Sleep disturbance and daytime sleepiness predict
Peter C Elwood,1Antony J Bayer,2Mark Fish,2Janet Pickering,1Clive Mitchell,1
John E J Gallacher1
Background Disturbed sleep is common throughout the
community and is associated with an increase in daytime
sleepiness, both of which, in turn are associated with an
increased risk of ischaemic vascular disease. The
hypothesis that sleep disturbances are predictive of
dementia, and in particular vascular dementia was
tested in a large community-based cohort of older men.
Methods A questionnaire on sleep disturbances was
administered to 1986 men aged 55e69 years in the
Caerphilly Cohort Study and 10 years later the men were
examined clinically for evidence of dementia or cognitive
impairment with no dementia (CIND).
Findings Approximately 20% of the men reported
disturbed sleep and 30% reported ‘severe’ daytime
sleepiness. Ten years later 1225 men (75% of the
surviving men in the cohort) were tested and 268 (22%)
were found to be cognitively impaired with 93 (7.6%)
showing clear evidence of dementia and the remaining
175 (14.3%) showing evidence of CIND. After
adjustment for possible confounding, including cognitive
function and the taking of sleeping tablets at baseline,
sleep disturbances appeared to be predictive of
dementia and CIND of vascular origin, while there was
no suggestion of prediction of non-vascular cognitive
impairment by sleep. Prediction of vascular dementia
appeared to be particularly strong for daytime
sleepiness, with an adjusted OR of 4.44 (95% CI 2.05 to
9.61). Further adjustments for psychological distress at
baseline reduced the size of the relationships, but the
ORs remain large, consistent with a direct positive effect
of sleep disturbance on vascular dementia.
Interpretation Sleep disturbances, and in particular
severe daytime sleepiness, appear to be strongly
predictive of vascular dementia, but have no predictive
power for non vascular dementia.
Sleep disturbances are common in the community,
and daytime sleepiness, which is to a large extent
a consequence of poor sleep, affects perhaps up to
30% of the general community.1e3Yet these effects
have been judged to be neglected, underdiagnosed
and the possible long-term
consequences of sleep disturbances appear to have
received little attention.
We have already reported that in the Caerphilly
cohort of older men, sleep disturbances are predic-
tive of ischaemic stroke, (relative odds of up to 1.97;
95% confidence limits 1.26, 3.09) and daytime
sleepiness is associated with an increase in vascular
disease events (relative odds: 1.41; 1.04, 1.92).5In
this paper we examine relationships between both
sleep disturbances and daytime sleepiness and
The Caerphilly Cohort Study is based on a repre-
sentative population sample of older men, born
between 1920 and 1935 and resident in a typical
small town in South Wales. The men were first seen
between 1979-83 and the initial response rate was
89%. The primary aims of the study were to eval-
uate life-style, dietary, haemostatic, lipid and other
factors predictive of ischaemic heart disease and
The men have been re-examined approximately
every 5 years. In the third follow-up examination,
when the men were aged 60e74 years, they were
asked to complete the Wisconsin Sleep Question-
naire8with help from their partners. This asks
about the severity and frequency of symptoms of
insomnia, restless legs, snoring, episodes of apnoea
and daytime sleepiness as defined in table 1. The
questionnaire allows for the grading of symptoms
into ‘mild’ and ‘severe,’ based largely on the
frequency of occurrence. Because the questionnaire
was self administered and gave opportunity for the
reporting of trivial symptoms, it was decided to
ignore the ‘mild’ and ‘infrequent’ symptoms
throughout. Several questionnaires on aspects of
mood were also administered, including the General
Health Questionnaire (GHQ)9which enabled the
estimation of psychological distress, namely a total
score on the GHQ of >4.
