Public health and clinical interventions for obesity in free-living adults may be diminished by individual compensation for the intervention. Approaches to predict weight outcomes do not account for all mechanisms of compensation, so they are not well suited to predict outcomes in free-living adults. Our objective was to quantify the range of compensation in energy intake or expenditure observed in human randomized controlled trials (RCTs).
We searched multiple databases (PubMed, CINAHL, SCOPUS, Cochrane, ProQuest, PsycInfo) up to 1 August 2012 for RCTs evaluating the effect of dietary and/or physical activity interventions on body weight/composition. Inclusion criteria: subjects per treatment arm ⩾5; ⩾1 week intervention; a reported outcome of body weight/body composition; the intervention was either a prescribed amount of over- or underfeeding and/or supervised or monitored physical activity was prescribed; ⩾80% compliance; and an objective method was used to verify compliance with the intervention (for example, observation and electronic monitoring). Data were independently extracted and analyzed by multiple reviewers with consensus reached by discussion. We compared observed weight change with predicted weight change using two models that predict weight change accounting only for metabolic compensation.
Twenty-eight studies met inclusion criteria. Overfeeding studies indicate 96% less weight gain than expected if no compensation occurred. Dietary restriction and exercise studies may result in up to 12–44% and 55–64% less weight loss than expected, respectively, under an assumption of no behavioral compensation.
Compensation is substantial even in high-compliance conditions, resulting in far less weight change than would be expected. The simple algorithm we report allows for more realistic predictions of intervention effects in free-living populations by accounting for the significant compensation that occurs.
Obesity is a serious and prevalent public health concern.1 New public health and clinical interventions to reduce obesity are frequently advocated or implemented based on hypothetical estimates of an outcome that may have little empirical support (for example, the 3500 kcal rule). For example, imagine an initiative from a large company that replaces its 250 kcal candy bars in its vending machines with 50 kcal protein bars to reduce energy intake (EI) from snacking among its employees. This initiative can be expected to produce (in those who consume at least 250 kcal per day from such snacks), on average, 5.7 kg of weight loss after one year (for example, for a 35-year old man who is 183 cm tall and weighs 100 kg at baseline, body mass index=30). This estimate is based on one of the mathematically validated prediction models2 sometimes used to justify such interventions.3 But is this estimate realistic?
On the basis of the evidence, this estimate is likely optimistic because current models for predicting weight change are not well suited for use in free-living subjects. A common rule of thumb used for decades to predict weight change outcomes is that losing or gaining one pound of fat requires a deficit of 3500 kcals of energy.4 This rule does not consider that human energy balance is a dynamic and adaptable system or that lean and fat mass is lost during negative energy balance, and this leads to an underestimation of the change in EI or energy expenditure (EE) needed to produce weight change.5, 6, 7, 8 Recently, more sophisticated models have been developed to predict weight changes, which consider the metabolic adaptations that occur during weight change.9, 10, 11, 12 To accurately predict weight change in free-living individuals, however, both metabolic and behavioral compensatory mechanisms must be accounted for.
Specifically, we define the modes of possible compensation as follows:
It is a compensation for an energy balance intervention through physiological changes in metabolism. For example, current mathematical models account for changes in resting metabolic rate, fluid balance, the thermic effect of food and spontaneous physical activity resulting from an energy balance intervention.11, 12, 13
It is a compensation for an energy balance intervention through behavior changes. For example, when a dietary or physical activity intervention attempts to create negative energy balance, an individual may respond by reducing voluntary EE and/or increasing EI if these avenues are not strictly controlled. Similarly, during an energy balance intervention of added energy, voluntary EE may increase and/or EI may decrease from other sources.
