physiology in the causes and consequences
of
dis-
rupted sleep. Identification
of
conditions that act as triggers for sleep restriction can guide
individuals and caregivers to avoid, detect, and cope with the situations that stimulate sleep
restriction. Insights into the bearing that the extensive knowledge about stress ecology and
physiology has on understanding the sources and sequelae
of
sleep behavior may resolve
old questions and change scientific, clinical, and popular views
of
why and how we sleep.
HUMAN SLEEP
For most people, sleep occupies about a third
of
the day and, as such, represents the most
common human behavior. Outwardly, sleepers are quietly disengaged from the world,
eyes closed, limbs relaxed, and habitually withdrawn to a designated comfortable loca-
tion. Yet the apparent behavioral quiescence
of
sleep belies its characteristic intense,
complex, and patterned physiological activity (Table 16-1). A brief review
of
this com-
plex state provides valuable background to understanding the nature and ecology
of
sleep
and how it may
be
disrupted (reviewed
in
Buysse, 2005; Hobson & Pace-Schott, 2002;
Rama, Cho, & Kushida, 2006). Virtually all systems and their functions are altered as
sleep sequences through distinctive physiological patterns that run
in
90- to lOO-minute
cycles between phases
of
nonrapid eye movement (NREM) and rapid eye movement
(REM). Usually, sleep begins with a progression through the four stages
of
NREM sleep,
moving from a brief period
of
Stage 1 drowsy sleep
(3-8%
of
sleep), to Stage 2 light sleep
(45-55%), to the deep and very deep slow wave (Bdelta) sleep comprising Stages 3 and 4
(15-20%). In the coma-like depths
of
slow wave sleep, several body functions (e.g., res-
piration and heart rate, thermoregulation) are slowed, muscles relax, and directed thought
is sharply diminished. Brain activity alters, and not only
in
the distinctive overall elec-
troencephalographic (EEG) signatures
of
each sleep stage: some brain areas active
in
waking become inactive, while others inactive
in
waking become active. The contrast
between external and internal activity states becomes greatest in REM sleep, during
which a very active brain occupies an immobilized body. Thermoregulation and muscle
tone are nearly absent, heart rate and respiration become slow and more irregular, and
eyes move
in
characteristic staccato bursts. REM sleep hosts dreaming. The qualitatively
distinctive mental activity experienced
in
this stage features hallucinatory over directed
thought, absence
of
self-reflective awareness, attenuated analytical thought, and lack
of
voluntary control over dream content.
Sleep Regulation
How does the body "know" when to sleep and to wake? Orienting to the world and main-
taining appropriate levels
of
arousal constitute critical features
of
effective functioning
for any organism. Hence, these features are subject to redundant mechanisms that
negotiate meeting immediate demands such
as
evading a predator
or
foraging for food

295
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EVOLUTIONARY
MEDlCINEAND
HEALTH
TABLE
16-1
Characteristics
of
Wake
and
Sleep
States
Behavioral state
Wake
NREM
Functional
state
Awake--somnolent
Stages
1-4
REM
Tonic-phasic
Physiological
EEG Fast, low voltage Slow, high voltage Fast, low voltage
Brain activity
+++
(vary by
+++
(vary by
+++
(vary by
region) region) region)
Eye movement Varies with vision Slow 1irregular Rapid, phasic
Muscle tone ++ + 0
Heart rate, blood pressure, + + + (variable) + + (regular) + (variable)
respiration
Response to hypoxia,
+++
++
hypercarbia
Thermoregulation
+++
++ Oto +
Physiological + Physiological, Physiological
behavioral sweat/shiver
Behaviorol
Eyes Open, blink Closed Closed
Posture Erect Recumbent Recumbent
Body movement Continuous, voluntary Episodic, involuntary Immobile-twitches
Responsiveness
+++
+1++
0/+
Cognitive
Mental activity Vivid, external origin Absent or dull Vivid, internal origin
Conscious thought Logical, progressive Logical, perseverative lllogical, distorted
Memory Acquisition. retrieval Consolidation Consolidation
(declarative and (declarative and
nondeclarative) nondeclarative)
Proportion
of
sleep period
Infancy (I6-18h1day) Gradual consolidation, 50%
reduction
of
sleep
quota
Adolescence (9 h/day) IntenseSWS 20-25%
Adulthood (7-Sh/day)
<5%
75-80% 15-25%
Source:
Buysse
2005;
Hobson
& Pace-Scholl
2002;
Rosenthal
2006;
Roth
2004,
Walker
&
StickgoJd
2006.
against ongoing homeostatic needs that are met during sleep_ Accordingly, regulation
of
sleep and wake states is the product
of
two interacting mechanisms, a circadian pace-
maker
and
homeostatic drive.
The
internal circadian pacemaker manages alertness and
operates through the suprachiasmatic nucleus
of
the hypothalamus: entrained primarily
external environmental light, the nucleus tracks ambient time and synchronizes activ-
ity
of
the
body's
systems and organs to
both
clock time and seasons (Pace-Schott &
Hobson, 2002; Richardson, 2005). Circadian drive for alert
wakefulness-indexed
activity
of
arousal systems in brain stem, basal forebrain, and
hypothalamus-peaks
at
8-9 p.m. and thereafter drops precipitously to a minimum during the latter
half
of
the
habitual sleep period,
or
between 3 and 6 a.m., whereafter it rises throughout the day
(Wright, Hull, Hughes, Ronda, & Czeisler, 2006).
