Lifestyle modifications to prevent and control hypertension. 5. Recommendations on dietary salt. Canadian Hypertension Society,Canadian Coalition for High Blood Pressure Prevention and Control,Laboratory Centre for Disease Control at Health Canada,Heart and Stroke Foundation of Canada

OBJECTIVE: To provide updated, evidence-based recommendations concerning the effects of dietary salt intake on the prevention and control of hypertension in adults (except pregnant women). The guidelines are intended for use in clinical practice and public education campaigns. OPTIONS: Restriction of dietary salt intake may be an alternative to antihypertensive medications or may supplement such medications. Other options include other nonpharmacologic treatments for hypertension and no treatment. OUTCOMES: The health outcomes considered were changes in blood pressure and in morbidity and mortality rates. Because of insufficient evidence, no economic outcomes were considered. EVIDENCE: A MEDLINE search was conducted for the period 1966-1996 using the terms hypertension, blood pressure, vascular resistance, sodium chloride, sodium, diet, sodium or sodium chloride dietary, sodium restricted/reducing diet, clinical trials, controlled clinical trial, randomized controlled trial and random allocation. Both trials and review articles were obtained, and other relevant evidence was obtained from the reference lists of the articles identified, from the personal files of the authors and through contacts with experts. The articles were reviewed, classified according to study design and graded according to level of evidence. In addition, a systematic review of all published randomized controlled trials relating to dietary salt intake and hypertension was conducted. VALUES: A high value was placed on the avoidance of cardiovascular morbidity and premature death caused by untreated hypertension. BENEFITS, HARMS AND COSTS: For normotensive people, a marked change in sodium intake is required to achieve a modest reduction in blood pressure (there is a decrease of 1 mm Hg in systolic blood pressure for every 100 mmol decrease in daily sodium intake). For hypertensive patients, the effects of dietary salt restriction are most pronounced if age is greater than 44 years. A decrease of 6.3 mm Hg in systolic blood pressure and 2.2 mm Hg in diastolic blood pressure per 100 mmol decrease in daily sodium intake was observed in people of this age group. For hypertensive patients 44 years of age and younger, the decreases were 2.4 mm Hg for systolic blood pressure and negligible for diastolic blood pressure. A diet in which salt is moderately restricted appears not to be associated with health risks. RECOMMENDATIONS: (1) Restriction of salt intake for the normotensive population is not recommended at present, because of insufficient evidence demonstrating that this would lead to a reduced incidence of hypertension. (2) To avoid excessive intake of salt, people should be counselled to choose foods low in salt (e.g., fresh fruits and vegetables), to avoid foods high in salt (e.g., pre-prepared foods), to refrain from adding salt at the table and minimize the amount of salt used in cooking, and to increase awareness of the salt content of food choices in restaurants. (3) For hypertensive patients, particularly those over the age of 44 years, it is recommended that the intake of dietary sodium be moderately restricted, to a target range of 90-130 mmol per day (which corresponds to 3-7 g of salt per day). (4) The salt consumption of hypertensive patients should be determined by interview. VALIDATION: These recommendations were reviewed by all of the sponsoring organizations and by participants in a satellite symposium of the fourth International Conference on Preventive Cardiology. They have not been clinically tested. SPONSORS: The Canadian Hypertension Society, the Canadian Coalition for High Blood Pressure Prevention and Control, the Laboratory Centre for Disease Control at Health Canada, and the Heart and Stroke Foundation of Canada.     

