Eighteen studies, including around four hundred patients, have looked at the effects of sodium restriction on fasting plasma insulin concentrations. In one study of 147 people with normal weight and blood pressure, salt restriction caused increases in insulin, uric acid, LDL, and total cholesterol levels. Fasting insulin was higher in twenty-two of the twenty-seven groups (thirteen statistically significant), unchanged in two, and lower in three (not statistically significant). Egan and colleagues found that low-salt diets increase both fasting and postglucose insulin by about 25 percent compared to high-salt diets, an effect that has been duplicated and confirmed—that is, proven—in many later studies and meta-analyses of randomized controlled trials. Even those few people whose blood pressure might go down on low-salt diets—the “salt-sensitive” among us—experience significant increases in insulin. One of the mechanisms that could be at work here is salt’s ability to actually improve our cells’ ability to use glucose. Animal studies indicate that salt restriction worsens the body’s ability to use glucose correctly while also increasing body weight, body fat, and fatty acid levels. A high salt intake likely increases the glucose transporter GLUT4 in insulin-sensitive tissues and thus allows greater glucose disposal. Indeed, high-salt diets have been found to increase GLUT4 protein in both fat tissue and muscle. This is a good thing, because it allows your body to pull more glucose out of the bloodstream, reducing insulin levels and minimizing the damage that high glucose levels would have on the blood vessels. While a low-salt diet has been shown to impair insulin signaling, a high-salt diet has been proven to enhance insulin signaling. Salt-restriction studies in humans have found adverse effects on glucose and lipid metabolism. One animal study even found that a low-salt diet increased body weight, belly fat, and blood glucose and plasma insulin levels, while it induced insulin resistance in the liver and muscle tissue. Low-salt diets have also been found to increase liver fatty acid synthesis, which can contribute to nonalcoholic fatty liver disease (NAFLD), commonly known as “fatty liver,” as well as organ fat storage, compared to a normal salt intake. Researchers found that the activity of brown adipose tissue—the “good fat” that burns calories—was reduced on a low-salt diet, indicating that low-salt diets may lower our basal metabolic rate, and possibly contribute to accelerated aging. Worse, many obese patients begin their weight-loss programs by trying to cut their carbohydrate intake. Cutting carbs causes you to become a “salt waster,” excreting more salt than you would on a more balanced diet, especially when you hit ketosis (near 50 grams of carbohydrates per day or less). Thus, if you are going to cut your carbohydrate intake, you want to increase your salt intake to match the additional salt loss by the kidneys and to help prevent the subsequent rise in insulin levels to compensate for this loss. Sadly, most doctors will pair recommendations to lose weight with recommendations to reduce salt at the same time. But it appears that most people need an additional 2 grams of sodium per day compared to their normal sodium intake during the first week of carbohydrate restriction, and around an additional 1 gram of sodium per day during the second week to match increased salt losses.
In this excerpt, the author talks about how pairing our weight loss efforts by eating clean meals might actually make it harder for ourselves if we intake less salt than we actually need. In fact, your body will require more salt especially if you are taking a low carbs diet (as popular now with fads like the keto diet).
