O6.9 Nutrition

Nutritional management of COPD is complex, as both malnutrition and obesity are highly prevalent and both contribute to the patient’s 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: Low body weight and/or low fat free mass (FFM) is common in COPD, particularly in those patients with severe disease, 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 the energy costs of breathing and the metabolic costs of respiratory tract infections (Sridhar 2006).  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 conducted 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]. 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 (6MWD) in all patients (Ferreira 2012) [evidence level I]. Hence high calorie nutritional supplements should be considered in COPD, particularly those who are malnourished.

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) 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. Weight loss interventions have not been tested in COPD to date and no recommendations are currently available.Considering the improved prognosis for severe COPD patients with increasing BMI, weight loss strategies need to be considered with caution.

Other nutritional interventions: Various other nutritional interventions have being evaluated in COPD. However 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. Two RCTs manipulating fruit and vegetable intake have been conducted in COPD. A 12 week study in 81 COPD subjects showed no effect of a high fruit and vegetable intake on FEV1, systemic inflammation or airway oxidative stress (Baldrick 2012). However, a 3 year study in 120 COPD patients revealed an improvement in the high fruit and vegetable group compared to the control group (Keranis 2010), suggesting that longer term intervention provides a therapeutic effect [evidence level III-1].

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). 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) [evidence level II].

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 subjects 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). The other study compared the effects of 8 weeks supplementation with 3g omega-3PUFA/day versus a placebo in 102 COPD subjects 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). Hence omega-3PUFA supplementation may be a useful adjunct to COPD rehabilitation programmes [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-2]. As a result, 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). In an RCT using high-dose vitamin D (100,000 IU per month) administered over 1 year to 186 COPD patients, there was no improvement in exacerbation frequency, lung function, quality of life or mortality rate compared to placebo (Lehouck 2012). However, in the same trial, this vitamin D regimen resulted in an improvement in inspiratory muscle strength and oxidative metabolism compared to the placebo group, in patients undergoing pulmonary rehabilitation (Hornikx 2012) [evidence level II]. A prespecified subgroup analysis in a multi-centre study of COPD patients demonstrated that those subjects (148 subjects of a total of 240 COPD patients recruited from London clinics) who had baseline serum 25-hydroxyvitamin D levels below 50nmol/L had a 43% reduction in moderate and severe exacerbations when taking 3mg of vitamin D orally 2 monthly, over 12 months (Martineau 2015). Vitamin D deficiency should be considered with a view to supplementary replacement in COPD patients [evidence level III].

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 subjects 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-2]. Whey protein, rich in the amino acid cysteine and other essential amino acids, was trialled in a 16 week RCT in COPD subjects 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. In patients with COPD with weight loss, anabolic steroids have been shown to increase body weight and lean body mass but have little or no effect on exercise capacity (Yeh 2002, Weisberg 2002) [evidence level II].

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 subjects who are undernourished. Benefits have been demonstrated for 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 programme. However, level I evidence supporting the use of these other interventions does not yet exist and further research is needed to confirm efficacy.

Eating strategies

For all COPD patients the 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 have been recommended:

  • 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
  • Eat slowly
  • Choose softer foods that are easier to chew and swallow, eg mashed potato, soups, bananas
  • Limit foods that can cause bloating, eg 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 (eg Sustagen)
  • Referral to a dietitian for individual advice may be beneficial

Other tips to avoid aspiration can be found in O7.6 Aspiration