Others have shown that behavioral compensation occurs for physical activity interventions.14 Behavioral compensation may also occur for interventions that reduce caloric intake or add calorie-containing foods to the diet.15, 16 Current prediction models are intended for use where interventions are implemented with high fidelity (that is, intended intervention exposure was achieved) in isolation, and when metabolic compensation is the only route of compensation for the intervention possible. During interventions in free-living subjects, however, compensation can occur through metabolic compensation and through behavioral compensation. Behavioral compensation may diminish the effects of an intervention, making it important to quantify and account for when predicting outcomes in free-living populations. It is imperative that more realistic models be used for predicting outcomes for the reasons stated recently:
“…to establish a less controversial legacy for this important field, we should avoid past traps and be explicit about reasonable expectations. Implausible results that are ‘too good to be true’ still threaten nutritional research on many fronts, including survey measurements, observational associations, treatment effects in randomized trials, and estimates of the impact on populations.”17
We therefore set out to build an empirically based model to predict weight change outcomes in free-living subjects, and to quantify the extent to which observed weight change in free-living subjects differs from that predicted under the assumption of no behavioral compensation. The approach we took was to use systematic review techniques to collect study data and conduct meta-regression on studies meeting a priori inclusion criteria. These criteria guided identification of high-fidelity interventions implemented in free-living adults. The subjects had some ability to behaviorally compensate for the intervention, yet the reported information about the intervention and compliance verification allowed for a high degree of confidence in treatment fidelity. For our main analysis, we compared the predictions from models that assume no active compensation2, 18 with the observed outcomes as an estimate of the effects of behavioral compensation.
Materials and Methods
Systematic review of the literature and study selection
Articles, abstracts and doctoral dissertations were retrieved using searches performed on the following electronic databases: PubMed, Cochrane Library, SCOPUS, PsycInfo, Cumulative Index to Nursing and Allied Health Literature (CINAHL) and Dissertation Abstracts. We searched PubMed without MeSH headings to identify publications for inclusion, using the following limits: dated 1 August 2012 back to earliest records of human studies. Detailed search methods are provided on the PROSPERO registry website (Registry #CRD42013002912). No ethics committee approval was required as the data used are published summary statistics.
All studies were evaluated according to the following inclusion criteria: (1) the data were from adult human randomized controlled trials in free-living subjects, (2) the intervention was either a prescribed amount of over- or underfeeding given and reported (or could be converted) in kcal and/or supervised or monitored physical activity was prescribed and verified, (3) an objective verification method was used to verify the intervention at ⩾80% (for example, observation, electronic monitoring and provision of food with returned unused portions), (4) the study had a total sample size of at least five participants at enrollment, (5) the study protocol included an intervention period of at least 7 days, (6) the publication was available in the English language and (7) the study was published and listed in the above databases on or before 1 August 2012.
Our exclusion criteria are detailed in the online Supplementary Material. Briefly, we excluded studies on samples that were completely or predominantly made up of individuals younger than 18 years old or older than 60 years or having any health conditions that may affect weight. The filtering process of the initial search results is detailed in Figure 1 and also described in more detail in the online supplement.
Quantifying the effect of behavioral compensation—comparison with metabolic compensation models
We entered sample demographic and intervention data into each of the metabolic compensation model calculators to most closely represent each intervention as described in the published papers to estimate weight changes that would occur if only metabolic compensation occurred. As we included data that had samples of both men and women where separate baseline data and results were not reported (only combined summaries), we entered the data for both genders and mathematically adjusted the outputs for the relative proportions of men and women. For the NIDDK simulator,2 we assumed a baseline value (when not otherwise reported) of sedentary activity level (1.4 metabolic equivalents). The difference between the observed weight change for each study and the weight change predicted by these models is indicative of the degree of behavioral compensation that is observed for the interventions in free-living adults included in our review and meta-analysis.
All model data were analyzed with R routines19 and descriptive summaries were generated with Microsoft Excel version 2010. Further details of statistical approaches used for the predictive model building are on the online supplement. Risk of bias was assessed by two authors (EJD and KAK) independently and discrepancies were discussed until consensus was reached.
Role of funding source
The funding agency (International Life Science Institute—North America) had no role in the design, conduct, analysis, manuscript preparation or decision to publish the results of this study.
