There is strong evidence for a causal relationship between salt intake and blood pressure. Randomized trials demonstrate that salt reduction lowers blood pressure in both individuals who are ...hypertensive and those who are normotensive, additively to antihypertensive treatments. Methodologically robust studies with accurate salt intake assessment have shown that a lower salt intake is associated with a reduced risk of cardiovascular disease, all-cause mortality, and other conditions, such as kidney disease, stomach cancer, and osteoporosis. Multiple complex and interconnected physiological mechanisms are implicated, including fluid homeostasis, hormonal and inflammatory mechanisms, as well as more novel pathways such as the immune response and the gut microbiome. High salt intake is a top dietary risk factor. Salt reduction programs are cost-effective and should be implemented or accelerated in all countries. This review provides an update on the evidence relating salt to health, with a particular focus on blood pressure and cardiovascular disease, as well as the potential mechanisms.
Suboptimal diets are a leading risk factor for death and disability. Nutrition labelling is a potential method to encourage consumers to improve dietary behaviour. This systematic review and network ...meta-analysis (NMA) summarises evidence on the impact of colour-coded interpretive labels and warning labels on changing consumers' purchasing behaviour.
We conducted a literature review of peer-reviewed articles published between 1 January 1990 and 24 May 2021 in PubMed, Embase via Ovid, Cochrane Central Register of Controlled Trials, and SCOPUS. Randomised controlled trials (RCTs) and quasi-experimental studies were included for the primary outcomes (measures of changes in consumers' purchasing and consuming behaviour). A frequentist NMA method was applied to pool the results. A total of 156 studies (including 101 RCTs and 55 non-RCTs) nested in 138 articles were incorporated into the systematic review, of which 134 studies in 120 articles were eligible for meta-analysis. We found that the traffic light labelling system (TLS), nutrient warning (NW), and health warning (HW) were associated with an increased probability of selecting more healthful products (odds ratios ORs and 95% confidence intervals CIs: TLS, 1.5 1.2, 1.87; NW, 3.61 2.82, 4.63; HW, 1.65 1.32, 2.06). Nutri-Score (NS) and warning labels appeared effective in reducing consumers' probability of selecting less healthful products (NS, 0.66 0.53, 0.82; NW,0.65 0.54, 0.77; HW,0.64 0.53, 0.76). NS and NW were associated with an increased overall healthfulness (healthfulness ratings of products purchased using models such as FSAm-NPS/HCSP) by 7.9% and 26%, respectively. TLS, NS, and NW were associated with a reduced energy (total energy: TLS, -6.5%; NS, -6%; NW, -12.9%; energy per 100 g/ml: TLS, -3%; NS, -3.5%; NW, -3.8%), sodium (total sodium/salt: TLS, -6.4%; sodium/salt per 100 g/ml: NS: -7.8%), fat (total fat: NS, -15.7%; fat per 100 g/ml: TLS: -2.6%; NS: -3.2%), and total saturated fat (TLS, -12.9%; NS: -17.1%; NW: -16.3%) content of purchases. The impact of TLS, NS, and NW on purchasing behaviour could be explained by improved understanding of the nutrition information, which further elicits negative perception towards unhealthful products or positive attitudes towards healthful foods. Comparisons across label types suggested that colour-coded labels performed better in nudging consumers towards the purchase of more healthful products (NS versus NW: 1.51 1.08, 2.11), while warning labels have the advantage in discouraging unhealthful purchasing behaviour (NW versus TLS: 0.81 0.67, 0.98; HW versus TLS: 0.8 0.63, 1). Study limitations included high heterogeneity and inconsistency in the comparisons across different label types, limited number of real-world studies (95% were laboratory studies), and lack of long-term impact assessments.
Our systematic review provided comprehensive evidence for the impact of colour-coded labels and warnings in nudging consumers' purchasing behaviour towards more healthful products and the underlying psychological mechanism of behavioural change. Each type of label had different attributes, which should be taken into consideration when making front-of-package nutrition labelling (FOPL) policies according to local contexts. Our study supported mandatory front-of-pack labelling policies in directing consumers' choice and encouraging the food industry to reformulate their products.
