Dataset Information

Longer term effects of very low energy diet on obstructive sleep apnoea in cohort derived from randomised controlled trial: prospective observational follow-up study.

ABSTRACT:

Objective

To determine whether initial improvements in obstructive sleep apnoea after a very low energy diet were maintained after one year in patients with moderate to severe obstructive sleep apnoea.

Design

Single centre, prospective observational follow-up study.

Setting

Outpatient obesity clinic in a university hospital in Stockholm, Sweden.

Participants

63 men aged 30-65 with body mass index (BMI) 30-40 and moderate to severe obstructive sleep apnoea defined as an apnoea-hypopnoea index ≥ 15 (events/hour), all treated with continuous positive airway pressure.

Intervention

A one year weight loss programme, consisting of an initial very low energy diet for nine weeks (seven weeks of 2.3 MJ/day and two weeks of gradual introduction of normal food) followed by a weight loss maintenance programme.

Main outcome measure

Apnoea-hypopnoea index, the main index for severity of obstructive sleep apnoea. Data from all patients were analysed (baseline carried forward for missing data).

Results

Of 63 eligible patients, 58 completed the very low energy diet period and started the weight maintenance programme and 44 completed the full programme; 49 had complete measurements at one year. At baseline the mean apnoea-hypopnoea index was 36 events/hour. After the very low energy diet period, apnoea-hypopnoea index was improved by -21 events/hour (95% confidence interval -17 to -25) and weight by -18 kg (-16 to -19; both P<0.001). After one year the apnoea-hypopnoea index had improved by -17 events/hour (-13 to -21) and body weight by -12 kg (-10 to -14) compared with baseline (both P<0.001). Patients with severe obstructive sleep apnoea at baseline had greater improvements in apnoea-hypopnoea index (-25 events/hour) compared with patients with moderate disease (-7 events/hour, P<0.001). At one year, 30/63 (48%, 95% confidence interval 35% to 60%) no longer required continuous positive airway pressure and 6/63 (10%, 2% to 17%) had total remission of obstructive sleep apnoea (apnoea-hypopnoea index <5 events/hour). There was a dose-response association between weight loss and apnoea-hypopnoea index at follow-up (β = 0.50 events/kg, 0.11 to 0.88; P = 0.013).

Conclusion

Initial improvements in obstructive sleep apnoea after treatment with a very low energy diet can be maintained after one year in obese men with moderate to severe disease. Those who lose the most weight or have severe sleep apnoea at baseline benefit most. Trial registration Current Controlled Trials 70090382.

SUBMITTER: Johansson K

PROVIDER: S-EPMC3106149 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:The roles of central nervous mechanisms and cortical output in obstructive sleep apnoea remain unclear. We addressed corticomuscular coupling between cortical sensorimotor areas and lower facial motor units as a mechanistic pathway and as a possible surrogate marker of corticoperipheral motor control in obstructive sleep apnoea. In this exploratory cross-sectional retrospective study, we analysed EEG (C3 and C4 leads) and chin EMG from polysomnography recordings in 86 participants (22 females; age range: 26-81 years): 27 with mild (respiratory disturbance index = 5-15 events/h), 21 with moderate (15-30 events/h) and 23 with severe obstructive sleep apnoea (>30 events/h) and 15 control subjects (<5 events/h). By computing C3-/C4-EEG-chin EMG coherence of signal dynamics in time and frequency domains, we investigated corticomuscular coupling between cortical sensorimotor areas and lower facial motor units with increasing obstructive sleep apnoea severity during the entire sleeping time, during different sleep stages and during obstructive respiratory events, including 5 s before (stable breathing) and after events (breathing resumption). In addition, we studied a possible influence of body mass index and autonomic nervous system activation. We found that both average and respiratory event-specific corticomuscular coupling between cortical sensorimotor areas and lower facial motor units weakened significantly with increasing obstructive sleep apnoea severity, was strongest during N3 and weakened in N1, N2 and rapid eye movement stages (in decreasing order). Coupling increases significantly during the obstructive respiratory events compared with coupling just before and following them. Results were independent of body mass index or autonomic nervous system activation. We conclude that obstructive respiratory events in obstructive sleep apnoea are very strongly associated both quantitatively and temporally with the degree of disconnection within the cortical sensorimotor areas-lower facial motor units pathway. This quite coordinated activity pattern suggests a cortical sensorimotor area-driven obstructive respiratory event pattern generator and a central motor output disorder in obstructive sleep apnoea.