Restoring Sleep Homeostasis to Lower Blood Pressure

Cutting back on sleep duration has developed into a common, highly prevalent habit in the
adult population, and may lead to a major health problem. Large epidemiological studies have
demonstrated that short sleep duration is associated with increased risk of cardiovascular
disease (CVD). The investigators' preliminary data on the effects of experimental sleep
reduction have shown elevation of blood pressure (BP) and inflammatory markers, such as
interleukin-6 (IL-6) and C reactive protein (CRP), suggesting that both may play an
important role in linking sleep loss and CVD risk. With this background, the investigators
hypothesize that restoring sleep homeostasis, i. e. getting adequate amounts of sleep, is an
effective behavioral intervention in the treatment of elevated BP.

The investigators will test this hypothesis in subjects with BP above normal and with short
habitual sleep duration, as verified by sleep logs and actigraphic recordings. Subjects will
either undergo 6 weeks of mild sleep extension, in which 60 min of bedtime will be added to
the habitual sleep duration, or subjects will maintain their habitual sleep duration for the
following 6 weeks.

Regarding their first specific aim, the investigators expect that sleep extension across 6
weeks will lower BP, inflammatory (IL-6, CRP, cell adhesion molecules) and autonomic markers
(catecholamines). In particular, the investigators expect that in subjects with mild BP
elevation, i. e. with pre-hypertension, sleep extension leads to normalization of BP.

This study presents a very first approach in using sleep behavior components for the
treatment of elevated BP. Therefore, the investigators' second specific aim will
characterize the strength of associations between changes in sleep duration, BP, and
inflammation, and they will explore factors that are predictive for these changes. In
particular, adiposity, as measured by percent body fat, has frequently been shown to be
related to short sleep duration and inflammatory processes, but the role of adiposity in
modulating the physiological consequences of changes in sleep duration has never been
addressed.

If the investigators' hypothesis is correct, sleep extension may be considered as an
additional component in current lifestyle intervention programs in combating and preventing
hypertension.