Salt intake: More complicated than you think

Salt intake – A cautionary tale

Most nutritional guidelines advocate restricting our salt intake to less that 100 mmol/day. This is about half of what most adults get each day from their diet. In those with high blood pressure, diabetes, kidney or heart disease lower targets are recommended ( less than 65mmol/day).

The rationale for such recommendations is straightforward: our daily salt intake correlates with our blood pressure levels. The more salt we eat, the higher our blood pressure. And high blood pressure damages blood vessels, which can lead to cardiovascular disease and stroke.

In fact, along with smoking and diabetes, hypertension is one of the biggest killers of hearts and minds. Consequently, if we reduce our salt intake, we’d also reduce our blood pressure and the risk of having a heart attack or stroke.

While such logic is appealing, especially as a low-cost public health message, the actions of salt on human physiology are more complicated, and certainly extend beyond blood pressure regulation.

Keeping things constant and balanced

Millions of years ago, our ancestors emerged from the salty oceans, and took part of it with them. Homeostasis of our inner sea is a fundamental part of our physiology. We can eat our salt and vinegar chips or drink gallons of fresh water, but our salt content hardly changes. We survive(d) by keeping things constant.

Our kidneys are the key regulators of this balance, filtering and reabsorbing more than 25,000 mmol of salt every day, losing only 0.5% through urine.

In healthy individuals, this loss equates almost exactly with the amount of salt they eat (~100-200 mmol/day). Consequently, if we eat salty chips (an extra 30 mmol of salt) it’s not a major effort excrete sodium into our urine. And if we didn’t get much salt today, it’s not hard to increase reabsorption slightly to maintain the salt and water balance.

This balance is under tight neuro-hormonal control, involving a range of chemical signals between the kidneys, heart, adrenal glands and brain. The most well-known are the renin angiotensin system (RAS) and the sympathetic nervous system (SNS). If you reduce salt intake, these homeostatic pathways signal the kidneys to retain more salt. If you increase salt intake, these pathways are suppressed to increased salt excretion and offset increases in blood pressure that would otherwise occur.

These same neuro-hormonal pathways are implicated in the development and progression of human disease, from cardiovascular disease and diabetes, to cancer and mental illness. Indeed, the wide clinical utility and effects of drugs that block the RAS or SNS stand as testament to the importance of these pathways, beyond simply regulating blood pressure. But if this is true, then by implication, salt intake must also have pleiotropic actions beyond those on blood pressure.

Salt reformers and salt skeptics

Many observational studies have looked at the association between salt intake with heart disease and the risk of premature mortality. Some have shown that high salt intake is associated with poor health, some have found no effect at all, while others have found that individuals with a low salt intake have worse clinical outcomes. This is despite trials clearly showing that salt restriction lowers blood pressure.

This inconsistency forms the basis of the so-called “salt wars”, an unscientific and often vitriolic war of words between (blood-pressure centric) salt reformers and (pleiotropic) salt skeptics. Each has some scientific data to support their stance, and sound scientific reasons for doubting the opposing viewpoint.

For example, one well-known advocate for restricting salt responded to an article in JAMA, which showed modestly reduced survival in individuals on a low-salt diet, saying: “it doesn’t make (any) sense … it’s like saying we don’t think cigarettes are harmful! … I don’t think this is worth paying attention to”.

He went on to say: “Everything else that has been shown to lower blood pressure is beneficial in terms of heart attacks and strokes.” So why should salt intake be any different?

Salt skeptics argue that this is not always true. For example, a clinical trial of lowering blood pressure in patients with diabetes (ACCORD) failed to show effects on cardiovascular events or mortality, despite achieving very significant falls in blood pressure. Moreover, many drugs are readily ascribed blood pressure-independent effects on health outcomes. Why not salt?

A parable once told by Michael Alderman (a notable skeptic) goes something like this:

Weight loss is safe and effective for lowering blood pressure in obese and overweight individuals. So once upon a time, pregnant women were advised to limit their weight gain in order to reduce their risks from hypertension during pregnancy (known as eclampsia). From a blood pressure centric point of view, this worked very well. But while eclampsia was prevented and blood pressure lowered, fetal mortality was dramatically increased. So no one now recommends weight restriction during pregnancy. It might be lowering the blood pressure, but what else is salt restriction doing?

The likely truth is that some individuals will benefit from restricting salt in their diet, while others may not.

For some, salt-sensitive hypertension is more important than neuro-hormonal activation. One example is in the elderly, in whom low-renin hypertension and renal impairment predominates. Here, restricting salt is a logical and important health message. In other contexts, neuro-hormonal activation may have primacy over blood pressure, and salt restriction may lead to less favorable or even adverse outcomes.

It is unlikely that anyone will accept this middle ground in an inconclusive and ongoing war. Either salt is a weapon of mass destruction or it is the spice of life. Ultimately, consumers are left in a quandary, unsure who to believe and taking each new piece of information with or without a pinch of salt.

Last reviewed 24/Feb/2017