Reciprocally, homeostatic sleep drive constitutes sleep pressure that accumulates dur-
ing wakefulness and resolves during sleep (Borbely & Achermann, 2000). Homeostatic
Chapter
16:
Evolutionary
Ecology
of
Sleep
regulation
of
slow wave activity,
or
slow oscillations in membrane potential
of
cortical neu-
rons
during sleep, manifests inincreased slow wave activity after wakefulness and declines
to baseline during sleep. Slow wave activity
may
reflect synaptic changes that generate
the
cellular "drive" for sleep (Tononi, 2005). Thus, slow wave activity increases during
sleep in specific brain regions after learning tasks that target those regions (Huber, Ghilardi,
Massimini, & Tononi, 2004). In
this
homeostatic model
of
sleep need, the longer the time
since the last sleep episode, the greater the drive; conversel
y,
the longer the time elapsed in
a sleep bout, the lower the homeostatic drive for sleep. Further, insufficient sleep incurs
a "sleep debt" reflected in residual sleep drive manifested in subjective sleepiness and
objective latency to fall asleep (Littner et al., 2005) and produced by inhibition
of
wakeful-
ness-promoting neurons as adenosine levels rise with duration
of
wakefulness (Basheer,
Strecker, Thakkar, & McCarley, 2004). Hunger
and
food consumption provide a well-
studied behavioral parallel: the greater the hunger, the more intense the feeding, and the
more that has been eaten, the lower the hunger drive (Lima, Rattenborg, Lesku, &Amlaner,
2005). The physiological bases
of
homeostatic sleep drive are uncertain, but biomarkers for
extent
of
sleep drive comprise amount and intensity
of
slow wave activity, or delta
EEG
activity during
NREM
sleep, and possibly the amount
of
EEG theta activity during wake-
fulness (Buysse, 2005). Sleep loss potentiates a compensatory catch-up response mani-
fested
in
more and greater intensity
of
slow
Wave
sleep and longer sleep episode, In snm,
current fonnulations
of
sleep drive aim to explain patterns
of
sleepiness, but the physiolog-
ical bases remain fuzzy: the gap in our understanding
of
the bases
of
sleep need leads to
reliance on amount and timing
of
slow wave sleep as markers
of
sleep drive or deficit.
Interactions
of
the circadian pacemaker and homeostatic drive direct the
sleep-wake
cycle through inputs to hypothalamic nuclei regulating wakefulness, particularly the
hypocretinlorexin system, to adaptively adjust the amount and timing
of
sleep (Saper,
Cano, & Scammell, 2005). Yet sleep is also immediately reversible. Capacity forreversibil-
ity inheres in the neuroarchitecture
of
sleep and permits acute demands, such as the cry
of
a hungry infant
or
the ring
of
an alarm clock,
to
counterbalance
the
ascendant states
of
arousal regulating systems. Brain activity states that potentiate condition-specific arousal
responses (micro-arousals) are systematically distributed throughout sleep and alter the
threshold
for
reaction to external stimuli: the cyclic alternating pattern
of
such states
in
NREM sleep is thought to permit sleep reversibility even during the otherwise coma-like
periods
of
deep sleep (reviewed in Halasz, Terzano, Parrino, & B6dizs, 2004). Generally,
micro-arousals may organize a capacity for filtered monitoring
of
the external environ-
ment during sleep by sensitizing endogenous processes
of
sleep to internal
and
external
conditions_ Density
of
micro-arousals is increased after a stressful day
or
in
anxious indi-
viduals and has been associated with nomestorative sleep (poor sleep quality) even where
sleep efficiency (percent actual sleep during sleep period) is maintained: treatments that
reduce micro-arousals in insomniacs improve subjective sleep quality (Halasz, Terzano,
Parrino, & B6dizs, 2004).
The picture
of
sleep that emerges, then,
is
of
a behavior state that is highly regulated
and structured through endogenous neurological processes, yet is entrained
by
external
cues and acutely reversible
by
momentary demands. In other words. perhaps more than
any other behavior, sleep combines powerful physiological regulation with inbuilt
sensitivity
to
context, both internal and external. Unlike other behaviors, the course and
content
of
sleep lies largely outside voluntary control (Hobson & Pace-Schott, 2002),

296
EVOLUTIONARY MEDICINE
AND
HEALTH
EVOLUTIONARY BACKGROUND
Regular
or
cyclic variation in the environment (diurnal, seasonal, trophic) presents adap-
tive opportunities and challenges for resident organisms. Accordingly, life fonus univer-
sally display capacities to vary activity states
in
synchrony with patterns
of
light-dark,
warm-cold,
or
feeding opportunities. Although sleep has been studied most extensively
in
mammals, characteristic sleep-like behavior has been observed in invertebrates such
as
cockroaches and fruit flies, amphibians and fish such as tree frogs
or
carp, and reptiles and
birds such as lizards
or
hummingbirds (Lesku, Rattenborg, & Amlaner, 2006;
2000). Data on the comparative physiology
of
sleep and activity states remain patchy but
can be generalized to suggest that the hallmarks
of
sleep-like behavior include character-
istic posture, reduced activity, altered arousal thresholds, and homeostatic regulation man-
ifested in rebound
or
compensatory responses after rest/sleep deprivation. Despite the
ubiquity
of
behavior that meets these criteria, substantial variation in sleep budget,
or
the
amount and distribution
of
sleep behavior, has been observed both within and between
taxa. Species-characteristic sleep quotas,
or
daily amount
of
sleep, vary among mammals
from 3 hours in horses and 4 hours in elephants to
19
hours in opossum and nearly
20
hours
in brown bats (Siegel, 2005 source materials). The underlying architecture and physiology
of
sleep differ among taxa
as
well.
At
one extreme, dolphins and other cetaceans lack REM
and are never completely asleep; rather, one hemisphere goes into slow wave "sleep" and
the contralateral eye closes while swimming and navigation continue. Other extremes
include short wake cycles in small animals, down to 7 minutes in 15.5 g big brown bats,
and long ones in large animals, up to 2 hours in 3500
kg
Asiatic elephants (Siegel, 2005).
Debated Functions
of
Sleep
Of
the many functions ascribed to sleep, the most prominent concern rest and recupera-
conservation
of
energy, safety and predator avoidance, and memory consolidation
and affective processing (Siegel, 2005). Those who emphasize that sleep is by the brain for
the brain underscore a role in brain development and function (Walker & Stickgold,
2(06).
While there is evidence that some
of
these functions are necessary, none has been found to
be a sufficient role for sleep.
For
instance, the primacy
of
rest is undercut by observations
that periods
of
hibernation
or
torpor, such as in bears
or
hummingbirds, are followed by
profiles
of
brain activity in sleep indicative
of
sleep deprivation. A role for energy sparing
is limited by the high energetic cost
of
REM and the observation that "[tJhe metabolic sav-
ings
of
sleep over quiet wakefulness has been estimated at approximately 10 to
15
percent;
from the standpoint
of
energy savings, a night
of
sleep for a 200-pound person is worth a
cup
of
milk" (Rechtschaffen, 1998, p. 364). Absence
of
sleep in newborn dolphins and
killer whales argues against the crucial role
of
sleep in brain development (Siegel, 2005).