Results of publication search
We retrieved citations dated back to 1935, but more than two-thirds of the initial publications retrieved were published after 2001. The final data set for building the predictive model consisted of 28 studies published between 1987 and 2012, including 15 exercise studies, 9 studies with added energy, 3 dietary restriction studies and 2 studies that included both dietary restriction and exercise in the intervention (see Table 1 for a complete listing of included studies with selected summary data and intervention descriptions). The primary reasons for exclusion after full text review were studies not being truly randomized or not having a control group, followed by reliance only on self-report for EI or physical activity without any objective verification of compliance. Studies were all published journal articles, except for two dissertations.20, 21 Eleven studies had samples that were either 100% men or 100% women. Three other studies reported results by gender separately if both males and females were included in the sample. Only six studies (21%) reported the racial makeup of the samples; therefore, this factor was excluded from further analysis. Mean ages of the samples ranged from 20.6 to 60 years. Mean baseline body mass index of the samples ranged from 22.6 to 35.1 kg m−2.
Building a predictive model
We expected to find enough studies to build a robust regression model, incorporating mean participant characteristics and evaluating any significant interactions. However, the relatively low number and sparsely distributed data prevented reliable estimates from our final model. Details of the model and its estimations can be found in the online supplement, Supplementary Figure S1 and Supplementary Tables S1a and S1b.
Comparison with metabolic compensation models—estimating behavioral compensation
To address our main research question (What is the effect of behavioral compensation that occurs in free-living subjects who receive an energy balance intervention on weight outcomes?),we generated output for each study using the NIDDK and Pennington weight change prediction calculators2, 18 to estimate weight changes that would occur if only metabolic compensation occurred. The difference between the observed weight loss for each study and the weight change predicted by these models is indicative of behavioral compensation occurring during the intervention. The NIDDK and Pennington models are highly correlated (Pearson’s r=0.98, P<0.0001) in predicted weight change (Supplementary Figure S2). In general, the Pennington calculator is slightly more conservative than the predictions made by the NIDDK calculator.
The overall degree of behavioral compensation estimated by the gap between the observed and metabolic compensation-only predicted values is illustrated in Supplementary Figure S3, panels A and B. Both slopes being less than 1 (that is, 0.344 and 0.399 for the NIDDK and Pennington Models, respectively) indicate that the observed weight change is less than predicted after accounting for metabolic compensation. This quantifies the degree of behavioral compensation that is occurring (that is, the compensation that is in addition to the metabolic compensation, resulting in less weight change than expected).
The degree of behavioral compensation appears to differ depending on intervention type. As shown in Supplementary Figure S3, panels A and B, all types of interventions demonstrated less weight change than either the Pennington or NIDDK calculators predicted. The plot of overfeeding trials has a slope (95% confidence interval) of 0.06 (−0.04, 0.16) and 0.07 (−0.05, 0.18), plotted against the NIDDK and Pennington calculators, respectively (Figure 2, panels a and b). A slope of 1 would indicate that, on average, the interventions produced exactly as much weight change as expected from the mathematical models, which assume no behavioral compensation. As such, this suggests that behavioral compensation may result in as much as 96% less weight gain than predicted by metabolic calculators when adding energy to the diet. The slopes of the plots for dietary restriction and exercise studies are more similar to each other. Specifically, slopes (95% confidence interval) of 0.56 (0.17, 0.96) and 0.88 (0.36, 1.40) were plotted against the NIDDK and Pennington calculators, respectively, for dietary restriction studies (Figure 2). For exercise intervention studies, slopes (confidence interval) of 0.38 (0.16, 0.60) and 0.46 (0.19, 0.72) were plotted against the NIDDK and Pennington calculators, respectively (Figure 3). Thus, behavioral compensation may result in up to 12–44% less weight loss than predicted for dietary restriction studies and 55–64% less weight loss than predicted for exercise intervention studies.
Risk of bias assessment for included studies
See online supplement for risk of bias summary and detailed rating figure (Supplementary Figure S4) for each included study. The greatest proportions of study aspects with high risk of bias were judged to be due to the lack of analysis for incomplete data (attrition bias—for example, use of intention-to-treat analysis) and lack of attention placebo for control groups. Four studies reported results using intention-to-treat analysis.
We generated simple adjustment factors to predict weight change resulting from energy balance interventions in free-living adult populations, with the ability to compensate both behaviorally and metabolically, using 73 treatment and control arm group outcomes from 28 studies. One of the notable findings was the small number of studies meeting our inclusion criteria (that is, where compliance was objectively measured), making it difficult to study the role of behavioral compensation in a free-living context beyond a very basic level. Although our estimates are the only ones for this purpose to date based on the currently available literature, this highlights a gap in the literature of studies designed to determine the impact of energy balance perturbations in humans in the context of a full range of compensation that prevents a more precise estimate. As these studies are crucial to understanding the effect of public health interventions, their limited quantity underscores a need for future research in this area.
