Using Salt to Optimize Mental & Physical Performance

The episode opens by introducing salt, also called sodium, as more than a seasoning or something to avoid. The host notes that most people link salt with blood pressure. He says the discussion will cover blood pressure, and also how the brain controls our appetite for salt or our aversion to it. He adds a less familiar claim: how we sense salty tastes affects how much sugar we crave, and whether we eat more or less sugar than we need.

He describes a "salt system": the cells and connections in the brain and body that drive salt craving and avoidance. He presents it as affecting many parts of health and performance, including athletic and cognitive performance, and he says he will touch on aging and dementia. He warns that some themes may be controversial and promises to label them when they are. He stresses that the new data point only to a possibility.

for some people, more salt might help them in terms of health, cognitive and bodily functioning. And for other people, less salt is going to be better.

He frames any guidelines as things to use together with a physician. He says listeners should absolutely talk to their physician before adding or changing anything in their diet or supplement routine. The planned topics include neurobiology, hormone biology, liver function, kidney function and brain function.

Before turning to salt, the host describes work from Diego Bohórquez's lab at Duke University, which studies how the gut and brain interact. The lab is known for finding neuropod cells. These are nerve cells in the gut that detect substances such as fatty acids and amino acids, and some of them sense sugar.

According to the lab's earlier work as the host summarizes it, sugar-sensing neuropod cells respond to ingested sugar and send electrical signals along their axons, through the vagus nerve, into the brain. Further processing in the brain leads to dopamine release. The host describes dopamine as a molecule known to promote craving, motivation and action. These cells are thought to push us to seek out and eat more sugary foods. He stresses that this happens without awareness.

This is a taste system in the gut that is not available to your conscious awareness.

He describes two systems that work in parallel. One is the taste of sweet food in the mouth. The other is the gut sensing its contents below conscious awareness and signaling the brain. He suggests this second system matters for hidden sugars and other ingredients in processed foods that may make the gut send signals that increase craving for those foods. His point to sugar lovers is that the craving is not only about how sugar tastes.

The new study was published on February 25, 2022, in Nature Neuroscience, under the title "The preference for sugar over sweetener depends on a gut sensor cell." The host reports that the lab found a category of neuropod cells that can tell apart sweet substances in the gut that contain calories, such as sugar, from sweet substances that do not, such as aspartame and sucralose. He notes that the researchers did not test every sweetener, including plant-based noncaloric ones such as stevia and monkfruit. He says the findings "ought to pertain" to all sweet noncaloric substances. That is his extrapolation, not something the study tested.

The central finding, in his summary, is that noncaloric sweeteners produce a distinct pattern of signals from the gut to the brain. So the gut can tell caloric from noncaloric sweetness below conscious awareness. He states that what this sensing leads to further down the line is not yet clear. His broader point is that food and drink cravings come partly from how things taste and partly from biochemical and neural events that start in the body and act on the brain. As a result, people may crave sugar or artificially sweetened foods without knowing why.

The host calls artificial sweeteners a somewhat controversial topic. He recalls an earlier discussion of Yale University School of Medicine studies on conditioning the insulin system, in which artificial sweeteners could trigger an insulin response under certain conditions. He says that coverage drew some pushback and that he welcomes pushback because it forces a closer look at a topic.

He makes several qualifications:

He says he does not demonize artificial sweeteners. Animal studies suggest artificial sweeteners can disrupt the gut microbiome, but those studies used fairly high doses, and whether this applies to humans is unclear and has not been investigated thoroughly. People differ: some dislike the taste, some like it, and some find sweeteners help them avoid eating too many calories. Some people believe sweeteners can change the insulin response in all people, but he stresses there still isn't evidence for that.

He says the new data show a need to understand how the gut registers artificial sweeteners and how that changes brain function. He connects this to a common experience: sweeteners at first taste "sort of not right," but over time people come to crave the taste. He describes drinking a lot of aspartame-sweetened diet soda in graduate school and feeling that he needed it. He allows that the cause may have been caffeine, sweetness or carbonation. After quitting for reasons unrelated to any fear of sweeteners, he no longer liked the taste. Now he drinks diet soda only occasionally, usually on a plane when nothing else is available.

He also says he consumes stevia, a plant-based noncaloric sweetener, in a number of supplements and foods. He places himself among people who are curious about sweeteners, somewhat wary of them, and still consume them in small amounts, and he guesses most people fall into that group. He notes that food manufacturers add sweeteners such as sucralose to foods for reasons that have always been unclear. He then points out that sweet taste can drive more craving for sweet foods even without calories, and suggests there "may be a logic or a strategy" behind the practice. He presents this as a question to explore, not a finding.

He links this to the main topic: salt sensing, both conscious and unconscious, can change how much we crave other things such as sugar and water. He calls nutritional neurobiology an emerging field and describes the Bohórquez Lab as one of its premier laboratories.

In a sponsor segment for the electrolyte drink LMNT, the host describes sodium, magnesium and potassium as electrolytes critical for neuronal function and many other biological functions. He says he favors appropriate salt intake, meaning intake matched to a person's baseline blood pressure, activity level, sweating and cognitive and physical demands. He also says that salt intake, water intake and hydration are closely linked.

He then lists salt's functions. It regulates fluid balance: how much fluid we want and how much we excrete. It also regulates salt appetite itself, which he calls homeostatically driven. We tend to crave salty foods and drinks when salt stores are low and avoid them when stores are high. He notes that this does not always hold: people sometimes keep craving salt when they don't need it, or even when they need to get rid of salt. Salt also affects appetite for other nutrients, such as sugar and carbohydrates.

He separates table salt from sodium. Salt is technically a mineral, and he says he will use "salt" and "sodium" interchangeably except when discussing specific intake recommendations. He gives a conversion figure:

one gram of table salt contains about 388 milligrams of sodium.

He warns that assuming grams of table salt equal grams of sodium causes confusion and can even cause trouble. He then outlines the rest of the discussion: the neural mechanisms behind salt appetite, how the brain and body interact in seeking and avoiding salt, how to tell when more or less salt is needed, and kidney function.

The explanation starts in the brain. Small clusters of neurons, called nuclei, sense salt levels in the brain and body. The host says the regions that do this are special because they lack the protective barrier around most of the brain: the blood brain barrier, or BBB. Most substances circulating in the body, especially large molecules, cannot simply pass into the brain.

He compares the brain with the ovaries and testes, which also have strict barriers, and gives reasons for each. For the brain, he argues that most of it cannot regenerate after injury. He acknowledges neurogenesis, the birth of new neurons, which has been shown in animal models. In humans it occurs to some extent in a few places, such as the olfactory bulb, and probably in a small subregion of the hippocampus. He says most of the strong data point to little neuron turnover in humans, so the neurons a person is born with are used for most, if not all, of life.

He adds that people are born with many more neurons than they keep. A normal, healthy process of cell death called apoptosis removes them during development. He says estimates vary, but anywhere from a third to maybe half or even two-thirds of neurons die across development, depending on the brain area. He presents this pruning as part of how an infant becomes able to walk, talk and calculate. Because the brain must use its cells for the whole lifespan, he calls the BBB absolutely critical.

For the ovaries and testes, he says the barrier is assumed to exist because they hold the genetic material passed to offspring. Mutated cells there could lead to mutations in children, which is costly in evolutionary terms. That explains why the body would keep mutagens away from the brain, ovaries and testes.