Some of us can never resist a packet of chips.
In fact, most of us fail to curb our salty cravings: the average adult in America eats about 8.1g of sodium a day, far above the 5g limit recommended by the WHO.
And scientists may have discovered why.
A research team at the Beth Israel Deaconess Medical Center in Boston has found a specific group of neurons that drives our appetite for sodium.
They say the finding offers hope of developing drugs that target these neurons in people who have a hormone deficiency which could make them think they need more sodium than they should.
A research team at the Beth Israel Deaconess Medical Center in Boston has found a possible explanation for why the average adult eats far more sodium than they should
It is still unclear, however, how these neurons affect obesity or vice versa.
The neurons lie in an area known as the NST (nucleus of the solitary tract) 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.
‘We identified a specific circuit in the brain that detects sodium deficiency and drives an appetite specific for sodium to correct the deficiency,’ co-first author Dr Jon Resch said.
‘In addition, this 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.’
The breakthrough reported in Neuron follows a major 12-year study published last month that found a high-salt diet can double the risk of heart failure.
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.
Most people eat well in excess of this – anything from 80 to 140 percent more than they should, it says.
According to the World Health Organization, consuming less than 5g a day ‘helps to reduce blood pressure and risk of cardiovascular disease, stroke and coronary heart attack.’
The principal benefit of lowering salt intake is a corresponding reduction in high blood pressure which affects about one-in-four adults in the UK.
Humans can’t survive without salt as it helps balance the body’s water content as well as playing a critical role in regulating blood pressure and cellular function.
As salt is lost through excretion and other metabolic processes hormones are released in response to sodium deficiency.
But exactly how these work on the brain to trigger salt-seeking and salt-consuming behavior has remained a mystery.
Now 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.
The subset of neurons – known as NTSHSD2 – were discovered a decade ago by co-corresponding author Prof Joel Geerling, formerly of BIDMC and now a leading neurologist at Iowa University.
In a series of experiments the researchers demonstrated these neurons 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.
Dr Resch explained: ‘These neurons appear to be highly influenced by these hormones and less so by inputs from other neurons – though further study is warranted.
‘This is a unique and very unexpected feature of these NTSHSD2 neurons.’
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.
This is a chemical which is also released by the body during sodium deficiency.
From this the researchers concluded another set of neurons sensitive to angiotensin II likely plays a role in salt appetite. These have yet to be identified.
The findings demonstrated a combined relationship between the two distinct sets of neurons that respond to aldosterone and angiotensin II causes salt cravings.
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.
He said: ‘Several questions remain with regard to how sodium appetite works but a major one is where angiotensin II is acting in the brain and how the signal works in concert with NTSHSD2 neurons that respond to aldosterone.
‘We have already begun work to help us close these gaps in our knowledge.’
Member states of the WHO have agreed to reduce the global population’s intake of salt by 30 per cent by 2025 because of the health benefits.
Foods usually high in salt include anchovies, bacon, cheese, gravy granules, olives, pickles, prawns and soy sauce.
Pasta sauces, chips, ready-made sandwiches, sausages and ketchup can also have large amounts.
Even dissolvable vitamin supplements and painkillers can contain up to a gram of salt in each tablet.