Desperate Diseases Call for Drastic Diets
Abstract & Commentary
By Barbara A. Phillips, MD, MSPH. Dr. Phillips is Professor of Medicine, University of Kentucky; Director, Sleep Disorders Center, Samaritan Hospital, Lexington; she serves on the speakers bureaus for Cephalon, Resmed, and Respironics. This article originally appeared in the June 29, 2011 issue of Internal Medicine Alert. At that time it was peer reviewed by Gerald Roberts, MD, Assistant Clinical Professor of Medicine, Albert Einstein College of Medicine, New York, NY. Dr. Roberts reports no financial relationship to this field of study.
Synopsis: A very low energy diet followed by a weight maintenance program results in significant improvements in weight, obstructive sleep apnea, metabolic factors, and quality of life for at least a year.
Source: Johansson K, et al. Longer term effects of very low energy diet on obstructive sleep apnea in cohort derived from randomised controlled trial: Prospective observational follow-up study. BMJ 2011;342:d3017.
This report is an extension of a shorter-term study conducted to assess the effects of a very low energy (or calorie) diet on obstructive sleep apnea. The study was conducted at the Obesity Unit at Karolinska University Hospital in Sweden. The participants were all obese men with moderate-to-severe obstructive sleep apnea who were stable on continuous positive airway pressure (CPAP). Patients were randomized to a very low energy diet or a control group for the first 9 weeks, but then the control group was also started on the very low calorie diet after 9 weeks. After a 9-week very low energy diet period, both groups entered a weight loss maintenance program. Since the control group was only a control for the first 9 weeks, data from both groups were pooled for this 1-year follow-up analysis.
The very low energy weight loss diet was a 2.3 MJ/day (about 550 calories) liquid energy intake protocol (Cambridge Weight Plan, Northants, UK) for 7 weeks, followed by 2 weeks' gradual introduction of normal food to reach 6.3 MJ/day (about 1500 calories) at week 9. Patients were also scheduled for six visits with clinical examinations and group sessions. The maintenance program started right after the very low energy diet period and was essentially behavior modification group therapy supplemented with a self-help manual. Each group included 13-15 patients and was led by a research nurse and a dietitian. Each patient also was seen by a nurse for anthropometry measurements and a dietitian for individual dietary advice.
The protocol specified use of partial meal replacement as a first option (exchanging one or two daily meals with an approximately 140 calorie meal replacement) if the patient's weight had increased by more than 2 kg since the last visit. (Of note, almost all [86%] of the participants reported using partial meal replacement at least once). The secondary option was sibutramine or orlistat prescription, but orlistat was prescribed to only one patient.
Of the original 63 patients in the study, 49 completed sleep and adiposity follow-up measures (this included five people who dropped out of the weight maintenance program but were willing to follow-up), and 44 completed a full year of treatment.
At baseline, the majority of patients had severe obstructive sleep apnea, metabolic syndrome, hypertension, and dyslipidemia. Slightly more than half were obese; 56%, 41%, and 3% had BMIs of 30-34.9, 35-39.9, and ≥ 40, respectively. Their physical quality-of-life component was lower than in the general male Swedish population while the mental component was similar.
During the very low energy diet and full treatment program, weight, BMI, waist circumference, neck circumference, and percentage body fat all decreased significantly, but all these variables increased significantly during the weight maintenance period. Of the participants analyzed at the 1-year follow-up, one was normal weight (BMI < 25), 27 were overweight, and 35 (56%) remained obese (BMI ≥ 30).
All sleep variables improved significantly after the very low energy diet period and full treatment program, but then worsened significantly during the weight maintenance period. However, neither the weight nor the sleep-disordered breathing returned to baseline severity during 1 year of follow-up. Overall, the apnea- hypopnea index (AHI) fell by 58% after 9 weeks of a very low energy diet and was still statistically and clinically reduced (by 47%) at 1 year. At the 1-year follow-up, six patients (10%) had total remission of obstructive sleep apnea and 30 (48%) patients no longer required CPAP (23 of these did not need any further treatment and 7 shifted to treatment with an oral appliance). Improvements in the AHI were larger in those men with severe obstructive sleep apnea at baseline than in those with moderate disease. Patients who lost ≥ 15 kg had larger improvements in the AHI at 1 year than patients who lost less, but even modest weight loss resulted in significant improvement in AHI.
