Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate (2005) / Chapter Skim
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6 Sodium and Chloride
6 Sodium and Chloride
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/day in Northern Japan. The ability to survive at extremely low levels of sodium intake re flects the capacity of the normal human body to conserve sodium by markedly reducing losses of sodium in the urine and sweat.
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Concerns have been raised that a low level of sodium intake ad versely affects blood lipids, insulin resistance, and cardiovascular disease risk. However, at the level of the AI, the preponderance of evidence does not support this contention.
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/day. While blood pressure, on average, rises with increased sodium intake, there is well-recognized heterogeneity in the blood pres sure response to changes in sodium chloride intake.
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It is well-recognized that the current intake of sodium for most individuals in the United States and Canada greatly exceeds both the AI and UL. Progress in achieving a reduced sodium intake will likely be incremental and will require changes in individual be havior towards salt consumption, replacement of high salt foods with lower salt versions, increased collaboration of the food indus try with public health officials, and a broad spectrum of additional research.
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With reduced salt intake, reduced blood volume, or reduced blood pressure, the renin-angiotensin-aldosterone axis is stimulated. When the renin-angiotensin-aldosterone system is less responsive, as with advancing age, there is a greater blood pressure reduction from a reduced intake of sodium chloride (Cappuccio et al., 1985; Weinberger et al., 1993a)
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, which accounts for approximately 90 percent of the total sodium intake in the United States. Sodium bicarbonate is used as an ingredient in foods.
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. INDICATORS CONSIDERED FOR ESTIMATING THE REQUIREMENTS FOR SODIUM AND CHLORIDE The following section reviews the potential markers for adverse effects resulting from insufficient sodium intake in apparently healthy individuals.
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. Urine and Feces In nonsweating individuals living in a temperate climate who are in a steady-state of sodium and fluid balance, urinary sodium excretion is approximately equal to sodium intake (i.e., 90 to 95 percent of total intake is excreted in urine)
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. One study provided detailed information on sweat losses at three levels of dietary sodium intake (Allsopp et al., 1998)
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for 5 d, 3 levels of sodium intake/d 1.5 g (66 mmol)
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279 SODIUM AND CHLORIDE Sodium Concentration in Sweat, Sweat Sodium Loss, mmol/L (g/L) mmol/d (g/d)
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. Some infants presented with hypokalemia, metabolic alkalosis, hematuria, hyperaldosteronism, and increased plasma renin levels (Roy, 1984)
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Not determined Serum or Plasma Sodium Concentration A number of studies have reported the concentrations of serum or plasma sodium by level of dietary sodium intake. Changes in sodium intake can influence serum or plasma levels of sodium, but the changes are relatively small and do not lead to pathological conditions, such as hyponatremia.
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. In a meta-analysis that only included trials lasting for 4 or more weeks and excluding those trials with extremely low sodium intakes, sodium reduction led to an average increase in plasma renin activity of 0.36 ng/mL/ hour from a median value of 1.55 ng/mL/hour (He and MacGregor, 2002)
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. Some investigators have interpreted the rise in plasma renin activity from a reduced sodium intake as a deleterious response that mitigates the potential benefits of sodium reduction on blood pressure (Alderman et al., 1991)
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1–2 d Ruppert et al., 1991 98 salt-resistant men and women 7-d crossover Cappuccio et al., 1997 18 men and women 4-wk crossover Hypertensive individuals Mark et al., 1975 6 men with borderline HT 10-d crossover
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285 SODIUM AND CHLORIDE Urinary Sodium,b Dietary Sodium, Plasma Renin Activity, g/d (mmol/d) g/d (mmol/d)
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. Further research is needed before plasma renin activity can be used as a marker of adequacy for sodium intake.
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reductions in blood pressure in response to reduced sodium intake. Those with the greatest reductions in blood pressure have been termed "salt sensitive," while those with little or no reduction in blood pressure have been termed "salt resistant." Some investigators have reported that blood pressure might rise in response to sodium reduction, potentially because of activation of the renin-angiotensinaldosterone system.
