No doubt the UK's anti-salt publicity machine was feeling pleased with their success in generating headlines for a recent piece that suggested that infants need to cut their salt in half. That is, until junkfoodscience called their bluff.

We don't know if blogger-nurse Sandy Szwarc knew anything about the multi-million pound British anti-salt ad campaign featuring "Sid, the Slug," a cartoon reminder of one of the 14,000 beneficial uses of salt -- to kill slugs. Szwarc suggests the public "pour salt on it" -- the study in question. As she laments:

Such extraordinary claims require extraordinary evidence. Does this study hold up?

This study is said to be the "first ever meta-analysis of salt reduction studies in children." And it epitomizes every caveat of these types of studies. MacGregor and He "developed a strategy" of their own design to look for words in several databases and through reference lists at the end of articles to find studies of salt reduction in children. They only used studies published in English and of the 33 they found, decided to use 10 on children for this report. The studies all had different designs, with only one being a double-blind trail and only 9 were randomized; the studies varied in length from 2 weeks to 3 years; compliance with salt reductions appeared poor in two of the studies; we have no information on the racial/ethnic mix of the children and if it is representative of the general population; and only 3 measured 24-hour urinary sodium levels - which the researchers admitted is "the only accurate way to assess dietary salt intake." Simplifying what they did next, they pooled the data on blood pressures and net changes in salt intake, and used statistics to estimate the changes as needed to fill in missing data. Then, they applied two computer models to plot the results and more statistical analyses to reach their findings.

What they reported was that cutting salt intake by 42% reduced systolic blood pressures in the children by 1.17 mmHg. Most parents and children would consider such a salt reduction - nearly in half - to be extreme; while most doctors would debate the clinical significance of a mere 1 point reduction in blood pressure. Taking blood pressures in young children is an imprecise task at best and the children in these different studies were also at varying stages of development, with corresponding variable changes in blood pressures over the study durations, according to their growth and size.

The researchers stated that the "physiological need for salt intake in children has not been studied," but concluded anyway that "current salt intake in children is unnecessarily high and is very likely to predispose children to develop hypertension later."

They went on to declare that these results "provide strong support for a reduction in salt intake for children. [And] if continued, may well lessen the subsequent rise in BP with age and prevent the development of hypertension. This would result in major reductions in cardiovascular disease."

Their press release promised possible "massive population health gains."

·But this study did not examine a single child.

·It conducted no clinical research to learn how much salt is needed or might be harmful for children.

·It offered no clinical evidence to know if a lower blood pressure reading of 1 point means anything for children's health or is maintained as a child grows.

·It offered no proof that a blood pressure reading during childhood has any bearing on adult blood pressures or heart disease.

·And worse, it didn't follow a single child to see if there were any health effects from the salt restrictions they are recommending.

In other words, this study offered no clinically meaningful evidence, only speculations. ...

Shouldn't we have something tenable to go on before experimenting on an entire generation of children? I suspect most parents would think so.

She notes approvingly the award-winning expose of games-playing by the anti-salt crowd as documented in Science magazine and recent research showing that low-salt diets may be creating additional risk .

Beginning in 2007, the American Journal of Hypertension will have a new Editor-in-Chief, replacing its founder, Dr. John Laragh, a Time magazine cover story subject for his breakthrough work on blood pressure and heart disease. Laragh will be succeeded by Dr. Michael Alderman who has just completed his stint as president of the International Society of Hypertension.

In his parting editorial, Dr. Laragh says:

It is a pleasure for me to announce that Dr. Michael Alderman will replace me as Editor-in-Chief of the American Journal of Hypertension effective January 1, 2007. Dr. Alderman is a world-renowned epidemiologist who is unique among his peers because he has been especially interested in asking pathophysiologic questions in performing his population trials. This penchant led him to demonstrate, in a classic eight-year trial of 1717 hypertensive worksite employees, that the height of the entry ambulatory plasma renin level was directly related to the subsequent occurrence of a myocardial infarction (MI). At the same time, he found that no MI's occurred in the 251 patients who had low entry plasma renin levels. This led Alderman to do a confirming follow up study showing that dietary salt-depleted hypertensives with consequent higher renin values and lower urinary sodium values had proportionally higher heart attack rates than did those who ate more salt, and therefore had progressively lower renin values.

Dr. Alderman's research rightly questions the popular wisdom of unselectively advising salt avoidance for all hypertensives, and for all normotensive people, - a popular public health strategy which will surely chronically raise all of their plasma renin values and may have other unintended adverse consequences. Furthermore, this research has clearly reaffirmed the existence of only two mechanistically different types of long-term hypertension, each one of which is caused and sustained by either a body sodium (plasma and ECF fluid-volume) excess or instead by a plasma renin-angiotensin excess. This construction is supported by evidence that the hypertensive states caused by a body salt excess or a plasma renin excess are each quite selectively correctable respectively by giving a natriuretic drug or instead an antirenin antihypertensive drug.