- Email: [email protected]
Comment to: Luo et al. (2013) Int J Cardiol. 168(4):4454–6
512
Letters to the Editor
Fig. 1 A. Mother's transesophageal echocardiogram showing supraaortic stenosis. B: Cardiac CT showing supraaortic stenosis (arrow). C and D: Transthoracic echocardiogram in her oldest son revealed supraaortic stenoisis with maximum gradient of 118 mmHG.
0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.01.050
Comment to: Luo et al. (2013) Int J Cardiol. 168(4):4454–6 Cidália Dionísio Pereira a, Maria Carmen Collado b, Emanuel Passos a,c, Isabel Azevedo a, Rosário Monteiro a, Maria João Martins a,⁎ a b c
Department of Biochemistry (U38/FCT), Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal Institute of Agrochemistry and Food Technology, Spanish National Research Council (IATA-CSIC), Department of Biotechnology, 46980 Paterna, Valencia, Spain Research Centre in Physical Activity, Health and Leisure, Faculty of Sport, University of Porto, 4200-450 Porto, Portugal
a r t i c l e
i n f o
Article history: Received 9 January 2014 Accepted 10 January 2014 Available online 23 January 2014 Keywords: Mineral-rich water Minerals Fructose Metabolic syndrome Cardiovascular disease
Luo et al. [1] interestingly demonstrated in International Journal of Cardiology (October issue) that consumption of low-mineral bottled ⁎ Corresponding author. Tel.:/fax: 351 22 5513624. E-mail address: [email protected] (M.J. Martins).
water is associated with the increase of cardiovascular disease risk biomarkers, namely pathological lesions in the heart and aortic arch in rabbits and increased serum homocysteine levels and worsening of lipid profile in men. As stressed by Luo et al., there is not enough valid scientific evidence on the impact of water-supplied minerals on the human health. Nevertheless, natural mineral-rich waters are excellent sources of highly bioavailable minerals [2,3]. Adding to Luo et al.'s results, low-mineral intake is acknowledged as a factor associated with Metabolic Syndrome (MetSyn) increasing incidence [4]. In fact, high-energy density Western-diets, rich in sugars and fats, possess low-mineral content [4]. As widely studied, MetSyn is a risk factor for cardiovascular disease. Regarding natural mineral-rich water ingestion, some data highlight beneficial effects on MetSyn isolated parameters [5–8], but not in the MetSyn itself. The consumption of sodium bicarbonate containing/ rich mineral waters decreased systolic blood pressure in mildly hypertensive men (3 L/day, 7 days) [6] and mean arterial blood pressure in elderly normotensive individuals (1.5 L/day, 4 weeks) [8].
Letters to the Editor
Additionally, the ingestion of natural mineral water, sulfate, calcium, magnesium and bicarbonate-rich (at least 1 L/day, 2–4 weeks), reduced systolic and diastolic blood pressure in adults with borderline hypertension and low urinary magnesium and calcium excretion levels [7]. Vaquero et al. showed that, in moderately hypercholesterolemic young adults, the ingestion of bicarbonated natural mineral water, rich in sodium, chloride and potassium (1 L/day, 8 weeks), reduced systolic blood pressure (an effect already seen after 4 weeks), apolipoprotein-B, total-cholesterol and LDL-cholesterol fasting serum levels as well as total-cholesterol and LDL-cholesterol to HDLcholesterol ratios [6]. The same group showed, in healthy postmenopausal women, that a) the ingestion of the previous water (1 L/day, 2 months), increased HDL-cholesterol and decreased endothelial dysfunction markers, glucose, total-cholesterol and LDL-cholesterol fasting serum levels as well as total-cholesterol and LDL-cholesterol to HDL-cholesterol ratios, and b) the consumption of sodium bicarbonate-rich mineral waters (0.5 L each) with a standard fatrich meal decreased postprandial insulin levels (more distinctly in women with higher homeostasis model assessment index values) and lipemia [6]. Both a decrease in lipid and protein oxidation products and an increment of total antioxidant capacity and total thiol plasma levels were observed in healthy individuals drinking a sulfurous mineral water (0.5 L/day, 2 weeks) [5]. Given the current scenario, and using an opposite approach than that applied by Luo et al., we focused on the possible beneficial effects of the intake of natural mineral-rich water (MW) on the development or aggravation of MetSyn features. We used adult