-IBIS-1.7.6-
tx
respiratory system
emphysema
Nutrition
dietary guidelines
eating principles:
moderately low fat
low sugar
high complex whole carbohydrates
protein 12-15% diet
vegetarian cleansing diet or short fasts
foods rich in Vitamins A and E
therapeutic foods:
garlic, onions, leeks, turnips, grapes, pineapple, honey, green leafy vegetables (Jensen, p. 61)
fresh juices:
carrot
carrot, parsnip, potato, and watercress (Walker, p. 136)
avoid:
food intolerances (Rowe. Dis. Chest 1965;48:609.)
cow's milk and other dairy products, white bread, refined foods, processed foods, sugar and sweets, catarrh-forming foods: oranges, tofu, tomatoes; meat, ice cream, shellfish
supplements
Vitamin C: 3 g once daily.
Vitamin A: 50,000 IU once daily. Some research indicates that beta-carotene may increase the risk of lung cancer among smokers.
Vitamin E: 400 IU three times daily.
Antioxidants: Free radicals are generally considered to be associated with COPD, especially for smokers. It would seem that antioxidants would be beneficial in reducing COPD risk and might alleviate its symptoms. Individuals whose dietary intake of fruits and vegetables is rich in alpha-tocopherol and beta-carotene appear to be at reduced risk for developing COPD. However, according to one double-blind study, supplementation with synthetic alpha-tocopherol or beta-carotene provided no benefit against the symptoms of chronic obstructive pulmonary disorders.
(Eiserich JP, et al. Am J Clin Nutr. 1995 Dec;62(6 Suppl):1490S-1500S; Rautalahti M, et al. Am J Respir Crit Care Med 1997;156:1447-1452.)
Magnesium: Intravenous magnesium is a potent bronchodilator. Even though research indicates that magnesium deficiency may be common among those with COPD, oral supplementation has not been proven to be effective in treating the condition.
(Fiaccadori E, et al. Crit Care Med 1988;16:751-760; Okayama H, et al. JAMA 1987;257:1076-1078; Rolla G, et al. Magnesium Trace Elem 1990;9:132-136; Skorodin MS, et al. Arch Intern Med 1995;155:496-500.)
Zinc picolinate: 30 mg twice daily.
Coenzyme Q10: 20-60 mg, three times daily, prevents fatty acid oxidation, protects heart muscle through anti-oxidant action, and assists development of increased exercise tolerance.
(Satta A, et al. Clin Ther. 1991 Nov-Dec;13(6):754-757; Fujimoto S, et al. Clin Investig 1993;71(8 Suppl):S162-S166.)
Lecithin: 1200 mg three times daily, improves lung surfactant.
L-carnitine: (Dal Negro R, et al. Int J Clin Pharmacol Ther Toxicol 1986;24:453-456; Dal Negro R, et al. Int J Clin Pharmacol Ther Toxicol 1988;26:269-272.)
N-acetyl cysteine (NAC): helps break down mucus and exerts antioxidant activity. 400 mg, three times daily.
(Boman G, et al. Eur J Respir Dis 1983;64:405-415; Multicenter Study Group. Eur J Respir Dis 1980;61:111:93-108; Pela R, et al. Respiration. 1999 Nov-Dec;66(6):495-500; van Overveld FJ, et al. Inflamm Res. 2000 Jan;49(1):8-13.)
Omega-3 fatty acids: flaxseed oil, 2 Tbsp once daily.
NOTE: Rule out cadmium toxicity and allergy. (Marz R. 324, 1997.)
footnotes
[No author listed.] Preliminary study on the relation between allergy and chronic bronchitis. Chin Med J 1976;2:63-68.
Abrahamson EL, Viswanath M, Kovar IZ, Jawad SA. Unilateral pulmonary interstitial emphysema and treatment with colfosceril palmitate. Lancet. 1993 Jun 19;341(8860):1603.
Alatyrtseva SG, Pukhovskaia NV. [Surfactant and its role in the pathogenesis of lung diseases]. Vopr Okhr Materin Det. 1973 Oct;18(10):51-55. Review) [Article in Russian]
Boman G, Bäcker U, Larsson S, et al. Oral acetylcysteine reduces exacerbation rate in chronic bronchitis: a report of a trial organized by the Swedish Society for Pulmonary Diseases. Eur J Respir Dis 1983;64:405-415.
Businco L, Businco E. Allergic pathogenesis in chronic bronchitis. Allergol Immunopathol (Madr) 1975 Jan-Feb;3(1):1-8.
