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Sleep apnea is a disorder that commonly
afflicts more than 12 million people in the United States.
It takes its name from the Greek word apnea, which means
"without breath." People with sleep apnea literally stop
breathing repeatedly during their sleep, often for a minute
or longer and as many as hundreds of times during a single
night. Sleep apnea can be caused by either complete obstruction
of the airway (obstructive apnea) or partial obstruction
(obstructive hypopnea-- hypopnea is slow, shallow breathing),
both of which can wake one up. There are three types of
sleep apnea — obstructive, central, and mixed. Of these,
obstructive sleep apnea (OSA) is the most common. OSA occurs
in approximately 2 percent of women and 4 percent of men
over the age of 35.
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2002
West Roxbury VA Medical Center and
Harvard Medical School, 1400 VFW Parkway, West Roxbury,
MA 02132, USA.
Aging produces a loss in a number
of behavioral and cognitive functions, including sleep.
Hypocaloric diet is one of the few methods that have been
shown to retard the effects due to age. However, the effects
of such a diet on sleep have never been investigated.
In the present study, 21 months old male F344 rats fed
a 60% calorie-reduced diet continued to have a significant
reduction in delta power (0.3-4 Hz EEG), less sleep following
12 h total sleep deprivation (TSD) and increased sensitivity
to caffeine compared to young rats (3 months) fed a similar
diet. These results indicate that caloric restriction
is unable to prevent the decline in sleep that occurs
with aging. Copyright 2002 Elsevier Science Inc.
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1998
Department of Otolaryngology, Kuopio
University Hospital, Finland.
The aim of this study was to examine
the effect of a very low-calorie diet (VLCD)-induced weight
loss on the severity of obstructive sleep apnoea (OSA),
blood pressure and cardiac autonomic regulation in obese
patients with obstructive sleep apnoea syndrome (OSAS).
A total of 15 overweight patients (14 men and one woman,
body weight 114 +/- 20 kg, age 52 +/- 9 years, range 39-67
years) with OSAS were studied prospectively. They were
advised to follow a 2.51-3.35 MJ (600-800 kcal) diet daily
for a 3-month period. In the beginning of the study, the
patients underwent nocturnal sleep studies, autonomic
function tests and 24-h electrocardiograph (ECG) recording.
In addition, 15 age-matched, normal-weight subjects were
studied. They underwent the Valsalva test, the deep-breathing
test and assessment of heart rate variability at rest.
The sleep studies and autonomic function tests were repeated
after the weight loss period. There was a significant
reduction in weight (114 +/- 20 kg to 105 +/- 21 kg, P
< 0.001), the weight loss being 9.2 +/- 4.0 kg (range
2.3-19.5 kg). This was associated with a significant improvement
in the oxygen desaturation index (ODI4) during sleep (31
+/- 20-19 +/- 18, P < 0.001). Before the weight loss the
OSAS patients had significantly higher blood pressure
(150 +/- 18 vs. 134 +/- 20, P < 0.05, for systolic blood
pressure, 98 +/- 10 vs. 85 +/- 13, P < 0.05, for diastolic
blood pressure) and heart rate (67 +/- 10 beats min-1
vs. 60 +/- 13, P < 0.05) at rest than the control group.
They had also lower baroreflex sensitivity (4.7 +/- 2.8
ms mmHg-1 vs. 10.8 +/- 7.1 ms mmHg-1, P < 0.01). During
the weight reduction, the blood pressure declined significantly,
and the baroreflex sensitivity increased by 49%. In conclusion,
our experience shows that weight loss with VLCD is an
effective treatment for OSAS. Weight loss improved significantly
sleep apnoea and had favourable effects on blood pressure
and baroreflex sensitivity that may have prognostic implications.
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