Sprague–Dawley male rats drinking 10% (w/v) fructose (F) solution (well-validated MetSyn animal model), either in tap water (TW; total mineralization: 148–151, sodium: 200, calcium: 30.5–40.2, magnesium: 3.6–9.2, potassium: 2.6 and chloride: 250 mg/L) or MW [2855, 591, 92.5, 26.2, 29.9, 30.8 (respectively) and bicarbonate 2013 mg/L]; controls drank tap water. All groups (7 rats each) ingested pellet food (2014 Teklad Global 14% Protein, Harlan Interfauna Iberica, Spain) ad libitum for 8 weeks. MW-supplementation reduced the magnitude of the increasing effect seen in TW + F-treated animals versus controls on heart rate and plasma triacylglycerols, insulin and leptin levels (along with a reduction of the strong decreasing tendency of the insulinsensitivity index). In MW + F-treated animals, no significant differences occurred versus controls. MW intake was also able to reduce the alterations found in hepatic oxidative stress biomarkers induced by F-treatment, which resulted in increased catalase activity and reduced glutathione peroxidase activity and oxidized glutathione content [9]. The deleterious effects observed in hepatic and adipose tissue glucocorticoid and insulin signaling-pathways of TW + F-treated animals versus controls were prevented/counteracted by MW-supplementation, which also induced metabolically beneficial stress pathways (Table 1, data under review). Regarding endothelial dysfunction, MW-supplementation increased smooth muscle cell proportion and tended to increase sirtuin 1 expression in the erectile tissue, in comparison with TW + F and/or control rats [10]. As widely known, menopause substantially increases MetSyn incidence; obesity is a relevant cardiovascular risk factor in both. So, we extended our research to adult Sprague–Dawley ovariectomized (O) female rats (5 groups of 6 rats each): sham-operated, TW or MW-treated O rats, with or without F, for 10 weeks, regarding feces microbiome and short chain fatty acids (SCFA) composition/levels. Higher Firmicutes to Bacteroidetes ratio has been associated with obesity in mice and humans [11] and higher levels of SCFA occur in obese individuals [12]. Lower levels of Bacteroidetes and higher levels of Proteobacteria, Actinobacteria and TM7 occurred in TW-O rats and higher levels of Firmicutes and lower levels of Bacteroidetes were observed in TW-OF versus sham-operated rats. In general, MW turned back changes in TW-O and TW-OF groups, more clearly and
513
Table 1 Hepatic and adipose tissue glucocorticoid and insulin signaling-pathways evaluation by Western blot in fructose-treated groups compared to controls. Tissue
Glucocorticoid and insulin signaling-pathways
TW-F
MW-F
Global P
Liver
PGC1-α Sirt1 p-IRS1 IRS1 p-IRS1/IRS1 p-JNK JNK p-ERK/ERK ERK GR
↓↓ ↓↓ ↓↓ t↓ t ↓↓ t↑ ↓↓ t↑ ↑↑ ↔
t↓ ↑↑ t↓ t↓ t↓ ↔ ↔ ↑↑ t↑ ↑↑
0.004 b0.001 0.005 0.056 0.078 0.058 b0.001 0.009 0.016 0.009
Visceral adipose tissue
↓↓ and ↑↑: significant decrease or increase versus control; t ↓↓: tendency to decrease versus control; t ↓ and t ↑: slight decrease or increase versus control; ↔: no effect; ERK: extracellular-signal related kinase; GR: glucocorticoid receptor; IRS1: insulin receptor substrate 1; JNK: C-jun N-terminal kinase; MW-F: 10% fructose/mineral water; p-ERK: phosphorylated extracellular-signal related kinase; p-IRS1: phosphorylated insulin receptor substrate 1; p-JNK: phosphorylated C-jun N-terminal kinase; PGC1-α: peroxisome proliferator-activated receptor gamma coactivator 1-alpha; Sirt1: sirtuin 1; TW-F: 10% fructose/tap water.
relevantly in the latter. TW-OF showed the highest Firmicutes to Bacteroidetes ratio compared to the other groups, while MWsupplementation reduced this ratio in TW-OF and TW-O groups. Sham-operated rats showed the lowest ratio, with no difference observed versus MW-O rats. The Principal Coordinates Analysis differentiated MW from TW groups, sham-operated rats microbiota being similar to MW groups (MW-O and MW-OF) microbiota. On the other hand, MW reduced total SCFA levels observed in the TWOF model. MW groups showed a tendency for lower body weight increase than the corresponding TW groups, more evidently in Ftreated rats. In conclusion, and reinforcing Luo et al.'s findings, drinking water mineral content appears as a subject of high relevance for health, natural mineral-rich waters probably constituting a valuable resource to reduce the risk of cardiovascular disease.