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FIGURE 6-2a Distribution of blood pressure differences between two points in time when sodium intake was similar. Each 5 mm Hg bar is centered.
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. An apparent rise in blood pressure in some individuals when sodium intake is reduced has been interpreted as a pressor response, potentially as a result of an overactive renin-angiotensin-aldosterone system.
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Furthermore, the standard deviation of the distribution of change in blood pressure was similar, 8.4 versus 8.6 mm Hg, respectively, suggesting that much of the variability in blood pressure response to a reduced sodium intake (including an apparent increase in blood pressure in some individuals) results from random factors unrelated to sodium intake.
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reported that while a rise in plasma renin activity and aldosterone concentration were observed in all subjects placed on a reduced sodium diet, the largest increases were observed in those whose blood pressure increased. Those who have the greatest reduction in blood pressure as a result of a reduced sodium intake appear to have a less responsive reninangiotensin-aldosterone system (Cappuccio et al.
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Insulin Resistance A possible adverse effect of reduced sodium intake on insulin resistance has been postulated, potentially as a result of increased sympathetic nervous system activity. It has also been hypothesized that this phenomenon might be more prevalent in certain subgroups -- those individuals who experience little or no reduction in blood pressure from a reduced sodium intake (salt-resistant individuals)
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Longer-term studies at relevant sodium intakes are needed to assess the effects of sodium intake on insulin resistance. FACTORS AFFECTING SODIUM AND CHLORIDE REQUIREMENTS Physical Activity and Temperature Physical activity can potentially affect sodium chloride balance, mostly from increased losses in sweat.
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individuals Masugi et al., 1988 8 patients with essential HT 5-d parallel Del Rio et al., 1993 30 men 2-wk crossover Boero et al., 2000 13 men and women, 21–64 yr 2-wk crossover Grobbee et al., 1987 40 young adult men and women with mildly elevated blood pressure 6 wk Geleijnse et al., 1995 89 men and women, 55–75 yr 24-wk parallel Nonhypertensive and hypertensive individuals Harsha et al., 2004 390 men and women 4-wk crossover feeding study a LDL = low-density lipoprotein, HDL = high-density lipoprotein, TC = total cholesterol. b Differed significantly at p < 0.05.
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300 → 20 Total and LDL cholesterol greater in counter-regulators with sodium reduction 185 vs. 52 No difference in total or LDL cholesterol 220 → 20 Total cholesterol 4.26 → 4.52b LDL cholesterol 2.86 → 3.13b HDL cholesterol 0.89 → 0.85 105 vs.
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strenuously in the heat on a daily basis can lose substantial amounts of sodium. The loss of sodium in sweat is dependent on a number of factors, including overall diet, sodium intake, sweating rate, hydration status, and degree of acclimatization to the heat (Allan and Wilson, 1971; Allsopp et al., 1998; Brouns, 1991)
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. Sodium sweat loss was reported to be significantly greater when subjects performed a running exercise than when the subjects sat in a climatic chamber at 40°C (104°F)
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The joint effects on sodium loss of physical activity (or temperature) with dietary sodium intake has received little attention.
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. A similar lack of effect of calcium supplementation on urinary sodium excretion was seen over a longer (8 week)
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While there is some evidence that an extremely reduced sodium intake to 0.46 g (20 mmol) /day can decrease insulin sensitivity, there is little evidence of the adverse effects of sodium reduction to levels of ≈ 1.2 g (50 mmol)
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Issues debated have been the extent to which sodium is required in infancy for normal growth and the possibility that adult hypertension results from excess sodium intake during early years (Dahl, 1968; de Wardener and MacGregor, 1980)
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Hence the quantitative impact of sodium intake on growth in healthy, full-term infants cannot be ascertained from the available literature described above. It has been suggested that changes in extracellular fluid volume in infants in response to sodium intake could be a measure of adequacy of sodium, and possibly excess as well (Bernstein et al., 1990)
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The authors concluded that dietary sodium was required in sufficient quantities to permit normal expansion of the extracellular fluid volume that accompanies tissue growth. Chloride As stated earlier, chloride requirements are generally met due to the presence of sodium chloride in processed foods and infant formula.
