05P-0450

A fascinating example of this mechanism at work was made on July 10, 2006, when scientists discovered the reason why gorillas eat decayed wood, a behavioral characteristic of these primates that puzzled researchers for decades.  The researchers analyzed the wood and found that it was the source of over 95 % of the gorilla's dietary sodium, even though it represented only a tiny fraction of their food intake.  Other animals exhibit the same behavior to satisfy their sodium needs. All animals appear to instinctively know that sodium is a necessity for life.

 In order for our circulatory system to function, it must have an adequate volume of blood that is under sufficient pressure to supply all our tissues with the nutrients they need and to remove all the toxic byproducts of metabolism. It is a precisely tuned balance of water and salt that allows this to occur. Any amount of water or salt that is consumed in excess of our critical needs is quickly eliminated through our kidneys.  Our capacity to eliminate excess salt is truly extraordinary.  As highlighted in the Institute of Medicine (IOM) report, “Dietary Reference Intakes For Water, Potassium, Sodium, Chloride, and Sulfate”[1], researchers Valtin and Schafer reported that the normal human kidney was able to filter 25,000mmols of sodium each day[2].  This amounts to 1,500 grams or more than two full retail cans/boxes of salt per person per day! 

  Not only are we capable of eliminating that tremendous surplus of sodium, but by extremely precise mechanisms, our kidney filtration system is capable of reabsorbing 99% or more of it if we need to.  Why did we evolve such an incredibly efficient and vigorous system for the elimination and turnover of sodium?

 An equally important issue is the converse situation, that is, ensuring that we have ingested sufficient water and salt to make up for any losses we experience, because this, too, may lead to a loss of volume or an imbalance of electrolytes that will affect the osmotic pressure of our extracellular fluid.

 During the course of vertebrate evolution, precise complex osmoregulatory mechanisms emerged to maintain a specific level of sodium in the extracellular fluid.  These processes went through several transitions in the course of evolution from marine to brackish to freshwater to land environments.  The renin-angiotensin-aldosterone system (RAAS) first appeared in the bony fishes and has been strengthened through every major evolutionary leap.

 When salty foods are freely available, all animals (including humans) will spontaneously intake more that is required for immediate need and any excess sodium or water is excreted in the urine.  The extent of  this excess intake can be influenced by a prior history of sodium deficiency[3] or prenatal experience with maternal illness during pregnancy[4]^, [5]. 

 In parallel with the osmoregulatory mechanisms, our bodies have developed an additional capacity to react to sodium and water depletion through the development of a strong appetite drive.  This is manifested through the mechanisms controlling the thirst for water and the appetite for salt.  Salt is a critical nutrient to our diet.  Not only is it essential to our metabolism through the maintenance of plasma homeostasis, but its bitterness moderation character has a strong positive impact on the palatability of other foods that are highly nutritious, but somewhat bitter, such as cruciferous vegetables.  In contrast with other essential minerals such as potassium, iodine and magnesium, salt is the only mineral that animals have an innate craving for.  

 The impact of an inherent salt appetite is particularly important for herbivores and vegetarians. Carnivores receive a large part of their sodium by virtue of the sodium contained in the muscles and vicera of the animals they eat.  Vegetarians and herbivores do not. Human evolution is very likely to have been highly influenced by the development of the salt appetite and hormonal regulatory mechanisms required for sodium conservation, because from the earliest hominid period onward, the diet was predominantly vegetarian.  Even at the height of the hunter-gatherer period,  vegetable matter made up the majority of the calories consumed.  Because of this, selection pressure favored the development of a strong salt appetite in order to ensure consumption and retention of salt for the purpose of osmoregulation. 

 Aptly, our appetite for salt brought on by sodium  deficiency is specifically stimulated by the taste of salt.  Sodium deficient animals will always choose salt over potassium or calcium chloride even though both the latter salts have a certain degree of salt-like taste.

 One of the earliest and most striking examples of increased salt appetite was observed in a clinical setting in 1940 by Wilkins and Richter[6].  A child, suffering an undiagnosed adrenal disease, had an extreme and persistent desire to consume salt and water from an early age.  From the time he could first speak, he demanded salt on everything he ate.  He had no desire for sugar or candies, but always insisted on salt.  He was taken to hospital in order to determine what the cause of his affliction might be.  Unfortunately, soon after he was admitted, he was forced by the staff  to eat a standard hospital diet and was denied free access to salt.  He promptly died. (His adrenal condition was discovered only at autopsy.)

 The latest research publication in this field[7] of salt appetite shows that this mammalian multi-factorial system is very robust and includes failsafe mechanisms that permits it to continue functioning even after sections of its system are shut down.  Employing a complex cascade of physiological functions from hormones to pressure sensitive receptors in the brain, these thirst for water and appetite for salt mechanisms moderate our behavior so that we are driven to quickly replenish the volume and osmotic balance of our blood, in order to pressurize it sufficiently for our heart to pump it through our circulatory system.

 When fluids and electrolytes are lost, such as with sweating, physical exertion, diarrhea or other circumstances, we immediately get a water thirst signal. In response, we drink water to make up the loss. After a slight delay, our sensors detect a change in plasma osmolarity and our salt appetite kicks in to ensure that we consume salt so that the sodium ion levels are replaced. If we don’t respond on time to our salt appetite, the consequences are dire as seen in the previous examples. 

In order to explain salt appetite, Geerling et al have proposed a model with three central components^[8]. Initially, chronic sodium deficiency provoke specific groups of neurons to signal increased sodium need, resulting in heightened salt-seeking behavior.  Once a salt source is detected, a signal of recognition is generated.  Finally these two signals are integrated to drive salt ingestion activity.  Currently, research is focused in finding the specific locations in the brain responsible for carrying out these functions.  Progress towards defining the brain sites responsible for regulation will provide a foundation to explain the neural basis for salt appetite.

 The presence of a salt appetite working together with our hormonal osmoregulatory systems illustrates our capacity to bring our extracellular fluid into osmotic balance and maintain it there.  Just as we are designed to take in salt or water when we need it, the body’s feedback mechanisms also alert us to cease consumption once the proper balance is achieved.

 As an example, the peptide oxytocin, released into the blood from the posterior lobe of the pituitary gland, actively serves to limit salt intake^[9],[10].  Research findings clearly suggest that salt appetite is thus controlled by multiple physiological input signals, both positive and negative, that are incorporated into a highly specialized and individually tuned neural network that regulates our thirst for water and our consumption of salt.

 For each person, the activity of their salt/water regulatory system will differ according to their individual need, dictated by diet, stature, environment, genetics, stress and physical activity.  This system is the total opposite to a “one size fits all” paradigm.  It is a system that is a specifically tailored response to individual, personal needs.

 For this very reason, any imposed national policies or recommendations limiting the amount of salt consumed is utterly contrary to the biological need.  Any such recommendations may impede and ultimately render ineffectual the finely tuned mechanisms we have evolved over the eons to fit our individual needs and unintentionally result in harm.

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