The perils of Salt

Dialysis finally forced recognition of its importance in kidney disease

The Amazonian Yanomami Indians famously manage on only 50mg (1 mmol) of sodium chloride per day, while in more developed societies we struggle to keep our average intake below 100 times that level. Humans probably mostly evolved on diets more like that of the Yanomami. In response to this, Yamomami Indians have been found to have persistently high levels of circulating renin and aldosterone, driving maximum salt retention in the kidney.

Interestingly, although the perils of salt overloading were well understood in the setting of acute renal failure in the 1940s, in chronic renal disease many nephrologists were very late to pick up the importance of salt restriction.  Addis (1949) and de Wardener (1958) identified control of salt intake as important in oedema, but both dismissed it as not very relevant to chronic renal failure, even in malignant hypertension. Soon after the introduction of dialysis for end stage (as opposed to acute) renal failure it was discovered that limitation of salt intake, and its removal by dialysis, controlled the severe hypertension that was universal in young patients with end stage renal disease in the 1960s.  There were very few other effective and tolerable treatments at that time – blood pressure charts from that era are scary.  Most longterm survivors from 1960s and 1970s have experienced prolonged periods of severe hypertension. One of the earliest patients, Robin Eady, describes the transformation when he went to the world’s first chronic dialysis unit in Seattle in 1963, where Belding Scribner had determined the importance of sodium and volume balance in controlling blood pressure.  That lesson has been re-learned several times since.  Chronic salt and fluid overload is a major contributor to the high rate of heart failure in dialysis patients. 

Observations in human populations with low salt intake, and chimpanzees on similarly fruit or vegetable-rich, salt-poor diets, find lower average blood pressures, and a lack of the rise of blood pressure with age that we now expect during adult life.  Studies with the DASH diet and other low-salt diets show that they can lower blood pressure in hypertensive patients.  These diets tend to have other potentially good things about them too though. 

We have also learned that lowering salt intake increases the effects of ACE inhibitors, not only on blood pressure but also on proteinuria.  Other discoveries have included that most genetic causes of hypertension act through increasing sodium retention by the kidney; and that mild kidney disease is much more common in the population than we previously suspected.  Salt sensitivity may be an early change in kidney disease, and a large proportion of the population may be susceptible. 

Should we all be eating less salt, or only those of us with high blood pressure or kidney disease? For the general population there has been an extraordinary resistance to further lowering salt intake, though there seems little to lose, and potentially a lot of gain. Some blame this on pressure and scheming from food manufacturers and the salt industry. Salt gives food longer shelf life, gives low quality food more taste, and the water sucked in increases the weight of many products (notably meat products).
We seemed programmed to like salty foods, perhaps because our species lived for millenia in environments where salt was scarce and treasured. But it’s probably bad for many of us. 

Further reading

Oliver WJ, EL Cohen, JV Neel, 1975. Blood pressure, sodium intake, and sodium related hormones in the Yanomamo Indians, a ‘no-salt” culture.  Circulation 52:146-51.

Eady R  2001 The dawn of dialysis: reminiscences of a patient. . See also The Record Holders on this blog.

MacGregor GA, HE de Wardener, 1998  Salt, diet and health. Cambridge University Press, Cambridge

De Wardener HE, 1958.  The Kidney (1st edition).  Churchill, London

Addis T 1948.  Glomerular nephritis.  Macmillan, New York.

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