Nutritional management of COPD is complex, as both malnutrition and obesity are highly prevalent and both contribute to patient morbidity and mortality risk. In addition, poor eating habits, sedentary lifestyle, smoking and corticosteroid use can lead to poor nutritional status in COPD, with deficiencies in various nutrients such as vitamins and minerals, fatty acids and amino acids. The randomised controlled trials (RCTs) that have been conducted with the aim of achieving a healthy weight, improving nutritional status and functional outcomes in COPD are discussed below.
Malnutrition: Malnutrition is an independent predictor of mortality and healthcare use in COPD patients (Hoong 2017) [evidence level III-2]. Low body weight and/or low fat free mass (FFM) is common in COPD, particularly in those patients with severe disease and those who are socially deprived (Collins 2018), due to an inadequate nutritional intake compared to energy expenditure. Energy intake may be reduced due to breathlessness during eating, hyperinflation of lungs causing pressure on the stomach and loss of appetite induced by drugs (Sridhar 2006). At the same time, energy demands may be increased due to factors such as the energy costs of breathing, the metabolic costs of respiratory tract infections increased nutrient-induced thermogenesis and catabolic effects of systemic inflammation (Sridhar 2006, Akner 2016). As a result, low BMI and loss of FFM are common in COPD patients and this increases COPD mortality risk, being inversely associated with respiratory and peripheral muscle function, exercise capacity and health status (Vestbo 2006, Schols 2005). Two meta-analyses have shown that high calorie nutritional support has small, yet beneficial effects in COPD, particularly in those who are undernourished. A systematic review which included 13 RCTs of nutritional support included a meta-analysis that showed a pooled increase in mean weight, which was greatest in undernourished patients [1.94 (95%CI 1.43-2.45) kg]. There were also increases in grip strength 5.3% (p < 0.05) and small effects on fat free mass and skin fold thickness (Collins 2012) [evidence level I]. In a follow-up meta analysis which focused on functional outcomes, nutritional support led to improvements in inspiratory muscle and expiratory muscle strength (Collins 2013) [evidence level I]. A Cochrane Review updated in 2012 also demonstrated in a meta-analysis of data from 17 RCTs, that nutritional therapy resulted in body weight gain in undernourished patients [1.65 (95% CI 0.14-3.16) kg] and improved FFM index and exercise tolerance (6-minute walk distance (6MWD)) in all patients. Importantly, the increase in 6MWD reached the minimum clinically important difference in severe COPD patients (Ferreira 2012) [evidence level I]. Hence high calorie nutritional supplements should be considered in COPD, particularly those who are malnourished and/or have severe disease. Importantly, those with undernutrition are most likely to benefit from nutrition therapy before an undernutrition state is established (Akner 2016).
Obesity: At the other end of the spectrum, obesity is becoming increasingly prevalent in COPD. Obesity complicates COPD management and in addition to the negative metabolic consequences, is associated with decreased expiratory reserve volume (ERV) and functional residual capacity (FRC), increased use of inhaled medications, increased dyspnoea and fatigue, decreased heath related quality of life and decreased weight bearing exercise capacity (Cecere 2011, Ramachandran 2008, Ora 2009). Despite these negative effects, obesity has been associated with reduced mortality risk in severe COPD, (Landbo 1999, Guo 2016) which may be due to a reduction in static lung volumes (Casanova 2005) and /or the increase in FFM (Poulain 2008) that occurs in obesity due to over-nutrition and increased weight bearing. A meta-analysis of 17 studies evaluated the dose-response relationship between BMI and mortality. Compared to healthy weight COPD individuals, the RR for death in the underweight was 1.40 (95% CI 1.20-1.63; p=0.0001), whereas the risk of death was reduced in those in that were overweight (RR 0.80, 95% CI 0.67-0.96; p=0.0001) and obese (RR 0.77, 95% CI 0.62-0.95; p=0.0162). There was a nonlinear relationship between mortality and BMI categories. Those with a BMI <21.75 kg/m2 had the greatest risk of dying. Once BMI exceeded 32 kg/m2 the protective effect of high BMI was no longer evident (Guo 2016).
No weight loss RCTs have been conducted in COPD to date, however, a recent pre-post study has demonstrated the potential benefits of weight loss. In this uncontrolled trial, dietary energy restriction coupled with resistance exercise training led to clinically significant improvements in BMI, exercise tolerance and health status, while preserving FFM (McDonald 2016b) [evidence level III]. Definitive RCTs are needed in this area in order to formulate clinical guidelines for managing obese COPD patients.