Within a few days of the administration of these
questionnaires, tests of cognitive function were
administered in a quiet room in the home of each
man, by a specially trained nurse. These were:
ethe AH4, a test of fluid IQ assessed by verbal and
ethe National Adult Reading Test (NART), which
tests crystallised IQ;11
ea Choice Reaction Time test (CRT) in which
stimuli are presented within a grid shown on
a computer screen, and the subject has to press the
In the fifth examination, the men being aged
65e79 years, the tests of cognitive function were
repeated, and those men who had a score on the
Cambridge Cognitive (CAMCOG) Examination12
of less than 83, a decline in CAMCOG score of 10 or
more, together with subjects who failed to
complete the CAMCOG were selected for a clinical
assessment (by MF).
Full details of the clinical assessment of the
selected men are reported elsewhere.13In brief: this
1Department of Primary Care
and Public Health, Cardiff
University, Cardiff, UK
2Department of Medicine,
Cardiff University, Cardiff, UK
Professor Peter Elwood, School
of Medicine, Cardiff University,
University Hospital of Wales,
Cardiff CF14 4XN UK;
Accepted 28 March 2010
Published Online First
30 July 2010
820J Epidemiol Community Health 2011;65:820e824. doi:10.1136/jech.2009.100503
included a modified Cambridge Mental Disorders of the Elderly
Examination interview of subject and informant;12the Rosen-
revised Hashinski Ischaemic score (HIS),14neurological exami-
nation with Frontal Assessment Battery,15Clinical Dementia
Rating,16and the Informant Questionnaire on Cognitive Decline
in older people.17Available medical records were reviewed for
details of relevant medical history, evidence of functional
impairment due to cognitive impairment, and results of neuro-
imaging and other relevant investigations.
Subjects with vascular cognitive impairment comprised those
diagnosed as having vascular dementia, mixed Alzheimer’s and
vascular dementia and vascular cognitive impairment with no
dementia (CIND). Subjects diagnosed as having vascular
dementia fulfilled the National Institute of Neurological
nationale pour la Recherché et l’Enseignement en Neurosciences
criteria for possible or probable vascular dementia.18Subjects
diagnosed as having mixed Alzheimer’s and vascular dementia
had a clinical course in keeping with Alzheimer’s dementia as
well as clinical features to suggest cerebrovascular disease.19
Cognitively impaired subjects who did not meet the full
dementia criteria with an HIS $3, including a history of stroke
or consistent lateralising neurological signs, were classified as
vascular CIND. Impaired subjects diagnosed as having dementia
or CIND were classified as non-vascular if they had no clinical
features to suggest cerebrovascular disease operationalised as
a HIS score $2 and an absence of cerebral infarction on available
neuroimaging. Subjects diagnosed as having Alzheimer’s disease
needed to fulfil this criterion as well as the National Institute of
Neurological and Communicative Disorders and Stroke and the
Alzheimer’s Disease and Related Disorders Association criteria
for probable Alzheimer’s disease.20
standardised diagnostic criteria for other dementing conditions
were categorised accordingly. Those who screened positive but
with cognitive symptoms and/or functional impairment insuf-
ficient to warrant dementia diagnosis were classified as CIND.
Due to the small numbers, all non-vascular conditions were
combined in the analyses which follow.
The power of sleep disturbances and daytime sleepiness at
baseline to predict dementia 10 years later was examined. ORs
for dementia within the various subgroups of men with the
sleep disturbances and daytime sleepiness were estimated, and
these were adjusted to allow for differences in age, social class
(based on most recent occupation), smoking (grouped as non
smoker, ex-smoker and current smoker), weekly alcohol
consumption (expressed as average cc/day), height and weight,
a number of measures of vascular disease and the regular taking
of sleeping tablets as reported at the time of the baseline
examinations. The effects of adjustments for psychological
distress at baseline were then examined.
Subjects who fulfilled
Prevalence of sleep disorders in 1986 men aged 55e69 years
No* of men without the symptom,
or the symptom only occasionally
No* of men (%) with
Snoring: Having been told, and being aware of oneself of snoring on a few nights per month or more
Insomnia: Difficulty in getting to sleep and waking repeatedly once or twice a week, or more often.
Restless legs: Experiencing ‘restless legs or bothersome twitches’ once or twice a week or more.
