Research conducted by Beth Israel Deaconess Medical Center in Boston discover specific group of neurons that increase appetite for sodium.
Let’s face it, for some of us, that packet of chips is always irresistible.
Now, a study discovers why most of us fail to curb our salty cravings.
A research, conducted by the Beth Israel Deaconess Medical Center in Boston has discovered a specific group of neurons that increases our appetite for sodium.
The research may help developing a drug that target neurons in people who had a hormone deficiency which makes them think they need more sodium than they actually should.
The neurons lie in an area known as NST that plays an important role in the cardiovascular system.
The team pinpointed this sub-population of cells that respond to salt - or sodium - deficiency and mapped the circuitry that increases intake.
One of the lead authors of the study Dr Jon Resch said that they identified a specific circuit in the brain that detects sodium deficiency and drives an appetite specific for sodium to correct the deficiency.
He further add that the work establishes that sodium ingestion is tightly regulated by the brain, and dysfunction in these neurons could lead to over or under consumption of sodium - which could lead to stress on the cardiovascular system over time.'
According to the World Health Organization an estimated 2.5 million deaths a year could be prevented if people reduced their consumption of salt to its recommended level of 5g.
While most people consume more than necessary, it is true that humans can't survive without salt as it helps balance the body's water content and help in regulating blood pressure and cellular function.
Dr Resch and colleagues in the Division of Endocrinology, Diabetes and Metabolism at the teaching hospital of Harvard Medical School have shed new light on the process in which neurons regulate sodium intake.
In a series of experiments the researchers demonstrated these neurons called NTSHSD2 were activated when mice were deficient in salt.
The presence of the hormone aldosterone - which the body releases during salt deficiency - also increased the response of these brain cells.
The researchers also revealed the neurons are not solely responsible for driving salt appetite.
Using mice not deficient in the mineral showed when they were activated artificially consumption was only triggered in the presence of the hormone angiotensin II.
Dr Resch said the sodium-appetite circuity he and colleagues have revealed provides a physiological framework for a hypothesis put forward in the early 1980s.