Perhaps, the most robust finding from our study most relevant to public health is that currently available predictions consistently overestimate weight change, which is evidence of significantly diminished weight change resulting from behavioral compensation. This is in spite of some instances where explicit instructions were given to make no other changes in routine habits, a form of compliance that is less commonly tracked or verified. In particular, the treatment effect of added calories was only, on average, ~5% of the weight gain predicted from models assuming no behavioral compensation. Several included studies reported a mean weight loss effect from added energy. This indicates that even if a new food is introduced to the diet, for example, adding a daily snack or beverage, EI and/or EE can be adjusted reasonably well, resulting in very little weight gain relative to how much would be expected if this behavioral compensation did not occur. Behavioral compensation for negative energy balance interventions such as exercise or dietary restriction is also evident from our analysis, and results in 37–45% and 56–88% of the weight loss predicted from metabolic-only compensation models. In our initial example of reducing EI via snacks by 200 kcals per day for the hypothetical man, the adjusted estimate of weight change after 1 year would be closer to 3.2 kg. This is lower than the 5.7 kg estimate given by the body weight simulator that predicts metabolic compensation only.
Therefore, our results suggest that current public health interventions or clinical interventions that alter one aspect of energy balance, without holding other aspects constant, may result in more modest weight changes than predicted or desired. A similar approach has been reported in pediatric studies,3 but it did not attempt to account for both behavioral and metabolic compensation components. It is important to take all modes of compensation into consideration when planning an intervention with targeted amounts of weight change and when anticipating its outcomes. It is likely that increased doses of energy perturbations are required. Increased control over compliance and compensation is necessary to achieve target outcomes. Estimates of what is required to achieve a specific weight change may be made more accurate for the purposes of public health recommendations if the present estimations are considered.
Our results suggest that there might be a differential effect of treatment type on the degree of behavioral compensation. However, an aspect of our data set needs to be considered in interpreting this result. Dietary restriction interventions are associated with greater treatment effects, and less behavioral compensation, than either exercise or overfeeding interventions. However, this finding may be because the dietary restriction interventions included in our analysis only allowed for behavioral compensation through EE changes, whereas all exercise and overfeeding interventions allowed for behavioral compensation through both dietary intake and EE changes.
Our approach has strengths and limitations. First, our inclusion criteria were rigorous. All included studies have at least 80% compliance with the prescribed intervention, with compliance verified objectively (no reliance solely on self-report). In addition, the dose was corrected in our calculations for the level of compliance reported in the study. Further, included studies were randomized controlled trials, and our outcome for generating the predictive model and for comparing with metabolic compensation models was the control group-adjusted weight change. Therefore, our models are built to assess true treatment effect, and are corrected for any weight change due to factors such as regression to the mean, maturation, historical factors and behaviors that result from simply participating in a study, rather than from the treatment itself.
Several limitations should also be considered when interpreting our analysis. Weight was not always the primary outcome in studies that met our inclusion criteria. This is particularly true for those with added EI in the form of nuts. Differences in stated outcomes of interest, time with researchers and other factors may affect weight outcomes for individual studies. In addition, body composition may be an important outcome that we were not able to adequately analyze because of the limited number of studies including body composition measurements such as changes in fat mass and fat-free mass. Because of our rigorous inclusion criteria, our data set is small (28 studies). The types of studies we selected are necessary for making definitive conclusions about the impact of perturbations in one aspect of energy balance on body weight. Studies also tended to be shorter in duration, thus it is difficult to make conclusions about long-term effects. This is a large gap in the literature, and a more systematic approach to large, well-controlled studies to answer these questions is warranted. In addition, 16 of the 28 studies reported data only for those participants who completed the intervention period, and across all studies there was a 17.8% dropout rate (Table 1), which may have biased our estimates of weight change toward overestimation. We used the intention to treat data when reported (four studies). Eight studies reported no dropouts.
