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 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.
Results
After crossing over to a very low energy diet, the patients who had served as controls in the randomised phase10 achieved the same weight loss (−20 v −19 kg; mean difference −1 kg, 95% confidence interval −3 to 1; P=0.34) and improvement in the apnoea-hypopnoea index (−21 v −25 events/hour; mean difference −4, −12 to 5; P=0.38) as the first intervention group. The find- ing of greater improvements in patients with severe versus moderate disease10 was also replicated after crossover of the controls (−26 v −13 events/hour, P=0.02).
By pooling the two intervention groups, 58 of 63 patients completed the very low energy diet period (two patients never started and three dropped out). At one year 49 patients had completed sleep and adiposity follow-up measures, and 44 had completed the one year treatment.
At baseline the majority of patients had severe obstructive sleep apnoea, metabolic syndrome, hyper- tension, and dyslipidaemia (table 1, and 56%, 41%, and 3% had a BMI of 30-34.9, 35-39.9, and ≥40, respec- tively. Those with moderate and severe obstructive sleep apnoea had a mean apnoea-hypopnoea index of 23 and 46 events/hour, respectively. The physical quality of life component (as measured with SF-12) was lower than in the general male Swedish population (47 v 51 units, P<0.001), while the mental component was similar (53 v 54 units, P=0.57).
Kari Johansson, PhD student 1, Erik Hemmingsson, postdoctoral research fellow 1, Richard Harlid, physician 2, Ylva Trolle Lagerros, physician 1,3, Fredrik Granath, statistican 3, Stephan Rossner, professor 1, Martin Neovius, associate professor 3
1 Obesity Unit, Department of Medicine (Huddinge), Karolinska Institute, SE-141 86 Stockholm, Sweden
2 Aleris Fysiologlab, Stockholm
3 Clinical Epidemiology Unit, Department of Medicine (Solna), Karolinska Institute, Stockholm
Cite this as: BMJ 2011;342:d3017
doi:10.1136/bmj.d3017
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