Sleep apnoea: Having been told of gasping, choking or snorting on one night each week or more, and/or
stopping breathing or breathing abnormally a few nights each month or more; and/or waking suddenly with
a feeling of gasping or choking on a few nights each month or more
Daytime sleepinessy: Feeling today a little foggy, or slowed down, or loosing the struggle; and/or at least
once a week not feeling rested and/or feeling excessive sleepiness and/or a need for coffee or other stimulant
1347 639 (32%)
*Totals differ slightly because some men did not answer all the questions.
yDaytime sleepiness is a consequence of a sleep disturbance in about 50% of the men (see text).
Relationships between baseline factors and sleep disturbances and daytime sleepiness
Sleeping disturbance etc. Mean age (years)Social class* (percentage manual)Smoking (%) Mean alcohol intake (cc/week)Mean BMI (kg/m2)
*Social class is based on the most recent occupation of each man, divided into manual and non-manual occupations.
J Epidemiol Community Health 2011;65:820e824. doi:10.1136/jech.2009.100503821
The sleep questionnaire was completed by 1985 men aged
55e69 years. Around one-third of the men reported at least one
symptom suggestive of sleep disturbance, and one-third reported
severe daytime sleepiness (table 1). About 55% of the men with
a sleep disturbance complained of daytime sleepiness suggesting
that daytime sleepiness is largely a consequence of sleep
disturbance. However, 17% of the men with no sleep distur-
bance reported severe daytime sleepiness.
Significant associations were found with social class and with
BMI (table 2), and in what follows adjustments were made for
these, together with age, smoking, alcohol intake, neck
circumference, angina, ECG ischaemia, chest pain and the
regular taking of sleeping tablets.
Table 3 summarises cross-sectional relationships between
sleep disturbances and cognitive function at baseline, adjusted
for confounding as indicated in a footnote to the table. Fluid
IQ,18crystallised IQ19and choice reaction time all showed a very
similar pattern. Subjects who admitted insomnia, restless legs or
apnoea have scores which are lower or reaction times which are
slower than those of men without these symptoms, by about
10e30% of an SD. For snoring, apart from an unexpected faster
choice reaction time, which we cannot explain, no important
association with cognitive function was found.
Ten years after the baseline questionnaire on sleep had been
completed, 1225 men (75% of the surviving men) were tested,
and 268 men (22%) were examined clinically. In 93 of these men
(7.6%), it was judged that there was clear evidence of dementia,
while in a further 175 (14.3%) men, there was cognitive
impairment which did not fulfil the definition of dementia
(CIND). In 44 men with dementia and 39 with CIND, the
symptoms were judged to have a vascular basis, a total of 83
(6.8% of the cohort).
The prediction of these conditions by sleep disturbance and by
daytime sleepiness 10 years previously is indicated by the data in
table 4. Although the numbers are small, the general pattern of
results is fairly clear. After adjustment for possible confounding,
including cognitive function at baseline, sleep disturbances
appear to be predictive of dementia and CIND of vascular origin,
while there is no suggestion that non-vascular cognitive
Sleep disturbance and cognitive function at baseline
AH4 adjusted differences
(with 95% CI) (%SD)
National Adult Reading Test adjusted
differences (95% CI) (%SD)
Choice reaction time adjusted
differences (95% CI) (%SD)
Mean (SD)in total cohort(1865 men)
25.9 SD 10.46
?2.31 (?3.90 toe0.72)(22% of SD)
?2.47 (?3.64 to ?1.30)(24% of SD)
+0.73 (?0.25 to 1.72)(7% of SD)
?1.43 (?2.65 to ?0.22)(14% of SD)
?2.62 (?3.69 to ?1.56)(25% of SD)
106.11 SD 9.75
?3.13 (?4.63 to e1.63)(32% of SD)
?2.82 (?3.91 toe1.72)(29% of SD)
?0.26 (?1.18 to 0.67)(3% of SD)
?1.24 (?2.38 to e0.10)(13% of SD)
?2.42 (?3.42 toe1.42)(25% of SD)
918 SD 247
+1.00 (?42 to 43)(0.4% of SD)
+39 (8 to 70)(16% of SD)
?29 (?545 toe3)(12% of SD)
+18 (?14 to 50)(7% of SD)
+38 (9 to 66)(15% of SD)
Restless legs(365 men)
Daytime sleepiness(493 men)
The overall mean scores and SD for the cognitive function tests in all the men are shown. Then, for each sleep disturbance the adjusted differences (95% CI) from the overall mean are shown.