Future research is needed to understand potential differences in compensation between dietary interventions (added or reduced energy), different food forms and macronutrient compositions. Also, certain factors should be considered as potential confounders when quantifying the compensatory response to a specific intervention. For example, bioavailability of energy in food, efficiencies in physical activity and food utilization, seasonal effects and durations of interventions may all influence both the metabolic and behavioral compensatory response to an intervention. It is also unclear whether compensation would remain constant over time. Moreover, evaluating the influence of participant characteristics related to eating behavior (cognitive restraint, disinhibition and hunger) and compensation during interventions is needed as this may hold promise for optimizing treatment effectiveness.
To conclude, we have presented the first empirically based, quantitative estimation for the range of behavioral compensation that may be observed for energy balance interventions. This information may assist in the estimation of weight outcomes of clinical health interventions. It may also inform public health projections for obesity interventions or public health initiatives.
Flegal KM, Carroll MD, Kit BK, Ogden CL . Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999-2010. JAMA 2012; 307: 491–497.
National Institute of Diabetes and Digestive and Kidney Diseases. Body weight simulator, 2013. Available at http://bwsimulator.niddk.nih.gov/ (accessed on 28 September 2013).
Wang YC, Hsiao A, Tracy Orleans C, Gortmaker SL . The caloric calculator: average caloric impact of childhood obesity interventions. Am J Prev Med 2013; 45: e3–e13.
Wishnofsky M . Caloric equivalents of gained or lost weight. Am J Clin Nutr 1958; 6: 542–546.
Hall KD . What is the required energy deficit per unit weight loss? Int J Obes (Lond) 2008; 32: 573–576.
Hall KD, Chow CC . Why is the 3500 kcal per pound weight loss rule wrong? Int J Obes (Lond) 2013; 37: 1614.
Thomas DM, Martin CK, Lettieri S, Bredlau C, Kaiser K, Church T et al. Response to 'Why is the 3500 kcal per pound weight loss rule wrong?'. Int J Obes (Lond) 2013; 37: 1614–1615.
Thomas DM, Martin CK, Lettieri S, Bredlau C, Kaiser K, Church T et al. Can a weight loss of one pound a week be achieved with a 3500-kcal deficit? Commentary on a commonly accepted rule. Int J Obes (Lond) 2013; 37: 1611–1613.
Hall KD, Butte BA, Swinburn BA, Chow CC . Dynamics of childhood growth and obesity: development and validation of a quantitative mathematical model. Lancet Diabetes Endocrinol 2013; 1: 97–105.
Hall KD, Chow CC . Estimating changes in free-living energy intake and its confidence interval. Am J Clin Nutr 2011; 94: 66–74.
Thomas DM, Ciesla A, Levine JA, Stevens JG, Martin CK . A mathematical model of weight change with adaptation. Math Biosci Eng 2009; 6: 873–887.
Thomas DM, Schoeller DA, Redman LA, Martin CK, Levine JA, Heymsfield SB . A computational model to determine energy intake during weight loss. Am J Clin Nutr 2010; 92: 1326–1331.
Hall KD . Predicting metabolic adaptation, body weight change, and energy intake in humans. Am J Physiol Endocrinol Metab 2010; 298: E449–E466.
Thomas DM, Bouchard C, Church T, Slentz C, Kraus WE, Redman LM et al. Why do individuals not lose more weight from an exercise intervention at a defined dose? An energy balance analysis. Obes Rev 2012; 13: 835–847.
Martin CK, Heilbronn LK, de Jonge L, DeLany JP, Volaufova J, Anton SD et al. Effect of calorie restriction on resting metabolic rate and spontaneous physical activity. Obesity (Silver Spring) 2007; 15: 2964–2973.
Alper CM, Mattes RD . Effects of chronic peanut consumption on energy balance and hedonics. Int J Obes Relat Metab Disord 2002; 26: 1129–1137.
Ioannidis JP . Implausible results in human nutrition research. BMJ 2013; 347: f6698.
Multisubject weight change predictor. Pennington Biomedical Research Center. Available at: http://www.pbrc.edu/research-and-faculty/calculators/mswcp/ (accessed on 28 September 2013).
Team RDC R: A Language and Environment for Statistical Computing. R Foundation for Statistical Computing: Vienna, Austria, 2009.
