Journal of Human Hypertension (2008) 22, 13 & 2008 Nature Publishing Group All rights reserved 0950-9240/08 $30.

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COMMENTARY

Salt and blood pressure in children

MH Alderman
Albert Einstein College of Medicine, Department of Epidemiology & Population Health, Bronx, New York, USA
Journal of Human Hypertension (2008) 22, 13; doi:10.1038/sj.jhh.1002269; published online 6 September 2007

The relationship of dietary sodium to blood pressure in adults is well established by substantial epidemiological and clinical data,12 as well as various pathophysiological studies.3,4 Not surprisingly, considerably less is known about the relationship in children. In this issue of the Journal of Human Hypertension, He et al.5 analysed the salt to blood pressure link in a cross-sectional study of a large representative sample of British children. They found that, in children 418 years old, sodium, potassium, and energy intake, body mass index, arm circumference and all measures of blood pressure, increase with age. In the group as a whole, a significant direct relationship between salt intake and blood pressure was found, even after the adjustment for multiple potential confounders. Specifically, a difference in salt intake of 1 g was associated with a 0.4 mm Hg rise in blood pressure. However, the significance of this relationship disappeared after correction for energy intake. Stratification by 5-year age tertiles suggested a similar tendency towards a positive salt to blood pressure relation within each group. Interestingly, discretionary salt use, either at table or in cooking, was not associated with blood pressure in these youngsters. The kidney, in normal circumstances, accommodates wide variations in sodium intake through compensatory excretion. In healthy humans, this occurs without change in systemic blood pressure.6 In practice, the short-term pressure response of individuals varies substantially with variations in sodium intake.7 Not surprisingly, therefore, it has been difficult in observational studies to demonstrate a meaningful or consistent link between dietary salt and blood pressure. Nonetheless, these limitations of observational studies are of little moment since randomized clinical trials, the clearly preferred method to establish causality and draw clinical inferences, have defined the population impact of salt restric-

Correspondence: Dr MH Alderman, Albert Einstein College of Medicine, Department of Epidemiology and Population Health, 1300 Morris Park Avenue, Bronx, New York 10461, USA. E-mail: alderman@aecom.yu.edu

tion.8 In fact, the link of blood pressure to dietary sodium is based on pretty strong stuff. More than 100 well designed and executed randomized clinical trials, and meta-analyses thereof, have unequivocally demonstrated, in adults, that a 75100 mmol reduction in daily sodium intake can, on average reduce blood pressure by 34/o1 mm Hgmore in older, hypertensive, or black persons.8 It should also be noted that blood pressure response to dietary change in sodium is hardly consistent. In some, blood pressure actually rises, and in most, a change in pressure is undetectable. Moreover, the blood pressure effect of substantial and sustained decrease in sodium consumption tends to attenuate over time and, in a 3-year randomized trial, virtually disappeared at the end of the study.9 In short, and with some caveats, there can be no quibble with the claim that sodium intake contributes to variation in blood pressure, and that this relationship is modulated by genetics, behaviour and environment. The findings here are consistent with this settled dogma. The study has the strength of size, representativeness and multiple (7) daily dietary records to estimate sodium intake. Its muted findings reflect the difficulty, in cross-sectional study, of identifying a robust association of sodium intake to blood pressure. For example, the strong correlation of energy intake and sodium has made separating the impact of these (like almost all other nutrients) factors difficult if not impossible. Interestingly, the 1980 clinical study by Cooper on 73 black and white school children in Chicago detected what the authors described as a quantitatively weak (although their findings of a 1 mm Hg per gram of sodium increase was greater than seen here) but significant (P 0.045) relation of sodium to blood pressure.10 In Chicago, as opposed to the current study, urine collection replaced dietary recall as the basis of estimating sodium intake. Because the earlier study did not capture energy intake and could not assess its potentially confounding effect. On the other hand, creatinine excretion was available. Its inclusion in the analysis eliminated the significance of the relationship between sodium and blood pressure in these children. He et al.5 appropriately pointed out the inability to determine

