Not the packaged kind, but the real kind. Source
I dedicate this to all of you ramen lovers out there (which includes me). If you don’t love ramen, then… I’m sorry. OK, I’m not sorry. Ramen is not real food so there is no reason why I should be apologizing. But it’s still damn good, in my opinion.
Wait, my conscious said something to me: “It is real food, damnit!” OK. It’s real. Just look at the picture.
In the first post of this series, I went a little bit into what salt is and how dietary salt affects your health through blood pressure manipulation. Studies upon studies have been conducted trying to verify that salt restriction leads to blood pressure reduction, thus leading to a decreased risk of cardiovascular disease. It’s true that salt does mingle with blood pressure and that high blood pressure is a pretty darn good indicator of heart disease; but so do other things. In this post, I will talk about these other things—namely stress. I also talked about how context plays a huge part in how your body responds to salt—if you’re leading a generally unhealthy lifestyle, salt will harm you. If not, you probably don’t have much to worry about.
Sometimes when I read research, I feel as if investigators are just moving from one target to another, like a firing squad. They hit one target, liked what they saw then moved onto the next—first fat, now salt. It’s not a surprise given that blood pressure control is a HUGE market for pharmaceutical companies; literally, billions of dollars.
What’s the issue then?
Experts often talk about how we need this nutrient and that nutrient, or throw out a blanket statement such as, “decrease sodium to decrease blood pressure”. Many times, these messages are often lost in translation and people will concede without analyzing why they’re doing said modification. Worse yet, many will read a single article on a popular mass media outlet, not do any additional research, and talk about an issue with utmost confidence while citing the source. That’s cool. Only problem with that is that it has many problems. Take nutritional research with a grain of salt.
So, do we take into consideration our overall dietary and lifestyle habits or just throw salt out with the baby and the bathwater? We have a hard time considering context, making us miss the forest for the trees. And not surprisingly, this ‘lack of salt knowledge’ is actually driving people to eat less salt, which has its own shortcomings (more on this later).
Eating too much of anything is bad, unless it’s popcorn shrimp (but then you may get HBP). Based on my amazing logic, eating too much salt is obviously bad. Legend has it that too much salt intake leads to a condition called ‘hypertension’, or high blood pressure, which is then intricately linked to an increased risk of heart disease and stroke. Considering I have a family history of strokes, I hold this topic close and dear to my heart (get it?).
Guess what else is bad for you? Breathing. Too much exercise. Eating too many Brussels sprouts. A few years ago, a Chinese woman was rushed to the emergency room due to thyroid failure because she ate 2-3 pounds of raw bok choy for a few months. Hey, at least she was getting her vitamin C. See the trend? Things that are good for you in moderation will send you quicker to the grave than the Undertaker.
His name is Extreme and he’s coming for you. Source
The battle wages on
Salt is a victim to dichotomy. Though, there is a somewhat solid connection between high salt intake and blood pressure, we see some studies refuting the proposal that deep salt restriction is actually beneficial. Some studies actually showed no difference between high and low salt intakes between two different groups of people. This is not surprising, given that normal people with a normally functioning kidney do not exhibit increases in blood pressure compared to someone who is sick or is salt-sensitive (Azak; Weinberger; Franco). But the real question is whether salt actually leads someone to be hypertensive in the first place.
The battle between the high-salt/low-salt clans is like a good arm-wrestling match: there’s a lot of back and forth going on. Since there seems to be an association between increased blood pressure and risk of cardiovascular disease, researchers wanted to see if the opposite is true in the clinical setting: that too little salt is harmful. A good deal of the retort is based on speculation and basic physiology of the body’s salt regulation system; in particular, the RAAS. As you will read below, other reports show that restricting salt worsens clinical outcomes, overactivates the RAAS, leads to electrolyte imbalances.
I mentioned in my earlier post that the RAAS is crucial for survival, and proper function of it will determine how long you live and the quality of life. Its primary responsibility is the regulation of electrolyte balance through hormone action (Atlas).