References [1] Luo J, Zhao Q, Zhang L, et al. The consumption of low-mineral bottled water increases the risk of cardiovascular disease: an experimental study of rabbits and young men. Int J Cardiol 2013;168:4454–6. [2] Bohmer H, Muller H, Resch KL. Calcium supplementation with calcium-rich mineral waters: a systematic review and meta-analysis of its bioavailability. Osteoporos Int 2000;11:938–43. [3] Karagulle O, Kleczka T, Vidal C, et al. Magnesium absorption from mineral waters of different magnesium content in healthy subjects. Forsch Komplementmed 2006;13:9–14. [4] Odermatt A. The Western-style diet: a major risk factor for impaired kidney function and chronic kidney disease. Am J Physiol Renal Physiol 2011;301:F919–31. [5] Benedetti S, Benvenuti F, Nappi G, et al. Antioxidative effects of sulfurous mineral water: protection against lipid and protein oxidation. Eur J Clin Nutr 2009;63:106–12. [6] Perez-Granados AM, Navas-Carretero S, Schoppen S, Vaquero MP. Reduction in cardiovascular risk by sodium-bicarbonated mineral water in moderately hypercholesterolemic young adults. J Nutr Biochem 2010;21:948–53. [7] Rylander R, Arnaud MJ. Mineral water intake reduces blood pressure among subjects with low urinary magnesium and calcium levels. BMC Public Health 2004;4:56. [8] Schorr U, Distler A, Sharma AM. Effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and metabolic parameters in elderly normotensive individuals: a randomized double-blind crossover trial. J Hypertens 1996;14:131–5. [9] Pereira CD, Severo M, Araújo JR, et al. Relevance of a hypersaline sodium-rich naturally sparkling mineral water to the protection against metabolic syndrome induction in fructose-fed Sprague–Dawley rats: a biochemical, metabolic, and redox approach. Int J Endocrinol 2014, http://dx.doi.org/ 10.1155/2014/384583. [10] Pereira CD, Severo M, Rafael L, Martins MJ, Neves D. Effects of natural mineral-rich water consumption on the expression of sirtuin 1 and angiogenic factors in the erectile tissue of rats with fructose-induced metabolic syndrome. Asian J Androl 2014, http://dx.doi.org/10.4103/1008-682X.122869.
514
Letters to the Editor
[11] Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Microbial ecology: human gut microbes associated with obesity. Nature 2006;444:1022–3.
[12] Schwiertz A, Taras D, Schafer K, et al. Microbiota and SCFA in lean and overweight healthy subjects. Obesity (Silver Spring) 2010;18:190–5.
0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.01.044
Renin–aldosterone paradox in patients with myalgic encephalomyelitis and orthostatic intolerance Kunihisa Miwa a,⁎, Masatoshi Fujita b a b
Department of Internal Medicine, Miwa Naika Clinic, Toyama, Japan Department of Cardiology, Uji Hospital, Kyoto, Japan
a r t i c l e
i n f o
Article history: Received 6 January 2014 Accepted 10 January 2014 Available online 23 January 2014 Keywords: Chronic fatigue syndrome Orthostatic intolerance Myalgic encephalomyelitis Small heart Low cardiac output Aldosterone
The etiology of chronic fatigue syndrome (CFS) is unknown. Recent studies have confirmed that almost 90% of CFS patients experience symptoms related to orthostatic intolerance (OI), which primarily predicts functional capacity in CFS [1]. Many symptoms of OI appear to be related to reduced cerebral blood flow. Also a small heart with low cardiac output has been reported to be common in CFS patients [2–4]. Recently, central nervous dysfunction due to myalgic encephalomyelitis (ME) has been postulated to be the cause of CFS. The International Consensus Criteria for ME differentiate patients with ME from those who are depressed and identify patients who are more physically debilitated and have greater physical and cognitive impairments [5]. Impaired activation of renin– aldosterone system may be included in the pathophysiology of ME. ME was diagnosed according to the International Consensus Criteria proposed by the International Consensus Panel in 2011 [5]. Plasma renin activity and aldosterone concentrations were determined in 10 ME patients (group ME), compared to 10 sedentary control subjects (Controls). All the ME patients complained of symptoms of OI, which was defined as the instability to maintain normal consciousness without significant symptoms such as disabling fatigue, dizziness, diminished concentration, tremulousness, sweating, light-headedness, visual disturbance, palpitations and nausea during upright position. Left ventricular (LV) morphology and function were determined echocardiographically. All of the study participants gave informed consent, and the study protocol conformed to the ethical guidelines of the 1975 Declaration of Helsinki and was approved by the ethics committee at our institution. All the study ME patients underwent a conventional active standing test. After a 10-min period of rest in the supine position, patients were asked to stand up actively by themselves and keep upright for 10 min. A total of 3 patients stopped before completing the conventional 10-min ⁎ Corresponding author at: Department of Internal Medicine, Miwa Naika Clinic, 1-43 Shintomicho, Toyama 930-0002, Japan. Tel.: +81 76 482 3014; fax: +81 76 482 3016. E-mail address: [email protected] (K. Miwa).