Compelling evidence for the role
of
sleep in brain plasticity and memory consolidation
(Hairston
et
al., 2005; Huber, Ghilardi, Massimini, & Tononi, 2004; Wright, Hull, Hughes,
Ronda, & Czeisler, 2006) nevertheless fails to account for the near-absence
of
postpartum
maternal sleep
or
sleep rebound in cetaceans (Siegel, 2005).
The continued mystery surrounding its function motivates interest in the comparative
study
of
sleep for clues from its evolutionary history. Comparative evolutionary approaches
have focused on features thought to
be
related to the putative functions
of
sleep. Thus,
1
~~'
1
Chapter
16:
Evolutionary Ecology
of
Sleep
297
~~'
brain and body size, metabolic rate, diet (cami-, omni-, and herbivore), and neonatal i
characteristics (birth weight, altriciality) all have been considered as life history traits
Ie
that influence the need for energy conservation, predator avoidance through inactivity
ii
and concealment, buffering
or
restoration
of
wear and tear, or demands
of
development, 1
1-
l
especially brain development. As such, taxonomic correlations between these life history
traits and key parameters
of
sleep (sleep quota, amount
of
NREM and
of
REM sleep, and
cl
duration
of
sleep cycle) have been consulted to identify possible functional constraints
that shape the evolution
of
sleep (Allison & Cicchetti, 1976; Tobler, 2000). Phylogenetic
studies have concentrated on the more extensive data available for the well-studied mam-
malian order and repeatedly have linked taxonomic variation in sleep parameters with
size
of
body and brain, metabolic rate, and neonatal characteristics (Elgar, Pagel, & Harvey,
1988; Zepelin, 2000). A recent definitive multivariate analysis has superceded previous
reports by taking the critical step
of
accounting for evolutionary effects related to body
size,
or
allometry, as well as removing statistical artifacts (Capellini, Barton, McNamara,
& Nunn, in press). Capellini and colleagues' results, summarized in Table 16-2, demon-
strate the pervasive effects
of
allometry on sleep parameters and substantially clarify
evolutionary relationships. In particular, this clarified view prunes the list
of
candidate
functions for sleep. That brain mass is unrelated to any sleep parameters refutes direct
functions
of
sleep for brain restorative processes. Similarly, absence
of
association
between neonatal brain mass and sleep parameters militates against a direct role for sleep
in
brain development (Rechtschaffen, 1998). The failure to find constraints on sleep para- ,
meters related to metabolic rate argues against hypothesized restorative need for relief
of
1
oxidative stress from metabolic turnover (Siegel, 2005)
as
well as against a straightfor-
ward role in energy conservation for sleep (Berger & Phillips, 1995).
Most prominent among Capellini and colleagues' findings that support proposed sleep
functions are the multiple relationships
of
life history characteristics to sleep param-
eters that suggest effects
of
predator pressure (Lima, Rattenborg, Lesku, & Amlaner,
2005): short gestation length and low birth weight are related to lower sleep quotas, both
TABLE 16-2 Comparative Evolutionary Analysis
of
the Correlates
of
Mammalian Sleep
Phenotypic
Sleep cycle
feature Sleep
quota
NREM
REM
length
Body
mass
Negative Positive
Brain mass X X
Basal Metabolism X X X
Gestation length Negative Negative Negative X
Body
mass,
neonatal Negative Negative X
Brain
mass,
neonatal X X
Total sleep Negative
NREMquota Positive
REM
quota
Negative
Association tested.
not
significant.
X.
Association removed by controlling
for
allometry.
Blank, rest
for
association
not
reponed. presumably positive.
Source: Data from Capellini
et
al.. in press.

298
EVOLUTIONARY MEDICINE AND
HEALTH
REM and NREM, which may reflect reduced investment in maintenance. Then, the asso·
ciation
of
longer sleep cycles with less total and REM sleep supports the proposed trade·
off
between vigilance and sleep need whereby the reduced vigilance characteristic of
REM is more widely spaced and diminished when total sleep is increased. Nevertheless,
as Capellini and colleagues emphasize (Capellini, Barton,
McNam~
& Nunn, in press),
the phenotypic features included in their analysis account for little taxonomic variation
in sleep parameters (9-40%): that so
much
diversity remains unexplained powerfully
indicates that other factors are at work and much remains to be explored.
For
instance, the
greater the body mass, the longer the length
of
sleep cycle. This association mediates all
other phenotypic relationships
to
cycle length; even so, the body mass-cycle length rela·
tionship explains only a third
of
the phylogenetic variance in cycle length.
Note
also that
phylogenetic analyses
of
this global kind cannot evaluate possible brain
region-
or
func·
tion·specific roles such as memory consolidation (Walker & Stickgold, 2006) or cortical
plasticity (Hobson & Pace·Schott, 2002) and suggest the need
to
ally physiological with
field research to link experimental with phenotypic, demographic, and ecological infor-
mation and accelerate progress on understanding the functions
of
sleep.
Viewed from a comparative evolutionary perspective, the characteristics
of
human
sleep are not distinctive (Siegel, 2005). Given both the brain-based understandings of
sleep and that so much else in human behavior and cognition has been considered extraor-
dinary, its unexceptional character in humans is worth remarking. Quotas for total, REM,
and NREM sleep, ratio
of
REM
to NREM, and sleep cycle length
do
not stand out in
phylogenetic analyses, although overall and specific regional size and organization
of
the
human brain
do
(Allison & Cicchetti, 1976; Rilling, 2006).
The strong focus
on
sleep
architecture-structure
of
the sleep cycle by stage and
NREMlREM-by
comparative studies for insight into function has tended to over·
shadow the role
of
ecological factors in the evolution
of
sleep behavior and physiology.
