A few more recent ones..
1) Salt & health
Effect of lower sodium intake on health: systematic review and meta-analyses. BMJ. 2013 Apr 3;346:f1326. doi: 10.1136/bmj.f1326.
Free Articlehttp://www.bmj.com/content/346/bmj.f132 ... d=23558163
OBJECTIVE: To assess the effect of decreased sodium intake on blood pressure, related cardiovascular diseases, and potential adverse effects such as changes in blood lipids, catecholamine levels, and renal function.
DESIGN: Systematic review and meta-analysis.
DATA SOURCES: Cochrane Central Register of Controlled Trials, Medline, Embase, WHO International Clinical Trials Registry Platform, the Latin American and Caribbean health science literature database, and the reference lists of previous reviews.
STUDY SELECTION: Randomised controlled trials and prospective cohort studies in non-acutely ill adults and children assessing the relations between sodium intake and blood pressure, renal function, blood lipids, and catecholamine levels, and in non-acutely ill adults all cause mortality, cardiovascular disease, stroke, and coronary heart disease. STUDY APPRAISAL AND SYNTHESIS: Potential studies were screened independently and in duplicate and study characteristics and outcomes extracted. When possible we conducted a meta-analysis to estimate the effect of lower sodium intake using the inverse variance method and a random effects model. We present results as mean differences or risk ratios, with 95% confidence intervals.
RESULTS: We included 14 cohort studies and five randomised controlled trials reporting all cause mortality, cardiovascular disease, stroke, or coronary heart disease; and 37 randomised controlled trials measuring blood pressure, renal function, blood lipids, and catecholamine levels in adults. Nine controlled trials and one cohort study in children reporting on blood pressure were also included. In adults a reduction in sodium intake significantly reduced resting systolic blood pressure by 3.39 mm Hg (95% confidence interval 2.46 to 4.31) and resting diastolic blood pressure by 1.54 mm Hg (0.98 to 2.11). When sodium intake was <2 g/day versus =/>2 g/day, systolic blood pressure was reduced by 3.47 mm Hg (0.76 to 6.18) and diastolic blood pressure by 1.81 mm Hg (0.54 to 3.08). Decreased sodium intake had no significant adverse effect on blood lipids, catecholamine levels, or renal function in adults (P>0.05). There were insufficient randomised controlled trials to assess the effects of reduced sodium intake on mortality and morbidity. The associations in cohort studies between sodium intake and all cause mortality, incident fatal and non-fatal cardiovascular disease, and coronary heart disease were non-significant (P>0.05). Increased sodium intake was associated with an increased risk of stroke (risk ratio 1.24, 95% confidence interval 1.08 to 1.43), stroke mortality (1.63, 1.27 to 2.10), and coronary heart disease mortality (1.32, 1.13 to 1.53). In children, a reduction in sodium intake significantly reduced systolic blood pressure by 0.84 mm Hg (0.25 to 1.43) and diastolic blood pressure by 0.87 mm Hg (0.14 to 1.60).
CONCLUSIONS: High quality evidence in non-acutely ill adults shows that reduced sodium intake reduces blood pressure
and has no adverse effect on blood lipids, catecholamine levels, or renal function, and moderate quality evidence in children shows that a reduction in sodium intake reduces blood pressure. Lower sodium intake is also associated with a reduced risk of stroke and fatal coronary heart disease in adults. The totality of evidence suggests that most people will likely benefit from reducing sodium intake.
2) Salt impairs the endothelium
High dietary sodium intake impairs endothelium-dependent dilation in healthy salt-resistant humans. J Hypertens. 2012 Dec 20. [Epub ahead of print] PMID:23263240
BACKGROUND:: Excess dietary sodium has been linked to the development of hypertension and other cardiovascular diseases. In humans, the effects of sodium consumption on endothelial function have not been separated from the effects on blood pressure. The present study was designed to determine if dietary sodium intake affected endothelium-dependent dilation (EDD) independently of changes in blood pressure.
METHOD:: Fourteen healthy salt-resistant adults were studied (9M, 5F; age 33 ± 2.4 years) in a controlled feeding study. After a baseline run-in diet, participants were randomized to a 7-day high-sodium (300-350 mmol/day) and 7-day low-sodium (20 mmol/day) diet. Salt resistance, defined as a 5 mmHg or less change in a 24-h mean arterial pressure, was individually assessed while on the low-sodium and high-sodium diets and confirmed in the participants undergoing study (low-sodium: 85 ± 1 mmHg; high-sodium: 85 ± 2 mmHg). EDD was determined in each participant via brachial artery flow-mediated dilation on the last day of each diet.
RESULTS:: Sodium excretion increased during the high-sodium diet (P < 0.01). EDD was reduced on the high-sodium diet (low: 10.3 ± 0.9%, high: 7.3 ± 0.7%; P < 0.05). The high-sodium diet significantly suppressed plasma renin activity (PRA), plasma angiotensin II, and aldosterone (P < 0.05).
