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et al., 2007) found that consumption of diet rich in cocoa, but not tea drinking, reduced blood pressure, confirming the potential favourable effect of polyphenols and other food components derived from cocoa and cocoa extracts on risk of cardiovascular diseases. However, the possible association between consumption of chocolate and risk of cardiovascular disease has not been adequately studied. To our knowledge, only a cohort study based on 470 men and 314 deaths, including 152 deaths for cardiovascular disease, analysed the issue (Buijsse et al., 2006). That study showed an inverse association between cocoa intake and blood pressure, cardiovascular and all cause mortality (Buijsse et al., 2006). We investigated the issue considering data from a case control study on acute myocardial infarction (AMI), including a specific question on consumption of chocolates and bars of chocolate (Tavani et al., 2006). Between 1995 and 2003, we conducted a casecontrol study on AMI in greater Milan, Italy (Tavani et al., 2006). Cases were 760 patients (580 men and 180 women) in hospital with a first episode of non-fatal AMI, and controls were 682 patients (439 men and 243 women), admitted to the same hospitals for acute conditions unrelated to AMI risk factors (30% traumas, 25% non-traumatic orthopaedic disorders, 18% surgical conditions, 18% eye, nose, throat or teeth disorders and 9% miscellaneous other illnesses unrelated to diet). Information on diet was based on a reproducible and validated food frequency questionnaire (FFQ) (Tavani et al., 2006). The odds ratios (OR) and corresponding 95% confidence intervals (CI) were derived by unconditional multiple logistic regression models after allowance for age, sex, education, diabetes, obesity, hypertension, hyperlipidaemia, cholesterol level, body mass index, cigarette smoking, alcohol and coffee drinking, and family history of AMI in first-degree relatives. Compared to the consumption of o2 chocolates per day, the multivariate OR was 0.49 (95% CI: 0.221.10) for 2, and 0.23 (95% CI: 0.080.65) for X3 chocolates/day (w2 trend 10.57, P 0.001). The OR for an increment of one chocolate per day was 0.81 (95% CI: 0.690.96). In our study, the FFQ was satisfactorily valid and reproducible (Spearmans correlation coefficient for intake frequency of chocolate consumption was 0.47), cases and controls were interviewed in the same hospitals and came from the same geographic area, participation was over 95%, and a different recall of chocolate consumption on the basis of the disease status is unlikely. These data confirm findings from small intervention studies showing that cocoa-containing foods protect against cardiovascular mortality (Buijsse et al., 2006; Taubert et al., 2007). S Gallus1, A Tavani1 and C La Vecchia1,2 Istituto di Ricerche Farmacologiche Mario Negri, Via La Masa 19, Milan, Italy and 2Istituto di Statistica Medica e Biometria, ` Universita degli Studi di Milano, Milan, Italy E-mail: gallus@marionegri.it

References
Buijsse B, Feskens EJ, Kok FJ, Kromhout D (2006). Cocoa intake, blood pressure, and cardiovascular mortality: the Zutphen Elderly Study. Arch Intern Med 166, 411417. Strandberg TE, Strandberg AY, Pitkala K, Salomaa VV, Tilvis RS, Miettinen TA (2008). Chocolate, well-being and health among elderly men. Eur J Clin Nutr 62, 247253. Taubert D, Roesen R, Schomig E (2007). Effect of cocoa and tea intake on blood pressure. Arch Intern Med 167, 626634. Tavani A, Gallus S, Negri E, Parpinel M, La Vecchia C (2006). Dietary intake of carotenoids and retinol and the risk of acute myocardial infarction in Italy. Free Radic Res 40, 659664.

