American Journal of Kidney Diseases
Volume 55, Issue 4 , Pages A31-A32, April 2010

Salt Appetite

  • Philip J. Klemmer, MD

      Affiliations

    • Corresponding Author InformationAddress for correspondence: CB#7155 University of North Carolina, Chapel Hill, NC 27514

Chapel Hill, NC

Article Outline

 

“Would you like salt on your fries?”

In North Carolina, the answer to this question is the same as to the “Do you want slaw on your barbeque?” question: “Yeah, boy!”

Like most Southerners, and, for that matter, most human beings, I love salt. So when I convinced one of our renal fellows to join me in adopting a Paleolithic salt-free diet, I already knew what he was thinking: now Don Quixote is looking for companionship in a folie à deux experiment requiring the adoption of a hunter-gatherer cuisine. I suspected that he had grown weary of my incessant historical examples of salt science, ranging from the Yamamano Indians with their astonishingly low salt intakes and blood pressures, Derek Denton's chimpanzees with their salt-induced hypertension, and the Brazilian viper with an ACE inhibitor in its venom. My enthusiasm aside, I have always found guidance in the observation of Theodosius Dobzhansky, the father of modern evolutionary biology. He said that nothing in biology makes sense except through the lens of natural selection and evolution. Our attraction to salt, I believed, was an evolved addiction rather than a physiologic requirement. Salt-containing processed foods dominate the lower level of our contemporary food pyramid. Indeed, the author Michael Pollan has suggested that most of what we currently consume should not be considered food. Diet is but one important component of culture and culture can not be readily altered by evidence-based science. Avoiding salt in the modern world would clearly be a daunting task.

To my surprise, my fellow not only agreed to join me but also managed to round up 4 additional members of our division to serve as normal controls. We hoped that our IRB-approved pilot experiment would demonstrate the effect of different levels of dietary sodium on extracellular volume and aldosterone in normal individuals. Against this referent we would compare humans suffering the most extreme natriuretic handicap: anuric dialysis patients. During the low-salt phase we adopted a diet for which the renin-angiotensin-aldosterone system most surely was evolved: <10 mEq/L of sodium per day. All 5 of us had very similar baseline levels of urinary sodium excretion (average of 150 mEq/L per day), typical for most contemporary Americans. Surprisingly, our cultural diversity—2 East Indian Americans, 1 Middle Easterner, and 2 cheeky Northeastern Yankees—did not result in differences in salt appetite or salt intake. Some have speculated that this reflects a normal, physiologic level of salt intake driven by genetically determined salt appetite. I prefer an alternative explanation: our contemporary food chain has been contaminated with this level of salt in order to make processed foods more appealing to our taste and therefore more profitable to food manufacturers. Salt stimulates not only thirst but also the sale of high fructose beverages. To me, reclassifying an addiction as a physiological requirement doesn't pass muster with salt any more than it does for nicotine.

Rather than foraging for twigs and wild berries, we eliminated all processed and fast foods. For me, it also meant forsaking sushi on Friday night with my bemused wife. We also eliminated breads, cereals, milk, cheese, condiments, and hospital cafeteria food. Instead, we grazed on steamed vegetables, fresh and dried fruits, unsalted nuts, beans and rice, and a little meat, but not too bloody. Thank God, India pale ale was permitted. To add flavor we discovered what Christopher Columbus sought on his failed voyage to India: spices! Liberal use of spices, garlic, and vinegar all helped compensate for the absence of that not-so-salubrious substance to which we had all become accustomed.

Our sodium intake plummeted to 10 mEq/L per day (estimated from our 24-hour urine sodium measurements). We all felt great, lost on average 1.4 kg (saline weight), and in no way resembled our patients suffering from Bartter or Gitelman syndromes or other rare, salt-wasting conditions. Although we endured some mockery from our salt-consuming colleagues, we resembled our Patheolithic ancestors both hormonally and biochemically: appropriately high renin and aldosterone secretion with low urinary sodium excretion. Our kidneys bravely defended our sodium balance. Our hemoglobin concentrations increased by 0.9 g/dL, a result of a contraction of our extracellular volumes from 44% of total body water on 150 mEq/L per day sodium intake to 39% on 10 mEq/L per day (we did volume measurements with bioimpedance technology). We were all in the lower range of normotension on our low-salt diet, and none of us swooned during rounds. We were reminded that we live by blood flow, not by blood pressure. Personally, I felt that I had briefly reunited with our forgotten pre-agricultural ancestor and, for that matter, all other free-living mammals.

At the end of the experiment, I walked home across campus thinking about salt. The history of salt is well documented. Roman soldiers were paid in salt, leading to the word “salary.” Revolutions in France and India were triggered by taxation on salt. As I walked I came upon a memorial dedicated to James Pettigrew, one of our school's former faculty who fought at Gettysburg and died during his homeward retreat. Had James Pettigrew been employed in the extraction of salt from the ocean water on the North Carolina coast, a key wartime task, he would have been spared conscription into the Confederate Army and might have lived to see refrigeration displace salt as a food preservative. Yet today, copious amounts of salt remain in our diets. Now we are engaged in a more subtle civil (sometimes not so civil) war fought on the pages of our journals and in the popular press—The Great Salt War. Could we or should we try to reduce the level of sodium in our food chain? This question reflects much more than an omnivore's dilemma about food choices, as Michael Pollan would have it: it is a matter of public health policy based on compelling, but still inconclusive, scientific evidence. Furthermore, there is perhaps no one-size-fits-all answer. Some of us fare well on a high-salt diet, while others are salt sensitive and respond with blood pressure elevation and vascular inflammation.

As for me, all I can do is advise my patients with defects in sodium excretion to try to reduce their dietary sodium intakes. I instruct them explicitly on how to accomplish this—eat as your great-grandmother did; namely, reduce consumption of processed foods. As for our group of normal controls, we celebrated the completion of our experiment in 21st century style. We went out for barbeque—with slaw!

 This essay was based on a pilot research project supported by the Renal Research Institute.

 Dr Klemmer is a nephrologist and clinical researcher in the UNC Kidney Center and Professor of Medicine at the University of North Carolina at Chapel Hill.

PII: S0272-6386(10)00120-4

doi:10.1053/j.ajkd.2010.02.001

American Journal of Kidney Diseases
Volume 55, Issue 4 , Pages A31-A32, April 2010