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REVIEW ARTICLE
Year : 2006  |  Volume : 23  |  Issue : 2  |  Page : 78-81 Table of Contents   

COPD and nutrition


Divison of Chest Medicine, St John's Medical College Hospital, Sarjapur Road, Bangalore 560034., India

Correspondence Address:
Brinnell Caszo
Divison of Chest Medicine, St John's Medical College Hospital, Sarjapur Road, Bangalore 560034.
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-2113.44414

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How to cite this article:
Caszo B, D'Souza GA. COPD and nutrition. Lung India 2006;23:78-81

How to cite this URL:
Caszo B, D'Souza GA. COPD and nutrition. Lung India [serial online] 2006 [cited 2020 Oct 25];23:78-81. Available from: https://www.lungindia.com/text.asp?2006/23/2/78/44414


   Introduction Top


The presence of cachexia indicates a poor outcome in terms of morbidity, quality of life (QOL) and mortality in patients with chronic obstructive pulmonary disease (COPD). Interest in this field is considerable, as simple nutritional supplementation does not always successfully reverse the cachexia. It is commonly seen in patients with many chronic diseases such as congestive cardiac failure COPD tuberculosis, rheumatoid arthritis, cystic fibrosis, and Crohn's disease [1],[2] . Generally it is taken to mean that there is an extensive loss of muscle mass. These conditions are associated with changes in body composition, general metabolism and immune status. The functional consequences are in term of quality of life, endurance and strength, exercise capacity, general morbidity and mortality.


   Mechanisms of malnutrition in COPD Top


Weight loss seen in COPD involves all body compartments. The cause of weight loss is believed to be energy deficiency due to a hypermetabolic state. This hypermetabolic state is due to an increased energy expenditue required because of the mechanical disadvantages of increased resistance to airflow and hyperinflation. However studies done on resting energy expenditure show no significant increase and the energy expenditure is not influenced by severity of COPD, oxygen cost of breathing or total energy expenditure [3],[4],[5],[6] .

Other mechanisms thought to produce weight loss are believed to be mediated by pulmonary inflamation and tissue hypoxia [7] . Studies done in this area attempt to link loss of muscle mass/ body weight to status of inflammatory markers [8] . AbduRah et al showed that loss of free fat mass (FFM) and skeletal muscle mass is related to an increase in cytokines, particularly tumor necrosis factor a (TNFa) and interleukin 6 (IL-6). When seen in the light of impaired lung functions of these patients i.e.reduced Total Lung Capacity, forced expiratory volume in the first second (FEV [1] and Diffusion Co-efficeint, it appears that these markers may be associated with lung injury. There is evidence of increased protein turnover in patients with even stable COPD. However a direct causal link between weight loss in COPD and pro-inflammatory and inflammatory markers is yet to be conclusively proven. [7],[9],[10]

There is growing evidence that COPD is a chronic inflammatory disease. This suggests the role of inflammation and oxidative stress in the pathogenesis of COPD. Studies have shown that there is an imbalance in the redox status in the plasma of COPD patients with elevated levels of lipid per oxidation products [11] . Molecules of adhesion on neutrophils as well as G-proteins were also increased in a cohort of COPD patients [12] . There was also an increase in cytochrome oxidase in circulating lymphocytes. Other pro inflammatory markers like TNFa, IL-8 and acute phase proteins are found elevated in COPD patients [13],[14] In acute exacerbations these markers are further elevated.

Cytokines and pro-inflammatory mediators exert systemic effects in addition to their immunologic functions. Anorexia may result from central action on the hypothalamic nuclei and alteration of feeding behavior. Cytokines may cause other effects through release of other mediators such as serotonin, leptin or corticotropin releasing hormone, which have an effect on feeding.

Leptin has a major role in this regard. Studies show that there is a link between cytokines and leptin as signals that have an influence on the nutritional status [15],[16] . Leptin is a protein that is released by the adipocytes and regulated by the expression of the ob gene. Leptin binds to receptors present in the hypothalamic nuclei that influences feeding behavior; in animals binding of leptin to receptors causes decrease in food intake. However leptin is now believed to play a larger role by interactions with appetite stimulating neuropeptide Y and satiety stimulating melanocyte-stimulating hormone (MSH). Since weight loss in COPD involves both losses in FM and FFM as well as anorexia, there may be an increase in circulating leptin or an insensitivity to changes in circulating leptin levels. On the other hand, the inflammatory cytokines seen in COPD may effect the expression of leptin [17],[18],[19],[20] .