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The AI for sodium for older infants is determined by estimating the sodium intake from human milk (sodium concentration × 0.6 L/day) and from complementary foods (Chapter 2)
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b Bold values also used in determining sodium concentration for months 7 through 12. Sodium and Chloride AI Summary, Ages 0 Through 12 Months AI for Sodium for Infants 0–6 months 0.12 g (5 mmol)
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Given that little data are available indicating that in normal children, inadequate sodium intakes result in specific identifiable markers, and that, as with adults, normal kidney function can maintain sodium balance at extremes of sodium intake, the AI is set based on meeting nutrient needs for other essential nutrients. The AI is thus extrapolated down from the adult AI of 1.5 g/day (65 mmol/day)
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, which requires an indicator of adequacy evaluated at multiple levels of intake, and an assessment of the level at which approximately half of the individuals in the life stage group would demonstrate inadequacy for that indicator. However, available evidence supports an AI of 1.5 g (65 mmol)
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diet and the DASH diet. Both provided an average sodium intake of approximately 1.5 g (65 mmol)
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as estimated by mean urinary excretion. The sodium intake of each participant was indexed to calorie level (0.9 to 1.8 g/d (39 to 78 mmol, corresponding to 1,600 to 3,600 kcal/d)
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. The clinical significance of this impaired response may be considerable when older individuals must quickly adapt to the reduced sodium intakes that are often seen during illnesses or following surgery.
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Increased blood pressure has been directly associated with increased sodium intake. Blood pressure, on average, rises with increased sodium intake (see subsequent discussion)
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sodium intake in persons older than 45 years compared with those 45 years of age or younger has also been noted (Vollmer et al., 2001)
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. There are major differences of opinion on the interpretation of these volume changes that occur during normal pregnancy and their relationship to sodium intake and thus requirements.
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. Of interest is a study in which pregnant women decreased their sodium intake to approximately 0.23 g (10 mmol)
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as well as that seen in nonpregnant women. At the opposite extreme of sodium intake, it is evident that in cultures with virtually no sodium intake (e.g., the Yanomamo Indians)
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The estimated median energy intake of lactating women (2,066 kcal/day [IOM, 2002]
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. Sodium intake invariably rises with increased energy intake in physically active individuals and this increase usually is enough to compensate for sweat sodium losses.
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INTAKE OF SODIUM Sources Sodium chloride (salt) is the primary form of sodium in the diet.
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. Only about 12 percent of the total sodium chloride consumed is naturally occurring (Mattes and Donnelly, 1991)
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These intake ranges are equivalent to 7.8 to 11.8 g/ day of sodium chloride for men and 5.8 to 7.8 g/day of sodium chloride for women. The estimated dietary sodium intakes of both white and African American men and women in the United States were similar (Appendix Tables D-9 and D-10)
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321 SODIUM AND CHLORIDE TABLE 6-10 Daily Sodium Intake from a Diet Providing 2,200 kcal Meal Food/Beverage Consumed Calories (kcal) Sodium (mg)
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. There is a lack of data on average sodium intakes during pregnancy and only a few studies have reported sequentially measured urinary sodium excretion.
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The ratio then rises rapidly to just above two for children 4 through 8 years of age, and remains above two into adulthood, but then drops somewhat in middle- and older-aged adults. The progressive rise in this ratio at an early age reflects a greater increase in dietary sodium intake compared with the increase in dietary potassium intake.
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years years 32 32 50-59 50-59 years years Stroke Mortality Stroke Mortality 16 16 8 8 4 4 2 2 1 1 120 140 160 180 70 80 90 100 110 Usual systolic blood Usual diastolic blood pressure (mm Hg) pressure (mm Hg)
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Although only one blood pressure-reduction trial with a clinical endpoint has been conducted in nonhypertensive individuals (PCG, 2001) , several analyses have estimated the potential benefits from population-wide application of therapies, such as sodium reduction.
