Zout en de kans op hartziekte of doodgaan*
Uit verschillende studies blijkt dat beperking van de zoutinname mogelijk meer nadelen heeft dan voordelen. Minder zout doet de bloeddruk weliswaar iets dalen en vaak nog alleen bij mensen met duidelijk
hoge bloeddruk. Hoge zoutinname verhoogt wel de bloedwaarden cholesterol en triglyceriden en zorgt ervoor dat de nieren meer renine en het hormoon aldosteron gaan produceren, stoffen die in verband staan met hoge bloeddruk. Hierdoor zou de kans op hartziekten eerder toenemen dan afnemen. Bij mensen met een normale bloeddruk heeft het verminderen van de zoutconsumptie mogelijk meer nadelen dan voordelen, zo besluiten de onderzoekers. Uit een andere studie blijkt weer eens dat een goed
kalium-natrium verhouding nog wel belangrijker is dan minder zout. Het zijn vooral lage
kaliumwaarden die slecht zijn voor u gezondheid. Uit een analyse van verschillende studies blijkt dat zes maanden lang de zoutinname verlagen leidt tot meer hart- en vaatziektes en het doodgaan.
Reduced dietary salt for the prevention of cardiovascular disease
Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S
Cardiovascular disease includes heart attacks, strokes, and the need for heart surgery and is a major cause of premature death and disability. This review set out to assess whether intensive support and encouragement to cut down on salt in foods reduced the risk of death or cardiovascular disease. This advice did reduce the amount of salt eaten which led to a small reduction in blood pressure by six months. There was not enough information to detect the expected effects on deaths and cardiovascular disease predicted by the blood pressure reductions found. There was limited evidence that dietary advice to reduce salt may increase deaths in people with heart failure. Our review does not mean that asking people to reduce salt should be stopped. People should continue to strive to do this. However, additional measures - reducing the amount of hidden salt in processed foods, for example – will make it much easier for people to stick to a lower salt diet. Further evidence of measures to cut dietary salt is needed: (1) randomised controlled trials of advice to reduce salt in individuals with heart failure assessing mortality and cardiovascular events and (2) experimental or observational studies of population based interventions to reduce salt in hypertensives or healthy individuals assessing mortality and cardiovascular events.
Background:
An earlier Cochrane review of dietary advice identified insufficient evidence to assess effects of reduced salt intake on mortality or cardiovascular events.
Objectives:
1. To assess the long term effects of interventions aimed at reducing dietary salt on mortality and cardiovascular morbidity.
2. To investigate whether blood pressure reduction is an explanatory factor in any effect of such dietary interventions on mortality and cardiovascular outcomes.
Search strategy:
The Cochrane Library (CENTRAL, Health Technology Assessment (HTA) and Database of Abstracts of Reviews of Effect (DARE)), MEDLINE, EMBASE, CINAHL and PsycInfo were searched through to October 2008. References of included studies and reviews were also checked. No language restrictions were applied.
Selection criteria:
Trials fulfilled the following criteria: (1) randomised with follow up of at least six-months, (2) intervention was reduced dietary salt (restricted salt dietary intervention or advice to reduce salt intake), (3) adults, (4) mortality or cardiovascular morbidity data was available. Two reviewers independently assessed whether studies met these criteria.
Data collection and analysis:
Data extraction and study validity were compiled by a single reviewer, and checked by a second. Authors were contacted where possible to obtain missing information. Events were extracted and relative risks (RRs) and 95% CIs calculated.
