Nutritional Evaluation in Chronic Obstructive Pulmonary Disease Patients
Malnutrition is a common problem in moderate or severe Chronic
Obstructive Pulmonary Disease (COPD) patients which affects body composition
and food intake of these patients. In this study, the relationship of the stage
of COPD with nutritional intake and body mass index in COPD patients were investigated
and compared with healthy people and Dietary Reference Intake tables. A total
of 93 COPD patients were referred by pulmonary physicians in Motahari and Faghihi
medical centers. Pulmonary Function Test (PFT) was used in order to confirm
the diagnosis of COPD and also categorize the patients into three categories
(mild, moderate and sever). The control group consisted of 108 adults matched
to the cases by age and gender. Anthropometric indices and physical activity
and a 24 h dietary recall were recorded. All analyses were performed using the
SPSS 14. All data presented as means (±SD). The mean intake of energy
(p = 0.002), protein (p<0.001), fat (p = 0.007), vitamin C (p = 0.003), vitamin
E (p<0.001), magnesium (p<0.001) and omega-3 (p<0.001) was significantly
lower in COPD patients compared with controls. The mean BMI of the severe group
was significantly lower than the controls (p = 0.016). The mean intake of energy,
carbohydrate, fat, vitamin E, magnesium and omega-3 was significantly lower
in both case and control groups compared to the RDA (p<0.001) for all of
the mentioned nutrients). Vitamin C intake was lower than RDA in the case (p<0.001)
and also in the control males (p<0.001). In COPD patients, there is a significant
relationship between the stage of COPD and nutrients intake and their BMI.
Received: June 30, 2012;
Accepted: September 14, 2012;
Published: October 06, 2012
Chronic Obstructive Pulmonary Disease (COPD) is characterized by obstruction
of the airways which is progressive and is associated with an anomalous inflammatory
response of the lungs to harmful gases or particles, primarily tobacco smoke
(Agusti et al., 2003). COPD is a leading cause
of morbidity and mortality worldwide (Asia Pacific COPD
Roundtable Group, 2005) and the fourth leading cause of mortality in the
United States and in Europe (Murray and Lopez, 1997).
COPD will be the third leading cause of death worldwide by 2020 (Murray
and Lopez, 1997). Exacerbations in COPD patients lead to an increase in
the need for medical care and hospitalization, thereby causing increases in
health-care costs (Siafakas et al., 1995). Attention
to nutritional status in patients with respiratory diseases is important because
of malnutrition has direct effect on the lungs function, respiratory muscles
and the lung parenchyma, consequently contributing to worsening of the disease
(Batres et al., 2007). There is Malnutrition
in at least one third of moderate or severe cases of COPD. Malnutrition affect
functional performance and quality of life of these patients and independent
of other aspects of the disease it is indicator of both morbidity and mortality
(Foley and ZuWallack, 2001). Imbalance in dietary intake
and energy expenditure contributed to weight loss. In contrast to an adaptive
decreased energy metabolism during starvation, total daily energy expenditure
has been increased in COPD patients (Slinde et al.,
2003). The low intake in these patients can be explained by a cytokine leptin
link leading to increased levels of leptin. These increased leptin levels lead
to reduced food intake and higher energy demand and therefore, poor response
to nutritional support (Saudny-Unterberger et al.,
1997). It seems that patients with COPD are at high risk for malnutrition,
making it essential that these patients undergo careful assessment and screening
to identify those who require dietary treatment. So in this study, we evaluated
the nutritional status in COPD patients and compared it with healthy control
MATERIALS AND METHODS
Participants: The study was conducted in two therapeutic centers, Motahari
and Faghihi, in Shiraz during 1 year. A total of 93 COPD patients were diagnosed
and referred by pulmonary physicians. In order to confirm the diagnosis of COPD
and categorize the patients into three categories (mild, moderate and sever)
pulmonary function test (PFT: was used to measure the intensity and reversibility
of obstruction of airways in COPD patients) and the Global Initiative for Chronic
Obstructive Lung Disease (GOLD) stages (Asia Pacific COPD
Roundtable Group, 2005) were used. The control group consisted of 108 adults
from the same domain as the cases. The controls were matched to the cases by
age (within 5 years) and gender and their health was confirmed by physicians.
