Following yesterday's blog, I just came across another article attributing "salt-sensitivity" to abnormally high levels of aldosterone . Admittedly, this research was carried out on mice, but their mamallian renin-angiotensin-aldosterone system works similarly to that of humans. The report states that mice lacking normal components of circadian clock controls (the 24-hour cycle of biochemical, physiological, or behavioral processes) show salt-sensitive hypertension due to the production of abnormally high levels of aldosterone by the adrenal glands. In fact, the authors recommend this to be a new hypertension risk factor in mice. Based upon the evidence, high aldosterone levels should move way up the chain of risk factors for humans as well.

This is another example where salt-sensitivity is not an independent medical condition, but an overt manifestation of a more profound physiological disturbance resulting in excessive aldosterone production. It is control over aldosterone levels which will be the critical strategy for treatment.

The evidence continues to build....

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.

Well, at long last the data are in. In a paper published in the American Journal of Clinical Nutrition (pdf 135.14 kB) , Harvard researchers Adam Bernstein and Walter Willett found that the amount of sodium consumed by Americans over the past 4 decades has remained unchanged, while the rates of high blood pressure have increased greatly. The result, based upon the most reliable form of data - the 24 hour urinary sodium analysis - was a real shock. So upsetting was this data that the authors parsed it in the following way:

"Sodium intake in the US adult population appears to be well above current guidelines and does not appear to have decreased with time."

No statement can be more reflective of a fixed ideology than that. In the first instance, they fully expected to see a significant increase in salt - but they did not - salt consumption has remained unchanged - why did they not simply say salt has not increased with time? If high blood pressure increased significantly but salt consumption did not, then it is obvious that the Dietary Guidelines regarding salt are totally baseless, yet once again they remain entrapped in a flawed doctrine that has proven to be wrong time and time again.

In fact, their most telling, but grudging admission comes near the end of their publication:

"Thus, despite the increase in processed foods in the US marketplace over the past 50 y, total caloric imbalance and the resultant epidemic of obesity may be a more important determinant of the increased prevalence of hypertension than sodium intake."

In other words, the sodium-hypertension link is not what it was quacked up to be!

Not surprisingly, Dr Graham MacGregor (University of London, UK), the spiritual father of WASH (World Action on Salt and Health) feels there must be something wrong with the data . The man behind the worldwide campaign to denigrate salt, has typically tried to cast doubt upon the data because it blows away his anti-salt agenda and his lifelong work.

One thing we know for certain. These data are real and confirms that on a population-wide basis, salt does not contribute to high blood pressure except for a minority of the population that is salt sensitive. I await the day when researchers shake loose from their arbitrary dogma and willingly admit the truth. We will all be better off.