Is salt-sensitivity a misnomer?
One of the most misunderstood phenomenons related to hypertension is commonly termed “salt-sensitivity.” It has never been explained to everyone’s satisfaction, it is complicated to characterize and most people who are diagnosed with it are unaware they have it. Why is that? Could it be that salt-sensitivity is not an independent medical condition per se but rather a coupled overt manifestation of a far more profound physiological disturbance?
We have long known that many people of African decent have a heightened tendency towards hypertension. In what has become almost a knee-jerk reaction, these individuals are routinely prescribed a low-salt diet with highly variable degrees of success. Now, researchers Kammerer and Pratt have looked more closely onto the matter and have determined that many Africans have a genetic predisposition to high aldosterone levels, which is a significant contributor to hypertension.
The rennin-angiotensin-aldosterone system (RAAS) evolved as a means of physiologically controlling the amount of sodium in the blood. When we consume sufficient sodium (salt), the excess is simply excreted in the urine. When we do not consume sufficient sodium, several receptor systems in the body are stimulated to activate the RAAS, which produces aldosterone, which in turn signals the kidneys to start recouping the sodium that was destined to be excreted in the urine and send it back to the circulatory system. That is the sodium control mechanism that has evolved for humans and many other animal species. For most people, the RAAS begins to be activated when our consumption of salt falls below 6-8 g per day.
While aldosterone plays this very important sodium-control function, its presence at elevated levels in our blood is not benign. High levels of circulating aldosterone are associated with several negative consequences including hypertension, degeneration of arterial epithelium, metabolic syndrome and Type II diabetes.
Of particular interest is the combination of elevated aldosterone and normal to high salt consumption which routinely results in increased blood pressure.
Researchers Kammerer and Platt believe the genetic tendency for Africans to have elevated aldosterone levels is the evolutionary result of coming from an environment that was traditionally low in salt, thereby necessitating a continual need to conserve all available salt within the body. This chronically elevated level of aldosterone has resulted in high rates of hypertension and a symptomatic sensitivity to salt.
The conventional first course of treatment – severe reduction of salt in the diet – may have a positive impact on reducing some of the blood pressure, but it does nothing to reduce the chronically-high levels of aldosterone. On the contrary, reducing salt may stimulate even more aldosterone production with all the attendant negative consequences.
Salt reduction is a very poor and somewhat thoughtless strategy in this circumstance and the most likely reason for its inevitable selection is the dogmatic attachment to the concept of “salt-sensitivity.”
Labeling chronic elevated aldosterone as “salt-sensitivity” is a bit like calling the genetic tendency to accumulate cholesterol as “schmaltz-sensitivity.” The basic problem is neither the salt nor the schmaltz – it is the genetically-moderated tendency to produce excessive amounts of harmful metabolites.
Just as we routinely treat cholesterol conditions with statins, we have to consider our first treatment strategy for chronically-elevated aldosterone to be ACE inhibitors and aldosterone blockers such as spironolactone. Rather than treating only one of the manifestations of the conditions, by going after the real culprit all of the consequences of elevated aldosterone will be managed.