   Measuring Nutritional Status Top


The use of simple measures of nutritional status such as body weight and body weight corrected for height (Body Mass Index, BMI) is preferable in the clinical setting, as use of established and more accurate methods such as deuterium dilution, hydro density and total body potassium may be of limited practicality. Whereas body weight and BMI are simple, the main drawback is that changes in body composition cannot be assessed. In patients with COPD, these changes could be further distorted by fluid retention. Reduction in muscle mass is also associated in depletion of respiratory muscles and strength. This will further reduce respiratory function. Such changes have been demonstrated in patients who have low body weight [21] . There is reduced capacity for work, increased fatigability and a poor quality of life [22],[23],[24],[25] . Another method that can be used to measure body composition is measurement of skin fold thickness as described by Durnin and Womersly. This method involves the measurement of skin fold thickness using a pair of calipers, and then using a reference table to calculate the fat mass. This method is based on the principle that a constant fraction of the mid-arm circumference is composed of fat. The tables are population specific and inter observer error is high. Bioimpedance can also be used to measure and assess body composition. Here the principle is that the body behaves as a volume conductor and FFM has a higher conductivity as it contains all the electrolytes and fluid as compared to fat. Theoretically FFM is found to correlate with height 2 /- resistance or height 2 / impedance. A disadvantage of the procedure is the lack of a convenient and accurate in vivo reference method. Main advantages include that it can be used what ease, is non-invasive and needs no positive participation on the part of the patient. This method has been used by Schols et al 38 and compared with deuterium dilution and found to be quite satisfactory. The same study shows that skin fold derived FFM is overestimated when compared with BIA derived FFM [4],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16]

Other studies show that it is the muscle mass itself and not body weight that predicts outcome in COPD patients with cachexia. Marquis et al have shown that the cross-sectional area at the mid-thigh level is a better predictor of mortality, compared to an index such as BMI. In this study corns-sectional areas was determined using computerized tomography. In those patients with a FEV 1 less than 50% predicted, cross-sectional area was a better predicor of mortality. However whether this was a reflection of total muscle mass or function could not be clarified [26] .

Muscle atrophy and dysfunction are features associated with weight loss and changes in body composition in COPD. A decrease in muscle strength has been shown when compared with matched controls [22],[23],[24],[25],[26],[27] . There is also reduced endurance [22],[23] , and increased fatigability. Studies also show that there is fatigability and a reduced exercise capacity [25] . Since other treatment options are relatively limited, a study of these factors particularly in relation to nutritional stauts is a new strategy in the management of COPD. These features may be attributed in part to disuse, as COPD patients find their exercise capacity limited, and this in turn could further perpetuate inactivity and further disuse atrophy. Medications such as steroids, which may cause myopathies, may also have a role to play [27] . Further injury may be caused by hypoxia; increased oxidative stress, and reduced capacity of oxidative enzymes [28] . Finally nutritional depletion due to inadequate intake and the hyper metabolic state of the disease process itself may worsen exercise capacity.

Exercise training may help to prevent deconditioning of skeletal muscles. A programme including endurance training could be useful, as in normal individuals, endurance training produces increase in capillary density, increase in the mitochondria and muscle fibre type [29] . A suitable training programme that would be tolerated by the patient and be of sufficient intensity to cause benefit would have to be considered. Prevention of hypoxia can also improve exercise capacity [30] . The role of nutritional supplementation in combination with an exercise-training programme would need to be studied. Nutritional supplementation has been shown to increase body weight, however there is little evidence to show suitable change in body composition.


   Nutritional Intervention in COPD Top


Weight loss, loss in FFM and low BMI have been associated with a much poorer outcome in COPD patients. Hence addressing these issues by means of supplementation have been studied in some detail. Randomized controlled trials have been done, comparing outcomes such as lung function tests, quality of life and exercise tolerane [31] . Generally it is observed that short-term studies (2 to 3 weeks) show supplementation increases exercise tolerance, QOL and lung fucntion tests. However in the long-term the benefits of such a strategy are questionable as shown in one particular study where patients particularly resistant to refeeding programmes were put on aggressive nocturnal gastrostomy feeds. Weight gain in this group was minimal. The authors propose that this is so because of the "hyper-metabolic" and "hyper-catabolic" status of these patients. Therefore, coupling of refeeding with an anabolic stimulus like exercise would make sense. One study used endurance training along with supplementation and showed a higher weight gain [32] .

The use of other anabolic agents such as the oral anabolic steroid stanozolol in randomized controlled studies showed that patients in the treatment group had improvement in body weight as well as inspiratory muscle strength as compared to those patients in the control group [33],[34] . Recombinant growth hormone has also been investigated in this role and the results indicate no substantial increase in body weight or muslce mass or performance [35] . The consumption of polyunsaturated fatty acids in the diet has also been shown to be related to a low incidence of lung disease in general. Communities whose diets have a high content of fish oils show similar trends. The presence of these fatty acids is believed to displace precursors of leukotrienes and other inflamamatory mediators form the cell membrane lipids and lower the production of inflammatory mediators [36],[37] .

The role of supplemental oxygen has been shown clearly in increasing quality of life and decreasing morbidity and mortality of COPD patients. There is a decrease in dyspnea and a consequent increase in appetite and food intake. However it is advisable to use the least concentration of oxygen as the extent of possible oxidative damage to lungs has not been assessed completely.


   Conclusion Top


COPD patients commonly suffer from muscle wasting, loss of body weight and a poor quality of life. The low body weight and loss of muscle mass have a negative impact on quality of life, morbidity and mortality. Hence a nutritional assessment in such patients should be an important component of management. In addition to BMI more sensitive tests are required for the assessment of these patients, as oedema seen often in COPD patients make it not so useful. Bioimpedance and mid-thigh cross sectional area are two such methods which need to be assessed in a wider section of COPD patients. An approach encompassing all aspects including assessment of nutritional status, nutritional supplementation, anabolic stimulants including exercise training and use of domiciliary oxygen should be considered part of any effective pulmonary rehabilitation program. Exercise training and nutritional supplementation should be considered in the appropriate patient and their effects need to be better characterized.

 
   References Top

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