Also shown are the adjusted differences as proportions of the appropriate SD. All relationships were adjusted for age, social class, smoking, alcohol intake, BMI, neck circumference, angina,
ECG ischaemia, chest pain and the use of sleeping tablets.
men with no sleeping problems at baseline
Sleep disturbances and dementia 10 years later OR for dementia in men who had had sleeping problems 10 years previously, relative to 920
Vascular dementia plus
Non vascular dementia
plus non-vascular CIND
Snoring1.18 (0.57 to 2.46)
1.19 (0.54 to 2.65)
1.92 (0.65 to 5.64)
1.34 (0.42 to 4.24)
2.39 (1.10 to 5.20)
1.87 (0.80 to 4.37)
2.01 (0.86 to 4.67)
1.80 (0.72 to 4.54)
1.30 (0.59 to 2.88)
1.24 (0.55 to 2.81)
3.11 (1.07 to 9.01)
2.81 (0.94 to 8.40)
2.26 (0.99 to 5.15)
1.96 (0.81 to 4.72)
2.93 (1.23 to 6.97)
2.56 (1.04 to 6.28)
2.41 (1.05 to 5.51)
1.96 (0.80 to 4.80)
1.23 (0.70 to 2.15)
1.22 (0.67 to 2.22)
2.32 (1.05 to 5.11)
1.91 (0.84 to 4.36)
2.24 (1.24 to 4.05)
1.80 (0.96 to 3.37)
2.34 (1.24 to 4.41)
2.04 (1.05 to 3.98)
3.15 (1.76 to 5.63)
2.17 (1.15 to 4.11)
1.00 (0.47 to 2.14)
0.89 (0.40 to 1.96)
1.04 (0.30 to 3.61)
0.80 (0.22 to 2.96)
0.86 (0.33 to 2.24)
0.69 (0.26 to 1.89)
0.96 (0.36 to 2.53)
0.88 (0.32 to 2.38)
1.13 (0.49 to 2.62)
0.88 (0.35 to 2.23)
0.76 (0.48 to 1.21)
0.86 (0.52 to 1.41)
0.97 (0.48 to 1.97)
0.74 (0.33 to 1.65)
1.04 (0.62 to 1.73)
0.91 (0.52 to 1.61)
1.06 (0.60 to 1.85)
1.04 (0.57 to 1.90)
1.36 (0.85 to 2.18)
1.26 (0.74 to 2.16)
0.81 (0.54 to 1.23)
0.87 (0.56 to 1.34)
1.02 (0.54 to 1.94)
0.79 (0.39 to 1.63)
1.01 (0.63 to 1.61)
0.88 (0.52 to 1.47)
1.02 (0.61 to 0.69)
0.99 (0.58 to 1.69)
1.35 (0.88 to 2.07)
1.23 (0.76 to 2.00)
Daytime sleepiness 4.44 (2.05 to 9.61)
2.65 (1.12 to 6.29)
The first figures are ORs adjusted for base-line levels of age, social class, smoking, alcohol intake, BMI, angina, ECG ischaemia and chest pain and National Adult Reading Test. The second
figures are ORs adjusted for all the above factors, plus psychological distress estimated from the General Health Questionnaire (see text).
CIND, cognitive impairment with no dementia.
822 J Epidemiol Community Health 2011;65:820e824. doi:10.1136/jech.2009.100503
impairment is predicted by sleep. The relationship appears to be
particularly strong for daytime sleepiness (4.44; 2.05 to 9.61 for
vascular dementia and 2.41; 1.05 to 5.51 for vascular).