standing test complaining OI. Of these patients, 2 had neurally mediated hypotension and the other 1 had delayed orthostatic hypotension. The other 7 patients completed the standing test despite moderate symptoms of OI. Postural orthostatic tachycardia syndrome (POTS) with an increase of pulse rate ≥30 beats/min was diagnosed in 4 of the patients. The mean cardiothoracic ratio, systolic and diastolic blood pressures, LV end-diastolic dimension, stroke volume, cardiac output and index, and LV mass index were all significantly smaller in ME than in Controls (Table 1). The mean values of heart rate, fractional shortening and LV ejection fraction were comparable between the groups. As shown in Table 1 and Fig. 1, there was no significant difference in plasma renin activity between ME and Controls. The mean plasma aldosterone concentration was significantly lower in ME than in Controls. There was no significant difference in the mean serum K level between the two groups (ME: 4.0 ± 0.6 vs. Controls: 4.2 ± 0.3 mEq/L, p = 0.20). However, the mean serum Na level was significantly higher in ME than in Controls (143 ± 1 vs. 141 ± 1 mEq/L, p = 0.001). It has been reported that patients with OI have deficits in their blood volume and some patients improve their symptoms after acute or chronic plasma volume expansion [6]. In response to hypovolemia, plasma renin activity and aldosterone concentration would be expected to increase to
Table 1 Hemodynamic and echocardiographic data of the study subjects.
Number of patients Male/female Age (years) Cardiothoracic ratio (%) Heart rate (beats/min) Systolic blood pressure (mm Hg) Diastolic blood pressure (mm Hg) IVST (mm) PWT (mm) LVEDD (mm) LVESD (mm) LAD (mm) AoD (mm) RVD (mm) Stroke volume (mL) Stroke volume index (mL/m2) Cardiac output (L/min) Cardiac index (L/min/m2) Fractional shortening (%) LV ejection fraction (%) LV mass index (g/m2)
Controls
ME
p value
10 3/7 33 ± 12 43 ± 3 70 ± 9 120 ± 11 75 ± 7 8±1 8±1 47 ± 2 28 ± 2 28 ± 5 27 ± 4 16 ± 4 72 ± 9 41 ± 5 5.1 ± 1.2 2.9 ± 0.5 40 ± 3 71 ± 3 73 ± 19
10 3/7 31 ± 9 40 ± 3 68 ± 13 108 ± 12 66 ± 8 7±1 7±1 43 ± 5 26 ± 4 25 ± 4 26 ± 4 15 ± 3 57 ± 13 35 ± 8 3.8 ± 0.6 2.3 ± 0.3 39 ± 6 69 ± 7 58 ± 13
0.60 0.047 0.63 0.02 0.04 0.24 0.91 0.02 0.27 0.24 0.52 0.60 0.009 0.06 0.004 0.005 0.58 0.51 0.02
CTR: cardiothoracic ratio; IVST: interventricular septum thickness; PWT: left ventricular (LV) posterior wall thickness; LVEDD: LV end-diastolic dimension; LVESD: LV end-systolic dimension; LAD: left atrial dimension; AoD: aortic root dimension; RVD: right ventricular dimension.
