Maintenance diets following rapid weight loss in obstructive sleep apnea: a pilot 1‐year clinical trial
Randomized controlled trials have shown that obesity reduction is effective in reducing obstructive sleep apnea (OSA) severity and improving associated cardiovascular risk factors (Chirinos et al., 2014; Johansson et al., 2009; Kajaste et al., 2004; Kemppainen et al., 2008; Nerfeldt et al., 2008a; Tuomilehto et al., 2009), making it a viable alternative, given the poor compliance with continuous positive airway pressure (CPAP), which is the gold standard for OSA treatment (Weaver and Grunstein, 2008). It is well established that use of a very low energy diet (VLED) is an efficacious means of inducing significant and rapid weight reduction in patients with and without OSA (Barnes et al., 2009; Johansson et al., 2009; Kajaste et al., 2004; Larsen et al., 2010; Nerfeldt et al., 2008b; Parretti et al., 2016; Tuomilehto et al., 2009). However, maintenance of this weight loss is challenging, and obese cohorts typically experience regain after 6 months (Anderson et al., 2001; Franz et al., 2007; Tsai and Wadden, 2006). Furthermore, the deployment of such intensive weight loss strategies in obesity and speciality clinics poses difficulties, and the translation of this model to real‐world settings is not without inherent challenges (Appel et al., 2011; Tsai et al., 2015; Wadden et al., 2013). Previous randomized controlled trials in patients with OSA using a VLED have not specifically addressed eventual weight regain. The reasons include too short a follow‐up period (Chirinos et al., 2014; Kansanen et al., 1998; Nerfeldt et al., 2008a) or lacked implementation of a formal weight loss maintenance programme that included both prescribed diet and exercise to explicitly prevent weight regain (Barnes et al., 2009; Chirinos et al., 2014; Johansson et al., 2011; Kajaste et al., 2004; Kansanen et al., 1998; Nerfeldt et al., 2010). Of the studies that included a formal weight maintenance programme, the intensive visit schedule precludes their translation to clinical practice due to high patient burden (Johansson et al., 2011; Tuomilehto et al., 2010). These two studies were also not generalizable, in that they were limited exclusively to either mild or treated OSA. It has been hypothesized that OSA might be obesogenic and could impede weight loss with limited improvements in cardiometabolic health (Borel et al., 2012). It is therefore important to test whether common dietary prescriptions, when combined with exercise, maintain weight loss and associated benefits in patients with the full range of OSA severity, regardless of treatment.
The primary hypothesis of our study is that weight loss maintenance using two commonly prescribed diets is feasible, tolerable and efficacious in patients with OSA. Following rapid weight loss with a VLED, our primary aim was to maintain the reduction in central obesity (determined by our primary outcome of waist circumference) for 10 months. Given the potential for OSA treatment to modulate weight loss we deliberately included treated and untreated OSA patients in the study. We also aimed to assess OSA and cardiometabolic function and to determine whether sympathetic activity at baseline or following the VLED were associated with the amount of overall weight loss or the degree of weight regain. We chose to test the programme efficacy with two specific maintenance diets used commonly in Australia [the Australian Guide to Healthy Eating (AGHE; Dixon et al., 2012) and the low glycaemic index high‐protein diet (LGHP, Larsen et al., 2010)] to facilitate the translatability of these findings into clinical practice. Importantly, however, it was not an aim of this pilot trial to compare these dietary approaches, because we did not have a hypothesis that these diets are different and we did not have enough patients to test for equivalence.