Sodium intake, specifically how much one should consume, continues to be a highly debated subject that is mainly spurred by higher sodium intakes thought to be associated with high blood pressure and cardiovascular disease. While the recommendations of government and medical organizations alike have been pushing for all of us to consume less sodium, the science is not actually very clear on if this is really effective at meaningfully reducing high blood pressure and cardiovascular disease/events in the general public. A look at the literature may surprise you. I know it surprised me!
Currently the WHO and the American Heart Association recommend that we consume no more than about 2-2.5 grams of sodium daily (about 1 teaspoon of table salt), and for certain populations the recommendations go down to about 1.5 grams (about 0.7 tsp of table salt). Currently the average intake of sodium in the US is somewhere between 3-4 grams a day.
To get a better understanding, let's look at 3 of the most cited general population studies on sodium the INTERSALT study and the Scottish Heart Study (both 1988, BMJ) and a review of the Framingham Offspring Study (AJE, 2017):
INTERSALT - This study showed a very moderate association between sodium intake and blood pressure with only a 0.9 mmHg increase in systolic BP per 1 gm of salt intake. (To put that in perspective, according to this study, if my blood pressure was 120/60 mgHg eating 2 grams of sodium daily, then it would be 120.9/60 eating 3 grams of sodium and 121.8/60 eating 4 grams of sodium)
The Scottish Heart Study - This study showed no association between sodium intake and blood pressure, but rather showed an association with age, BMI, alcohol and potassium intake.
Framingham Offspring Study- This review showed those who consumed the recommended 2-2.5 grams of sodium daily actually had higher blood pressure than those that took in more than the recommended sodium intake.
Next, if we look at controlled studies, one of the most famous is the DASH (2001) study. But on further look, this study showed that only when potassium was low did restricting sodium help blood pressure, but with a high potassium intake, the negative blood pressure effects of a higher sodium intake were mitigated. In other words, the story is more complicated than just sodium.
Further, in a 2011 Cochrane Review looking at 71 studies of normotensive people revealed significant heterogeneity in if sodium restriction helped blood pressure (some showed no effect, some a positive and some a negative effect) Of the studies that did show that reducing sodium lowered blood pressure, it was surprisingly only a modest lowering of 1.27 mmHg (0.3 mmHg per 1 g of sodium reduction).
Finally, in another large international study (NEJM, 2014) that estimated sodium intake in over 100,000 people, it was shown that low sodium intakes which are consistent with officially recommended levels were surprisingly associated with higher cardiovascular events and mortality, even in people with high blood (Lancet, 2016). Additionally, The Prospective Urban Rural Epidemiology study also showed sodium intake was associated with cardiovascular disease and strokes only in communities where mean intake was greater than 5 g/day (Lancet, 2018).
This is not to say that there is not evidence for salt restriction with certain medical conditions like kidney failure or congestive heart failure, but that is beyond the focus of this post.
All of this said, none of these studies looked at sodium intake while on a ketogenic diet and with all the debate, one thing is very clear and should be noted; when you are on a ketogenic diet, restricting sodium, in the words of the American Nutrition Association, “is a recipe for failure.” The body has many ways to deal with varying sodium intakes by adjusting the amount of sodium excreted by the kidneys in the urine. Additionally, sodium regulation is controlled by many other factors as well that actually have nothing to do with how much sodium is consumed. Two of these factors are insulin and ketones. High insulin and low ketones result in a higher level of sodium retention, while low insulin and high ketones results in an increase in the excretion of sodium. The clinical term to describe this loss of sodium in the urine on a ketogenic diet (or during fasting) is called natriuresis.
It is important to take this point a bit further. When the sodium is removed from the body at a higher rate while on a ketogenic diet, the body compensates by excreting more fluid in an effort to keep its fluid to sodium concentrations balanced. Initially this reduction in fluid retention is a good thing that contributes to weight loss, reduced need for diuretic medication for those that take it, and improved blood pressure; but, it is important to realize that this increase in sodium excretion continues for as long as one remains in nutritional ketosis and can result in sodium and plasma volume depletion. This can result in people feeling dizzy, fatigued, constipated and to have headaches. This loss of sodium and fluid further can lead to compensatory hormonal changes that then lead to potassium and magnesium loss leading to muscle cramps, irregular heartbeats, loss of muscle mass and neuromuscular dysfunction. These symptoms are often referred to as the “keto flu.”
What are the takeaways?
1. How much sodium to consume is a highly debated subject, and current guidelines are being challenged by the literature.
2. Eating a low carbohydrate diet naturally lowers insulin levels and leads to the production of ketones, both of which stimulate an increase of sodium excretion in the urine.
3. This loss of sodium causes a loss of fluid as well and is a major driver of what is commonly referred to as the “keto-flu.”
4. RESTRICTING SODIUM WHILE ON A KETOGENIC DIET IS A “RECIPE FOR FAILURE.”
Next week we will go further into what the keto-flu is and more importantly, how to avoid it, so make sure and stay tuned!