Sleep is a risky behavior, because it includes periods
of
blunted awareness, relative phys·
ical unresponsiveness, reduced
or
absent thermoregulation, and a stationary site (Lima,
Rattenborg, Lesku, & Arnlaner, 2005). Sites, surfaces, and social groupings for sleep all
would have direct bearing on important ecological challenges incurred for sleep, includ-
ing thermal exposure, physical safety and comfort, and vulnerability to predators and par.
asites (Anderson, 1998). Extensive field studies
of
primates document that avoidance
of
predation drives selection
of
sleeping sites, exemplified
by
use
of
tree holes
by
prosimians
and tamarins, cliff faces by Hamadryas baboons, and tree crowns
or
outer branches
by
many primates, from smaller monkeys
to
apes (Anderson, 1998; Kappeler, 1998).
Widespread practice
of
nest building among the great apes even may represent evidence
for instrumental tool use and observational learning,
or
culture (Fruth & Hohmann, 1996).
Sleep in Human Evolution
The record
of
evolutionary history for human sleep is sketchy (see Nadel et al., 2004).
Sleep sites, whether nests in trees
or
beds on the ground, leave little,
jf
any, trace in the
fossil record. Skeletal evidence provides clues to where hominids might have slept:
advancing skeletal modifications in the evolution
of
bipedalism diminished agility in
trees and decreased access to and usability
of
arboreal sleeping sites. Loss
of
hair that
limited infant capacity for clinging would have
made
tree occupation even more
,
Chapter
16:
Evolutionary Ecology of Sleep
299
cumbersome and dangerous. Hair loss also increased thermal pressure from heat loss
during sleep and required sources
of
heat
or
covering in exposed arboreal settings. The
ground-dwelling ancestral ape lineages became ground-sleeping in hominids, who have
been presumed to have relied
on
protection from tools, social groupings, then fire. and
eventually physical structures
to
fend
off
predators during waking and sleeping. Thence,
one must turn
to
the record
of
occupation sites themselves. Residence in and exchange
with social groups is seen as characteristic
of
the human lineage: an influential theory
proposed that emergence
of
a home base for convergence after foraging and sharing
of
food, information, and sociality formed a crucial step in social evolution (Isaac, 1981).
But sharing and other features
of
home base are not unique
to
humans, and unambiguous
identification
of
such home bases in the paleoantbropological record has proven difficult
(Sept, 1998). Disputed evidence for hominid association with fire begins in Africa 104-1.5
million years ago and is uncontestably accepted as widespread systematic, controlled
use at around the onset
of
the last Ice Age in the later middle Pleistocene (-110.000-130,000
B.P.) in conjunction with appearance
of
anatomically modern humans (Wrangham.
Jones, Laden, Pilbeam, & Conklin-Brittain. 1999). ConvergentIy, characteristic human
occupation sites that combine use for living. production, and food sharing also appear
during the same period in sub-Saharan
Mrica.
Use
of
caves and traces
of
posts for huts
around hearths appear
by
500,000 B.P. (Nadel et al., 2004).
For
much
of
human evolution, security in sleep depended upon sources other than fire
or housing, which undoubtedly have shaped the features
of
sleep and sleeping behavior.
Features
of
the evolutionary bioecology
of
human sleep are summarized in Thble 16-3.
Although limitations in the archeological record may produce conservative estimates
of
the dates by which humans customarily used fire and lived in physical structures that
TABLE 16-3 Elements of Human Sleep Ecology
Microecology
Proximate physical ecology
Bedding
Presence
of
fire
Sleeping place or structure
Proximate social ecology
Sleeping arrangements
Separation
of
sleep--wake states
Biotic macro- and microecology
Domestic animals
Parasites
and
nighttime pests
Macropredators (animal, human)
Macroecology
Labor demands
Social activity
Ritual practices
Beliefs about sleep and dreaming
Status (social status, class, gender)
Life history, lifespan processes
Ecology, climate
Demography and settlement patterns
Evolutionary Bioecology
Group living
Ground dwelling
Subsistance foraging
Equatorial
Intense social relations
Sharing, reciprocity
Food
Labor
Infonnation
Protection and care
Use of tools and (later) fire
Dual inheritance

300 301
EVOLUTIONARY
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HEALTH
afforded protection from predators and the elements, these practices nonetheless came
late in the evolution
of
human sleep. Thence, an evolutionary picture
of
human sleep ecol-
ogyas
"extremely safe" and safer than
in
any other mammal (Allison & Cicchetti, 1976)
would appear overoptimistic.
COMPARATIVE PERSPECTIVES
Surprisingly, anthropology
and
behavioral ecology have not systematically engaged the-
most
prevalent
of
human behaviors.
In
consequence, the empirical grounds for compara-
tive analysis
of
sleep behavior are exceedingly thin. Documentation
of
cross-cultural
patterns and variation
in
sleep, sleep quota, napping, objective
and
subjective sleep qual-
ity, sleep architecture, and life course trajectory has barely begun (see BaHamman,
2003; Liu. Liu, & Wang, 2003; McKenna, 1986, 2000; McKenna & McDade, 2005;
McKenna, Mosko, Dungy, & McAnninch, 1991; McKenna
et
al., 1993; Reimao et al.,
2000a, 2000b; Reimao, Souza, Medeiros, & Almirao, 1998; Worthman & Brown, 2007
(see also Chapter 12).
The
physical and social ecology
of
sleep is, by contrast, more
accessible in ethnographic and historical accounts (Ekirch, 2005; McKenna et al., 1993).
Humans inhabit a wide range
of
physical settings
and
distinctive cultures associated with
strikingly different personal
and
social landscapes
of
meaning, thought, and action. The
pervasive impact
of
culture extends to sleep and informs where, when, how, and with
whom
one will sleep at any age
and
physical
or
social condition, along with the meanings
and interpretations
of
sleep
and
its wider social-emotional frame. With ethnographic
information from colleagues having society-specific expertise (Robert Bailey, Fredrik
Barth, Magdalena Hurtado, Bruce Knauft, Mel Konner,
and
John Wood) and using an
analytical framework outlined in Table 16-3 (left side), we undertook a preliminary com-
parative analysis
of
human sleep ecology (Worthman & Melby, 2002). This analysis
revealed areas
of
commonality and diversity in the proximal conditions
or
microecology
under which people sleep and documented the pervasive effects
of
social, CUltural, and
physical ecological factors,
or
macroecology,
on
patterns
of
sleep.