Inclusion criteria were as follow: age between 55-75 years and having COPD
diagnosis as the primary limiting illness within the past four years. Exclusion
criteria were diabetes, renal failure, liver diseases, dementia, Parkinson disease,
cancer and other cachexic conditions, current dental problem, parenteral or
enteral feeding and multivitamin-multimineral supplement consumption.
The objective and protocol of the study were explain to the participants and
written informed consent provided from them. The study was approved by the ethics
committee of the School of Public Health and Nutrition of Shiraz University
of Medical Sciences.
Instruments: A face-to-face interview with each participant was conducted
by using a structured questionnaire. The first part of the questionnaire included
demographic information on age, gender, educational level, occupation, cigarette
smoking (never smoker; ex-smoker; current smoker) and duration of smoking (data
not shown). In the second part of the questionnaire, dental status, nausea,
vomiting and anorexia during the period of disease and medication use were recorded.
In the third part, anthropometrical measures; height (m), weight (kg) and weight
reduction in previous months were assessed. Body weight was assessed with a
beam scale to the nearest 0.1 kg while they were worn light clothing. Height
was measured by a clinical stadimeter in standing position. BMI, defined as
weight (kg) divided by the square of height (m), was calculated. The forth part
was about physical activity, history of supplement consumption and a 24 h dietary
recall. Dietary intake was measured by dietary recall that is a validated measure
to assess habitual food consumption. In the 24 h dietary recall, some questions
about food preparation were also asked. Dietary intakes were monitored by 3
day 24 h food recall, including 2 week day and 1 weekend day. To analyze the
dietary data we used DFP (Dorosty food processor: which is a software to calculate
the amount of calorie and nutrient intake in the diet). The last part was the
result of their spirometry test.
Statistical analysis: For statistical analysis, SPSS program version
11.5 (SPSS Inc., Chicago, IL, USA) was used and for comparison of continuous
variables in the two groups, we used independent samples t-test for normally
distributed data and non-parametric Mann-Whitney U test for variables showing
non-normal distribution. One-sample t-test was used to compare the mean of continuous
variables with standard numbers. For qualitative variables the Chi-square test
was used for each contingency table. A two-tailed p<0.05 was considered statistically
Table 1 presents the anthropometric status of the cases and
controls. The mean BMI of the severe group was significantly lower than the
controls (p = 0.016). About weight loss, more subjects in the case group (mild,
moderate and sever) had weight loss in previous months than the controls (p<0.001).
Table 2 presents the comparison of nutrient intake in the
case and control groups. The mean intake of energy (p = 0.027), carbohydrate
(p<0.001), vitamin E (p<0.001) and omega-3 (p<0.001) in the mild group
was significantly lower than the controls.
|| Mean intake of energy, macro and micro-nutrients in COPD
patient and control group
|P1: Mild vs. control, P2: Moderate vs. control, P3: Severe
vs. control, P4: Total group vs. control group, Values are Mean±SD
|| Body mass index (BMI) and weight loss with COPD exacerbation
in COPD patients and healthy people
|P1: Mild vs. control, P2: Moderate vs. control, P3: Severe
vs. control, P4: Total group vs. control group, Values are Mean±SD
|| Comparing the Mean intake of energy, macro and micro-nutrients
in COPD patient and control group with DRI tables
|P1: Male COPD vs. DRI, P2: Female COPD vs. DRI, P3: Male healthy
vs. DRI, P4: Female healthy vs. DRI, Values are Mean±SD
In the moderate group, the mean intake of carbohydrate (p = 0.004) and vitamin
E (p<0.001) was lower than the control group. But there were not any significant
difference in the intake of other nutrients. And the severe group had a lower
mean intake of energy and all other nutrients that were analyzed in this study.
