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Suckling R.J.,Blood Pressure Unit
Cochrane database of systematic reviews (Online) | Year: 2010

There is strong evidence that our current consumption of salt is a major factor for increased blood pressure (BP) and a modest reduction in salt intake lowers BP whether BP levels are normal or raised. Tight control of BP in diabetics lowers the risk of strokes, heart attacks and heart failure and slows the progression of diabetic kidney disease (DKD). Currently there is no consensus in restricting salt intake in diabetic patients. To evaluate the effect of altered salt intake on BP and markers of cardiovascular disease and DKD. In January 2010, we searched the Cochrane Renal Group's Specialised Register, CENTRAL (in The Cochrane Library), MEDLINE (from 1966) and EMBASE (from 1980) to identify appropriate articles. We included all randomised controlled trials of salt reduction in individuals with type 1 and type 2 diabetes. Two authors independently assessed studies and resolved differences by discussion with a third independent author. We calculated mean effect sizes using both the fixed-effect and random-effects models. Thirteen studies (254 individuals) met our inclusion criteria. These included 75 individuals with type 1 diabetes and 158 individuals with type 2 diabetes. The median reduction in urinary sodium was 203 mmol/24 h (11.9 g/day) in type 1 diabetes and 125 mmol/24 h (7.3 g/day) in type 2 diabetes. The median duration of salt restriction was one week in both type 1 and type 2 diabetes. BP was reduced in both type 1 and type 2 diabetes. In type 1 diabetes (56 individuals), salt restriction reduced BP by -7.11/-3.13 mm Hg (systolic/diastolic); 95% CI: systolic BP (SBP) -9.13 to -5.10; diastolic BP (DBP) -4.28 to -1.98). In type 2 diabetes (56 individuals), salt restriction reduced BP by -6.90/-2.87 mm Hg (95% CI: SBP -9.84 to -3.95; DBP -4.39 to -1.35). There was a greater reduction in BP in normotensive patients, possibly due to a larger decrease in salt intake in this group. Although the studies are not extensive, this meta-analysis shows a large fall in BP with salt restriction, similar to that of single drug therapy. All diabetics should consider reducing salt intake at least to less than 5-6 g/day in keeping with current recommendations for the general population and may consider lowering salt intake to lower levels, although further studies are needed. Source

Polonia J.J.,University of Porto | Polonia J.J.,Blood Pressure Unit | Magalhaes M.T.,ULS | Senra D.,ULS | And 3 more authors.
Blood Pressure Monitoring | Year: 2013

Objective High salt intake has been associated with the development of arterial hypertension, but it still remains controversial as to how salt consumption relates with central haemodynamics and central pressures. For interventional purposes, it is crucial to identify the main food categories that contribute toward high salt consumption. Methods In 638 Caucasian hypertensive patients (age 50± 15 years, 329 women) enrolled for 7 years, we evaluate the independent relationship between urinary sodium (UNa+ , mean 207±78 mEq/24 h) or potassium (UK+ , mean 79±26 mEq/24 h) excretion measured in validated 24-h samples and office blood pressure (BP), 24 h BP, central pulse pressure, and parameters of central pulse wave analysis. A subgroup (n= 154) of this population (UNa+ , mean 205±75 mEq/24 h) was also subjected to structured validated food frequency questionnaires on dietary habits. Results Multiple regression analysis showed that UNa+ was associated independently with increases in 24-h systolic BP, central pulse pressure, and augmented aortic augmentation index (AIx) and associated inversely with pulse pressure amplification. In the subgroup, patients of the upper tercile of distribution of UNa+ (288±21 mEq/ 24 h) ate significantly higher amounts (g/day) of vegetables, sauces, bread, cheese, fries and sausages/ cold meat, yielding an estimation that bread could account for 20-27% of all daily salt intake. Conclusion Reduction of salt intake on the basis of the main food sources that we have identified could also influence cardiovascular risk throughout effects on 24-h and central pressures. Blood Press Monit 18:303-310 © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins. Source

McCarthy N.S.,Stephens College | McCarthy N.S.,University of Western Australia | Vangjeli C.,Stephens College | Cavalleri G.L.,Stephens College | And 12 more authors.
Circulation: Cardiovascular Genetics | Year: 2014

Background-Blood pressure (BP) is highly heritable, but our understanding of the genetic causes underlying variations in BP is incomplete. In this study, we explored whether novel loci associated with BP could be identified using a genecentric approach in 3 community-based cohorts with accurate BP measurements. Methods and Results-Genotyping of 1857 single nucleotide polymorphisms (SNPs) in 91 ion channel genes was performed in a discovery cohort (n=358). Thirty-four SNPs associated with BP traits (P≤0.01) were followed up in an independent population (n=387); significant SNPs from this analysis were looked up in another independent population (n=1010) and meta-analyzed. Repeated clinic and ambulatory measurements were available for all but the discovery cohort (clinic only). Association analyses were performed, with systolic, diastolic, and pulse pressures as quantitative traits, adjusting for age and sex. Quantile-quantile plots indicated that the genecentric approach resulted in an inflation of association signals. Of the 29 SNPs taken forward from the discovery cohort, 2 SNPs were associated with BP phenotypes with the same direction of effect, with experiment-wide significance, in follow-up cohort I. These were rs2228291, in the chloride channel gene CLCN2, and rs10513488, in the potassium channel gene KCNAB1. Both associations were subsequently replicated in follow-up cohort II. Conclusions-Using a genecentric design and 3 well-phenotyped populations, this study identified 2 previously unreported, biologically plausible, genetic associations with BP. These results suggest that dense genotyping of genes, in pathways known to influence BP, could add to candidate-gene and Genome Wide Association studies in further explaining BP heritability. © 2014 American Heart Association, Inc. Source

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