Serotonin,Eating Behavior,and Fat Intake

There is an intimate relationship between nutritional intake (eating) and serotonin activity. Experimental manipulations (mainly neuropharmacological) of serotonin influence the pattern of eating behavior, subjective feelings of appetite motivation, and the response to nutritional challenges. Similarly, nutritional manipulations (food restriction, dieting, or altered nutrient supply) change the sensitivity of the serotonin network. Traditionally, serotonin has been linked to the macronutrient carbohydrate via the intermediary step of plasma amino acid ratios. However, it has also been demonstrated that 5-HT drugs will reduce energy intake and reverse body weight gain in rats exposed to weight increasing high fat diets. 5-HT drugs can also reduce food intake and block weight gain of rats on a high fat cafeteria diet. Some diet selection studies in rats indicate that the most prominent reduction of macronutrient intake is for fat. These data indicate that 5-HT activity can bring about a reduction in fat consumption. In turn, different types of dietary fat can alter brain 5-HT activity. In human studies the methodology of food choice experiments has often precluded the detection of an effect of 5-HT manipulation on fat intake. However, there is evidence that in obese and lean subjects some 5-HT drugs can readily reduce the intake of high fat foods. Data also suggest that 5-HT activation can lead to a selective avoidance of fat in the diet. These effects of 5-HT on the intake of dietary fat may involve a pre-absorptive mechanism and there is evidence that 5-HT is linked to cholecystokinin and enterostatin. These proposals have theoretical and practical implications and suggest possible strategies to intensify or advance fat-induced satiety signals.     

Session on sodium and calcium in the management of hypertension summary of remarks of discussant and chairman

The evidence favouring a link between sodium and blood pressure, namely the interpopulation comparisons, the experimental animal models, and clinical trials of high sodium intake and very low sodium diets, appears to outweigh the evidence disputing this relationship. Differences between studies on the effect of sodium restriction on blood pressure may be explained by differences in a large number of factors including the nature of the study population, dietary sodium intake, amount of reduction of sodium, concurrent dietary intake of other ions and alcohol, and blood pressure at entry into the study. Further research is needed in order to answer the questions raised herein and to provide additional information on sodium and calcium management of hypertension.     

Blood pressure reduction by fish oil in adult rats with established hypertension--dependence on sodium intake.

The effects of fish oil combined with dietary sodium restriction on blood pressure and mesenteric vascular resistance were examined in a series of experiments with adult normotensive (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). Rats were fed normal or low sodium diets containing fish oil, olive oil or safflower oil. Small but significant reductions of blood pressure (measured directly in conscious rats) were seen in SHRSP but not in WKY after 8 weeks on a fish oil/low sodium diet, compared with rats fed olive or safflower oil diets with normal sodium content. This antihypertensive effect was not dependent on neurally mediated vasoconstriction but was associated with a reduction of basal resistance in the blood-perfused mesenteric artery. Subcutaneous injection of fish oil reduced blood pressure in adult SHRSP on a normal sodium diet. However, there was a further fall in blood pressure when sodium intake was reduced. The results indicate the antihypertensive effect of fish oil can be enhanced by restricting sodium intake.     

Differential effects of dietary sodium intake on blood pressure and atherosclerosis in hypercholesterolemic mice

The amount of dietary sodium intake regulates the renin angiotensin system (RAS) and blood pressure, both of which play critical roles in atherosclerosis. However, there are conflicting findings regarding the effects of dietary sodium intake on atherosclerosis. This study applied a broad range of dietary sodium concentrations to determine the concomitant effects of dietary sodium intake on the RAS, blood pressure, and atherosclerosis in mice. Eight-week-old male low-density lipoprotein receptor ?/? mice were fed a saturated fat-enriched diet containing selected sodium concentrations (Na 0.01%, 0.1%, or 2% w/w) for 12 weeks. Mice in these three groups were all hypercholesterolemic, although mice fed Na 0.01% and Na 0.1% had higher plasma cholesterol concentrations than mice fed Na 2%. Mice fed Na 0.01% had greater abundances of renal renin mRNA than those fed Na 0.1% and 2%. Plasma renin concentrations were higher in mice fed Na 0.01% (14.2±1.7 ng/ml/30 min) than those fed Na 0.1% or 2% (6.2±0.6 and 5.8±1.6 ng/ml per 30 min, respectively). However, systolic blood pressure at 12 weeks was higher in mice fed Na 2% (138±3 mm Hg) than those fed Na 0.01% and 0.1% (129±3 and 128±4 mmHg, respectively). In contrast, mice fed Na 0.01% (0.17±0.02 mm²) had larger atherosclerotic lesion areas in aortic roots than those fed Na 2% (0.09±0.01 mm²), whereas lesion areas in mice fed Na 0.1% (0.12±0.02 mm²) were intermediate between and not significantly different from those in Na 0.01% and Na 2% groups. In conclusion, while high dietary sodium intake led to higher systolic blood pressure, low dietary sodium intake augmented atherosclerosis in hypercholesterolemic mice.     