Finally, in the overall comparison of the case and controls, the mean intake
of energy (p = 0.002), protein (p<0.001), fat (p = 0.007), vitamin C (p =
0.003), vitamin E (p<0.001), magnesium (p<0.001) and omega-3 (p<0.001)
were significantly lower in the case group.
Table 3 shows the mean intake of energy and some nutrients
in the case and control groups by gender differentiation and also comparison
of their intake with Recommended Dietary Allowance (RDA). The mean intake of
energy, carbohydrate, fat, vitamin E, magnesium and omega-3 were significantly
lower in both the case and control groups compared to the RDA (p<0.001) for
all of the mentioned nutrients). Vitamin C intake was lower than RDA in the
case (p<0.001) and also in the control males (p<0.001).
In this case-control study, the intake of energy and nutrients that effect
COPD patients, was measured and compared with the control group and DRI tables.
Eating difficulties, higher metabolic rate and cost of ventilation, together
with oxidative stress causing systemic inflammation are important factors for
weight loss in these patients (Hallin et al., 2006).
One of the strengths of this study was spirometric measurements of the lung
function that were taken to ensure correct classification (mild, moderate, severe).
Another strength of the study was the comparison of dietary intake in both case
and control groups with DRI tables.
Body Mass Index (BMI) in the mild and moderate COPD patients have no significant
relationship with the control group but severe COPD patients have lower BMI
in comparison with the control group.
Furthermore, patients group have weight loss more than the control group. These
results indicate that with the exacerbation of the condition of COPD patients,
the basic metabolic rate increases and the energy intake decrease, causing the
lower BMI and higher weight loss in severe COPD patient as compared with the
control group. Hallin et al. (2006) also have
reported in agreement with our results. Because of reduced dietary intake and
increased in resting energy expenditure, severe patients have impaired energy
balance, consequently they have more weight loss (Vermeeren
et al., 1997). Systemic inflammation is another possible cause of weight
loss in severe patients (Schols et al., 1996)
and is more pronounced (Soler-Cataluna et al., 2005).
In a cohort study, they concluded that low BMI was an independent risk factor
for mortality in subjects with COPD and that the association was strongest in
the subjects with severe COPD (Landbo et al., 1999).
It is still difficult to know whether weight loss and low weight is a cause
or a consequence of exacerbations.
In normal-weight or overweight patients, it is more appropriate to measure
the Mid-arm muscle area because of the Muscle Mass Depletion (MD) is a better
predictor of mortality than BMI in patients with COPD (Agusti
et al., 2003).
All of the patients had lower intake of energy and protein than the healthy
control group. The epidemiological evidence also indicated lower food consumption
in these patients (Saudny-Unterberger et al., 1997;
Foley and ZuWallack, 2001; Slinde
et al., 2003; Batres et al., 2007).
In a recent study, found seven out of ten patients had insufficient food intake
which cause negative energy balance (Tang et al.,
2002). In one study, patients hospitalised for an exacerbation have been
found to be in negative nitrogen balance but some little gains were observed
with increased energy intake (Saudny-Unterberger et al.,
1997). Thus interventions for boosting energy intake may improve Health
of these patients.
The lower intake of proteins as compared with the control group was the same
as the result of Donna and Artemis (Palmer et al.,
2004). COPD patients also had lower intake of all macronutrient than DRI
tables except proteins. However, the energy intake of patients decreased but
the protein consumption has no significant relationship with DRI tables. It
seems its due to the vulgar belief more protein intake, more disease
recovery, so, they consumed more high protein foods.
There was no significant different between the intake of carbohydrate in COPD
patients and healthy group. The observed normal intake of carbohydrate by COPD
patients was not a consequence of eating well. Because of dysphagia and eating
difficulties, these patients prefer sugar drink rather than solid food.
The lower intake of fat than control group and DRI tables was seen in our study;
however, due to lower Respiratory Quotient (RQ), the increase of fat consumption
in these patients is more appropriable. It has to be noticed that the intake
of fat has to be from vegetable oil such as olive or canola oil to decrease
the risk of cardiovascular disease. In one study, Grigorakos and co-workers
reported, giving combination nutrition (including enteral and parenteral nutrition)
assisted with high amounts of fat cause positive nitrogen balance and prevent
development of malnutrition (Grigorakos et al., 2009).
