[Salt and blood pressure--centenarian bone of contention].
It is first discussed to what extent salt intake/metabolism may have been modulated since Homo sapiens' global spread from tropical Africa started some 200,000 years ago (10-15,000 generations). The effects on blood pressure, volume, heart rate etc. have been studied along with nearly 100-fold changes in salt intake. Disturbances and risks show up in both extreme ends of this intake range, as counterregulatory mechanisms are overswayed, but within a wide (15-20-fold) range mean pressure is usually changed only marginally, both in healthy man and in rats. When the biological setpoint for intake (salt appetite) has been tested in animals it corresponds--when adjusted to man's 65-70 kg bodyweight and metabolic rate--in sheep to 8-9 g/day and in rats to some 15 g, and it is moderately raised by mental stress. Therefore, human intakes around 10 g daily may, after all, reflect our biologically determined setpoint--rather than expressing a hedonistic abuse. When at different salt intakes not only blood pressure but also heart rate (unfortunately often neglected) are recorded, the percentage increase in pressure at high intakes is mostly less than the percentage decrease in heart rate--and vice versa at low intakes. Thus, as the long-term load on left heart and arteries can be approximated to the product of pressure and rate, low intakes often imply increases of long-term load--to which comes that the for the left ventricular coronary supply so important diastolic phase is shortened. Almost throughout such aspects have been overlooked at the--at best--modest reductions of pressure that have been reported at tolerable reductions of salt intake. The same is true concerning results showing how pressure is reduced considerably more by e.g. three weekly hours of physical activity which, in addition, has uniquely beneficial influences on metabolism, immune defences, sympatho-hormonal activity, etc. Towards such a background suggestions concerning overall reductions of salt intake are hardly justified, particularly as the induction of primary (essential) hypertension appears to be far more dependent on present-day psychosocial influences by means of central enhancements of neuro-endocrine activities.--It is a different matter that salt contents in processed foods should be declared, and kept low--first, because "salt sensitivity" is not uncommon, second, salt is then easy to add but impossible to eliminate.
Avdelningen för fysiologi, Sahlgrenska akademin, Göteborgs universitet.
Björn
B
Folkow
D000818:Animals; D005075:Biological Evolution; D001794:Blood Pressure / Q000187:drug effects*; D004039:Diet, Sodium-Restricted; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000139:chemically induced / Q000209:etiology / Q000517:prevention & control; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage / Q000009:adverse effects* / Q000378:metabolism; D013315:Stress, Psychological / Q000378:metabolism
D017673:Sodium Chloride, Dietary