The relationship of dietary sodium to blood pressure in adults is well established by substantial epidemiological and clinical data as well as various pathophysiological studies. Not surprisingly, considerably less is known about the relationship in children.
In this issue researches 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 4–18 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. In practice, the short-term pressure response of individuals varies substantially with variations in sodium intake. 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 restriction. 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 75–100 mmol reduction in daily sodium intake can, on average reduce blood pressure by 3–4/<1 mm Hg—more in older, hypertensive, or black persons.
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. 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 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. 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.
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.
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 elements—both 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. For example, researches note that 18-year-old British residents, in 1997, were consuming approx2.6-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. 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!
Guess is that the findings in adults—namely, that a large drop in sodium could produce a detectable fall in pressure—is 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 renin–angiotensin system, and increases aldosterone secretion.