PROSPERO (CRD42020161877).
Strong evidence indicates that reduction of salt intake lowers blood pressure and reduces the risk of cardiovascular disease (CVD). The WHO has set a global target of reducing the population salt ...intake from the current level of approximately 10 g daily to <5 g daily. This recommendation has been challenged by several studies, including cohort studies, which have suggested a J-shaped relationship between salt intake and CVD risk. However, these studies had severe methodological problems, such as reverse causality and measurement error due to assessment of salt intake by spot urine. Consequently, findings from such studies should not be used to derail vital public health policy. Gradual, stepwise salt reduction as recommended by the WHO remains an achievable, affordable, effective, and important strategy to prevent CVD worldwide. The question now is how to reduce population salt intake. In most developed countries, salt reduction can be achieved by a gradual and sustained reduction in the amount of salt added to food by the food industry. The UK has pioneered a successful salt-reduction programme by setting incremental targets for >85 categories of food; many other developed countries are following the UK's lead. In developing countries where most of the salt is added by consumers, public health campaigns have a major role. Every country should adopt a coherent, workable strategy. Even a modest reduction in salt intake across the whole population can lead to a major improvement in public health and cost savings.
The totality of evidence, including epidemiological studies, animal studies, randomised trials, and now out come studies all show the substantial benefits in reducing the average intake of salt.6-9 ...Most countries have adopted policies to reduce salt intake by persuading the food industry to reformulate food with less salt, as is occurring successfully in the UK,10 and also by encouraging people to use less salt in their own cooking and at the table.
Objective To determine the effects of longer term modest salt reduction on blood pressure, hormones, and lipids.Design Systematic review and meta-analysis.Data sources Medline, Embase, Cochrane ...Hypertension Group Specialised Register, Cochrane Central Register of Controlled Trials, and reference list of relevant articles.Inclusion criteria Randomised trials with a modest reduction in salt intake and duration of at least four weeks.Data extraction and analysis Data were extracted independently by two reviewers. Random effects meta-analyses, subgroup analyses, and meta-regression were performed.Results Thirty four trials (3230 participants) were included. Meta-analysis showed that the mean change in urinary sodium (reduced salt v usual salt) was −75 mmol/24 h (equivalent to a reduction of 4.4 g/day salt), and with this reduction in salt intake, the mean change in blood pressure was −4.18 mm Hg (95% confidence interval −5.18 to −3.18, I2=75%) for systolic blood pressure and −2.06 mm Hg (−2.67 to −1.45, I2=68%) for diastolic blood pressure. Meta-regression showed that age, ethnic group, blood pressure status (hypertensive or normotensive), and the change in 24 hour urinary sodium were all significantly associated with the fall in systolic blood pressure, explaining 68% of the variance between studies. A 100 mmol reduction in 24 hour urinary sodium (6 g/day salt) was associated with a fall in systolic blood pressure of 5.8 mm Hg (2.5 to 9.2, P=0.001) after adjustment for age, ethnic group, and blood pressure status. For diastolic blood pressure, age, ethnic group, blood pressure status, and the change in 24 hour urinary sodium explained 41% of the variance between studies. Meta-analysis by subgroup showed that in people with hypertension the mean effect was −5.39 mm Hg (−6.62 to −4.15, I2=61%) for systolic blood pressure and −2.82 mm Hg (−3.54 to −2.11, I2=52%) for diastolic blood pressure. In normotensive people, the figures were −2.42 mm Hg (−3.56 to −1.29, I2=66%) and −1.00 mm Hg (−1.85 to −0.15, I2=66%), respectively. Further subgroup analysis showed that the decrease in systolic blood pressure was significant in both white and black people and in men and women. Meta-analysis of data on hormones and lipids showed that the mean change was 0.26 ng/mL/h (0.17 to 0.36, I2=70%) for plasma renin activity, 73.20 pmol/L (44.92 to 101.48, I2=62%) for aldosterone, 187 pmol/L (39 to 336, I2=5%) for noradrenaline (norepinephrine), 37 pmol/L (−1 to 74, I2=12%) for adrenaline (epinephrine), 0.05 mmol/L (−0.02 to 0.11, I2=0%) for total cholesterol, 0.05 mmol/L (−0.01 to 0.12, I2=0%) for low density lipoprotein cholesterol, −0.02 mmol/L (−0.06 to 0.01, I2=16%) for high density lipoprotein cholesterol, and 0.04 mmol/L (−0.02 to 0.09, I2=0%) for triglycerides. Conclusions A modest reduction in salt intake for four or more weeks causes significant and, from a population viewpoint, important falls in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group. Salt reduction is associated with a small physiological increase in plasma renin activity, aldosterone, and noradrenaline and no significant change in lipid concentrations. These results support a reduction in population salt intake, which will lower population blood pressure and thereby reduce cardiovascular disease. The observed significant association between the reduction in 24 hour urinary sodium and the fall in systolic blood pressure, indicates that larger reductions in salt intake will lead to larger falls in systolic blood pressure. The current recommendations to reduce salt intake from 9-12 to 5-6 g/day will have a major effect on blood pressure, but a further reduction to 3 g/day will have a greater effect and should become the long term target for population salt intake.