The effects of further adjustment for psychological distress
were then examined (table 4). This leads to no significant change
in the relationships with non-vascular dementia. The prediction
of vascular impairment is reduced, and although the ORs remain
large for all the sleep disturbances, other than snoring, none is
statistically significant other than for apnoea and for daytime
The Caerphilly cohort is a large representative population
sample of men, and the present study is based on data collected
in repeated examinations of the men over a 10-year period. The
numbers of men examined declined during the course of the
study, mainly because of deaths, but every effort was made to
keep omissions to a minimum and maintain the representa-
tiveness of the cohort.
The prevalence of sleep disorders was around one-third. The
proportion who reported excessive daytime sleepiness is about
the same, and in about half the subjects the daytime sleepiness
may be a consequence of disturbed sleep. These prevalence
estimates are in reasonable agreement with those reported by
other authors. In a review of 154 published investigations,
Shamsuzzman et al2judged that 20% of adults have at least
‘mild’ sleep apnoea. In other studies the prevalence of ‘excessive’
daytime sleepiness was estimated to be 19%3and 30% in men
and 20% in women, increasing with age.1
The clinical relevance of symptoms which have a prevalence
as high as 20 or 30% can reasonably be questioned. However, the
exposure of subjects to frequent periods of noise, insufficient to
cause arousal, has been shown to raise blood pressure and, on
waking, to cause impairment of mental flexibility and atten-
tion.21This suggests that relatively minor disturbances, such as
some of those reported by many of the men in the present study,
can have important clinical effects.
The effects we describe on cognitive function (table 3) are
large. They are however similar in magnitude to those reported
in a population sample of 1026 subjects aged 60 years or over in
Paris. In this, 14% of subjects reported excessive daytime sleep-
iness, and compared with the other subjects, these had ORs of
around 2.0 for impaired cognitive function.22Any impairment of
cognitive function is important and will reduce the general
quality of life,1impair the performance of everyday activities22
and increase accident risk.23
Many reports have described disturbed sleep in patients with
dementia. The present results, however, indicate that sleep
apnoea, and possibly other disturbances, are predictive, but only
for dementia and CIND of vascular origin (table 4), and apart
from that with snoring, most of the ORs are relatively large, up
to 4.44 (2.05 to 9.61) for daytime sleepiness. The lack of
statistical significance in some of the other relationships with
vascular dementia and CIND may well be a consequence of the
relatively small numbers of subjects. In contrast, the relation-
ships with non-vascular disease are weak and none approaches
Foley et al24also studied the prediction of dementia by sleep
disturbances in a cohort of 2346 men aged 71 to 93 years. Three
years after base-line the men were re-assessed and 191 (8%) were
judged to have dementia and a further 21% to have cognitive
decline without dementia. Prediction by sleep disturbances was
not statistically significant: the adjusted ORs being 0.99 (0.70 to
1.41) for incident dementia and 1.14 (0.91 to 1.43) for cognitive
decline. Prediction by daytime sleepiness was however signifi-
cant: 2.19 (1.37 to 3.50) for incident dementia and 1.44 (1.01 to
2.08) for cognitive decline. This last is consistent with our
finding for daytime sleepiness (2.17; 1.15 to 4.11) for vascular
A major portion of the relationships described can be
explained on the grounds that sleep disturbances are associated
with an increased risk of stroke,25 26yet multi-infarct dementia
does not underlie all vascular dementia. Sleep disturbances have
also been shown to be associated with a higher blood pres-
sure.27 28Effects of sleep disturbances and a number of throm-
bosis-related factors have also been described.29 30At the same
time, there can be no certainty that sleep disturbances are causal,
and although we judge it unlikely, it could be that the distur-
bances are simply a very early marker of processes leading to
The inter-relationships between sleep disturbances and
cognitive performance are clearly complex, and the issue of
which is driving the relationships cannot be discerned with
confidence in these data. While it could be that psychological
distress (reflecting both anxiety and depression) is primary,
causing effects upon sleep and playing a part in the development
of dementia, it is equally reasonable to argue that sleep distur-
bances enhance psychological distress and are a causal factor in
dementia. The fact that significant relationships between sleep
disturbances and dementia remain after adjustments for
psychological distress (table 4) suggests that the second
conclusion is likely, namely that sleep disturbances directly
increase the risk of dementia of vascular origin.