Our comparative analysis yielded unexpected findings, particularly by identifying
unusual characteristics
of
contemporary sleep ecology and practices. Across societies we
reviewed, sleep settings were social and solitary sleep rare; bedtimes fluid and napping
common; bedding minimal; fire present; conditions dim
or
dark; and conditions rela-
tively noisy with people, animals, and little
or
no acoustic and physical barrier to ambi-
ent conditions. As such, sleep settings offered rich and dynamic sensory properties,
including security and comfort through social setting, fuzzy boundaries in time and
space,
and
little climate control. By contrast, postmodern industrial societies emerged
as having relatively impoverished, stable sensory properties including solitary
or
low-
contact sleep conditions, scheduled bed- and waketimes and consolidated sleep, padded
bed and profuse bedding, absence
of
fire, and darkness, silence, and high acoustic as well
as physical boundaries to sleep spaces. These much more static sleep conditions typically
offer security and comfort through physical setting, rigid boundaries in time and space,
and climate control. Although contemporary postmodern industrial Western conditions
did stand
out
as unusual, there were favorable contrasts that included the relative absence
of
parasites
and
vectors
of
disease, fear
of
predators
and
ambush, discomfort from harsh
Chapter
16:
Evolutionary Ecology
of
Sleep
temperatures
or
rough bedding,
or
disruptions from crowding, noise
or
activities
of
others. Other features may make sleep regulation more challenging, including habitual
solitary sleep
or
limited cosleep from infancy onwards; a "lie down and die" model
of
sleep
in
restricted intervals with few, brief sleep-wake transitions; and sensory depriva-
tion
of
physical
and
social cues
in
sleep settings.
An
untested question is whether these
unusual habits and settings place high and sustained burdens on sleep-wake regulation
systems that contribute to contemporary sleep problems and disorders.
Comparative analysis also reveals common features
of
sleep behavior among humans.
Human nights are filled with activity and significance, and nowhere
do
people typically
sleep from evening to dawn. Across cultures, humans also show a range
of
arousal states
that blur binary sleep-wake distinctions, including capacities for sustained somnolence
or resting wakefulness, for adjusting level
of
vigilance in sleep,
and
for nonconsolidated
sleep patterns including napping and night waking. When and as necessary, humans
can
and will restrict sleep for extended periods.
They
also will opportunistically sleep, toler-
ating long resting bouts they may not need.
The
risky conditions under which human sleep evolved likely promoted both com-
plexity
of
sleep architecture and capacity for vigilance
in
sleep (Lima, Rattenborg,
Lesku, & Amlaner, 2005).
We
know that a sure way
of
increasing the proportion
of
REM
is to lengthen the bout (Siegel, 2005), but
we
do not know how culture-based lifetime
differences in sleep patterns and settings influence sleep architecture,
or
amounts and
quality
of
sleep,
or
even memory, the capacity for state regulation, and mental health.
These compelling questions await future study.
NOT GETTING ENOUGH? SLEEP DIFFICULTIES
AND DYSFUNCTIONS
Sleep problems affect an estimated
50-70
million Americans (Strine & Chapman, 2005).
Sleep scientists and clinicians habitually point to dramatic statistics documenting national
and international escalation
in
sleep problems and threats to sleep adequacy (U.S.
Department
of
Health and Human Services, 2003). Recent Sleep
in
America Polls pro-
vide vivid evidence for the nature
and
extent
of
adult Americans , sleep problems and poor
sleep habits (National Sleep Foundation, 2005).
In
its most recent report, the survey
found that barely
half
of
Americans (49%) say that they regularly "had a good night's
sleep," and 17%
of
respondents reported that they felt tired
or
not
up
to
par
on
all
or
most
days. Unsurprisingly, respondents also reported a daily average consumption
of
2.5 caf-
feinated beverages. In another national survey, 26%
of
adults reported experiencing sleep
insufficiency
on
14
or more
of
the past 30 days (Strine & Chapman, 2005). Sleep prob-
lems constitute a personal and a public concern: they not only affect mental and physical
health and well-being, but also represent a major source
of
traffic and work-related
accidents and errors, and lateness
or
low productivity
at
work
or
school.
To the evident frustration
of
advocates, the public on the whole appears uumoved by
sleep matters, and sleep habits remain poor by scientific accounts. Before considering
further why sleep problems are so widespread
and
why they continue to advance
in
the
face
of
medical advice, a brief review
of
the nature and extent
of
sleep disruptions and
disorders is
in
order.

302 303
EVOLUTIONARY
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HEALTH
Sleep Difficulty
The most prominent sleep complaint is insomnia, defined
as
difficulty in entering
or
sus-
taining nighttime sleep or poor sleep quality (Brown, 2006). One third
of
contemporary
Americans report having one or more current insomnia symptoms (Ohayon, 2002), and
the
lifetime prevalence
of
having the disorder itself is 16.6% (Breslau, Roth, Rosenthal, &
Andreski, 1996). Prevalent as
it
is, insomnia arises from multiple causes and presents infor-
mative complexities that were brought to widespread attention by Mendelson's important
observation that patients taking benzodiazepine had objectively poor sleep but experienced
better subjective sleep quality (Mendelson, 1990). Cognitive processes since have been
recognized to play specific major roles in sleep quality and insomnia (Harvey, Tang, &
Browning, 2005). Related to Mendelson's observation, insomniacs' common experience of
sleep onset
as
more delayed and quality
of
sleep as lower than is objectively the case
pro-
vides further evidence for the significance
of
sleepers' distorted perception in poor sleep
quality. Studies that alter subjective sleep quality by using placebo, manipulating attribu-
tion,
or
modifying unhelpful beliefs about sleep have demonstrated the importance of
expectation. Associations
of
reduced reported sleep quality with selective attention
to
markers of delayed sleep onset and
of
poor sleep quality upon waking illustrate the con-
tributory role
of
attention in insomnia (Harvey, Tang, & Browning, 2005; Tang, Schmidt, &
Harvey, 2007).