Addington E . Aspartame- or Sugar-Sweetened Beverages. Effects on Food Appetites and Mood in Young Adults (Doctoral Dissertation). Kansas State University: Manhattan, KS, USA, 1998.
Crandall KJ . The Effects of Exercise Intensity on Energy-Derived Macronutrient Intake, Caloric Intake, Body Composition, and Body Weight in the Overweight (Doctoral Dissertation). University of Northern Colorado: Greeley, CO, USA, 1999.
Johnstone AM, Horgan GW, Murison SD, Bremner DM, Lobley GE . Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum. Am J Clin Nutr 2008; 87: 44–55.
Das SK, Saltzman E, Gilhooly CH, Delany JP, Golden JK, Pittas AG et al. Low or moderate dietary energy restriction for long-term weight loss: what works best. Obesity 2009; 17: 2019–2024.
Zachwieja JJ, Ezell DM, Cline AD, Ricketts JC, Vicknair PC, Schorle SM et al. Short-term dietary energy restriction reduces lean body mass but not performance in physically active men and women. Int J Sports Med 2001; 22: 310–316.
Moreira EA, Most M, Howard J, Ravussin E . Dietary adherence to long-term controlled feeding in a calorie-restriction study in overweight men and women. Nutr Clin Pract 2011; 26: 309–315.
Leon AS, Casal D, Jacobs D Jr . Effects of 2,000 kcal per week of walking and stair climbing on physical fitness and risk factors for coronary heart disease. J Cardiopulm Rehabil 1996; 16: 183–192.
Van Etten LM, Westerterp KR, Verstappen FT, Boon BJ, Saris WH . Effect of an 18-wk weight-training program on energy expenditure and physical activity. J Appl Physiol 1997; 82: 298–304.
Murphy MH, Hardman AE . Training effects of short and long bouts of brisk walking in sedentary women. Med Sci Sports Exerc 1998; 30: 152–157.
Shaw I, Shaw BS . Consequence of resistance training on body composition and coronary artery disease risk. Cardiovasc J S Afr 2006; 17: 111–116.
Kirk EP, Washburn RA, Bailey BW, LeCheminant JD, Donnelly JE . Six months of supervised high-intensity low-volume resistance training improves strength independent of changes in muscle mass in young overweight men. J Strength Cond Res 2007; 21: 151–156.
Whybrow S, Hughes DA, Ritz P, Johnstone AM, Horgan GW, King N et al. The effect of an incremental increase in exercise on appetite, eating behaviour and energy balance in lean men and women feeding. Br J Nutr 2008; 100: 1109–1115.
Guadalupe-Grau A, Perez-Gomez J, Olmedillas H, Chavarren J, Dorado C, Santana A et al. Strength training combined with plyometric jumps in adults: sex differences in fat-bone axis adaptations. J Appl Physiol 2009; 106: 1100–1111.
Alves JG, Gale CR, Mutrie N, Correia JB, Batty GD . A 6-month exercise intervention among inactive and overweight Favela-residing women in Brazil: the caranguejo exercise trial. Am J Public Health 2009; 99: 76–80.
Turner JE, Markovitch D, Betts JA, Thompson D . Nonprescribed physical activity energy expenditure is maintained with structured exercise and implicates a compensatory increase in energy intake. Am J Clin Nutr 2010; 92: 1009–1016.
Bell GJ, Harber V, Murray T, Courneya KS, Rodgers W . A comparison of fitness training to a pedometer-based walking program matched for total energy cost. J Phys Act Health 2010; 7: 203–213.
Vispute SS, Smith JD, Lecheminant JD, Hurley KS . The effect of abdominal exercise on abdominal fat. J Strength Cond Res 2011; 25: 2559–2564.
Hornbuckle LM, Liu PY, Ilich JZ, Kim JS, Arjmandi BH, Panton LB . Effects of resistance training and walking on cardiovascular disease risk in African-American Women. Med Sci Sports Exerc 2012; 44: 525–533.
Heydari M, Freund J, Boutcher SH . The effect of high-intensity intermittent exercise on body composition of overweight young males. J Obes 2012; 2012: 480467.
Thompson AM, Mikus CR, Rodarte RQ, Distefano B, Priest EL, Sinclair E et al. Inflammation and exercise (INFLAME): Study rationale, design, and methods. Contemp Clin Trials 2008; 29: 418–427.
Church TS, Earnest CP, Thompson AM, Priest EL, Rodarte RQ, Saunders T et al. Exercise without weight loss does not reduce C-reactive protein: the INFLAME study. Med Sci Sports Exerc 2010; 42: 708–716.
Lammert O, Grunnet N, Faber P, Bjornsbo KS, Dich J, Larsen LO et al. Effects of isoenergetic overfeeding of either carbohydrate or fat in young men. Br J Nutr 2000; 84: 233–245.
Martin A, Normand S, Sothier M, Peyrat J, Louche-Pelissier C, Laville M . Is advice for breakfast consumption justified? Results from a short-term dietary and metabolic experiment in young healthy men. Br J Nutr 2000; 84: 337–344.
Sabate J, Cordero-Macintyre Z, Siapco G, Torabian S, Haddad E . Does regular walnut consumption lead to weight gain? Br J Nutr 2005; 94: 859–864.
Whybrow S, Harrison CL, Mayer C, James Stubbs R . Effects of added fruits and vegetables on dietary intakes and body weight in Scottish adults. Br J Nutr 2006; 95: 496–503.
Whybrow S, Mayer C, Kirk TR, Mazlan N, Stubbs RJ . Effects of two weeks' mandatory snack consumption on energy intake and energy balance. Obesity 2007; 15: 673–685.
Sheridan MJ, Cooper JN, Erario M, Cheifetz CE . Pistachio nut consumption and serum lipid levels. J Am Coll Nutr 2007; 26: 141–148.
Casas-Agustench P, Lopez-Uriarte P, Bullo M, Ros E, Cabre-Vila JJ, Salas-Salvado J . Effects of one serving of mixed nuts on serum lipids, insulin resistance and inflammatory markers in patients with the metabolic syndrome. Nutr Metab Cardiovasc Dis 2011; 21: 126–135.
Maersk M, Belza A, Stodkilde-Jorgensen H, Ringgaard S, Chabanova E, Thomsen H et al. Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fat depot: a 6-mo randomized intervention study. Am J Clin Nutr 2012; 95: 283–289.
This project was sponsored by the International Life Sciences Institute—North America (EJD and KAK, co-PIs). We thank the following experts for their helpful comments on earlier versions of this manuscript: Steve Blair, Steve Heymsfield, Rick Mattes, Robert Matthews, Diana Thomas and Kevin Fontaine. Registry Information: PROSPERO (http://www.crd.york.ac.uk/prospero/search.asp) CRD42013002912.
EJD, KAK and DBA conceived the study and developed the design and selection criteria. KAK performed the literature searches. KAK and EJD reviewed the literature, selected studies, extracted data, evaluated risk of bias and wrote significant portions of the manuscript. ASA assisted with literature selection, data extraction and summary calculations. JAD and KDK performed the statistical analysis and wrote some portions of the manuscript. DBA directed the statistical analysis and wrote some portions of the manuscript.
DBA has received consulting fees and his university has received gifts, grants and donations from multiple non-profit and for-profit organizations with interests in obesity including publishers, litigators and food and pharmaceutical companies. KAK has received a speaker honorarium from Coca-Cola Iberia. The remaining authors declare no conflict of interest.
Supplementary Information accompanies this paper on International Journal of Obesity website
About this article
Cite this article
Dhurandhar, E., Kaiser, K., Dawson, J. et al. Predicting adult weight change in the real world: a systematic review and meta-analysis accounting for compensatory changes in energy intake or expenditure. Int J Obes 39, 1181–1187 (2015). https://doi.org/10.1038/ijo.2014.184
The Journal of Rural Health (2020)
Exceptional reported effects and data anomalies merit explanation from “A randomized controlled trial of coordination exercise on cognitive function in obese adolescents” by Liu et al. (2018)
Psychology of Sport and Exercise (2020)
Biobehavioural approaches to prevention and treatment: A call for implementation science in obesity research
Obesity Science & Practice (2020)
Environmental Health Perspectives (2020)
Current Addiction Reports (2019)