Inflammation is associated with COPD Pathogenesis. Omega-3 PUFAs acts as an
anti-inflammatory agent in the lung (Matsuyama et al.,
2005). We observed the lower intake of omega-3 PUFA in the diet of the whole
patients (mild, moderate, severe) than the control group and DRI tables. Matsuyama
concluded that nutritional support with the omega-3 could reduce inflammation
and improve exercise tolerance in COPD patients (Matsuyama
et al., 2005).
Normally, the lung exists in an oxygen-rich environment balanced between the
toxicity of oxidants (generated through normal cellular function or exposure
to prooxidants) and the protective activities of several intracellular and extracellular
antioxidant defense systems (Matsuyama et al., 2005).
Increase in oxidant stress or a impairment of antioxidant resources can initiate
a series of pathophysiologic events in the lung concluding cellular death and
dysfunction. Researchers have hypothesized that a diet low in antioxidants such
as |3-carotene and vitamins C and E may reduce natural defenses and increase
susceptibility to oxidant attack and airway inflammation. Higher intake of such
foods rich in antioxidants has been associated with a better lung function (Heffner
and Repine, 1989). Vitamin C and vitamin E are as important antioxidants
in people diet. A previous study by Schwartz and Weiss (1994)
suggested the significant statistical relationship between vitamin C and pulmonary
functional status. Walda and his co-workers have shown the results against of
Schwartz and our study (Walda et al., 2002).
This study have been shown that severe group of patients have lower intake of
vitamin C than the control group and standards.
Some minerals such as magnesium have the potential to promote bronchodilatation
and improve lung function in obstructive diseases. It is indicated that with
exacerbations in COPD patients, the intake of magnesium decreases. In the study
conducted by Do Amaral et al. (2008) magnesium
causes improvement in lung hyperinflation and respiratory muscle strength in
stable COPD patients.
This study indicated the importance of assessment of nutritional status and
monitoring weight changes in COPD patients. Lower BMI and higher weight loss
have been seen with exacerbations in COPD patients and have been shown that
COPD patients have low nutrient intake in compare with control group and DRI
tables. So, in patients with COPD nutritional intervention appears to be an
approach to obtaining anthropometric parameters improvement.
We would like to acknowledge the Students Research Committee of Shiraz University
of Medical Sciences for funding this study. We are also grateful to Dr. E. Mojtahedi
for their assistance in introducing the patients. We thank Motahari and Faghihi
Centerss staff and all people who gave up their time to participate in
our study. This article is derived from a thesis entitled Nutritional
evaluation in Chronic Obstructive Pulmonary Disease patients completed
by Ms. Neda Haghighat B.Sc. student of occupational health at Shiraz University
of Medical Sciences.
1: Agusti, A.G.N., A. Noguera, J. Sauleda, E. Sala, J. Pons and X. Busquets, 2003. Systemic effects of chronic obstructive pulmonary disease. Eur. Respir J., 21: 347-360.
Direct Link |
2: Batres, S.A., J.V. Leon and A.S. Rodolfo, 2007. Nutritional status in COPD. Arch. Bronconeumol., 43: 283-288.
3: Asia Pacific COPD Roundtable Group, 2005. Global Initiative for Chronic Obstructive Lung Disease strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease: An Asia-Pacific perspective. Respirology, 10: 9-17.
4: Do Amaral, A.F., A.L. Rodrigues-Junior, J. Terra Filho, H. Vannucchi and J.A. Martinez, 2008. Effects of acute magnesium loading on pulmonary function of stable COPD patients. Med. Sci. Monit., 14: CR524-CR529.
5: Foley, R.J. and R. ZuWallack, 2001. The impact of nutritional depletion in chronic obstructive pulmonary disease. J. Cardiopulm. Rehabil., 21: 288-295.