The treatment of sleep disturbances has been shown in
a randomised trial to lead to a reduction in blood pressure,31
but whether or not such treatment reduces the risk of
stroke, the loss of cognitive function and the risk of dementia
appears not yet to have been tested. We are therefore fully in
agreement with the comment of Silverberg et al: that sleep
disturbance is ‘a neglected, underdiagnosed and undertreated
What is already known on this subject
< Sleep disorders have been shown to be associated with an
increase in the risk of stroke, and daytime sleepiness to be
associated with an increase in ischaemic heart disease.
< Disturbed sleep is frequently a consequence of dementia, but
whether or not disturbed sleep is predictive of dementia is not
What this paper adds
< Sleep disturbances are predictive of an increase in cognitive
< Sleep disturbances are predictive of incident vascular
< There is no convincing evidence that sleep disturbances
predict non-vascular dementia.
< Evidence is now needed on the long-term effects of the
treatment of sleep disorders on the incidence of dementia.
J Epidemiol Community Health 2011;65:820e824. doi:10.1136/jech.2009.100503 823
Funding The Caerphilly Cohort Study was funded by MRC. The examination for
cognitive impairment was funded by the Alzheimer’s Society. The Caerphilly archive is
now maintained by the Department of Social Medicine in Bristol University.
Competing interests None.
Ethical approval Ethical approval was obtained from the Gwent Ethics Committee for
every phase of the work described.
Contributors PCE directed the Caerphilly Study. Overall responsibility for the work
described and chief author of the paper. AJB was actively involved throughout the
Caerphilly Cohort Study and had responsibility for the clinical examinations described
in the paper. MF conducted the clinical clinical examinations described in the paper.
JEJG directed the work within the Caerphilly Cohort Study which is the basis for this
paper. He now directs the work in Caerphilly. CM suggested the study, advised on the
analyses and assisted in preparation of the paper. JP analysed the data and
contributed to the writing of the paper.
Provenance and peer review Not commissioned; externally peer reviewed.
Baldwin CM, Griffith KA, Nieto FJ, et al. The association of sleep-disordered
breathing and sleep symptoms with quality of life in the Sleep Heart Health Study.
Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications
for cardiac and vascular disease. JAMA 2003;290:1906e14.
Empana J-P, Dauvilliers Y, Dartigues J-F, et al. Excessive daytime sleepiness is an
independent risk indicator for cardiovascular mortality in community-dwelling elderly.
Silverberg DS, Oksenberg A, Iaina A. Sleep related breathing disorders are common
contributing factors to the production of essential hypertension but are neglected,
underdiagnosed and undertreated. Am J Hypertens 1997;10:1319e25.
Elwood P, Hack M, Pickering J, et al. Sleep disturbance, stroke, and heart disease
events: evidence from the Caerphilly cohort. J Epidemiol Community Health
Lowe GDR, Rumley A, Sweetnam PM, et al. Fibrin D-dimer, markers of coagulation
activation and the risk of major heart disease in the Caerphilly Study. Thromb
Baker IA, Pickering J, Elwood PC, et al. Fibrinogen, viscosity and white blood cell
count predict myocardial infarction, but not cerebral infarction: evidence from the
Caerphilly and Speedwell cohort. Thromb Haemost 2002;87:421e5.
Young T. Epidemiology of daytime sleepiness: definition, symptomatology and
prevalence. N Engl J Med 1990;323:520e6.
Goldberg DP. The detection of psychiatric illness by questionnaire. London: Oxford
University Press, 1972.
Heim AW. (1970) AH4 Group Test of General Intelligence ASE: The NFER-Nelson.