Salt and blood pressure in children MH Alderman 2

whether energy or sodium intake provides the tenuous link to blood pressure. Regrettably, the current report provides little information regarding other associations to blood pressure or variations in other characteristics that might be associated with variations in sodium intake. For example, stature and physical maturation are associated with blood pressure. Bigger children may be muscular or pudgy. Children who exercise vigorously may have large energy (and sodium) intakes, and be taller and leaner than youngsters who have the same body mass index and different life styles. Cooper et al.10 postulated that the strong link of creatinine to blood pressure might reflect muscle mass and perhaps be a marker of body size. This, in turn, might be the most powerful determinant of blood pressure in childrenmore important than age or sodium. Perhaps, the best measure of growth and development available here is mid-arm circumference. The strong arm to blood pressure correlation may reflect muscle mass and suggests that diets high in energy (and therefore, among other things, sodium) may be conducive to physical maturation, along with a slightly higher blood pressure. In short, if this were the causal pathway, then higher pressure might even be a desirable sign in children. Dietary intake is complex, and to characterize it on the basis of one element may well oversimplify any assessment of its value. For example, given the high correlation of energy with virtually all other nutrients, it is possible that those consuming more sodium (and energy) had more satisfactory consumption of other important dietary elementsboth known and unknown. In any event, blood pressure is not the only measure of the health of children. The British Survey of Young People probably includes, in addition to physical and physiological data, information on other social, economic and developmental characteristics whose explanation might well inform our understanding of the relation of blood pressure, diet, health and development in these youngsters. Of note, He et al.5 also provide some other interesting information. For example, they note that 18-year-old British residents, in 1997, were consuming B2.6-g of sodium per day. That was similar to levels found in Chicago a decade earlier, and falls within the range of adult sodium intake seen world-wide in most countries and suggests that, a decade and 2 ago, these near adults were within that range. It is also interesting to note that measures of discretionary sodium use did not correlate with blood pressure. This supports the Cochrane Collaboration conclusion that there was not sufficient evidence for a general dietary recommendation to reduce sodium intake.11 Parenthetically, it is interesting to note that in countries where most sodium intake is discretionary, as parts of East Asia, sodium intake is much higher than in Britain, where most sodium is not discretionary, but consumed in our foods!
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The restricted focus of this report does not detract from the careful analysis and lucid presentation by He et al.5 It does, however, account for my dissent from the call for British youngsters to reduce their sodium intake. Observational data tells us something about associations, and can, when the data are particularly robust, even infer guilt. But that condition is not met here. My guess is that the findings in adultsnamely, that a large drop in sodium could produce a detectable fall in pressureis probably true for youngsters as well. But, it is also true that randomized clinical trials in adults have shown that lowering sodium intake increases sympathetic nerve activity, reduces insulin sensitivity, increases the activity of the reninangiotensin system, and increases aldosterone secretion.8,1214 Do these or other changes occur in children? This is critical because, of course, the health impact of any intervention is the sum total of all its consequences. While I remain an agnostic on that score, I continue to believe firmly that solid knowledge based on evidence of benefit and risk must precede any clinical or public health interventionparticularly when it comes to dependent children. Good observational studies, such as this one, generate hypotheses. They need to be tested in clinical trials. Absent such evidence, and absent some pressing public health challenge, therapeutic restraint may be the best and safest way to avoid doing harm.

References
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9 Trials of Hypertension Prevention Collaborative Research Group. Effects of weight loss and sodium reduction intervention on blood pressure and hypertension incidence in overweight people with high-normal blood pressure. Arch Intern Med 1997; 157: 657667. 10 Cooper R, Soltero I, Liu K, Berkson D, Levinson S, Stamler J. The association between urinary sodium excretion and blood pressure in children. Circulation 1980; 62: 97104. 11 Hooper L, Bartlett C, Smith GD, Ebrahim S. Systematic review of long term effects of advice to reduce dietary salt in adults. BMJ 2002; 325: 628.

12 Grassi G, DellOro R, Servalle G, Foglia G, Trevano FQ, Mancia G. Short- and long-term neuroadrenergic effects of moderate dietary sodium restriction in essential n. Circulation 2002; 106: 19571961. hypertensio 13 Petrie JR, Morris AD, Minamisawa K, Hilditch TE, Elliott HL, Small M et al. Dietary sodium restriction impairs insulin sensitivity in noninsulin-dependent diabetes mellitus. J Clin Endocrinol Metab 1998; 83: 15521557. 14 Cohen HW, Alderman MH. Sodium, blood pressure, and cardiovascular disease. Curr Opin Cardiol 2007; 22: 306310.

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