Other nutritional interventions: A number of large observational cohort studies have demonstrated that a healthy dietary pattern (including fruit, vegetables, fish and wholegrains) protects against lung function decline and COPD onset, while an unhealthy eating pattern (including refined grains, cured and red meats, desserts and French fries) has the opposite effect (Varraso 2015, Varraso 2007a, Varraso 2007b). Nutritional interventions targeting specific foods or nutrients in COPD are limited and to date, the level of evidence supporting these interventions is level II or less.
Fruit and vegetables: Fruit and vegetables are recognised as being part of a healthy diet as they are low in energy, yet dense in nutrients such as vitamins and minerals, fibre and phytochemicals. In a cohort study in 44,335 men followed for 13.2 years, high fruit and vegetable intake was associated with reduced risk of COPD. Current and ex-smokers with a high (≥ 5 serves per day) versus low (< 2 serves per day) had 40% and 34% lower COPD risk (Kaluza 2017) [evidence level III]. Two RCTs manipulating fruit and vegetable intake have been conducted in COPD. A 12 week study in 81 COPD patients showed no effect of a high fruit and vegetable intake on FEV1, systemic inflammation or airway oxidative stress (Baldrick 2012) [evidence level III]. However, a 3 year study in 120 COPD patients revealed an improvement in lung function in the high fruit and vegetable group compared to the control group (Keranis 2010) [evidence level III], suggesting that longer term fruit and vegetable intake provides a therapeutic effect.
Vitamin E: Vitamin E is a nutrient with antioxidant and anti-inflammatory properties. The ability for vitamin E to reduce biomarkers of oxidative stress in COPD has been demonstrated in one RCT (Daga 2003, but not another Wu 2007) [evidence level II]. In a large-scale RCT (Women’s Health Study, n=38597), the risk of developing chronic lung disease over a 10 year supplementation period was reduced by 10% in women using vitamin E supplements (600 IU on alternate days), suggesting benefit of long term supplementation (Agler 2011) [evidence level III].
Omega-3 fatty acids: Omega-3 fatty acids have been demonstrated to have diverse anti-inflammatory effects. Two RCTs have examined the effect of omega-3 polyunsaturated fatty acids (PUFA) in COPD. One RCT randomised 32 COPD patients to supplementation with 0.6g omega-3PUFA per day combined with low intensity exercise or a control group for 12 weeks. They reported an improvement in weight, exercise capacity, quality of life and inflammation in the omega-3PUFA/ exercise group compared to controls (Sugawara 2010) [evidence level II]. The other study compared the effects of 8 weeks supplementation with 2.6g omega-3PUFA/day versus a placebo in 102 COPD patients undergoing pulmonary rehabilitation. They reported an increase in exercise capacity in the omega-3PUFA group compared to the placebo group, but there were no effects on muscle strength, FEV1 or inflammation (Broekhuizen 2005) [evidence level II]. Hence omega-3PUFA supplementation may be a useful adjunct to COPD rehabilitation programs [evidence level II].
Vitamin D/ calcium: Vitamin D regulates calcium homeostasis and bone metabolism, as well as having roles in immune function, inflammation, airway remodelling and muscle strength. Vitamin D is frequently deficient in COPD due to factors including the use of oral corticosteroids, smoking, poor diet and reduced exposure to sunlight due to physical limitations. Vitamin D deficiency was associated with lower lung function and more rapid decline in FEV1 among smokers in a cohort of elderly men followed for 20 years (Lange 2012) [evidence level III]. In another cohort of 18,507 participants, lung function decline was faster, and COPD risk increased, in individuals with the lowest vitamin D levels (Afzal 2014). Corresponding with low vitamin D levels, osteoporosis is highly prevalent in COPD; in 658 COPD patients in the TORCH study, 23% were osteoporotic and 43% osteopenic (Ferguson 2009). While there are no COPD-specific treatment guidelines for osteoporosis, standard treatment guidelines apply, with patients using corticosteroids requiring treatment according to the guidelines for management of corticosteroid-induced osteoporosis, including daily calcium intake of 1200-1500 mg/day and vitamin D doses of 800-1000 IU per day (Grossman 2010).
A meta-analysis of individual patient data from three RCTs of 468 patients (Jolliffe 2019) was conducted to determine whether vitamin D supplementation reduced exacerbations of COPD. The authors reported that vitamin D supplementation did not reduce overall moderate or severe exacerbations, (adjusted IRR 0.94, 95% CI 0.78 to 1.13; p=0.52; n=469 in three studies, one step IPD meta-analysis), and results were similar for the two step analysis. There were however, protective effects of vitamin D supplementation in patients considered vitamin D deficient, [those with a baseline 25-hydroxyvitamin D level of <25 nmol/l (1.23 versus 2.10 events per person per year, aIRR 0.55, 95% CI 0.36 to 0.84 n=87 in three studies; within sub-group p=0.006] but not in those with baseline 25-hydroxyvitamin D levels ≥25 nmol/l (2.01 versus 1.94 events per person per year, p=0.71, aIRR 1.04, 95% CI 0.85 to 1.27; p for interaction=0.015, n=382,) [evidence level I].