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. Within-population studies of sodium and blood pressure generally lack statistical power, in large part because of large day-to-day variations in sodium intake and because of imprecise methods (e.g., use of a food-frequency questionnaire rather than a 24-hour urinary sodium excretion to assess sodium intake)
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NOTE: Studies include a sample size of at least 1,000 in which urinary sodium was measured. ment of the true relationship between sodium intake and blood pressure in observational studies.
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. Urinary sodium, blood pressure, and a number of potentially confounding variables were measured in 10,079 men and women, aged 20 to 59 years, from geographically diverse regions around the world with substantial variation in sodium intake.
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Only 10 trials tested three or more levels of dietary sodium intake (see Appendix I)
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330 DIETARY REFERENCE INTAKES TABLE 6-12 Intervention Studies on Sodium Intake and Blood Pressure in Nonhypertensive Adults in Order of Increasing Duration of Intervention Sodium (Na) Na/ Intake g/d Potassium Study Designa References (mmol)
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331 SODIUM AND CHLORIDE Blood Pressure SBP/DBPb Urinary Na Urinary K (mmol/d) (mmol/d)
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332 DIETARY REFERENCE INTAKES TABLE 6-12 Continued Sodium (Na) Na/ Intake g/d Potassium Study Designa References (mmol)
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333 SODIUM AND CHLORIDE Blood Pressure SBP/DBPb Urinary Na Urinary K (mmol/d) (mmol/d)
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Na-containing beverage or placebo, reduced dietary salt intake < 2.3 g (100 mmol/d) 4 wk Sacks et al., 208 men and women, DASH → 1.2 (50)
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335 SODIUM AND CHLORIDE Blood Pressure SBP/DBPb Urinary Na Urinary K (mmol/d) (mmol/d)
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Anderson, 6 mo Normal diet 1987 Hypertension 841 men and women, Na-kcal n = 126 Prevention aged 25–49 yr Control 3.3 Trial 6–36 mo Na reduction alone 3.4 Research Na-K n = 196 Group, 1990 Control 3.2 Na reduction alone 3.3 Na reduction with increased K 3.2 Kumanyika 744 men and women, Control 156 et al., 1993 no diet information; Na-reduced diet 155 behavior change counseling 6–18 mo He et al., 2000 128 men and women 18–96 mo Control diet Na-reduced diet TOHP 594 men and women 3.0 Collaborative 6–36 mo Research Group, 1997 a NTN = normotensive, HTN = hypertensive. b SBP = systolic blood pressure, DBP = diastolic blood pressure, MAP = mean arterial pressure, SS = salt sensitive, SR= salt resistant.
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337 SODIUM AND CHLORIDE Blood Pressure SBP/DBPb Urinary Na Urinary K (mmol/d) (mmol/d)
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338 DIETARY REFERENCE INTAKES TABLE 6-13 Intervention Studies on Sodium Intake and Blood Pressure in Hypertensive Adults, in Order of Increasing Duration of Intervention Sodium (Na) Na/ Intake g/d Potassium Study Designa References (mmol/d)
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(mmol/d) ↓ 47/↓ 21 0.43 mmol/L 88 mmol/L Also associated with weight loss 142d/92d 39 60 148d/98d 177 64 150d/96d 370 69 156d/104d 159d/105d 25 56 ↑ 9/↑ 6 122 60 MAP 107d 38 62 115e 334 67 119d/84d 15 68 120d/84d 343 67 MAP SS SR SS SR SS SR 105d 110d 3.7 10.5 56 63 124e 114e 215 259.7 60 72 MAP 92d 21 95d 214 SS SR 127d/82d 132d/85d 54 68 151e/95e 138d/90d 217 60 continued
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340 DIETARY REFERENCE INTAKES TABLE 6-13 Continued Sodium (Na) Na/ Intake g/d Potassium Study Designa References (mmol/d)
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341 SODIUM AND CHLORIDE Urinary Nab Urinary K Blood Pressure SBP/DBPc (mm Hg) (mmol/d)
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1992 sodium diet + placebo or 1.4 (61) 61 mmol Na supplement 4 wk Fotherby and 17 elderly men and women, 1.8 (80)
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343 SODIUM AND CHLORIDE Urinary Nab Urinary K Blood Pressure SBP/DBPc (mm Hg) (mmol/d)
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d,e,f Values with different superscripts differed significantly at p < 0.05. Individual trials that tested three or more levels of sodium intake provide the best evidence to assess dose-response relationships between dietary sodium intake and blood pressure.