Efficacy of magnesium in children with bronchial asthma

European Journal of Clinical Nutrition (2009) 63, 589590; doi:10.1038/sj.ejcn.1602947; published online 7 November 2007
I was pleased to read the original article entitled Oral magnesium supplementation in asthmatic children: a double-blind randomized placebo-controlled trial published in the European Journal of Clinical Nutrition in 2007 (61:5460) of a Brazilian group directed by Professor Gontijo-Amaral. Their conclusion was that the oral magnesium (Mg) supplementation helped to reduce bronchial reactivity to metacholine, to diminish the allergen-induced skin responses and to provide better symptom control in pediatric patients with moderate persistent asthma treated with inhaled fluticasone. The authors have mentioned that their study was the first performed in children aiming to investigate the effects of oral magnesium given on a regular basis. Let me bring to your notice that our paper entitled Urinary magnesium excretion in asthmatic children receiving magnesium supplementation: a randomized, placebo-controlled, double-blind study was published in Magnesium Research in 2003 (16 (4):262270). The aim of our study was to establish whether a Mg deficit is indicated by a decreased urinary Mg excretion and to determine whether continuous oral Mg European Journal of Clinical Nutrition

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supplementation over a 12-week period affects the Mg status, bronchodilator use, clinical symptoms and lung function in 89 randomized atopic children aged 416 years with stable bronchial asthma. The investigation ran over three 4-week treatment periods. During an initial 4-week period and the treatment period, the children ate their normal diet and short-term inhaled b2mimetics were administered if necessary. All of the patients met the inclusion criteria. At each visit they received placebo or Mg capsules according to a randomized, double-blinded protocol for the next 4-week period. The Mg intake was predetermined according to age within the groups. Children p7 years old received 200 mg, and children 47 years old received 290 mg Mg citrate daily (National Research Council (US), 1989), or 260 mg glucose as a placebo, in capsule form each evening. A significant decrease in daytime symptoms was experienced at 8 weeks in the Mg-treated patients which persisted at the end of the study. The bronchodilator was used significantly more often after 8 and 12 weeks in the placebo groups than in the Mg-treated patients with moderate asthma. We evaluated the alteration of the forced expiratory volume in 1 second (FEV1) during the study. FEV1 was significantly increased in the Mg group at 4 weeks and even higher at 12 weeks. Almost in parallel, a significant increase in FEV1 was also observed in the placebo-treated group at 8 weeks, which persisted at the end of the study. Magnesium deficiency resulting from an insufficient Mg intake develops in placebo-treated children with moderate asthma. In addition, b2-mimetic use proved significantly more frequent in placebo-treated than in Mg-treated moderately asthmatic children. b-Adrenergic agonists can stimulate Mg efflux in peripheral tissues (Khilnani et al., 1992; Romani and Scarpa, 1992; Ianello et al., 1998), which can aggravate the Mg deficit of the cells indicating a certain degree of Mg depletion. Determination of the 24-h urine Mg excretion is an important and simple way to assess a Mg deficiency. A suboptimal intake of dietary nutrients such as Mg was recently recognized to be a potential risk factor for asthma, especially in childhood (Baker and Ayres, 2000; Hijazi et al., 2000). Our study demonstrated that a large oral dose of Mg (with an atoxic nature) did not cause any disturbances. The Mg requirements may be greater in growing children, especially those with asthma. O Bede rgyi Medical Department of Paediatrics, Albert Szent-Gyo d, University of Szeged, Csongra Hungary E-mail: bedeolga@pedia.szote.u-szeged.hu

References
Baker JC, Ayres JG (2000). Diet and asthma. Respir Med 94, 925934. Hijazi N, Abalkhail B, Seaton A (2000). Diet and childhood asthma in a society in transition: a study in urban and rural Saudi Arabia. Thorax 55, 775779. Ianello S, Spina M, Leotta P (1998). Hypomagnesemia and smooth muscle contractility: diffuse oesophageal spasm in an old female patient. Miner Electrolyte Metab 24, 348356, (abstract). Khilnani G, Parchani H, Toshnival G (1992). Hypomagnesemia due to beta 2-agonist in bronchial asthma. J Assoc Physicians India 40, 346. (abstract). National Research Council (US) (1989). Recommended Dietary Allowances 10th edn. National Academy Press: Washington, DC, USA. Romani A, Scarpa A (1992). Regulation of cell magnesium. Arch Biochem Biophys 298, 112.

European Journal of Clinical Nutrition