Are Salt-Craving Neurons Driving Our Appetites?

    Salt is essential for life, but it can lead to serious health impacts when consumed in large amounts. Excessive salt consumption or having a “salt preference” can lead to chronic salt intake. This can result in an unhealthy imbalance of salt in one’s diet and a higher risk of developing cardiovascular disease. Researchers have taken interest in learning more about what causes unhealthy salt cravings. Is it possible to stem those cravings? The latest research leads scientists to believe that there are particular salt-craving neurons in the brain that are driving what has been named our “salt appetites”. Studies suggest that we may be wired to satisfy our salt cravings.

    What Is Sodium?

    Sodium is an ion found in table salt. It plays a key role in regulating body functions, including cardiovascular activity and nerve signaling. In every animal species, the body strictly regulates and maintains sodium levels. Since animals are unable to metabolically create sodium, ions must be consumed from external food sources. When the body is low on sodium, the brain triggers appetite signals that drive the consumption of sodium. 

    Sodium’s specific taste recognition system that drives humans to seek out sodium when deficient is unlike other minerals (e.g,. vitamins) for which there is no specific taste association. 

    According to Yuki Ola, an affiliated faculty member of the Tianqiao and Chrissy Chen Institute for Neuroscience at Caltech, “The desire to eat salt is the body’s way of telling you that your body is low on sodium.” He continues on to say, “Once sodium is consumed, it takes some time for the body to fully absorb it. So, it’s interesting that just the taste of sodium is sufficient to quiet down the activity of the salt-appetite neurons, which means that sensory systems like taste are much more important in regulating the body’s functions than simply conveying external information to the brain.”

    Essentially, sodium is required in order for a body to maintain homeostasis.

    Salt Appetite Explained

    Dr. Randall R. Sakai explored hormonal signals that are brought on when there is negative sodium balance, as well as their interaction with the central nervous system (CNS) to influence salt appetite. He found that sodium deprivation encourages both appetitive and consummatory behaviors which lead to a powerful appetite for salt. To demonstrate this, laboratory animals that were deprived of sodium and in a sodium-depleted state were studied. He found that, over time, these lab animals demonstrated an immense appetite for sodium after having been without. In addition, Kraus and colleagues found that average lick rates for a hypertonic NaCl solution increased when there was sodium depletion. This was not because of reflexive response, but because of voluntary motivated behavior.

    In a separate study, researchers found that rats who were sodium depleted increased operant response rates (e.g., running speed) to obtain a sodium reward. On the other hand, rats who had a severed connection between the forebrain and caudal brainstem or chronic supracollicular decerebrate (CD) rats would not increase intake of hypertonic sodium and appetitive response after being depleted. This would mean that sodium appetite behaviors are derived from higher order forebrain signaling. 

    In summary, laboratory studies show that sodium taste transduction mechanisms are key in the expression of a sodium-selective appetite. When blocked, this appetite is eliminated. 

    The Salt Appetite Brain Network      

    Salt appetite is subserved from the brain network, more specifically, the subfornical organ (SFO) that senses sodium needs. Sodium need indicates sodium deficiency or excess and encourages an organism to seek out or inhibit salt. A central sensor of salt depletion involves circumventricular organs. They lie in the forebrain, the subfornical organ (SFO), and organum vasculosum of the lamina terminalis (OVLT). These are of particular interest due to their high sensitivity to plasma osmolality changes as well as their composition, which includes a high density of angiotensin II type 1A receptor (AT1AR). Researchers found that sodium depletion elevates aldosterone and angiotensin II, resulting in sodium appetite stimulation.


    Research on sodium appetite remains ongoing. What is clear is that a sodium-selective appetite exists. Mechanisms related to sodium mineral cravings are unique to sodium since no other mineral is known to have a specific taste that arouses our nervous system. So what’s next? Scientists are working to understand how salt-craving neurons driving our appetites can be utilized to treat patients with chronic conditions for which an improved diet would prove beneficial.

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