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No trial lasted for more than one month, and several lasted only a few days (see Appendix Table I-2)
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The trial by Johnson and colleagues (2001) tested increasing levels of sodium intake from baseline by giving four different levels of sodium chloride (range of total intake: 0.9 g [40 mmol]
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. The average achieved levels of sodium intake, as reflected by 24-hour urinary sodium excretion, were 142, 107, and 65 mmol/day, respectively, corresponding to approximate intakes of 3.3 g, 2.5 g, and 1.5 g, respectively (Sacks et al., 2001)
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. Second, the DASH diet, compared with the control diet, blunted the effects of sodium on blood pressure, that is, over the same range of sodium intake, lowering sodium from 3.4 to 1.2 g (150 to 50 mmol)
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. In addition to the 10 trials that directly tested three or more levels of sodium intake, the Trials of Hypertension Prevention–Phase 1 (Kumanyika et al., 1993)
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These meta-analyses have provided consistent evidence that a reduced sodium intake lowers systolic and diastolic blood pressure in hypertensive individuals. However, the extent of blood pressure reduction in nonhypertensive individuals is less consistent.
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This meta-analysis documents the difficulties of sustaining a reduced sodium intake in free-living persons over the long-term. Because of the limited net reduction in sodium intake as evidenced by attained urinary sodium excretion, the efficacy of sodium reduction as a means to lower blood pressure cannot be assessed from this analysis.
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He and Randomized trials of modest 17 hypertensive trials and 11 MacGregor, Na reduction that lasted 4 or nonhypertensive trials 2002 more wk representing 954 subjects Hooper et al., Randomized trials of behavioral 3 nonhypertensive trials, 5 2002 interventions to reduce Na hypertensive trials intake that lasted at least (untreated) , and 3 treated 6 mo hypertensive trials representing 3,514 subjects Geleijnse Randomized trials with a 19 nonhypertensive trials, 28 et al., 2003 minimum duration of 2 wk hypertensive trials a SBP = systolic blood pressure, DBP = diastolic blood pressure, NT = nonhypertensive, HT = hypertensive.
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1.2 and 0.26 mm Hg, respectively, in NT individuals; (2) 3.9 and 1.9 mm Hg respectively in HT patients A high sodium chloride diet significantly increased SBP and DBP by 5.58 and 3.5 mm Hg, respectively A median reduction of urinary Na of 1.7 g/d (74 mmol/d)
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. For example, a downward shift in the population distribution of systolic blood pressure by 2 mm Hg would be expected to result in an annual reduction of 6 percent in mortality from stroke and 4 percent from coronary heart disease (Stamler, 1991)
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Results of this trial indicate that behavioral interventions can prevent hypertension over the long-term. Also, the pattern of incident hypertension at 6 and 18 months suggests that the effects of weight loss and reduced sodium intake, under optimal conditions of adherence, may be additive.
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. Greater and more sustainable reductions in sodium intake could be expected from a diminution in the amount of sodium added during food processing (approximately 80 percent of sodium consumed in westernized countries is derived from food products)
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. Given the current market availability of lowersodium food products, careful selection is necessary to lower sodium intake.
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. Urinary sodium excretion as obtained and reported in this study did not represent habitual dietary sodium intake.