Psychiatric manuals recognize a wide array
of
other sleep disorders with organic
and
psychiatric origins (Buysse, 2005), but only one will
be
considered here because
of
its
rising prevalence and visibility, namely sleep-related breathing disorders and partiCUlarly
obstructive sleep apneas. Epidemiological reports in the 1990s drew attention to these
conditions by finding a startlingly high prevalence in several countries. Characterized
by
frequent sleep-related apnea and hypopnea (obstructed/interrupted and shallow breath-
ing, respectively) with daytime sleepiness (Stradling & Davies, 2004), prevalence ranges
from 1 to 28%, depending on level
of
severity (Young, Peppard, & Gottlieb, 2002). Risk
factors include gender (men two- to threefold more often than women), overweight
and obesity, smoking, and age (Tesali & Van Cauter, 2002). The worldwide trends to
increased obesity, smoking, and aging population structure contribute to escalating rates
in obstructive sleep apnea. This condition, in tum, contributes to risk for hypertension
and other vascular disease, as well as exposure to the consequences
of
sleepiness
and
impaired cognition (Young, 2004).
Sleep Loss
By contrast with sleep difficulties, sleep loss is directly linked to psychological, behav-
ioral, and social-structural factors. The sleep quota among Americans has declined over
the last 24 years (1982-2005), from 8 to 6.9 hours a day (Kripke, Garfmkel, Wingard,
Klauber, & Marler, 2002; National Sleep Foundation, 2005).
In
a recent poll, modal
reported sleep per night was 6.8 hours, contrasting to the recommended
7-9
hours,
depending on age and other factors affecting need.
Yet
of
respondents to that poll, only
22% reported getting less sleep than they needed, and 40% said they got more than
needed (National Sleep Foundation, 2005).
Youth are a focus
of
particular concern because they appear especially vulnerable to
disordered sleep patterns associated with severe consequences reflected in spiking rates
Chapter 16: Evolutionary Ecology
of
Sleep
of accidents and suicide
or
even school failure (Dahl, 2006). Sleep need in adolescence
remains high (at around 9 hours), and youth show later onset and offset
of
sleep along
with an increased penchant for resisting sleep in favor
of
more stimulating pursuits
(Carskadon, 2002). Such youth-specific risks to educational, emotional, and physical
well-being are thought to have increased because the percentage
of
young adults who
sleep fewer than 7 hours per night has more than doubled during the last 40 years
(1960-2001), from 16 to 37% (Spiegel, Tasali, Penev, & Van Cauter, 2004).
Consequences
of
Sleep Loss
and
Disruption
Gauging the actual impact
of
sleep deprivation is challenged
by
the lack
of
a direct mea-
sure for sleep need
or
deficit
(Uttner
et al., 2005). The measurement problem relates to
ignorance about the "true" function
of
sleep, for how can sleep sufficiency
be
assessed or
lack
of
sleep detected when the target outcome is unknown (Young, 2004)? Nevertheless,
both intensive research and human experience recognize the effects
of
acute and chronic
sleep deprivation. Impact on cognitive performance includes gaps in attention and
responsiveness, rapid decay in performance on tasks, reduced capacity for multitasking,
errors in perception and response, increased variability in performance, and impaired
executive functioning, working
memory,
and emotion regulation (Durmer & Dinges,
2005). The greater the sleep deficit and the more disrupted the sleep episodes, the more
severe is the impact
of
sleep disruption and loss.
Sleep deprivation evokes distinctive compensatory neurophysiological profiles
in
sleep (Tobler, 2000): in particular, sleep latency is dramatically reduced and slow wave
sleep activity is increased, especially time in Stage 4 sleep. Lost sleep apparently can be
replaced with substantially less recovery sleep than the original deficit. For instance, up
to
10
days' sleep deprivation can be recouped within one to three 8-hour nights
of
sleep
(Bonnet, 2000).
Rapid recovery
of
sleep parameters from sleep restriction and the lack
of
parity
between sleep lost and compensatory sleep might imply that the "costs"
of
sleep loss
need not be fully repaid. Other consequences
of
sleep restriction contradict this conclu-
sion (Table 16-4). A burst
of
recent research has demonstrated that physiological effects
of
chronic sleep debt contribute to risk for and severity
of
chronic health problems
(Spiegel, Leproult, &
Van
Cauter, 1999). Indeed, merely 6 days
of
sleep restriction
induces endocrine and metabolic changes that may contribute to chronic conditions such
as
obesity, diabetes, and hypertension (Spiegel et al.,' 2004; Spiegel, Knutson, Leproult,
Tasali, & Van Cauter, 2005). The changes associated with sleep loss include decreased
glucose tolerance, increased sympathetic activity, increased cortisol, and decreased thy-
roid activity. Simply stated, sleep has been discovered to drive energy regulation, and
thus, sleep duration moderates body weight and metabolism (Taheri, Lin, Austin, Young,
& Mignot, 2004). Sleep restriction results in endocrine changes, including increased
ghrelin and decreased leptin, with a consequent increase in appetite (Spiegel, Tasali,
Penev, & Van Cauter, 2004). Unsurprisingly, multiple large popUlation studies have
found increased
BMI
or greater future risk for obesity among those who sleep less than
7 hours per day (Cizza, Skaarulis, & Mignot, 2005).
Brain and endocrine activity maintain a bidirectional relationship in sleep (Steiger,
2003), so sleep disruption alters endocrine profiles and vice versa. For instance, ghrelin
stimulates not only appetite, but also endocrine activity (growth hormone; cortisol and its

304
305
EVOLUTIONARY
MEDICINE
AND
HEALTH
TABLE 16·4 Correlates
of
Sleep Restriction
Parameter Change postrestrictioD
Acute
Endocrine Leptin
Ghrelin +
Catecholamines +
p.m.
cortisol +
Cortisol: diurnal variation
TSH:mean
TSH:
diurnal amplitude
Metabolic
a.m.
glucose tolerance
Insulin sensitivity
Autonomic Heart rate variability +
Sympathovagal tone +
(SlParaS)
Cognitive Hunger, appetite
Perceived stress +
o
Executive function,
working memory
Multitasking
Behavioral Response accuracy
Perlormance consistency
Chronic Obesity +
Metabolic syndrome +
Hypertension +
Source:
Brown,
2006;
Dunner
&:
Dinges,
2005;
Irwin,
1999; Sekine et
al.
2002; Spiegel
1999;
Spiegel,
Tasali
et al., 2004;
Spiegel,
Leprouit et
aI.,
2004;
Taheri
et
aI.