Abstract: Chronic bronchitis is a disease related to numerous etiologic factors: infections, climate influence, air pollution, cigarette smoking, etc. From a pathogenetic point of view, chronic bronchitis is generally considered as the phlogistic resultant of various irritative conditions, with a characteristic neutrophil component in the phlogistic pattern. Microbic involvement has up to now been considered a very important factor, with consequent wide utilization of antibiotic agents in basic therapy. Considerations of clinical nature induced us to consider unsatisfactory such pathogenetic concepts based on neutrophil phlogosis, while the involvement of an allergic mechanism became more acceptable. In order to solve this problem, we have carried out hitological studies on postmortem material from the respiratory tract of individuals whose death was attributable to chronic bronchitis or to concurrent chronic bronchitis. Results of our study conducted up to now on 60 cases may be summarized as follows: Bronchitis with lymphomonoplasmacytoid phlogosis of immunoallergic type (60%), bronchitis with neutrophil phlogosis of irritative-infective type (20%); bronchitis with mixed allergic-neutrophil phlogosis (20%). Lymphocytes, monocytes and plasma cells are directly involved in allergic tissue reactions, both of immediate and delayed type because they release active substances such as hsitamine, bradyquinine, quinine, etc., which will their multiple pharmacodynamic actions are responsible of various anatomic and functional changes in hypersensitivity. Infiltration of the bronchial mucosa with lymphomonoplasmacytary cells in chronic bronchitis, has a pattern of mixed allergic phlogosis of immediate and delayed type. Prophylaxis and management of chronic bronchitis should therefore be set up on new bases, with the various treatments used for hyperactive pathology.
Dal Negro R, Pomari G, et al. L-carnitine and rehabilitative respiratory physiokinesitherapy: metabolic and ventilatory response in chronic respiratory insufficiency. Int J Clin Pharmacol Ther Toxicol 1986;24:453-456.
Dal Negro R, Turco P, Pomari C, De Conti F. Effects of L-carnitine on physical performance in chronic respiratory insufficiency. Int J Clin Pharmacol Ther Toxicol 1988;26:269-272.
Eiserich JP, van der Vliet A, Handelman GJ, Halliwell B, Cross CE. Dietary antioxidants and cigarette smoke-induced biomolecular damage: a complex interaction. Am J Clin Nutr. 1995 Dec;62(6 Suppl):1490S-1500S.
Abstract: Epidemiologic evidence suggests that cigarette smoking is a major risk factor for chronic obstructive pulmonary diseases such as chronic bronchitis and emphysema, for carcinogenesis, and for cardiovascular disease. However, the precise mechanisms of these effects are incompletely understood. The gas phase of cigarette smoke contains abundant free radicals including nitric oxide. Hence, cigarette smoke may induce some of its damaging effects by free radical mechanisms. We report that exposure of plasma, a model for respiratory tract lining fluids, to gas-phase cigarette smoke causes depletion of antioxidants, including ascorbate, urate, ubiquinol-10, and alpha-tocopherol, and a variety of carotenoids, including beta-carotene. Gas-phase cigarette smoke induced some lipid peroxidation, as measured by cholesteryl linoleate hydroperoxide (18:2OOH) formation. Ascorbate was effective in preventing 18:2OOH formation. In contrast to the low concentrations of lipid hydroperoxides measured (< 1 mumol/L), protein carbonyl formation, a measure of protein modification, increased by approximately 400 mumol/L after nine puffs of cigarette smoke. Reduced glutathione inhibited protein carbonyl formation, whereas other plasma antioxidants, including ascorbate, were ineffective. alpha, beta-Unsaturated aldehydes (acrolein and crotonaldehyde) in cigarette smoke may react with protein -SH and -NH2 groups by a Michael addition reaction that results in a protein-bound aldehyde functional group. Gas-phase cigarette smoke is capable of converting tyrosine to 3-nitrotyrosine and dityrosine, indicating free radical mechanisms of protein damage by nitrogen oxides. Aldehydes and nitrogen oxides in cigarette smoke may be significant contributors to biomolecular damage, and endogenous antioxidants can attenuate some of these adverse effects.
Efthimiou J, Mounsey PJ, Bensen DN, et al. Effect of carbohydrate rich versus fat rich loads on gas exchange and walking performance in patients with chronic obstructive lung disease. Thorax 1992;47:451-456.
Fiaccadori E, Del Canale S, Coffrini E, et al. Hypercapnic-hypoxemic chronic obstructive pulmonary disease (COPD): influence of severity of COPD on nutritional status. Am J Clin Nutr 1988;48:680-685.
Fiaccadori E, Del Canale S, Coffrini E, et al. Muscle and serum magnesium in pulmonary intensive care unit patients. Crit Care Med 1988;16:751-760.