High salt intake is the major cause of raised blood pressure and accordingly leads to cardiovascular diseases. Recently, it has been shown that high salt intake is associated with an increased risk ...of obesity through sugar-sweetened beverage consumption. Increasing evidence also suggests a direct link. Our study aimed to determine whether there was a direct association between salt intake and obesity independent of energy intake. We analyzed the data from the rolling cross-sectional study-the UK National Diet and Nutrition Survey 2008/2009 to 2011/2012. We included 458 children (52% boys; age, 10±4 years) and 785 adults (47% men; age, 49±17 years) who had complete 24-hour urine collections. Energy intake was calculated from 4-day diary and misreporting was assessed by Goldberg method. The results showed that salt intake as measured by 24-hour urinary sodium was higher in overweight and obese individuals. A 1-g/d increase in salt intake was associated with an increase in the risk of obesity by 28% (odds ratio, 1.28; 95% confidence interval, 1.12-1.45; P=0.0002) in children and 26% (odds ratio, 1.26; 95% confidence interval, 1.16-1.37; P<0.0001) in adults, after adjusting for age, sex, ethnic group, household income, physical activity, energy intake, and diet misreporting, and in adults with additional adjustment for education, smoking, and alcohol consumption. Higher salt intake was also significantly related to higher body fat mass in both children (P=0.001) and adults (P=0.001) after adjusting for age, sex, ethnic group, and energy intake. These results suggest that salt intake is a potential risk factor for obesity independent of energy intake.
A reduction in salt intake lowers blood pressure (BP) and, thereby, reduces cardiovascular risk. A recent meta-analysis by Graudal implied that salt reduction had adverse effects on hormones and ...lipids which might mitigate any benefit that occurs with BP reduction. However, Graudal's meta-analysis included a large number of very short-term trials with a large change in salt intake, and such studies are irrelevant to the public health recommendations for a longer-term modest reduction in salt intake. We have updated our Cochrane meta-analysis.
To assess (1) the effect of a longer-term modest reduction in salt intake (i.e. of public health relevance) on BP and whether there was a dose-response relationship; (2) the effect on BP by sex and ethnic group; (3) the effect on plasma renin activity, aldosterone, noradrenaline, adrenaline, cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL) and triglycerides.
We searched MEDLINE, EMBASE, Cochrane Hypertension Group Specialised Register, Cochrane Central Register of Controlled Trials, and reference list of relevant articles.
We included randomised trials with a modest reduction in salt intake and duration of at least 4 weeks.
Data were extracted independently by two reviewers. Random effects meta-analyses, subgroup analyses and meta-regression were performed.