Main results:
Seven studies (including 6,489 participants) met the inclusion criteria - three in normotensives (n=3518), two in hypertensives (n=758), one in a mixed population of normo- and hypertensives (n=1981) and one in heart failure (n=232) with end of trial follow-up of seven to 36 months and longest observational follow up (after trial end) to 12.7 yrs. Relative risks for all cause mortality in normotensives (end of trial RR 0.67, 95% CI: 0.40 to 1.12, 60 deaths; longest follow up RR 0.90, 95% CI: 0.58 to 1.40, 79 deaths) and hypertensives (end of trial RR 0.97, 95% CI: 0.83 to 1.13, 513 deaths; longest follow up RR 0.96, 95% CI; 0.83 to 1.11, 565 deaths) showed no strong evidence of any effect of salt reduction. Cardiovascular morbidity in people with normal blood pressure (longest follow-up RR 0.71, 95% CI: 0.42 to 1.20, 200 events) or raised blood pressure at baseline (end of trial RR 0.84, 95% CI: 0.57 to 1.23, 93 events) also showed no strong evidence of benefit. Salt restriction increased the risk of all-cause death in those with congestive heart failure (end of trial relative risk: 2.59, 95% 1.04 to 6.44, 21 deaths). We found no information on participants health-related quality of life.
Authors' conclusions:
Despite collating more event data than previous systematic reviews of randomised controlled trials (665 deaths in some 6,250 participants), there is still insufficient power to exclude clinically important effects of reduced dietary salt on mortality or cardiovascular morbidity in normotensive or hypertensive populations. Further RCT evidence is needed to confirm whether restriction of sodium is harmful for people with heart failure. Our estimates of benefits from dietary salt restriction are consistent with the predicted small effects on clinical events attributable to the small blood pressure reduction achieved.
This record should be cited as:
Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S. Reduced dietary salt for the prevention of cardiovascular disease. Cochrane Database of Systematic Reviews 2011, Issue 7. Art. No.: CD009217. DOI: 10.1002/14651858.CD009217
Sodium and Potassium Intake and Mortality Among US Adults
Prospective Data From the Third National Health and Nutrition Examination Survey
Quanhe Yang, PhD; Tiebin Liu, MSPH; Elena V. Kuklina, MD, PhD; W. Dana Flanders, MD, ScD; Yuling Hong, MD, PhD; Cathleen Gillespie, MS; Man-Huei Chang, MPH; Marta Gwinn, MD; Nicole Dowling, PhD; Muin J. Khoury, MD, PhD; Frank B. Hu, MD, PhD
Arch Intern Med. 2011;171(13):1183-1191. doi:10.1001/archinternmed.2011.257
Background Several epidemiologic studies suggested that higher sodium and lower potassium intakes were associated with increased risk of cardiovascular diseases (CVD). Few studies have examined joint effects of dietary sodium and potassium intake on risk of mortality.
Methods To investigate estimated usual intakes of sodium and potassium as well as their ratio in relation to risk of all-cause and CVD mortality, the Third National Health and Nutrition Examination Survey Linked Mortality File (1988-2006), a prospective cohort study of a nationally representative sample of 12 267 US adults, studied all-cause, cardiovascular, and ischemic heart (IHD) diseases mortality.
Results During a mean follow-up period of 14.8 years, we documented a total of 2270 deaths, including 825 CVD deaths and 443 IHD deaths. After multivariable adjustment, higher sodium intake was associated with increased all-cause mortality (hazard ratio [HR], 1.20; 95% confidence interval [CI], 1.03-1.41 per 1000 mg/d), whereas higher potassium intake was associated with lower mortality risk (HR, 0.80; 95% CI, 0.67-0.94 per 1000 mg/d). For sodium-potassium ratio, the adjusted HRs comparing the highest quartile with the lowest quartile were HR, 1.46 (95% CI, 1.27-1.67) for all-cause mortality; HR, 1.46 (95% CI, 1.11-1.92) for CVD mortality; and HR, 2.15 (95% CI, 1.48-3.12) for IHD mortality. These findings did not differ significantly by sex, race/ethnicity, body mass index, hypertension status, education levels, or physical activity.
Conclusion Our findings suggest that a higher sodium-potassium ratio is associated with significantly increased risk of CVD and all-cause mortality, and higher sodium intake is associated with increased total mortality in the general US population.
Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride
Graudal NA, Hubeck-Graudal T, Jurgens G
We are commonly advised to cut down on salt. The previous version of this review looked at mostly short-term strategies to reduce salt intake. In the present updated version separate analyses of studies with a duration of 2 to 4 weeks or longer were performed. Low salt diets reduced systolic blood pressure by 1% in white people with normal blood pressure and by 3.5% in white people with elevated blood pressure. The effect was similar in trials of 4 weeks or longer. There were increases in some hormones and lipids which could be harmful if persistent over time. However, the studies were not designed to measure long-term health effects. Therefore we do not know if low salt diets improve or worsen health outcomes.
Most of the people who took part in the studies were whites, but in the small number of non-whites the blood pressure reduction was, if anything, greater. More research on reduced salt intake is required, particularly in non-white populations.
Background:
In spite of more than 100 years of investigations the question of reduced sodium intake as a health prophylaxis initiative is still unsolved.
Objectives:
To estimate the effects of low sodium versus high sodium intake on systolic and diastolic blood pressure (SBP and DBP), plasma or serum levels of renin, aldosterone, catecholamines, cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglycerides.
Search strategy:
PUBMED, EMBASE and Cochrane Central and reference lists of relevant articles were searched from 1950 to July 2011.
Selection criteria:
Studies randomizing persons to low sodium and high sodium diets were included if they evaluated at least one of the above outcome parameters.
Data collection and analysis:
Two authors independently collected data, which were analysed with Review Manager 5.1.
Main results:
A total of 167 studies were included in this 2011 update.
The effect of sodium reduction in normotensive Caucasians was SBP -1.27 mmHg (95% CI: -1.88, -0.66; p=0.0001), DBP -0.05 mmHg (95% CI: -0.51, 0.42; p=0.85). The effect of sodium reduction in normotensive Blacks was SBP -4.02 mmHg (95% CI:-7.37, -0.68; p=0.002), DBP -2.01 mmHg (95% CI:-4.37, 0.35; p=0.09). The effect of sodium reduction in normotensive Asians was SBP -1.27 mmHg (95% CI: -3.07, 0.54; p=0.17), DBP -1.68 mmHg (95% CI:-3.29, -0.06; p=0.04). The effect of sodium reduction in hypertensive Caucasians was SBP -5.48 mmHg (95% CI: -6.53, -4.43; p<0.00001), DBP -2.75 mmHg (95% CI: -3.34, -2.17; p<0.00001). The effect of sodium reduction in hypertensive Blacks was SBP -6.44 mmHg (95% CI:-8.85, -4.03; p=0.00001), DBP -2.40 mmHg (95% CI:-4.68, -0.12; p=0.04). The effect of sodium reduction in hypertensive Asians was SBP -10.21 mmHg (95% CI:-16.98, -3.44; p=0.003), DBP -2.60 mmHg (95% CI: -4.03, -1.16; p=0.0004).
In plasma or serum there was a significant increase in renin (p<0.00001), aldosterone (p<0.00001), noradrenaline (p<0.00001), adrenaline (p<0.0002), cholesterol (p<0.001) and triglyceride (p<0.0008) with low sodium intake as compared with high sodium intake. In general the results were similar in studies with a duration of at least 2 weeks.
Authors' conclusions:
Sodium reduction resulted in a 1% decrease in blood pressure in normotensives, a 3.5% decrease in hypertensives, a significant increase in plasma renin, plasma aldosterone, plasma adrenaline and plasma noradrenaline, a 2.5% increase in cholesterol, and a 7% increase in triglyceride. In general, these effects were stable in studies lasting for 2 weeks or more.
This record should be cited as:
Graudal NA, Hubeck-Graudal T, Jurgens G. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Cochrane Database of Systematic Reviews 2011, Issue 11. Art. No.: CD004022.
DOI: 10.1002/14651858.CD004022.pub3 (December 2011)
Reacties: