Obesity in COPD: Revealed and Unrevealed Issues

Figures & data

Table 1. Knowledge gaps and considerations for future studies.

Subjects	Knowledge gap	Available data	Considerations for future studies
Prevalence of obesity	What is the prevalence of obesity in COPD?	Variable prevalence rates (18%–54%).	-Large multicentre studies.
			-Including both COPD and non-COPD subjects.
			-Including all levels of COPD severity (GOLD I–IV).
			-Including both male and female.
			-Spirometry and physician made diagnosis of COPD.
	Is obesity more prevalent in COPD compared to non-COPD?	Most studies indicate higher prevalence in COPD; however, just two studies available with a direct comparison (including both COPD and non-COPD).
			-Measured height and length instead of self-reported data.
			-Well-defined sub-populations (severity of COPD, emphysema vs. bronchitis).
			-Longitudinal studies with follow-up of COPD patients and/or follow-up of obese patients
	Is there a causal link between obesity and COPD?	Unknown.
Role of obesity on dyspnea	Does obesity lead to more, similar or even less dyspnea in COPD?	No consensus, some indicate a negative effect of obesity on dyspnea, while others suggest that obesity does not influence dyspnea.	-Heterogeneity of COPD needs to be considered (e.g. emphysema vs. bronchitis; hyperinflation). For a fair comparison, groups should be matched for these factors.
			-Heterogeneity of obesity needs to be considered (e.g. adipose tissue distribution, FFMI, central vs. peripheral obesity). Groups should be matched for these variables.
			-Factors influencing dyspnea should be considered and be matched in groups. These include age, gender and comorbidities.
			-Consistency in questionnaires used to assess dyspnea.
Static lung volumes; obese vs. non-obese.	Does solely an increase in body fat contribute to less hyperinflation in obese COPD or do other factors influence this finding as well?	Obesity is associated with relatively less lung hyperinflation; however, more details are lacking.	-Evaluating the role of other factors on top of BMI, that may contribute in the pathogenesis of hyperinflation (e.g. FFMI, inflammation, etc.)
			-Clustering different phenotypes of COPD and identifying sub-populations that benefit from lower levels of hyperinflation.
			-Including patients with wide ranges of BMI in large cohorts.
	Which phenotype of COPD patients benefits the most of lower hyperinflation caused by obesity?	Unknown
	What is an ideal cut-off point in BMI where disadvantages of extra weight counterbalance the advantages of less hyperinflation in COPD?	In terms of survival, advantage seems to diminish with BMI > 32 kg/m^2 (Guo et al.). However, regarding symptoms and QoL definite answers are lacking.
Role of obesity in exercise capacity	Is 6MWT the right tool to measure functional capacity in obese COPD?	Obesity negatively influences weight-bearing tests (6MWT) and is associated with exercise induced desaturation. However, obesity seems not to influence weight-supported exercise (cycling).	-Studies exploring how to interpret 6MWT in obese COPD, does this give a realistic view on functional status and prognosis in obese COPD patients?
			-Translational studies for clinical practice, enabling us to advise obese COPD patients on proper exercise modality.
	What should be advised to obese COPD patients regarding weight- supported vs. weight-bearing exercise?
Role of obesity in exacerbation risk in COPD	What is the role of obesity on the risk of COPD exacerbations?	It seems that obesity is associated with better survival after hospitalization with AECOPD and lower risk of 30-day re-admission. However, whether obesity reduces the risk of exacerbations remains disputable.	-Prospective, longitudinal studies with follow-up of patients.
			-Diagnosis (COPD, exacerbation, obesity) based on measurements rather than self-reports or ICD coding.

Figure 1. Obese (OB) subjects with chronic obstructive pulmonary disease (COPD) (solid squares) had a rightward shifted dyspnea/ventilation (VE) slope in comparison with normal weight (NW) subjects with COPD (open squares). At an iso-VE of 25 L/minutes (vertical line with arrow), dyspnea intensity was 1.2 ± 1.1 versus 2.4 ± 1.6 Borg units in OB versus NW (p < 0.01). Reproduced from Ora J, Laveneziana P, Ofir D, Deesomchok A, Webb KA and O'Donnell DE. Combined effects of obesity and chronic obstructive pulmonary disease on dyspnea and exercise tolerance. Am J Respir Crit Care Med. 2009;180(10):964–71. Reprinted with permission of the American Thoracic Society. Copyright © 2017.

Figure 2. (A) Static lung volumes measured by body plethysmography at rest. Expiratory reserve volume (ERV) and functional residual capacity (FRC) (ERV + RV) were significantly (p < 0.05) lower in the obese (OB) group. (B) Lung volumes are shown from rest to peak exercise in OB patients COPD (closed squares) and in normal weight (NW) patients with COPD (open squares). In the OB compared with the NW group, end-expiratory lung volume (EELV) (standardized as a % of predicted TLC) was consistently lower (^*p < 0.01) at rest and throughout exercise; the OB group reached an EELV at peak exercise that was similar to that of the NW group at the pre-exercise resting level. IC = inspiratory capacity; IRV = inspiratory reserve volume; VT = tidal volume (shaded area); RV = residual volume. Values are means ± SE. Reproduced from Ora J, Laveneziana P, Ofir D, Deesomchok A, Webb KA and O'Donnell DE. Combined effects of obesity and chronic obstructive pulmonary disease on dyspnea and exercise tolerance. Am J Respir Crit Care Med. 2009;180(10):964–71. Reprinted with permission of the American Thoracic Society. Copyright © 2017.

Figure 3. The adjusted predicted MRC score is given for each subject. For every given severity of airflow obstruction, obese patients are more dyspneic than normal weight patients. Regression lines for each BMI category also shown. (Normal weight: black dots; Overweight: gravy dots; Obese: white dots). Reproduced from Cecere L, Littman A. Obesity and COPD: associated symptoms, health-related quality of life and medication use. COPD 2011;8(4):275–284. Reprinted with permission of Taylor & Francis Ltd, http://www.tandfonline.com. Copyright © 2017.

Figure 4. Post-bronchodilator lung volume components are shown divided by GOLD stage and BMI. UW = underweight; NW = normal weight; OW = overweight; OB = obese; RV = residual volume; ERV = expiratory reserve volume; IC = inspiratory capacity. Reproduced from O'Donnell DE, Deesomchok A, Lam YM, et al. Effects of BMI on static lung volumes in patients with airway obstruction. Chest. 2011;140 (2):461–8. Reprinted with permission of Elsevier. Copyright © 2017.

Figure 5. Main outcomes of cycle ergometry and 6-minute walk-test (6MWD) in normal weight and obese chronic obstructive pulmonary disease (COPD) patients. Reproduced from Maatman RC, Spruit MA, van Melick PP, et al. Effects of obesity on weight-bearing versus weight-supported exercise testing in patients with COPD. Respirology. 2016; 21(3):483–8. Reprinted with permission of John Wiley and Sons. Copyright © 2017.

Rutten EPA, Calverley PM, Casaburi R, Agusti A, Bakke P, Celli B, Coxson HO, Crim C, Lomas DA, Macnee W, et al. Changes in body composition in patients with chronic obstructive pulmonary disease: do they influence patient-related outcomes? Ann Nutr Metab. 2013;63(3):239–47.

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