Letters to the Editor
Fig. 1 A. Mother's transesophageal echocardiogram showing supraaortic stenosis. B: Cardiac CT showing supraaortic stenosis (arrow). C and D: Transthoracic echocardiogram in her oldest son revealed supraaortic stenoisis with maximum gradient of 118 mmHG.
0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.01.050
Comment to: Luo et al. (2013) Int J Cardiol. 168(4):4454–6 Cidália Dionísio Pereira a, Maria Carmen Collado b, Emanuel Passos a,c, Isabel Azevedo a, Rosário Monteiro a, Maria João Martins a,⁎ a b c
Department of Biochemistry (U38/FCT), Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal Institute of Agrochemistry and Food Technology, Spanish National Research Council (IATA-CSIC), Department of Biotechnology, 46980 Paterna, Valencia, Spain Research Centre in Physical Activity, Health and Leisure, Faculty of Sport, University of Porto, 4200-450 Porto, Portugal
a r t i c l e
i n f o
Article history: Received 9 January 2014 Accepted 10 January 2014 Available online 23 January 2014 Keywords: Mineral-rich water Minerals Fructose Metabolic syndrome Cardiovascular disease
Luo et al. [1] interestingly demonstrated in International Journal of Cardiology (October issue) that consumption of low-mineral bottled ⁎ Corresponding author. Tel.:/fax: 351 22 5513624. E-mail address: [email protected] (M.J. Martins).
water is associated with the increase of cardiovascular disease risk biomarkers, namely pathological lesions in the heart and aortic arch in rabbits and increased serum homocysteine levels and worsening of lipid profile in men. As stressed by Luo et al., there is not enough valid scientific evidence on the impact of water-supplied minerals on the human health. Nevertheless, natural mineral-rich waters are excellent sources of highly bioavailable minerals [2,3]. Adding to Luo et al.'s results, low-mineral intake is acknowledged as a factor associated with Metabolic Syndrome (MetSyn) increasing incidence [4]. In fact, high-energy density Western-diets, rich in sugars and fats, possess low-mineral content [4]. As widely studied, MetSyn is a risk factor for cardiovascular disease. Regarding natural mineral-rich water ingestion, some data highlight beneficial effects on MetSyn isolated parameters [5–8], but not in the MetSyn itself. The consumption of sodium bicarbonate containing/ rich mineral waters decreased systolic blood pressure in mildly hypertensive men (3 L/day, 7 days) [6] and mean arterial blood pressure in elderly normotensive individuals (1.5 L/day, 4 weeks) [8].
Letters to the Editor
Additionally, the ingestion of natural mineral water, sulfate, calcium, magnesium and bicarbonate-rich (at least 1 L/day, 2–4 weeks), reduced systolic and diastolic blood pressure in adults with borderline hypertension and low urinary magnesium and calcium excretion levels [7]. Vaquero et al. showed that, in moderately hypercholesterolemic young adults, the ingestion of bicarbonated natural mineral water, rich in sodium, chloride and potassium (1 L/day, 8 weeks), reduced systolic blood pressure (an effect already seen after 4 weeks), apolipoprotein-B, total-cholesterol and LDL-cholesterol fasting serum levels as well as total-cholesterol and LDL-cholesterol to HDLcholesterol ratios [6]. The same group showed, in healthy postmenopausal women, that a) the ingestion of the previous water (1 L/day, 2 months), increased HDL-cholesterol and decreased endothelial dysfunction markers, glucose, total-cholesterol and LDL-cholesterol fasting serum levels as well as total-cholesterol and LDL-cholesterol to HDL-cholesterol ratios, and b) the consumption of sodium bicarbonate-rich mineral waters (0.5 L each) with a standard fatrich meal decreased postprandial insulin levels (more distinctly in women with higher homeostasis model assessment index values) and lipemia [6]. Both a decrease in lipid and protein oxidation products and an increment of total antioxidant capacity and total thiol plasma levels were observed in healthy individuals drinking a sulfurous mineral water (0.5 L/day, 2 weeks) [5]. Given the current scenario, and using an opposite approach than that applied by Luo et al., we focused on the possible beneficial effects of the intake of natural mineral-rich water (MW) on the development or aggravation of MetSyn features. We used adult Sprague–Dawley male rats drinking 10% (w/v) fructose (F) solution (well-validated MetSyn animal model), either in tap water (TW; total mineralization: 148–151, sodium: 200, calcium: 30.5–40.2, magnesium: 3.6–9.2, potassium: 2.6 and chloride: 250 mg/L) or MW [2855, 591, 92.5, 26.2, 29.9, 30.8 (respectively) and bicarbonate 2013 mg/L]; controls drank tap water. All groups (7 rats each) ingested pellet food (2014 Teklad Global 14% Protein, Harlan Interfauna Iberica, Spain) ad libitum for 8 weeks. MW-supplementation reduced the magnitude of the increasing effect seen in TW + F-treated animals versus controls on heart rate and plasma triacylglycerols, insulin and leptin levels (along with a reduction of the strong decreasing tendency of the insulinsensitivity index). In MW + F-treated animals, no significant differences occurred versus controls. MW intake was also able to reduce the alterations found in hepatic oxidative stress biomarkers induced by F-treatment, which resulted in increased catalase activity and reduced glutathione peroxidase activity and oxidized glutathione content [9]. The deleterious effects observed in hepatic and adipose tissue glucocorticoid and insulin signaling-pathways of TW + F-treated animals versus controls were prevented/counteracted by MW-supplementation, which also induced metabolically beneficial stress pathways (Table 1, data under review). Regarding endothelial dysfunction, MW-supplementation increased smooth muscle cell proportion and tended to increase sirtuin 1 expression in the erectile tissue, in comparison with TW + F and/or control rats [10]. As widely known, menopause substantially increases MetSyn incidence; obesity is a relevant cardiovascular risk factor in both. So, we extended our research to adult Sprague–Dawley ovariectomized (O) female rats (5 groups of 6 rats each): sham-operated, TW or MW-treated O rats, with or without F, for 10 weeks, regarding feces microbiome and short chain fatty acids (SCFA) composition/levels. Higher Firmicutes to Bacteroidetes ratio has been associated with obesity in mice and humans [11] and higher levels of SCFA occur in obese individuals [12]. Lower levels of Bacteroidetes and higher levels of Proteobacteria, Actinobacteria and TM7 occurred in TW-O rats and higher levels of Firmicutes and lower levels of Bacteroidetes were observed in TW-OF versus sham-operated rats. In general, MW turned back changes in TW-O and TW-OF groups, more clearly and
513
Table 1 Hepatic and adipose tissue glucocorticoid and insulin signaling-pathways evaluation by Western blot in fructose-treated groups compared to controls. Tissue
Glucocorticoid and insulin signaling-pathways
TW-F
MW-F
Global P
Liver
PGC1-α Sirt1 p-IRS1 IRS1 p-IRS1/IRS1 p-JNK JNK p-ERK/ERK ERK GR
↓↓ ↓↓ ↓↓ t↓ t ↓↓ t↑ ↓↓ t↑ ↑↑ ↔
t↓ ↑↑ t↓ t↓ t↓ ↔ ↔ ↑↑ t↑ ↑↑
0.004 b0.001 0.005 0.056 0.078 0.058 b0.001 0.009 0.016 0.009
Visceral adipose tissue
↓↓ and ↑↑: significant decrease or increase versus control; t ↓↓: tendency to decrease versus control; t ↓ and t ↑: slight decrease or increase versus control; ↔: no effect; ERK: extracellular-signal related kinase; GR: glucocorticoid receptor; IRS1: insulin receptor substrate 1; JNK: C-jun N-terminal kinase; MW-F: 10% fructose/mineral water; p-ERK: phosphorylated extracellular-signal related kinase; p-IRS1: phosphorylated insulin receptor substrate 1; p-JNK: phosphorylated C-jun N-terminal kinase; PGC1-α: peroxisome proliferator-activated receptor gamma coactivator 1-alpha; Sirt1: sirtuin 1; TW-F: 10% fructose/tap water.
relevantly in the latter. TW-OF showed the highest Firmicutes to Bacteroidetes ratio compared to the other groups, while MWsupplementation reduced this ratio in TW-OF and TW-O groups. Sham-operated rats showed the lowest ratio, with no difference observed versus MW-O rats. The Principal Coordinates Analysis differentiated MW from TW groups, sham-operated rats microbiota being similar to MW groups (MW-O and MW-OF) microbiota. On the other hand, MW reduced total SCFA levels observed in the TWOF model. MW groups showed a tendency for lower body weight increase than the corresponding TW groups, more evidently in Ftreated rats. In conclusion, and reinforcing Luo et al.'s findings, drinking water mineral content appears as a subject of high relevance for health, natural mineral-rich waters probably constituting a valuable resource to reduce the risk of cardiovascular disease.