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Epidemiologic Follow-up Study to examine the relationship between sodium intake as obtained from self-reported dietary information and the subsequent risk of cardiovascular disease. They identified an inverse relationship between sodium intake and mortality from cardiovascular diseases (p = 0.09)
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Intakea (g/d) Reference Study Design Stroke Kagan Prospective cohort, 10-yr et al., follow-up, n = 7,895 Japanese 1985 men, multivariate analysis Perry and Intersalt study, cross-sectional, Beevers, n = 3,942 men and women 1992 Yamori CARDIAC Study, cross-sectional, et al., 14 countries 1994 Sasaki et al., Cross-sectional data collected 1995 from 24 published studies Alderman Prospective cohort, 3.8-yr Urinary Na (mmol/24 h)
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Positive correlation between urinary Na and rate of stroke mortality (p < 0.01 to p < 0.001) RR for Stroke 1.0 1.6 1.0 0.5 Positive correlation between Na intake and stroke mortality (p = 0.029)
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Reference Study Design Coronary heart disease Ikeda et al., Cross-sectional, 1,310 men and 1986 women from 49 regions in Japan Alderman Prospective cohort, 3.8-yr Urinary Na (mmol/24 h) et al., follow-up, 2,937 men and Men 1997 women Q1 < 89 Q2 89–126 Q3 127–174 Q4 > 174 Women Q1 < 66 Q2 66–97 Q3 98–138 Q4 > 139 Tunstall- Scottish Heart Health Study, Urinary Na (mmol/L/d)
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9.6 Adjusted hazard ratios for CHD, CVD, and Significant, direct relationships all-cause mortality in men and women of urinary Na excretion with associated with a 100 mmol/d increase in cardiovascular outcomes in urinary Na excretion were 1.56, 1.36, and overweight persons; 1.22, respectively nonsignificant in nonoverweight individuals
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, there were no significant relationships between sodium intake (as assessed by multiple 24-hour dietary recalls) and mortality from total cardiovascular disease, coronary heart disease, or stroke (Cohen et al., 1999)
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In a subsequent analysis of the NHANES database by He and colleagues (2002) , dietary sodium intake was a significant, independent risk factor for congestive heart failure in overweight individuals.
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, and, as discussed subsequently, sodium intake. Several cross-sectional studies have examined the relationship between sodium intake, typically as measured by urinary sodium excretion, and left ventricular mass or hypertrophy, as measured by echocardiography.
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. Four clinical trials assessed the effects of a reduced sodium intake on left ventricular mass in hypertensive individuals.
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b LVH = left ventricular hypertrophy, LVM = left ventricular mass. NOTE: Sodium intake estimated to be approximately equal to urinary excretion.
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. In summary, available data from cross-sectional studies in hypertensive individuals are consistent in documenting a progressive, direct, and independent relationship between sodium intake and left ventricular mass.
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et al., 1989 Low salt diet ± salt supplement 3.9 (170) 10 d Zarkadas 17 postmenopausal women 2.0 (89)
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0.15a 0.15a 0.26b 0.14a Control diet (mg Ca/g creatinine) DASH diet (mg Ca/g creatinine)
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. The effects of a reduced sodium intake in preventing bone fractures has not been tested.
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of these studies. More recently, the Intersalt study correlated gastric cancer mortality with sodium intake from 24 countries (Joossens et al., 1996)
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374 DIETARY REFERENCE INTAKES TABLE 6-20 Epidemiological Studies on the Effect of Sodium Intake on Calcium Excretion, Bone Mineral Density, and Kidney Stones Study Designa Effectb Reference Urinary calcium excretion Short et al., 12 men and women on 4 levels of Na and + 1988 constant Ca 3-d planned diet Nordin et al., 220 women + 1993 Itoh and Randomized population survey + Suyama, 1996 410 men, 476 women Dawson-Hughes Cross-sectional + et al., 1996 249 men, 665 women Bone density Greendale Longitudinal NS et al., 1994 258 women, 169 men Matkovic et al., Cross-sectional + 1995 381 women Devine et al., Longitudinal + 1995 124 women Jones et al., Population-based study NS 1997 34 men, 120 women Kidney stones Burtis et al., 124 subjects + 1994 1,000 mg Ca and defined diet or 1,000 mg Ca and usual diet Curhan et al., Prospective cohort + 1997 903,849 subjects
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and interocanter site (–0.003 × urinary Na + 7.86) in postmenopausal women Urinary Na correlated with urinary deoxypyridinoline and urinary Ca in men and women Urinary Na correlated with bone mineral content and density, but the association disappeared when adjusted for other confounders, especially body weight Urinary Ca excretion increased by 0.77 mg/23 mg of Na excreted in individuals with Ca oxalate kidney stones Relative risk for renal stones increased with increased intake of Na Q1 = 1.6 g/d Na, RR = 1.0 Q2 = 2.3 g/d Na, RR = 1.08 Q3 = 2.8 g/d Na, RR = 1.15 Q4 = 3.6 g/d Na, RR = 1.10 Q5 = 4.9 g/d Na, RR = 1.30 continued
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Results from the most rigorous dose-response trials (see Appendix I) have documented a progressive, direct effect of dietary sodium intake on blood pressure in nonhypertensive and hypertensive individuals.