Sodium and potassium intake and blood pressure.

Sodium and potassium intakes were increased in normotensive volunteers to assess the effects on their blood pressures. An approximately threefold increase in sodium intake for eight days had no effect on the blood pressures of seven volunteers, while a two-stage increase in potassium intake, by about 40% for eight days and a further 55% for 14 days, had no effect on the blood pressures of 21 volunteers. Renal electrolyte excretions and the blood pressures of all 28 subjects showed no statistically significant correlations between either sodium or potassium excretion and blood pressure. A weak negative correlation was found between the sodium: potassium ratio and systolic pressure. The small reductions in sodium intake and increases in potassium intake that might be achieved through propaganda and changes in food processing are unlikely to lower mean blood pressure in Western societies.     

Plasma Renin Activity and Blood Pressure in 89 Patients Receiving Maintenance Haemodialysis Therapy

Blood pressure, plasma renin activity, plasma sodium concentration, plasma potassium concentration, dietary sodium intake, and duration of dialysis have been measured under standard conditions in 89 patients on maintenance haemodialysis. No significant relation was found between plasma renin activity and blood pressure. Statistically significant correlations were found between plasma renin activity and plasma sodium concentration and between plasma renin activity and dietary sodium intake.Only one patient was found to have uncontrollable hypertension associated with a markedly raised plasma renin activity. Reasons are given for not performing bilateral nephrectomy in this patient. We believe the low incidence of uncontrollable hypertension and hyperreninaemia in our patients to be due to their slow introduction to haemodialysis, thus preventing violent swings in body weight, blood pressure, and renin secretion.Although plasma renin activity did fall with duration of dialysis, all 15 patients who have been on maintenance dialysis for longer than five years have normal levels.     

Nutritional effects on blood pressure

PURPOSE OF REVIEW: There has not been a thorough recent evaluation of the nutritional effects on blood pressure. Apart from outstanding clinical trials like Dietary Approaches to Stop Hypertension, there have been controversial papers on a number of factors influencing blood pressure. This paper is a systematic review of the current literature as it relates to hypertension. RECENT FINDINGS: Results from many meta-analyses and well controlled clinical trials on the effects of a variety of nutritional factors are presented in this review. Evidence suggests that dietary sodium intake needs reduction. There is a seemingly inverse relationship between protein intake and blood pressure, but data are inconclusive. High monounsaturated fat and fish oil appear to be beneficial. Several studies on dietary fiber indicate that the strongest evidence for blood pressure lowering effects is in hypertensive as opposed to normotensive participants. Vegetarians seem to have lower levels of hypertension and cardiovascular disease risk. Low carbohydrate diets show short-term beneficial effects but are not sustained. High levels of potassium, magnesium, calcium and soy seem to have some benefit, but results remain inconclusive. Weight reduction positively impacts blood pressure. SUMMARY: More compelling research defining specific factors is needed to inform the public as to steps needed to reduce blood pressure and improve cardiovascular risk.     

Long-chain omega 3 fatty acids, blood lipids and cardiovascular risk reduction

Increasing evidence suggests that omega 3 fatty acids derived from fish and fish oils may play a protective role in coronary heart disease and its many complications, through a variety of actions, including effects on lipids, blood pressure, cardiac and vascular function, prostanoids, coagulation and immunological responses. Interesting differences between the effects of highly purified eicosapentaenoic acid and docosahexaenoic acid are emerging, which may be relevant in the choice of omega 3 fatty acid for incorporation into food products. On the basis of our current knowledge, we believe it is justified to recommend, particularly to high-risk populations, an increased dietary intake of omega 3 fatty acids through the consumption of fish.     