Thirty-four trials (3230 participants) were included. Meta-analysis showed that the mean change in urinary sodium (reduced salt vs usual salt) was -75 mmol/24-h (equivalent to a reduction of 4.4 g/d salt), the mean change in BP was -4.18 mmHg (95% CI: -5.18 to -3.18, I (2)=75%) for systolic and -2.06 mmHg (95% CI: -2.67 to -1.45, I (2)=68%) for diastolic BP. Meta-regression showed that age, ethnic group, BP status (hypertensive or normotensive) and the change in 24-h urinary sodium were all significantly associated with the fall in systolic BP, explaining 68% of the variance between studies. A 100 mmol reduction in 24 hour urinary sodium (6 g/day salt) was associated with a fall in systolic BP of 5.8 mmHg (95%CI: 2.5 to 9.2, P=0.001) after adjusting for age, ethnic group and BP status. For diastolic BP, age, ethnic group, BP status and the change in 24-h urinary sodium explained 41% of the variance between studies. Meta-analysis by subgroup showed that, in hypertensives, the mean effect was -5.39 mmHg (95% CI: -6.62 to -4.15, I (2)=61%) for systolic and -2.82 mmHg (95% CI: -3.54 to -2.11, I (2)=52%) for diastolic BP. In normotensives, the mean effect was -2.42 mmHg (95% CI: -3.56 to -1.29, I (2)=66%) for systolic and -1.00 mmHg (95% CI: -1.85 to -0.15, I (2)=66%) for diastolic BP. Further subgroup analysis showed that the decrease in systolic BP was significant in both whites and blacks, men and women. Meta-analysis of hormone and lipid data showed that the mean effect was 0.26 ng/ml/hr (95% CI: 0.17 to 0.36, I (2)=70%) for plasma renin activity, 73.20 pmol/l (95% CI: 44.92 to 101.48, I (2)=62%) for aldosterone, 31.67 pg/ml (95% CI: 6.57 to 56.77, I (2)=5%) for noradrenaline, 6.70 pg/ml (95% CI: -0.25 to 13.64, I (2)=12%) for adrenaline, 0.05 mmol/l (95% CI: -0.02 to 0.11, I (2)=0%) for cholesterol, 0.05 mmol/l (95% CI: -0.01 to 0.12, I (2)=0%) for LDL, -0.02 mmol/l (95% CI: -0.06 to 0.01, I (2)=16%) for HDL, and 0.04 mmol/l (95% CI: -0.02 to 0.09, I (2)=0%) for triglycerides.
A modest reduction in salt intake for 4 or more weeks causes significant and, from a population viewpoint, important falls in BP in both hypertensive and normotensive individuals, irrespective of sex and ethnic group. With salt reduction, there is a small physiological increase in plasma renin activity, aldosterone and noradrenaline. There is no significant change in lipid levels. These results provide further strong support for a reduction in population salt intake. This will likely lower population BP and, thereby, reduce cardiovascular disease. Additionally, our analysis demonstrates a significant association between the reduction in 24-h urinary sodium and the fall in systolic BP, indicating the greater the reduction in salt intake, the greater the fall in systolic BP. The current recommendations to reduce salt intake from 9-12 to 5-6 g/d will have a major effect on BP, but are not ideal. A further reduction to 3 g/d will have a greater effect and should become the long term target for population salt intake.
Abstract Raised blood pressure is a major cause of cardiovascular disease, responsible for 62% of stroke and 49% of coronary heart disease. There is overwhelming evidence that dietary salt is the ...major cause of raised blood pressure and that a reduction in salt intake lowers blood pressure, thereby, reducing blood pressure-related diseases. Several lines of evidence including ecological, population, and prospective cohort studies, as well as outcome trials, demonstrate that a reduction in salt intake is related to a lower risk of cardiovascular disease. Increasing evidence also suggests that a high salt intake may directly increase the risk of stroke, left ventricular hypertrophy, and renal disease; is associated with obesity through soft drink consumption; is related to renal stones and osteoporosis; is linked to the severity of asthma; and is probably a major cause of stomach cancer. In most developed countries, a reduction in salt intake can be achieved by a gradual and sustained reduction in the amount of salt added to foods by the food industry. In other countries where most of the salt consumed comes from salt added during cooking or from sauces, a public health campaign is needed to encourage consumers to use less salt. Several countries have already reduced salt intake. The challenge now is to spread this out to all other countries. A modest reduction in population salt intake worldwide will result in a major improvement in public health.