References [1] Luo J, Zhao Q, Zhang L, et al. The consumption of low-mineral bottled water increases the risk of cardiovascular disease: an experimental study of rabbits and young men. Int J Cardiol 2013;168:4454–6. [2] Bohmer H, Muller H, Resch KL. Calcium supplementation with calcium-rich mineral waters: a systematic review and meta-analysis of its bioavailability. Osteoporos Int 2000;11:938–43. [3] Karagulle O, Kleczka T, Vidal C, et al. Magnesium absorption from mineral waters of different magnesium content in healthy subjects. Forsch Komplementmed 2006;13:9–14. [4] Odermatt A. The Western-style diet: a major risk factor for impaired kidney function and chronic kidney disease. Am J Physiol Renal Physiol 2011;301:F919–31. [5] Benedetti S, Benvenuti F, Nappi G, et al. Antioxidative effects of sulfurous mineral water: protection against lipid and protein oxidation. Eur J Clin Nutr 2009;63:106–12. [6] Perez-Granados AM, Navas-Carretero S, Schoppen S, Vaquero MP. Reduction in cardiovascular risk by sodium-bicarbonated mineral water in moderately hypercholesterolemic young adults. J Nutr Biochem 2010;21:948–53. [7] Rylander R, Arnaud MJ. Mineral water intake reduces blood pressure among subjects with low urinary magnesium and calcium levels. BMC Public Health 2004;4:56. [8] Schorr U, Distler A, Sharma AM. Effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and metabolic parameters in elderly normotensive individuals: a randomized double-blind crossover trial. J Hypertens 1996;14:131–5. [9] Pereira CD, Severo M, Araújo JR, et al. Relevance of a hypersaline sodium-rich naturally sparkling mineral water to the protection against metabolic syndrome induction in fructose-fed Sprague–Dawley rats: a biochemical, metabolic, and redox approach. Int J Endocrinol 2014, http://dx.doi.org/ 10.1155/2014/384583. [10] Pereira CD, Severo M, Rafael L, Martins MJ, Neves D. Effects of natural mineral-rich water consumption on the expression of sirtuin 1 and angiogenic factors in the erectile tissue of rats with fructose-induced metabolic syndrome. Asian J Androl 2014, http://dx.doi.org/10.4103/1008-682X.122869.
514
Letters to the Editor
[11] Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Microbial ecology: human gut microbes associated with obesity. Nature 2006;444:1022–3.
[12] Schwiertz A, Taras D, Schafer K, et al. Microbiota and SCFA in lean and overweight healthy subjects. Obesity (Silver Spring) 2010;18:190–5.
0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.01.044
Renin–aldosterone paradox in patients with myalgic encephalomyelitis and orthostatic intolerance Kunihisa Miwa a,⁎, Masatoshi Fujita b a b
Department of Internal Medicine, Miwa Naika Clinic, Toyama, Japan Department of Cardiology, Uji Hospital, Kyoto, Japan
a r t i c l e
i n f o
Article history: Received 6 January 2014 Accepted 10 January 2014 Available online 23 January 2014 Keywords: Chronic fatigue syndrome Orthostatic intolerance Myalgic encephalomyelitis Small heart Low cardiac output Aldosterone
The etiology of chronic fatigue syndrome (CFS) is unknown. Recent studies have confirmed that almost 90% of CFS patients experience symptoms related to orthostatic intolerance (OI), which primarily predicts functional capacity in CFS [1]. Many symptoms of OI appear to be related to reduced cerebral blood flow. Also a small heart with low cardiac output has been reported to be common in CFS patients [2–4]. Recently, central nervous dysfunction due to myalgic encephalomyelitis (ME) has been postulated to be the cause of CFS. The International Consensus Criteria for ME differentiate patients with ME from those who are depressed and identify patients who are more physically debilitated and have greater physical and cognitive impairments [5]. Impaired activation of renin– aldosterone system may be included in the pathophysiology of ME. ME was diagnosed according to the International Consensus Criteria proposed by the International Consensus Panel in 2011 [5]. Plasma renin activity and aldosterone concentrations were determined in 10 ME patients (group ME), compared to 10 sedentary control subjects (Controls). All the ME patients complained of symptoms of OI, which was defined as the instability to maintain normal consciousness without significant symptoms such as disabling fatigue, dizziness, diminished concentration, tremulousness, sweating, light-headedness, visual disturbance, palpitations and nausea during upright position. Left ventricular (LV) morphology and function were determined echocardiographically. All of the study participants gave informed consent, and the study protocol conformed to the ethical guidelines of the 1975 Declaration of Helsinki and was approved by the ethics committee at our institution. All the study ME patients underwent a conventional active standing test. After a 10-min period of rest in the supine position, patients were asked to stand up actively by themselves and keep upright for 10 min. A total of 3 patients stopped before completing the conventional 10-min ⁎ Corresponding author at: Department of Internal Medicine, Miwa Naika Clinic, 1-43 Shintomicho, Toyama 930-0002, Japan. Tel.: +81 76 482 3014; fax: +81 76 482 3016. E-mail address: [email protected] (K. Miwa).
