Laragh hands off to Alderman at American Journal of Hypertension
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.
