Abstract
Objective Short sleep duration may contribute to childhood obesity. Amenable to intervention, sleep thus provides a potential path for prevention. The authors aimed to determine the impact of a behavioural intervention that successfully reduced parent-reported infant sleep problems on adiposity at age 6.
Design 5-year follow-up of a previously reported population-based cluster randomised trial. Participant allocation was concealed to researchers and data collection blinded.
Setting Recruitment from well-child centres in Melbourne, Australia.
Participants 328 children (174 intervention) with parent-reported sleep problems at age 7–8 months drawn from 49 centres (clusters).
Intervention Behavioural sleep strategies delivered over one to three structured individual nurse consultations from 8 to 10 months, versus usual care.
Main outcomes at age 6 years Body mass index (BMI) z-score, percentage overweight/obese and waist circumference.
Analyses Intention-to-treat regression analyses adjusted for potential confounders.
Results Anthropometric data were available for 193 children (59% retention) at age 6. There was no evidence of a difference between intervention (N=101) and control (N=92) children for BMI z-score (adjusted mean difference 0.2, 95% CI -0.1 to 0.4), overweight/obese status (20% vs 17%; adjusted OR 1.4, 95% CI 0.7 to 2.8) and waist circumference (adjusted mean difference -0.3, 95% CI -1.6 to 1.1). In posthoc analyses, neither infant nor childhood sleep duration were associated with anthropometric outcomes.
Conclusions A brief infant sleep intervention did not reduce overweight/obesity at 6 years. Population-based primary care sleep services seem unlikely to reduce the early childhood obesity epidemic.
Trial registration ISRCTN48752250
Introduction
Around a quarter of Australian 5–17 year olds are overweight or obese. Interventions targeting childhood diet and physical activity levels have achieved very limited population success. Therefore, attention is broadening to factors associated with obesity that may prove more amenable to modification.
One topical factor is sleep. Secular trends towards rising childhood obesity have been parallelled by a steady decline in child sleep duration over the last 35 years. Many studies have shown weak-to-moderate associations between habitually short sleep and body mass index (BMI)/waist circumference. A 2008 systematic review of 17 observational studies yielded a pooled odds ratio of 1.6 (95% CI 1.3 to 2.0) for childhood overweight/obesity presenting with short sleep.
Chen's 2008 systematic review proposes a number of plausible mechanisms. Poor sleep could lead to higher BMI, for example, by: (1) fatigue, reducing subsequent physical activity; (2) increased evening and overnight intake of calorie-dense foods; (3) lower nocturnal leptin and higher ghrelin, thus increasing daytime appetite; (4) lower nocturnal growth hormone, decreasing lypolysis. Under the reverse hypothesis, obesity could contribute to shorter sleep via such mechanisms as obstructive sleep apnoea or lower activity levels leading to less fatigue and thence difficulty falling asleep. Currently, however, no single mechanism is endorsed or causal direction established because most studies are cross-sectional. Of the few longitudinal studies suggesting that short sleep precedes obesity, none focuses on infancy.
Despite this lack of robust evidence, the idea that poor sleep may play a causal role in childhood obesity is generating intense interest. Randomised trials could confirm causal associations if they successfully manipulate the predictor then measure its effect on overweight/obesity. Therefore, at least two ongoing trials aiming to lessen weight gain are incorporating infant sleep interventions that specifically target infant sleep problems and sleep duration (NCT00892983, New Zealand, and NCT00359242, Pennsylvania, USA). Regardless of their outcomes, anecdotally sleep is already being targeted clinically to reduce obesity.
In 2003–2005, we conducted a large, community-based, secondary prevention trial of a behavioural sleep intervention designed to improve infant sleep at 8–10 months of age. Drawing from a population-based sample recruited at age 4 months, all infants with parent-reported sleep problems at 7–8 months were eligible (see figure 1). Compared with controls, intervention parents reported fewer sleep problems at infant age 10 months (56% vs 68%, adjusted OR (adj OR) 0.6, 95% CI 0.4 to 0.9) and 12 months (39% vs 55%, adj OR 0.50, 95% CI 0.3 to 0.8). By age 2 years, the impact on sleep was less (27% vs 33%, adj OR 0.8, 95% CI 0.5 to 1.4) but a reduction in maternal depression was still apparent (15% vs 26%, adj OR 0.4, 95% CI 0.2 to 0.9). Because these benefits occurred across a broad sociodemographic range and at lower healthcare system cost, the government recently extended the programme to the entire state of Victoria.
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Figure 1.
Graphical depiction of components of the trial.
In this paper, we aimed to determine whether, by age 6 years:
this successful infant sleep intervention led to better anthropometric outcomes, ie:
lower mean BMI z-score
a smaller proportion of children overweight/obese
lower mean waist circumference
any observed intervention effects were mediated by parent-reported child sleep problems (yes/no) and/or sleep duration from baseline to 6 years