Objectives To determine the relationship between the reduction in salt intake that occurred in England, and blood pressure (BP), as well as mortality from stroke and ischaemic heart disease (IHD). ...Design Analysis of the data from the Health Survey for England. Setting and participants England, 2003 N=9183, 2006 N=8762, 2008 N=8974 and 2011 N=4753, aged ≥16 years. Outcomes BP, stroke and IHD mortality. Results From 2003 to 2011, there was a decrease in mortality from stroke by 42% (p<0.001) and IHD by 40% (p<0.001). In parallel, there was a fall in BP of 3.0±0.33/1.4±0.20 mm Hg (p<0.001/p<0.001), a decrease of 0.4±0.02 mmol/L (p<0.001) in cholesterol, a reduction in smoking prevalence from 19% to 14% (p<0.001), an increase in fruit and vegetable consumption (0.2±0.05 portion/day, p<0.001) and an increase in body mass index (BMI; 0.5±0.09 kg/m2, p<0.001). Salt intake, as measured by 24 h urinary sodium, decreased by 1.4 g/day (p<0.01). It is likely that all of these factors (with the exception of BMI), along with improvements in the treatments of BP, cholesterol and cardiovascular disease, contributed to the falls in stroke and IHD mortality. In individuals who were not on antihypertensive medication, there was a fall in BP of 2.7±0.34/1.1±0.23 mm Hg (p<0.001/p<0.001) after adjusting for age, sex, ethnic group, education, household income, alcohol consumption, fruit and vegetable intake and BMI. Although salt intake was not measured in these participants, the fact that the average salt intake in a random sample of the population fell by 15% during the same period suggests that the falls in BP would be largely attributable to the reduction in salt intake rather than antihypertensive medications. Conclusions The reduction in salt intake is likely to be an important contributor to the falls in BP from 2003 to 2011 in England. As a result, it would have contributed substantially to the decreases in stroke and IHD mortality.
The relation between sodium intake and cardiovascular disease remains controversial, owing in part to inaccurate assessment of sodium intake. Assessing 24-hour urinary excretion over a period of ...multiple days is considered to be an accurate method.
We included individual-participant data from six prospective cohorts of generally healthy adults; sodium and potassium excretion was assessed with the use of at least two 24-hour urine samples per participant. The primary outcome was a cardiovascular event (coronary revascularization or fatal or nonfatal myocardial infarction or stroke). We analyzed each cohort using consistent methods and combined the results using a random-effects meta-analysis.
Among 10,709 participants, who had a mean (±SD) age of 51.5±12.6 years and of whom 54.2% were women, 571 cardiovascular events were ascertained during a median study follow-up of 8.8 years (incidence rate, 5.9 per 1000 person-years). The median 24-hour urinary sodium excretion was 3270 mg (10th to 90th percentile, 2099 to 4899). Higher sodium excretion, lower potassium excretion, and a higher sodium-to-potassium ratio were all associated with a higher cardiovascular risk in analyses that were controlled for confounding factors (P≤0.005 for all comparisons). In analyses that compared quartile 4 of the urinary biomarker (highest) with quartile 1 (lowest), the hazard ratios were 1.60 (95% confidence interval CI, 1.19 to 2.14) for sodium excretion, 0.69 (95% CI, 0.51 to 0.91) for potassium excretion, and 1.62 (95% CI, 1.25 to 2.10) for the sodium-to-potassium ratio. Each daily increment of 1000 mg in sodium excretion was associated with an 18% increase in cardiovascular risk (hazard ratio, 1.18; 95% CI, 1.08 to 1.29), and each daily increment of 1000 mg in potassium excretion was associated with an 18% decrease in risk (hazard ratio, 0.82; 95% CI, 0.72 to 0.94).
Higher sodium and lower potassium intakes, as measured in multiple 24-hour urine samples, were associated in a dose-response manner with a higher cardiovascular risk. These findings may support reducing sodium intake and increasing potassium intake from current levels. (Funded by the American Heart Association and the National Institutes of Health.).
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