CONCLUSION:: These data demonstrate that excess salt intake in humans impairs endothelium-dependent dilation independently of changes in blood pressure.
3) Salt & blood pressure
Long-term effects of salt substitution on blood pressure in a rural North Chinese population. J Hum Hypertens. 2012 Dec 20. doi: 10.1038/jhh.2012.63. [Epub ahead of print] PMID:23254595
Dietary sodium and potassium intake can influence blood pressure. The effects of salt substitution on patients with hypertension and normotensive family member controls, however, have not been evaluated in a rural Chinese population.
The objective of this study, accordingly, was to assess the long-term effects of salt substitution on blood pressure.
We conducted a double-blind, randomized controlled trial among 200 families in rural China to establish the 2-year effects of a reduced-sodium, high-potassium salt substitute (65% sodium chloride, 25% potassium chloride, 10% magnesium sulfate) compared with normal salt (100% sodium chloride) on blood pressure.
Of the 462 individuals in the trial, 372 completed the study (81%). For normotensive subjects, the mean overall difference in systolic and diastolic blood pressure between the two groups at the 24-month follow-up was 2 mm Hg (95% confidence interval (CI) 0-4 mm Hg, P<0.05) and 2 mm Hg (95% CI 1-3 mm Hg, P<0.05), respectively. For subjects with hypertension, the mean overall decrease in systolic blood pressure showed a 4-mm Hg (95% CI 2-6 mm Hg, P<0.05) decrease between the two groups. Diastolic blood pressure was not affected by salt use in the hypertensive group.Salt substitution lowers systolic blood pressure in hypertensive patients and lowers both systolic and diastolic blood pressure in normotensive controls. Salt substitution, therefore, may be an effective adjuvant therapy for hypertensive patients and the potential efficacy in preventing hypertension in normotensive individuals.
4) Salt now linked to auto-immune disease
Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1.Nature. 2013 Apr 25;496(7446):513-7. doi: 10.1038/nature11984. Epub 2013 Mar 6.http://www.ncbi.nlm.nih.gov/pubmed/23467085
Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature. 2013 Apr 25;496(7446):518-22. doi: 10.1038/nature11868. Epub 2013 Mar 6.http://www.ncbi.nlm.nih.gov/pubmed/23467095
Immunology Exacerbating Autoimmune Disease with Salt
Sci. Signal., 30 April 2013 Vol. 6, Issue 273, p. ec97
EDITORS' CHOICEhttp://stke.sciencemag.org/cgi/content/ ... a051ac6c83
Science Volume 339, Number 6124, Issue of 8 March 2013
Dietary Salt Linked to Autoimmune Diseaseshttp://news.sciencemag.org/sciencenow/2 ... iseas.html
Salt in food may increase the risk of autoimmune diseases, according to provocative results reported this week in Nature. Immunobiologist David Hafler of the Yale School of Medicine and colleagues determined that a pinch of salt triggered cultures of unspecialized T cells to produce large numbers of destructive TH17 cells, which have been implicated in diseases such as psoriasis, rheumatoid arthritis, and multiple sclerosis. They also showed that a salt-rich diet makes mice more susceptible to experimental autoimmune encephalomyelitis (EAE), a rodent illness similar to multiple sclerosis.
A salt connection also crystallized when computational biologist Aviv Regev of the Broad Institute in Cambridge, immunologist Vijay Kuchroo of Harvard Medical School in Boston, and colleagues pieced together the molecular circuit that controls specialization of TH17 cells. An influential gene was SGK1, which helps cells manage sodium levels. And mice on high-salt rations developed a milder form of EAE if they lacked SGK1. The work doesn't establish that salt drives human autoimmune diseases, but "the stage is set to do precise experiments to test the hypothesis," Kuchroo says.
5) Salt and health
Salt in health and disease--a delicate balance.
N Engl J Med. 2013 Mar 28;368(13):1229-37. doi: 10.1056/NEJMra1212606.
Although it has been difficult to separate salt need from salt preference, current levels of salt consumption exceed salt need and are associated with adverse clinical outcomes. High salt intake is associated with high blood pressure and increased rates of cardiovascular disease. Experimental studies continue to provide information about mechanisms for these adverse effects of salt. In clinical trials, a reduction in salt intake is associated with reduced blood pressure, more so in persons with hypertension than in those with normal blood pressure. Although not discussed in the present review, it should be noted that reduced salt intake is associated with greater blood-pressure responses to antihypertensive drug therapy, including drug therapy in patients with resistant hypertension.85,86 Most, but not all, clinical trials have shown that reduced salt intake is also associated with decreased risks of cardiovascular events and death. Consequently, recommendations for reducing the currently high levels of salt consumption in the general population seem justifiable, although in terms of safety, the lower limit of salt consumption has not been clearly identified. It may be premature to dis-count the apparently paradoxical cardiovascular outcomes associated with low salt intake, particularly in specific clinical conditions (e.g., type 1 or type 2 diabetes and congestive heart failure that is aggressively treated with diuretic agents). Less-rigorous targets for salt reduction may be appropriate for these and other patient groups.