2004.
releasing hormone, adrenocorticotrophic hormone) (Schmid
et
al., 2005). In conse-
quence, increased ghrelin from sleep restriction leads to increased cortisol and growth
hormone, which, in turn, influence multiple systems, including metabolism. Reciprocally,
changes in ratios
of
the releasing hormones for growth hormone and cortisol alter sleep
propensity (Steiger, 2003).
These lines
of
inquiry have galvanized public health concerns that link the docu-
mented decline in the amount
of
daily sleep to the concurrent surge
in
national rates
of
obesity: during the dramatic rise in obesity rates over the last two decades, the proportion
of
adults
of
all ages whose nightly sleep averages 6 hours or less has increased from
roughly 20 to 30% (Centers for Disease Control and Prevention, 2005b). Obesity is
firmly associated with inactivity (Vioque, Torres, & Quiles, 2000), so why should sleep
reduction contribute to overweight?
Mounting laboratory, clinical, and statistical evidence for the health-eroding effects
of
sleep deprivation must confront a repeated set
of
epidemiological findings that fail to
confirm such evidence at the population level.
Tho
large epidemiological samples
(l
and
1.1
million adults, respectively) drawn 20 years apart and questioned prospectively found
essentially identical results linking mortality to sleep extension, rather than sleep restric-
tion (Kripke, Garfinkel, Wingard, Klauber, & Marler, 2002; Kripke, Simons, Garfinkel, &
Hammond, 1979). Mortality is lowest among men and women who report sleeping
7 hours (6.5-7.4 hours) daily.
At
more than 7.5 hours
of
reported daily sleep, mortality
Chapter
16:
Evolutionary Ecology
of
Sleep
steadily increases
as
amount
of
sleep increases. Remarkably, the mortality associated
with shorter sleep durations
of
4.5-6.5 hours was less than that
of
the near majority who
sleep longer than 7.5 hours. Insomnia was not related to mortality.
Quality
of
life aside, how can one reconcile these fmdings with the alarm sleep scien-
tists and clinicians express over the recent declines in sleep quota among Americans, given
that quotas have fallen from amounts (8 hours on average) associated with greater mortal-
ity risk to those (6.8 hours) associated with lowest risk? The analyses treat sleep behavior
independent
of
lifestyle and context; hence, one cannot know why individuals slept more
or less and whether factors that determine number
of
hours slept also influence well-being.
Sleep behavior may be as much a consequence as a cause in pathways to differential
health. Impact oflifestyle, including the eroding effects
of
poor health and environmental
quality that confront disadvantaged populations, will be considered below.
PERPLEXING PARADOXES OF SLEEP AND HEALTH
The course
of
the discussion so far has encountered several puzzles regarding human
sleep behavior and its relationships to well-being and health. These conundrums include:
• Why are humans able to rack up enormous sleep debts
if
the interest paid on that debt
is so high in terms
of
function, well-being, and health? Why do mechanisms that regu-
late sleep behavior fail to prevent accumulation
of
injurious sleep debt?
• Why are objective and subjective sleep quality dissociated?
• Contemporary Western populations are privileged, with perhaps the most uniformly
excellent health and living conditions in human history: why are rates
of
insomnia and
other sleep disorders so high?
• Why is sleep restriction related to obesity?
• Why are sleep researchers concerned about declining sleep quotas
if
the epidemiolog-
ical evidence links lower quotas to lower mortality risk?
• Given the statistics showing declining sleep quotas, why do nearly three quarters
of
Americans (72%) say that they get enough
or
more than enough sleep?
We
now turn to consider potential solutions for these puzzles suggested by evolutionary
adaptationist analyses, first by identifying a set
of
common threads that run through these
disparate questions, and then by extracting key underlying factors that contribute to sleep
problems and thus may merit greater attention in treatment and prevention.
SLEEP AND STRESS
Rapid reversibility distinguishes sleep from states such as coma, unconsciousness, or
hibernation. Yet the vital capacity for reversibility carries a sting: sleep can be fragile and
difficult to maintain
or
even to attain. Such difficulties can reach epidemic proportions,
as with the high prevalence
of
insomnia symptoms (Ohayon, 2002) and sleep-related
psychiatric disorders (Abad & Guilleminault, 2005). An adaptationist perspective

306
307
EVOLUTIONARY
MEDICINE
AND
HEALTH
emphasizes the value
of
stepping
back
to pose teleological questions
of
design concern-
ing the purposes
of
sleep, the impact
of
conditions
and
pressures
under
which
it
evolved
on
its organization and regulation, capacities for response to challenge,
and
sensitivities
to competing demands
or
functions. Such a perspective draws attention to two distin-
guishing features
of
sleep: (1) plasticity in sleep behavior
and
capacity to carry and
redress sleep debt
and
(2) regulation
by
convergent ecological, cognitive--emotional, and
physiological processes (Saper, Cano, & Scammell, 2005).
Sleep Disruption
as
a Response to Stressors
Many factors can influence the timing, duration, stability,
and
quality
of
sleep (see
Table 16-5), which contribute
to
the elasticity
of
sleep behavior
and
its capacity to
accommodate other life demands.
The
nature
of
these factors merits scrutiny and reveals
a common feature: the conditions that disrupt sleep represent stressors,
or
demands on
time, energy,
or
attention.
As
such, stressors challenge an adaptive response that com-
mands a reallocation
of
resources. Stressors related to sleep disruption operate in three
dimensions: as demands
on
time
and
energy, as cognitive demands
or
burdens, andlor
as
direct moderators
of
sleep/wake regulation. Sources
of
influence can
be
categorized in
these three dimensions by their dominant pathways for affecting sleep (Table 16-5,
columns on right). Thus, workload represents vital subsistence activity that directly
influences schedule
and
defines times for sleep. Shift work represents a conspicuous
example, including approximately 14.8%
of
U.S. workers
(-14.8
million persons) whose
hours fall
or
extend outside the regular daytime shift (6 a.m. to 6 p.m.) (United States
Census Bureau, 2006).
On
an
epic scale, globalizing shifts from agrarian
to
wage labor
are transforming daily schedules and altering sleep patterns worldwide.