In COPD patients, vitamin D deficiency should be considered and supplementation is recommended in deficient patients, particularly those with a 25-hydroxyvitamin D level <25 nmol/l.
Amino Acids: Amino acids are the building blocks of protein and hence an integral component of muscle tissue. Various types of amino acids and their derivatives have been assessed in intervention trials in COPD. In a 12 week RCT in 88 COPD out-patients, those who received essential amino acid supplementation had an improvement in FFM, muscle strength, physical performance and St George Respiratory Questionnaire (SGRQ) compared to placebo (Dal Negro 2010) [evidence level II]. Another RCT in 28 COPD patients examined outcomes following 12 weeks pulmonary rehabilitation, in patients with or without essential amino acid supplementation, including 5g/day branched chain amino acids. Body weight and FFM increased in the supplemented group compared to controls (Baldi 2010) [evidence level III]. Whey protein, rich in the amino acid cysteine and other essential amino acids, was trialled in a 16 week RCT in COPD patients who were undergoing exercise training for the last 8 weeks of the intervention. This resulted in increased exercise capacity and quality of life compared to placebo, but no changes in inflammation (Laviolette 2010) [evidence level II]. In a 6 week RCT in 16 COPD patients, the amino acid derivative L-carnitine was administered concurrent with pulmonary rehabilitation and resulted in improved exercise tolerance and inspiratory muscle strength compared to the placebo group (Borghi-Silva 2006) [evidence level II]. Conversely, the amino acid derivative creatine, has been shown in meta-analyses to have no effect on muscle strength, exercise tolerance or SGRQ in COPD (Al-Ghimlas 2010) [evidence level I]. In summary, based on level II evidence, essential amino acids, whey protein and L-carnitine may be beneficial in COPD, particularly when combined with exercise training.
Anabolic steroids: While anabolic steroids are not diet-derived, they have a potential role in FFM accretion. A recent systematic review and meta analysis reported that in COPD patients, 8-26 weeks intervention with anabolic steroids led to improvements in body weight, FFM and SGRQ, while there was no improvement in lung function, handgrip strength or 6MWD (Pan 2014) [evidence level I]. Hence some specific benefits are apparent, although possible adverse effects also need to be considered.
In summary, level I evidence exists for the use of high calorie nutritional supplementation in COPD, to achieve body weight gain, improve FFM index and exercise tolerance (6MWD), with results most significant for patients who are undernourished. Benefits have been demonstrated for healthy eating patterns, increasing fruit and vegetable intake and supplementing with n-3 PUFA, vitamin E, vitamin D, essential amino acids, whey protein and L-carnitine in COPD, particularly when the supplements are used in combination with a pulmonary rehabilitation program. However, level I evidence supporting the use of these other interventions does not yet exist and further research is needed to confirm efficacy.
For all COPD patients, a key goal of nutritional management is to eat a balanced diet and to achieve and maintain a healthy weight. Healthy eating means choosing a variety of foods from each of the five food groups every day, in suitable proportions including: vegetables and legumes/beans; fruit; grain foods, mostly wholegrain varieties, such as breads, cereals, rice and pasta; lean meats and poultry, fish, eggs, tofu, nuts and legumes; and dairy products such as milk, yoghurt and cheese. At the same time, foods that are high in saturated fat, sugar and sodium, such as highly processed and takeaway foods, should be limited.
To prevent dypsnoea while eating various strategies as shown in Box 7 below have been recommended:
|Box 7. Eating strategies which may prevent dyspnoea|
|Clear the airways of mucus before eating|
|If supplemental oxygen is used, make sure this is worn while eating|
|Avoid eating large meals, instead eat small nutritious meals and snacks more frequently|
|Avoid drinking with meals|
|Choose softer foods that are easier to chew and swallow, e.g. mashed potato, soups, bananas|
|Limit foods that can cause bloating, e.g. beans, onions, cauliflower, soft drinks|
|Rest for at least 15-20 minutes after eating in an upright position|
|In patients who are underweight, protein and calorie intake can be boosted using high energy, nutrient-rich foods that are easily accessible, such as milk powder, cheese, cream, custard, peanut butter and milkshakes or a nutritionally complete oral supplement (e.g. Sustagen)|
|Referral to a dietitian for individual advice may be beneficial|
Other tips to avoid aspiration can be found in O7.6 Aspiration< Prev Next >