Fujimoto S, Kurihara N, Hirata K, Takeda T. Effects of coenzyme Q10 administration on pulmonary function and exercise performance in patients with chronic lung diseases. Clin Investig 1993;71(8 Suppl):S162-S166.
Abstract: Serum coenzyme Q10 (CoQ10) levels were measured at rest and during incremental exercise in 21 patients with chronic obstructive pulmonary disease (COPD) and 9 patients with idiopathic pulmonary fibrosis (IPF). The mean serum CoQ10 levels at rest in patients with COPD and IPF were 0.56 +/- 0.20 and 0.45 +/- 0.16 microgram/ml, respectively. In both groups these levels were decreased compared with those of healthy subjects. In the patients with COPD, CoQ10 levels were significantly correlated with body weight, however, there was no correlation between CoQ10 levels and ventilatory function, PaO2, VO2/kg at rest, or maximal VO2. In eight of nine patients whose PaO2 at rest was lower than 75 torr, serum CoQ10 levels were lower than 0.5 microgram/ml. We studied the effects of the oral administration of CoQ10 at 90 mg/day for 8 weeks on pulmonary function and exercise performance in eight patients with COPD. Serum CoQ10 levels were significantly elevated in association with an improvement in hypoxemia at rest, whereas pulmonary function was unaltered. Oxygen consumption during exercise was not changed, whereas PaO2 was significantly improved, and heart rate was significantly decreased compared with the results obtained at an identical workload at baseline. Furthermore, lactate production was suppressed during the anaerobic exercise stage after CoQ10 administration, and exercise performance tended to increase. These data suggested that CoQ10 has favorable effects on muscular energy metabolism in patients with chronic lung diseases who have hypoxemia at rest and/or during exercise.
Krawczyk Z. Role of allergy of the immediate type in the pathogenesis of chronic bronchitis in adults. Penumonol Pol 1976;44:829-836. [Article in Polish]
Merritt TA, Hallman M, Berry C, Pohjavuori M, Edwards DK 3d, Jaaskelainen J, Grafe MR, Vaucher Y, Wozniak P, Heldt G, et al. Randomized, placebo-controlled trial of human surfactant given at birth versus rescue administration in very low birth weight infants with lung immaturity. J Pediatr. 1991 Apr;118(4 ( Pt 1)):581-594.
Miedema I, Feskens EJM, Heederik D, et al. Dietary determinants of long-term incidence of chronic nonspecific lung diseases. Am J Epidemiol 1993;138:37-45.
Multicenter Study Group. Long-term oral acetylcysteine in chronic bronchitis. A double-blind controlled study. Eur J Respir Dis 1980;61:111:93-108.
Okayama H, Aikawa T, Okayama M, et al. Bronchodilating effect of intravenous magnesium sulfate in bronchial asthma. JAMA 1987;257:1076-1078.
Pela R, Calcagni AM, Subiaco S, Isidori P, Tubaldi A, Sanguinetti CM. N-Acetylcysteine reduces the exacerbation rate in patients with moderate to severe COPD. Respiration. 1999 Nov-Dec;66(6):495-500.
Pingleton SK, Harmon GS. Nutritional management in acute respiratory failure. JAMA 1987;257(22):3094-3099.
Rautalahti M, Virtamo J, Haukka J, Heinonen OP, Sundvall J, Albanes D, Huttunen JK. The effect of alpha-tocopherol and beta-carotene supplementation on COPD symptoms. Am J Respir Crit Care Med. 1997 Nov;156(5):1447-1452.
Abstract: The effects of alpha-tocopherol (50 mg/d) and beta-carotene (20 mg/d) supplementation on symptoms of chronic obstructive pulmonary disease were studied among the 29,133 participants of the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study undertaken to investigate the effects of these two substances in the prevention of lung and other cancers. During the follow-up the supplementations did not affect the recurrence or incidence of chronic cough, phlegm, or dyspnea. The prevalence of chronic bronchitis and dyspnea at baseline was lower among those with high dietary intake of beta-carotene (OR = 0.78 and 0.67, respectively) or vitamin E (OR = 0.87 and 0.77) and high serum beta-carotene (OR = 0.59 and 0.62) and alpha-tocopherol (OR = 0.76 and 0.82). High intake and serum levels of retinol were associated with low prevalence of dyspnea (OR = 0.84 and 0.80, respectively) but not with chronic bronchitis. The results indicate no benefit from supplementation with alpha-tocopherol or beta-carotene on the symptoms of chronic obstructive pulmonary disorders but support the beneficial effect of dietary intake of fruits and vegetables rich in these compounds.