In contrast
to
social conditions, ecological factors such as day length operate largely
through physiological pathways, reflecting the deep evolutionary origins
of
activity-rest
regulation for adaptation
to
environmental conditions. Similarly, endogenous conditions
such as age, health,
or
neuroregulatory capacities directly influence regulation and
structure
of
sleep. lllness and infection, in particular, disrupt sleep patterns
by
inducing
lassitude
and
sleep via the potent prosomnogenic cytokines (particularly interleukin
[ILJ-Ij3
and
tumor
necrosis factor [TNFJ-a) produced during inflammatory responses
(Krueger, Majde, & Obat, 2003).
Thrning to psychological factors, both cognitive
and
affective processes powerfully
influence sleep. Cognitive loads
can
erode sleep budgets,
not
only
by
taking
up
time but
also by maintaining wakefulness for planning, problem solving,
or
rumination.
But
by far
the most powerful influence
on
wakefulness is emotional, particularly feelings
of
inse-
curity, threat,
and
fear. Anxiety-laden cognitive activity
and
the burden
from
perceived
threats are forceful stimulants to arousal that antagonize sleep (Semler & Harvey, 2004).
Whatever the objective validity
of
concerns
and
fears, cognitive framing translates social
and
personal experience into signals
of
reassurance
or
threat to the organism that inform
motivational states and arousal regulation (Saper, Cano, & Scammell, 2005). Social margin-
alization, uncertainty,
and
threat
or
shame are the key elicitors
of
physiological and affec-
tive stress responses (Dickerson & Kemeny, 2004; Sapolsky, 1998).
The
linkages are
adaptive because these emotions signal challenge and the potential
need
for response
(McNamara, 2004).
Chapter
16:
Evolutionary
ECOlogy
of Sleep
TABLE 16-5 Sources of Sleep Disruption
Time,
Cognition-
Source
Routes
of
influence
on
sleep emotion
Behavioral
Subsistence and domestic demands, X x
workload
Monitoring/tending the vulnerable X X
(juveniles, sick; livestock)
Food consumption patterns X
Context maintenance (fire, position) x X
Vigilance, defense x X
Social life, ritual pfactices X x
Ecological
Temperature X
Noise X x
Light X
Posture, physical discomfort X
Bed: substrate, covering, sharing X X
Psychological
Insecurity, threat, fear
Psychological (distress) X
Physical (malaise, self-monitoring) X
Social (rumination) X
Ecological (monitoring) X
Beliefs about sleeping, dreaming X
Planning, problem solving X X
Bad dreams, nightmares X
Endogenous
Infection, illness X X
Age (sleep quota, consolidation,
NREMIREM cycle, phase shift) X X
Genetic/organic conditions, state
regulation, need for sleep X
Sources:
Lima,
2005;
Stephan.
2002;
u.s.
DHHS,
2003.
Worthman
&
Melby,
2002.
X
Strong
association
x
Weak
association
Accordingly, SUbjective and objective sleep experience comprise related but distinct
aspects
of
sleep quality that are governed by divergent influences. Findings from recent
studies
of
American populations illustrate these contrasting dimensions. Influences
on
objective sleep quality include day length, body mass index, stimulant and medication
use, employment, level
of
sleep debt, prior emotion
and
learning states, and current
health status. Subjective sleep qUality is influenced by loneliness, depression,
poor
per-
ceived health, unemployment and economic difficulties,
back
pain, and obesity (Jacobs,
Cohen, Hammerman-Rozenberg, & Stress man, 2006; Tworoger, Davis, Vitiello, Lentz,
& McTiernan, 2005). As the literature
on
insomnia has discovered, cognitive processes
(beliefs, stressful thoughts, expectations, attributions, metacognition,
or
thinking about
thinking)
indeed
influence objective sleep onset
and
maintenance, but the influence pales
beside their eroding effects
on
recall
and
subjective experience
of
sleep
and
sleep qUality

308
EVOLUTIONARY
MEDICINE
AND
HEALTII
(Harvey, Tang, & Browning, 2005).
Poor
subjective sleep quality maintains the signal
that conditions are unfavorable
or
challenging and adjusts psychophysiological
and
behavioral responses accordingly (Capaldi, Handwerger, Richardson, & Stroud, 2005;
Fisher & Rinehart, 1990).
In
sum, the multiplicity
of
factors influencing sleep behavior and regulation pro-
motes adaptation to meet present demands and challenges. Whether they are demands
on
energy, time,
or
attention in important life domains, including subsistence and mate-
rial welfare, social status and integration, physical survival and well-being,
and
pursuits
of
meaning and value, such demands signal the need and capacity to reallocate resources
toward
or
away from sleep.
In
brief, all are stressors
or
markers
of
stressful conditions
that trigger an adaptive response at the physiological, cognitive, and behavioral levels.
This insight provides us with a possible answer to the puzzle about why sleep restriction
would
be
related
to
obesity. A review
of
the physiological responses to sleep restriction
listed in Table 16-4 confinns a profile
of
resource redeployment very similar to the
classic stress response, with elevated cortisol, increased sympathetic activity,
and
main-
tenance
of
blood sugar levels levied to meet immediate demands.
The
parallels to stress
extend further: the ability to restrict
or
adjust sleep to meet acute demands is a real
advantage in the short run,
but
this ability carries real costs
if
invoked too often. Similar
to effects
of
chronic stress and cumulative stress burden (allostatic load), potential
consequences include increased risk for the chronic conditions
of
diabetes, obesity, and
cardiovascular disease (McEwen & Seeman, 1999;
McEwen
& Wingfield, 2003). Sleep
debt is never fully repaid in the currency
of
sleep, but it
is
paid
in
the currency of
allostatic load.
A Human Propensity
for
Sleep
Debt
The
view
of
sleep regulation as designed to strike an adaptive balance among competing
demands and constrained resources furthennore suggests
an
answer to another set of
puzzles concerning why sleep is so vulnerable to restriction and why sleep regulation
is
not more robust against disruption. The very complexity
of
running dual systems
of
sleep
regulation, homeostatic drive, and circadian pacemaker both increases regulatory capac-
ity and flexibility and reduces resistance to overdetermination from acute external or
internal states. Furthennore, the complex three-stage neurointegration involved
in
regulating circadian rhythms is thought to permit flexible daily schedules (Saper, Cano,
& Scammell, 2005), coordinating sleep-wake states with patterns
of
food consumption,
temperature
and
light cycles,
and
physical activity