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For urinary calcium excretion, numerous trials documented that a reduced sodium intake lowers urinary calcium excretion, but urinary calcium excretion by itself is not a well-accepted surrogate marker for bone mineral density or dietary induced osteoporosis. Evidence that links sodium intake with gastric cancer is reasonably strong, but still insufficient to establish a UL.
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From page 378... ...
Likewise, the assessment of dose-response relationships in meta-analyses is subject to confounding. In this setting, the best available dose-response evidence comes from individual trials that specifically examined this issue (i.e., randomized trials that test the effects of three or more levels of sodium intake on blood pressure)
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Furthermore, the rise in blood pressure in response to increased dietary sodium intake is heterogeneous and is blunted in the setting of dietary potassium intakes in the range of the AI (4.7 g [120 mmol]
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. Nondietary factors, such as age, race, specific genes, and the presence of hypertension, diabetes, or kidney disease, also affect the blood pressure response to changes in dietary sodium intake.
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From page 381... ...
/day of sodium UL for Chloride for Adults 19–50 years 3.6 g (100 mmol) /day of chloride Older Adults and the Elderly Ages 51+ Years In observational studies, the rise in blood pressure in response to higher sodium intake increases with age (Law et al., 1991a)
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From page 382... ...
While the pathogenesis of preeclampsia remains uncertain, in the past attention has focused on nutritional factors, particularly a high sodium intake and low calcium intake as possible etiological factors. In fact, low sodium diets have been routinely prescribed as a means to prevent preeclampsia and its complications (Churchill and Beevers, 1999)
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From page 383... ...
Overall, there is inadequate evidence to support a different upper intake level for sodium intake in pregnant women from that of nonpregnant women as a means to prevent hypertensive disorders of pregnancy. Also, there are inadequate data to justify a different UL for lactating women.
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The data on the role of sodium intake during infancy on blood pressure in later years are also very limited. The most rigorous study was conducted with infants in Holland with a subsequent follow-up 15 years later.
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and food only. Children and Adolescents Concerns about adverse effects related to sodium intake in children are focused in two areas: first, does a higher level of dietary sodium result in increased blood pressure in children -- to the extent that there is a definable increase in risk of cardiovascular disease in children, and second, does increased dietary intake of sodium during childhood track to increased blood pressure during adulthood and thus increased risk for subsequent cardiovascular disease.
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with sodium intakes of 2.0 g (87 mmol) /day versus 2.9 g (130 mmol)
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From page 387... ...
/day of chloride Factors Affecting the Tolerable Upper Intake Level Salt Sensitivity As discussed previously, blood pressure, on average, is directly related to dietary sodium intake. However, evidence from a variety of studies, including observational studies and clinical trials, has demonstrated heterogeneity in the blood pressure responses to sodium intake.
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From page 388... ...
Further, the intake of these electrolytes, particularly potassium, may influence the blood pressure response to changes in dietary sodium intake. Sodium intake may also influence urinary excretion of these electrolytes.
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From page 389... ...
. The level of sodium intake may affect the blood pressure response to increased calcium intake, and conversely, the level of calcium intake may affect the blood pressure response to sodium.
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Available evidence is insufficient to adjust the UL based on obesity status. Gender Observational studies and clinical trials provide some evidence that the blood pressure response to a reduced sodium intake may differ by gender.