Rolla G, Bucca C, Bugiani M, et al. Hypomagnesiumia in chronic obstructive lung disease: effect of therapy. Magnesium Trace Elem 1990;9:132-136.
Rowe AH, Rowe A Jr, Sinclair C. Food allergy: its role in the symptoms of obstructive emphysema and chronic bronchitis. J Asthma Res 1967;5:11-20.
Rowe AH. Food allergy: its role in emphysema and chronic bronchitis. Dis Chest 1965;48:609.
Satta A, Grandi M, Landoni CV, Migliori GB, Spanevello A, Vocaturo G, Neri M. Effects of ubidecarenone in an exercise training program for patients with chronic obstructive pulmonary diseases. Clin Ther. 1991 Nov-Dec;13(6):754-757.
Abstract: A study was undertaken to determine the usefulness of ubidecarenone in pulmonary rehabilitation in exercise training programs in the management of chronic obstructive pulmonary disease (COPD). The subjects were 20 patients with COPD who had been participating in an exercise training program for at least four weeks. The patients were randomly assigned either to receive 50 mg of oral ubidecarenone daily or to enter a control group during the program. Oxygen consumption, expired volume, and heart rate were measured during exercise tests before and after training. Maximum oxygen consumption increased 13% in the ubidecarenone-treated patients and 7% in the controls, and maximum expired volume increased 10% in each group. The increases were significant in the ubidecarenone group but not in the controls. Heart rate increased 2% in both groups. It is concluded that ubidecarenone deserves further evaluation in exercise training programs for patients with COPD.
Shahar E, Folsom AR, Melnick SL, et al. Dietary n-3 polyunsaturated fatty acids and smoking-related chronic obstructive pulmonary disease. Atherosclerosis Risk in Communities Study Investigators. N Engl J Med 1994;331:228-233.
Skorodin MS, Tenholder MF, Yetter B, et al. Magnesium sulfate in exacerbations of chronic obstructive pulmonary disease. Arch Intern Med 1995;155:496-500.
Sridhar MK. Nutrition and lung health. Brit Med J 1995;310:75-76.
Theron A, Anderson R. Investigation of the protective effects of the antioxidants ascorbate, cysteine, and dapsone on the phagocyte-mediated oxidative inactivation of human alpha-1-protease inhibitor in vitro. Am Rev Respir Dis. 1985 Nov;132(5):1049-1054.
van Overveld FJ, Vermeire PA, De Backer WA. Induced sputum of patients with chronic obstructive pulmonary disease (COPD) contains adhesion-promoting, therapy-sensitive factors. Inflamm Res. 2000 Jan;49(1):8-13.
Abstract: OBJECTIVE: The aim of this study was to investigate whether sputum of COPD patients before and after treatment with inhaled corticosteroids (IHC) or N-acetylcysteine (NAC) exerts any effect on the adhesion of isolated polymorphonuclear cells (PMNs) to cultured endothelial cells. METHODS: A human endothelial cell line was grown to confluence before use in adhesion experiments. PMNs were obtained from normal, non-smoking volunteers and preincubated (30 min, 37 degrees C) with diluted sputum sol obtained from COPD patients before the cells were put on the endothelial cells. RESULTS: Basal adhesion of unstimulated PMNs after 30 min at 37 degrees C in 5% CO2 was 15.9+/-1.1% (mean +/- SEM, n = 9). A significant enhancement of the adhesion to 33.0+/-1.4% (n = 11, P<0.0001) was observed with sputum obtained from COPD patients before treatment with IHC, and 34.6+/-1.5% (n = 10, P<0.0001) before treatment with NAC. Administration of IHC for 8 weeks resulted in an adhesion of 27.7+/-2.4%, which is an inhibition of 31% (n = 11, P<0.05). However, treatment for 8 weeks with NAC showed no change in the adhesion of stimulated PMNs. Long-term treatment with NAC showed a gradual decrease of adhesion (n = 9, P<0.05), whereas long-term treatment with IHC lead to an increase in adhesion (n = 10, P<0.02). CONCLUSIONS: These results indicate that factors locally produced in the airways of COPD patients may promote adhesion of neutrophils to endothelium. They further suggest that glucocorticoids may only have a short-term transient effect on adhesion, whereas NAC showed effects on the adhesion after administration for longer periods.
Van Schayck CP, Dekhuijzen PNR, Gorgels WJMJ, et al. Are anti-oxidant and anti-inflammatory treatments effective in different subgroups of COPD? A hypothesis. Respir Med 1998;92:1259-1264.