Between baseline and 1-year follow-up, the physical component of the quality-of-life score had increased by 4 units (2 to 6; P < 0.001) and was similar to that of the general population. Between baseline and 1-year follow-up all measured metabolic variables improved significantly. Dyslipidemia disappeared in 11/59, insulin resistance in 10/20, and metabolic syndrome in 23/44. Of those with hypertension at baseline, resolution occurred in 8/36 (22%).
During the very low energy diet period, 13 patients had an adverse event classified as probably causally linked with the very low energy diet, including constipation (n = 3), increased alanine aminotransferase activity (n = 6), dizziness (n = 1), gout (n = 2), and dry lips (n = 1). All adverse events had disappeared by the visit 2 weeks after the very low energy diet period. During weight loss maintenance there were five additional adverse events probably causally linked to treatment with very low energy diet, including gallstones (n = 3), gout (n = 1), and kidney stones (n = 1). No patient discontinued treatment because of adverse events.
Obstructive sleep apnea has roughly the same prevalence as asthma,1 but is arguably more of a public health risk because it is associated not only with increased cardiovascular risk, but also with increased risk of moving vehicle crash.2-4 CPAP treatment is effective, but CPAP adherence while no worse than for any other medical treatment is not optimum. The original report of this cohort5 covered only 9 weeks of treatment, and the subjects were already regaining weight at the end of the first follow-up period after they left the very low energy diet and went to the maintenance program. I was among many skeptics who believed that neither the weight loss nor the improvement in sleep apnea would persist over time. This report has proved me wrong though there were dropouts and failures, as a whole, the patients had significant, persistent improvements not only in weight and sleep apnea, but also in metabolic factors and quality of life.
Indeed, while reading this report, I kept contrasting this approach to that of upper airway surgery such as uvulopalatopharyngoplasty (UPPP). UPPP has about the same short-term "cure" rate as is reported here (50%), but we don't know very much about its effects on blood pressure, metabolic factors, and quality of life. Indeed, long-term follow-up of those who undergo UPPP is uncommon, but we do know that relapse occurs, mostly related to weight gain.6 The weight loss protocol in this study was extensive and labor-intensive, but almost certainly cheaper than surgery. And the adverse events (dry lips, gallstones) for the very low calorie approach pale in comparison to those related to UPPP (speech change, palatal stenosis, and, er, death).
Talking to patients about weight loss is hard. Getting them into programs is even harder. But this report suggests that it can really make a difference. One of my favorite lines in clinic is, "You are a smart person, and you have struggled with this for a long time. If you were going to lose weight on your own, you would have done it by now. Let's get some help."
1. Young T, et al. Epidemiology of obstructive sleep apnea: A population health perspective. Am J Respir Crit Care Med 2002;165:1217-1239.
2. Marshall NS, et al. Sleep apnea as an independent risk factor for all-cause mortality: The Busselton Health Study. Sleep 2008;31:1079-1085.
3. Young T, et al. Sleep disordered breathing and mortality: Eighteen-year follow-up of the Wisconsin sleep cohort. Sleep 2008;31:1071-1078.
4. Tregear S, et al. Obstructive sleep apnea and risk of motor vehicle crash: Systematic review and meta-analysis. J Clin Sleep Med 2009;5:573-581.
5. Johansson K, et al. Effect of a very low energy diet on moderate and severe obstructive sleep apnoea in obese men: A randomised controlled trial. BMJ 2009; 339:b4609.
6. Phillips BA. Upper airway surgery does not have a major role in the treatment of sleep apnea. J Clin Sleep Med 2005;1:241-245.