standing test complaining OI. Of these patients, 2 had neurally mediated hypotension and the other 1 had delayed orthostatic hypotension. The other 7 patients completed the standing test despite moderate symptoms of OI. Postural orthostatic tachycardia syndrome (POTS) with an increase of pulse rate ≥30 beats/min was diagnosed in 4 of the patients. The mean cardiothoracic ratio, systolic and diastolic blood pressures, LV end-diastolic dimension, stroke volume, cardiac output and index, and LV mass index were all significantly smaller in ME than in Controls (Table 1). The mean values of heart rate, fractional shortening and LV ejection fraction were comparable between the groups. As shown in Table 1 and Fig. 1, there was no significant difference in plasma renin activity between ME and Controls. The mean plasma aldosterone concentration was significantly lower in ME than in Controls. There was no significant difference in the mean serum K level between the two groups (ME: 4.0 ± 0.6 vs. Controls: 4.2 ± 0.3 mEq/L, p = 0.20). However, the mean serum Na level was significantly higher in ME than in Controls (143 ± 1 vs. 141 ± 1 mEq/L, p = 0.001). It has been reported that patients with OI have deficits in their blood volume and some patients improve their symptoms after acute or chronic plasma volume expansion [6]. In response to hypovolemia, plasma renin activity and aldosterone concentration would be expected to increase to
Table 1 Hemodynamic and echocardiographic data of the study subjects.
Number of patients Male/female Age (years) Cardiothoracic ratio (%) Heart rate (beats/min) Systolic blood pressure (mm Hg) Diastolic blood pressure (mm Hg) IVST (mm) PWT (mm) LVEDD (mm) LVESD (mm) LAD (mm) AoD (mm) RVD (mm) Stroke volume (mL) Stroke volume index (mL/m2) Cardiac output (L/min) Cardiac index (L/min/m2) Fractional shortening (%) LV ejection fraction (%) LV mass index (g/m2)
Controls
ME
p value
10 3/7 33 ± 12 43 ± 3 70 ± 9 120 ± 11 75 ± 7 8±1 8±1 47 ± 2 28 ± 2 28 ± 5 27 ± 4 16 ± 4 72 ± 9 41 ± 5 5.1 ± 1.2 2.9 ± 0.5 40 ± 3 71 ± 3 73 ± 19
10 3/7 31 ± 9 40 ± 3 68 ± 13 108 ± 12 66 ± 8 7±1 7±1 43 ± 5 26 ± 4 25 ± 4 26 ± 4 15 ± 3 57 ± 13 35 ± 8 3.8 ± 0.6 2.3 ± 0.3 39 ± 6 69 ± 7 58 ± 13
0.60 0.047 0.63 0.02 0.04 0.24 0.91 0.02 0.27 0.24 0.52 0.60 0.009 0.06 0.004 0.005 0.58 0.51 0.02
CTR: cardiothoracic ratio; IVST: interventricular septum thickness; PWT: left ventricular (LV) posterior wall thickness; LVEDD: LV end-diastolic dimension; LVESD: LV end-systolic dimension; LAD: left atrial dimension; AoD: aortic root dimension; RVD: right ventricular dimension.