Sodium manipulation in the management of hypertension. The view against its general use

Extreme changes in sodium intake do have an effect on blood pressure of both normotensive and hypertensive individuals. Cross-population correlates of average sodium intake and mean population blood pressure are discordant with the results of studies within single populations and cannot be used as sufficient evidence to justify a reduction of dietary sodium intake in the general population to prevent hypertension. Both explanatory and management trials of sodium restriction have yielded contradictory results, and convincing evidence on the nature and size of subgroups of hypertensives with enhanced sodium sensitivity is lacking. The proportion of patients who will follow a moderately restricted sodium diet is low, unless expensive and time-consuming programs of instruction and monitoring are introduced. In light of this evidence, it is premature to recommend diets that are low in sodium as a public health measure and as initial and sole treatment of hypertension.     

Hypertension and nutrition in the young: early intervention?

The few studies, carried out on infants, children, and adolescents, relating blood pressure to sodium intake have shown a weak positive correlation in some but not all individuals. The effect of body size on blood pressure confounds the interpretation of the effect of dietary sodium on blood pressure. There appear to be sodium-sensitive and sodium-unsensitive infants, children, and adolescents and is probably genetically transmitted. Most infants, children, and adolescents in industrialized populations have a salt intake far greater than required, and reduction in dietary sodium is safe and may be beneficial to those individuals with a family history of primary hypertension.     

Dietary sodium induced cardiac hypertrophy.

In humans, high sodium intake not only increases the blood pressure, and thus can cause left ventricular hypertrophy (LVH), but also appears to increase LVH independent of this increase in blood pressure. In both normo- and hyper-tensive rats the hypertrophic effect of increased dietary sodium intake on the heart has been clearly established. In normotensive rats, this effect is strain and age dependent, and seems independent of hemodynamic effects of high sodium intake. In both rats and humans, dietary sodium appears to increase wall thickness, resembling pressure overload rather than an increased left ventricular diameter as expected of volume overload. The mechanisms through which high dietary sodium induces hypertrophy are still unknown. It is possible that dietary sodium increases either adrenergic stimulation and (or) enhances sensitivity for adrenergic stimulation and that this hypertrophic response mainly acts via stimulation of alpha 1-adrenergic receptors. Stimulation of the alpha 1-adrenergic receptors will increase the inositol phosphate-diacyl glycerol pathway and enhance the Na+/H+ exchange. The activity of this exchanger might play an important role in the development of dietary sodium induced cardiac hypertrophy.     

Dietary sodium restriction for mild hypertension in general practice.

Eighteen patients with stable mild hypertension (mean blood pressure 144/93 mm Hg) restricted their sodium intake for eight weeks while taking part in a double blind randomised crossover trial of slow sodium and placebo tablets. Mean 24 hour urinary sodium excretion was 143 mmol(mEq) during the period on slow sodium and 87 mmol during the period on placebo. Five patients were unable to reduce their sodium intake below 120 mmol, but the others had a mean 24 hour urinary sodium excretion of 59 mmol during the period on placebo. There was no significant difference in blood pressure between the slow sodium and placebo treatment periods, although the study had a power of 99% to detect a difference of 5 mm Hg in mean arterial pressure between the two periods. Moderate dietary sodium restriction does not lower blood pressure in patients with this degree of hypertension.     

Blood pressure control during weight reduction in obese hypertensive men: separate effects of sodium and energy restriction.

The separate and combined effects of dietary energy and sodium restriction on regulation of blood pressure were investigated in 30 middle aged obese men with essential hypertension attending the outpatient department. In group 1 (n = 15) a basal period with no dietary restriction was followed by a period taking an energy reduced diet (5.1 MJ; 1230 kcal), the sodium intake being supplemented and hence unchanged (1:ErSn). In group 2 (n = 15) the basal period preceded a control period with no intervention, which was followed by taking a diet restricted in energy (5.1 MJ; 1220 kcal) and sodium (2:ErSr). During period 1:ErSn there were reductions in heart rate and urinary noradrenaline output but not in systolic or diastolic blood pressure. Body weight decreased by 4.9-11.7 kg and urinary sodium excretion did not change. In period 2:ErSr urinary sodium output was reduced by 81.4 (SEM 17.8) mmol(mEq)/24 h and there was a weight loss of 8.2 (SEM 0.7) kg. Systolic and diastolic blood pressures fell significantly, as did the heart rate and urinary noradrenaline excretion. These results show that in hypertensive obese men a moderate weight reducing diet decreases indices of sympathetic nervous system activity. Reduction of blood pressure to the normotensive range was observed only when there was a concomitant restriction of sodium intake.     