Direct Link |
6: Grigorakos, L., E. Sotiriou, N. Markou, S. Stratouli, E. Boutzouka, G. Philntisis and G. Baltopoulos, 2009. Combined nutritional support in patients with chronic obstructive pulmonary disease (COPD), under mechanical ventilation (MV). Hepatogastroenterology, 56: 1612-1614.
Direct Link |
7: Hallin, R., U.K. Koivisto-Hursti, E. Lindberg and C. Janson, 2006. Nutritional status, dietary energy intake and the risk of exacerbations in patients with chronic obstructive pulmonary disease (COPD). Respir. Med., 100: 561-567.
8: Heffner, J.E. and J.E. Repine, 1989. Pulmonary strategies of antioxidant defence. Am. J. Respir. Dis., 140: 531-554.
9: Landbo, C., E. Prescott, P. Lange, J. Vestbo and T.P. Almdal, 1999. Prognostic value of nutritional status in chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med., 160: 1856-1861.
Direct Link |
10: Matsuyama, W., H. Mitsuyama, M. Watanabe, K. Oonakahara, I. Higashimoto, M. Osame and K. Arimura, 2005. Effects of omega-3 polyunsaturated fatty acids on inflammatory markers in COPD. Chest, 128: 3817-3827.
11: Murray, C.J.L. and A.D. Lopez, 1997. Alternative projections of mortality and disability by cause 1990-2020: Global burden of disease study. Lancet, 349: 1498-1504.
CrossRef | PubMed | Direct Link |
12: Palmer, N., D.H. Mueller, L. Gilson, A. Mills and A. Haines, 2004. Health financing to promote access in low income settings-how much do we know? Lancet, 364: 1365-1370.
13: Saudny-Unterberger, H., J.G. Martin and K. Gray-Donald, 1997. Impact of nutritional support on functional status during an acute exacerbation of chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med., 156: 794-799.
14: Schols, A.M., W.A. Buurman, A.J. Staal van den Brekel, M.A. Dentener and E.F. Wouters, 1996. Evidence for a relation between metabolic derangements and increased levels of inflammatory mediators in a subgroup of patients with chronic obstructive pulmonary disease. Thorax, 51: 819-824.
15: Schwartz, J. and S.T. Weiss, 1994. Relationship between dietary vitamin C intake and pulmonary function in the First National Health and Nutrition Examination Survey (NHANES I). Am. J. Clin. Nutr., 59: 110-114.
Direct Link |
16: Siafakas, N.M., P. Vermeire, N.B. Pride, P. Paoletti and J. Gibson et al., 1995. Optimal assessment and management of chronic obstructive pulmonary disease (COPD). The European Respiratory Society Task Force. Eur. Respir. J., 8: 1398-1420.
17: Slinde, F., L. Ellegard, A.M. Gronberg, S. Larsson and L. Rossander-Hulthen, 2003. Total energy expenditure in underweight patients with severe chronic obstructive pulmonary disease living at home. Clin. Nutr., 22: 159-165.
CrossRef | PubMed |
18: Soler-Cataluna, J.J., L. Sanchez-Sanchez, M.A. Martinez-Garcia, P.R. Sanchez, E. Salcedo and M. Navarro, 2005. Mid-arm muscle area is a better predictor of mortality than body mass index in COPD. Chest, 128: 2108-2115.
19: Tang, N.L., M.L. Chung, M. Elia, E. Hui and C.M. Lum et al., 2002. Total daily energy expenditure in wasted chronic obstructive pulmonary disease patients. Eur. J. Clin. Nutr., 56: 282-287.
20: Vermeeren, M.A., A.M. Schols and E.F. Wouters, 1997. Effects of an acute exacerbation on nutritional and metabolic profile of patients with COPD. Eur. Respir. J., 10: 2264-2269.
21: Walda, I.C., C.Tabak, H.A. Smit, L. Rasanen and F. Fidanza et al., 2002. Diet and 20-year chronic obstructive pulmonary disease mortality in middle-aged men from three European countries. Eur. J. Clin. Nutr., 56: 638-643.
CrossRef | Direct Link |