Nelson HE. National Adult Reading Test (NART) manual. Windsor, 1982.
Roth M, Tym E, Mountjoy CQ. CAMDEX: A standard instrument for the diagnosis of
mental disorder in the elderly with special reference to the early detection of
dementia. Brit J Psychiatr 1996;149:698e709.
Fish M, Bayer AJ, Gallacher JEJ, et al. Prevalence and pattern of cognitive
impairment min a community cohort of men in South Wales: methodology and
findings from the Caerphilly Prospective Study. Neuroepidemiology
Rosen WG, Terry RD, Fuld PA, et al. pathological verification of ischaemic score in
differentiation of dementias. Ann Neurol 1980;7:486e8.
Dubois B, Slachevsky A, Litvan I, et al. The FAB: a frontal assessment battery at
bedside. Neurology 2000;55:1621e6.
Berg L. Clinical dementia rating. Psychopharmacol Bull 1988;24:637e9.
Jorm AF, Jacomb PA. The informant questionnaire on cognitive decline in the elderly
(IQCODE): socio-demographic correlates, reliability, validity and some norms. Psychol
Roman GC, Tatemichi TK, Erkinjuntti T, et al. Vascular dementia: diagnostric criteria
for research studies. Report of the NINDS-AIREN International Workshop. Neurology
Rockwood K, Macknight C, Wentzel C, et al. The diagnosis of ‘mixed’ dementia in
the Consortium for the Investigation of Vascular Impairment of Cognition (CIVIC).
Ann NY Acad Sci 2000;903:522e8.
McKhann G, Drachman D, Folstein M, et al. Clinical diagnosis of Alzheimer’s
disease: report of the NINCDS-AIRDA Work Group under the auspices of the
Department of Health and Human Services Task Force on Alzheimer’s Disease.
Martin SE, Engleman HM, Deary IJ, et al. The effect of sleep fragmentation on
daytime function. Am J Respir Crit Care Med 1996;153:1328e32.
Ohayon MM, Caulet M, Phipip P, et al. How sleep and mental disorders are related
to complaints of daytime sleepiness. Arch Int Medicine 1997;157:2645e52.
Turkinton PM, Sidca M, Saralaya D, et al. Time course of changes in driving
simulator performance with and without treatment in patients with sleep apnoea
hypnoea syndrome. Thorax 2004;59:56e9.
Foley D, Monjan A, Masaki K, et al. Daytime sleepiness is associated with 3-year
incident dementia and cognitive decline in older Japanese-American men.
J Am Geriatr Soc 2001;49:1628e32.
Qureshi AI, Giles WH, Croft JB, et al. Habitual sleep patterns and risk for stroke and
coronary heart disease: a 10 year follow-up from NHANES I. Neurology
Marin JM, Carrizo SJ, Vicente E, et al. Long term cardiovascular outcomes in men
with obstructive sleep apnoea-hyponea with or without treatment with continuous
positive airway pressure: an observational study. Lancet 2005;365:1046e53.
Peppard PE, Young T, Palta M, et al. Prospective study of the association between
sleep disordered breathing and hypertension. N Engl J Med 2000;342:1378e84.
Nieto FJ, Young TB, Lind BK, et al. Association of sleep-disordered breathing, sleep
apnea and hypertension in large community based study: Sleep Heart Health Study.
Shamsuzzaman AS, Winnicki M, Lanfranchi P, et al. Elevated C-reactive protein in
patients with obstructive sleep apnea. Circulation 2002;105:2462e4.
Robinson GV, Pepperell JC, Davies RJ, et al. Circulating cardiovascular risk factors in
obstructive sleep apnoea: data from randomised controlled trials. Thorax
Faccenda JF, Mackay TW, Boon NA, et al. Randomised placebo-controlled trial of
continuous positive airway pressure on blood pressure in the sleep-hyponea
syndrome. Am J Respir Crit Care Med 2001;163:344e8.
824J Epidemiol Community Health 2011;65:820e824. doi:10.1136/jech.2009.100503