Self-selection of Dietary Threonine in the Rat and the Effect of Taste Stimuli on its Selection

The possible regulation of dietary threonine intake and the effect of a palatable (sodium saccharin) or aversive (quinine sulfate) taste stimulus on the manner of threonine selection were investigated in rats using a self-selection feeding method. Weanling rats were offered the choice of two diets differing only in threonine content for 2 weeks. Both weight gain and food consumption in the rats offered the choice of diets were quite comparable to each other and were the same as those in rats fed one diet containing sufficient threonine. Threonine intake of the self-selecting rats ranged from 0.43 to 1.90% of the food consumed. The threonine concentrations in the plasma and brain of the self-selecting rats increased proportionally with the threonine intake. When rats were offered a choice of two diets containing various amounts of threonine with taste materials, i.e., sodium saccharin or quinine sulfate, neither the dietary threonine nor their growth were ever affected.

These results indicate clearly that rats have an ability to regulate threonine intake to meet their requirement for the l-amino acid, and the threonine selection is not influenced significantly by the dietary addition of palatable or aversive taste materials.     

Sodium and potassium intake and blood pressure change in childhood.

OBJECTIVE--To assess the association between sodium and potassium intake and the rise in blood pressure in childhood. DESIGN--Longitudinal study of a cohort of children with annual measurements during an average follow up period of seven years. SETTING--Epidemiological survey of the population of a suburban town in western Netherlands. SUBJECTS--Cohort of 233 children aged 5-17 drawn at random from participants in the population survey. MAIN OUTCOME MEASURES--At least six annual timed overnight urine samples were obtained. The mean 24 hour sodium and potassium excretion during the follow up period was estimated for each participant and the sodium to potassium ratio calculated. Individual slopes of blood pressure over time were calculated by linear regression analysis. RESULTS--No significant association was observed between sodium excretion and the change in blood pressure over time. The mean systolic blood pressure slopes, however, were lower when potassium intake was higher (coefficient of linear regression -0.045 mm Hg/year/mmol; 95% confidence interval -0.069 to -0.020), and the change in systolic pressure was greater when the urinary sodium to potassium ratio was higher (0.356 mm Hg/year/unit; 95% confidence interval 0.069 to 0.642). In relation to potassium this was interpreted as a rise in blood pressure that was on average 1.0 mm Hg (95% confidence interval -1.65 to -0.35) lower in children in the upper part of the distribution of intake compared with those in the lower part. The mean yearly rise in systolic blood pressure for the group as a whole was 1.95 mm Hg. Urinary electrolyte excretion was not associated with diastolic blood pressure. CONCLUSION--Dietary potassium and the dietary sodium to potassium ratio are related to the rise in blood pressure in childhood and may be important in the early pathogenesis of primary hypertension.     