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From page 391... ...
In subgroup analyses of Phase 1 of the Trials of Hypertension Prevention, which enrolled adults aged 30 to 54 years, a reduced sodium intervention led to significantly greater systolic blood pressure reduction in women compared with men; this finding may have resulted from a lower achieved level of sodium intake in women (Kumanyika et al., 1993)
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. However, no randomized trial has specifically examined the effects of different levels of sodium intake on blood pressure and kidney function in the setting of chronic kidney disease.
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From page 393... ...
An example of a Mendelian disease associated with salt wasting is Gitelman's syndrome. In analyses that compared blood pressure and urinary sodium excretion in individuals from a large group of related persons who carried zero, one, or two copies of the mutant gene, lower blood pressure was seen in those with two copies of the mutant gene (homozygotes)
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From page 394... ...
. Angiotensinogen genotypes appeared to influence the effects of sodium intake on diastolic blood pressure, but not systolic blood pressure.
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appropriately designed, prospective observational studies that have linked sodium intake with subsequent cardiovascular disease. Still, others argue that sodium reduction has adverse metabolic effects (e.g., increased plasma renin activity and perhaps insulin resistance)
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• Better characterization of salt sensitivity as a phenotype and determination of its relationship to cardiovascular outcomes. • Influence of sodium intake during infancy and childhood on blood pressure later in life.
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1998b. Dietary sodium intake and mortal ity: The National Health and Nutrition Examination Survey (NHANES I)
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2001. Effects of reduced sodium intake on hypertension control in older individuals.
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2000. Metabolic effects of changes in dietary sodium intake in patients with essential hypertension.
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1986. Effect of increasing calcium intake on urinary sodium excretion in normotensive subjects.
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1984. A randomized trial on the effect of decreased dietary sodium intake on blood pressure in adolescents.
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1997. Randomized trials of sodium reduction: An overview.
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1989. Influence of sodium intake on left ventricular structure in untreated essential hypertensives.
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1987. Effect of sodium intake on blood pressure, serum levels and renal excretion of sodium and potassium in normotensives with and without familial predisposition to hypertension.
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1998. The effects of dietary sodium intake on biochemical markers of bone metabolism in young women.
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1999. Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults.
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From page 407... ...
1983. A randomized trial of sodium intake and blood pressure in newborn infants.
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1978. The effect of high sodium and low sodium intakes on blood pressure and other related variables in human subjects with idiopathic hypertension.
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1976. The effect of dietary sodium chloride on blood pressure, body fluids, electro lytes, renal function, and serum lipids of normotensive man.
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1998. Impact of dietary sodium intake on left ventricular diastolic filling in early essential hypertension.
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From page 411... ...
1997. Short-term effects of dietary sodium intake on bone metabolism in postmenopausal women measured using urinary deoxypyridinoline excretion.
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1989. Double-blind study of three sodium intakes and long-term effects of sodium restriction in essential hypertension.
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1981. Urinary calcium excretion at extremes of sodium intake in normal man.
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1984. Comparison of the effects of diuretic therapy and low sodium intake in isolated systolic hypertension.
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1982. Estimating sodium intake from food consumption data.
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1991. Blood pressure and renal blood flow responses to dietary calcium and sodium intake in hu mans.
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1990. Plasma atrial natriuretic peptide, aldosterone, and plasma renin activity responses to gradual changes in dietary sodium intake.
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1988. Influence of dietary sodium intake on urinary calcium excretion in selected Irish individuals.
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1994. Dietary sodium intake, airway responsiveness and cellular sodium transport.
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2001. Urinary sodium excretion and cardiovascular mortality in Finland: A prospective study.
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From page 421... ...
1982. The blood pressure-raising effects of high dietary sodium intake: Racial differences and the role of potassium.
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2001. Different asso ciations of blood pressure with 24-hour urinary sodium excretion among pre and post-menopausal women.
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1995. Chronic respiratory symptoms, bronchial responsiveness and dietary sodium and potassium: A population based study.
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Key Terms
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