Vitamin supplementation and blood pressure in Type 2 diabetes

Diabet. Med. 29, 1253-1259 (2012) ABSTRACT: Aims Vitamin D levels are inversely related to blood pressure. Given that low sun exposure can create a greater reliance on dietary sources of vitamin D, we aimed to determine whether dietary vitamin D and blood pressure associations differ between periods of low and high sun exposure. Methods Dietary intake, vitamin supplementation, blood pressure, and anthropometric parameters were assessed each season for 1?year (174 adults with Type 2 diabetes). Separate linear regression models were constructed for high and low sun exposure periods to examine associations of systolic blood pressure with dietary vitamin D intake and vitamin supplement use (adjusted for age, gender, BMI, ethnicity, smoking, alcohol, physical activity, antihypertensive medication and nutrient intake). Robustness of findings was confirmed with within-subject repeated measures analysis, including an interaction term for sun exposure period. Results Vitamin D intake from food sources was low year-round and no conclusive association with blood pressure was identified during either period. Systolic blood pressure was 5.1?mmHg lower during the low sun exposure period (95% CI 0.5-9.7) in daily supplement users compared with non-users. The interaction term between supplement use and sun exposure period was significant (low sun exposure* no supplement, P?=?0.02). Systolic blood pressure was relatively stable in users (low and high sun exposure periods, respectively, mean?±?SE: 135.2?±?2.6?mmHg and 134.2?±?2.5?mmHg), but not in non-users (140.2?±?2.7?mmHg and 130.5?±?2.5?mmHg). Conclusions Vitamin supplementation may stabilize systolic blood pressure in adults with Type 2 diabetes across seasons.     

Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium

Responses to acute sodium loading depend on the load and on the level of chronic sodium intake. To test the hypothesis that an acute step increase in total body sodium (TBS) elicits a natriuretic response, which is dependent on the chronic level of TBS, we measured the effects of a bolus of NaCl during different low-sodium diets spanning a 25-fold change in sodium intake on elements of the renin-angiotensin-aldosterone system (RAAS) and on natriuresis. To custom-made, low-sodium chow (0.003%), NaCl was added to provide four levels of intake, 0.03-0.75 mmol.kg(-1).day(-1) for 7 days. Acute NaCl administration increased PV (+6.3-8.9%) and plasma sodium concentration (~2%) and decreased plasma protein concentration (-6.4-8.1%). Plasma ANG II and aldosterone concentrations decreased transiently. Potassium excretion increased substantially. Sodium excretion, arterial blood pressure, glomerular filtration rate, urine flow, plasma potassium, and plasma renin activity did not change. The results indicate that sodium excretion is controlled by neurohumoral mechanisms that are quite resistant to acute changes in plasma volume and colloid osmotic pressure and are not down-regulated within 2 h. With previous data, we demonstrate that RAAS variables are log-linearly related to sodium intake over a >250-fold range in sodium intake, defining dietary sodium function lines that are simple measures of the sodium sensitivity of the RAAS. The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake.     

Dietary sodium and arterial blood pressure: evidence against genetic susceptibility.

Thirty five subjects with both parents in the top third of their age specific blood pressure distributions and 31 subjects with both parents in the bottom third of their blood pressure distributions restricted their intake of sodium for eight weeks while taking part in a double blind, randomised crossover trial of supplements of sodium and placebo. A comparison of two periods of four weeks at different intakes of sodium showed no differences in blood pressure in either the groups as a whole or the subgroups who complied best with the diet and tablets. In the compliant subgroups mean urinary sodium excretions were above 120 mmol(mEq) and below 50 mmol/day. The study provides evidence against the hypothesis that people with a family history of high blood pressure are more susceptible in their blood pressure response to dietary sodium.     

Sodium and potassium in essential hypertension.

A study was carried out of arterial pressure and body content of electrolytes in 91 patients with essential hypertension and 121 normal controls. Exchangeable sodium was found to be positively correlated with arterial pressure in the patients, the correlation being closest in older patients; values of exchangeable sodium were subnormal in young patients; and plasma, exchangeable, and total body potassium correlated inversely with arterial pressure in the patients, the correlations being closest in young patients. Three hypotheses were proposed to explain the mechanisms relating electrolytes and arterial pressure in essential hypertension--namely, a cell-salt hypothesis, a dietary salt hypothesis, and a kidney-salt hypothesis. It was concluded that two mechanisms probably operate in essential hypertension. In the early stages of the disease blood pressure is raised by an abnormal process related more closely to potassium than to sodium. A renal lesion develops later, possibly as a consequence of the hypertension. This lesion is characterised by resetting of pressure natriuresis and is manifest by an abnormal relation between body sodium and arterial pressure and by susceptibility to increased dietary sodium intake.