Health effects of too little salt
Before we move on, let’s see what is considered a “low-sodium diet”. According to research, a low-sodium diet can be anything under 2.3g of sodium per day. A high-sodium diet can be anything above. For instance, the U.S. average is 3.4g per day. This, according to health authorities, is far too much. If we cut intake to 1.5g per day, we would save over 400,000 lives per year (CDC).
Every system in the body exists for a reason (except maybe the appendix). If you know my philosophy, you know that I believe that finding a proper balance is the key to a long, healthy, and successful life. It’s no different with salt intake. If you’re constantly walking around in a drunken stupor, don’t exercise intelligently, eat like you’re the Michelin Man, and watch more TV than the dust on your couch, then managing certain nutrients in your diet will probably be a good idea.
One, big happy family. Source
Mismanagement of the RAAS, primarily through a low-sodium diet comes with its own risks. As much as some activation of the RAAS through moderate salt intake regulates arterial pressure and is involved in heart muscle contractions, too little sodium over-activates the RAAS, which forces it to release more renin and aldosterone, hormones that are directly responsible for fluid balance and urine retention.
This whole bit about the RAAS and cardiovascular disease stirs up quite a controversy. Quite a few studies looked at the interaction between the RAAS and health. So how exactly does over-activation of the RAAS through a low-sodium diet actually increase the risk of CVD? The proposed mechanism by which RAAS is thought to contribute to heart failure is because renin, a hormone released by the RAAS, preserves sodium by enhancing sodium reabsorption by the kidneys. Renin’s other functions include mediating extracellular fluid volume and arterial vasoconstriction. Having increased levels of renin in the blood dilates blood vessels; increases the concentration of water, shifting the balance towards hyponatremia (low sodium concentration); increases serum potassium levels; and reduces glomerular filtration rates (kidney) (Sealey). Asides from sodium, another major way that renin is secreted is through activation of the sympathetic nervous system.
To investigate whether too little salt and too much renin contributed to CVD, researchers of a 1997 study found that PRA (plasma renin activity) was independently associated with heart attacks; for every 2 units of PRA, heart attack risk went up by 25% (Aldermann). Another study done in 2010 again measured the risk of PRA and CV outcomes:
“The association of PRA with outcomes was observed after correction for hypertension, hyperlipidemia, diabetes, a family history of cardiovascular events, smoking, renal failure, and the use of statins. In conclusion, elevated baseline PRA is associated with cardiac morbidity and mortality in patients with coronary artery disease but normal left ventricular function and no previous MI or HF” (Muhlestein).
And then in a study done in 2011 and published in the European Heart Journal:
“The association of high NT-proBNP and high PRA identified a subgroup (22% of the study population) with the greatest risk of cardiac death. In conclusion, PRA resulted in an independent prognostic marker in patients with systolic heart failure additive to NT-proBNP level and ejection fraction” (Vergaro)
Along the same lines as the above study and published in the same journal:
“Analyses of specific causes of cardiovascular death showed that for each standard deviation increase in log-PRC there was a 22% (P = 0.006) increase in risk of sudden cardiac death and a 23% (P = 0.033) greater risk of death due to heart failure. The association of PRC with cardiovascular mortality remained stable after adjustment for established cardiovascular risk factors, ongoing antihypertensive medication, immunoreactive angiotensin II, and aldosterone levels” (Tomaschitz).
The HOPE study researchers also had this to say about PRA:
“High PRA is an independent predictor of major vascular events and mortality in a stable population of high-risk patients with atherosclerosis and/or diabetes. Although an increase in PRA could be a marker of more intense antihypertensive therapy, our results suggest that PRA may represent a risk marker and potential target for therapy in high-risk patients with atherosclerosis and/or diabetes” (Verma).
As a side note to the last quote, the first clause of the last sentence—“marker of more intense antihypertensive therapy”—signifies strategies that clinicians use to reduce BP, namely a low-sodium diet and medications. This is in stark contrast to the original HOPE studies that showed that Angiotension Converting Enzyme (ACE) inhibitors actually reduced the risk of heart disease.
Additionally, low-sodium diets increase levels of catecholemines—adrenaline and noradrenaline—and increase levels of cholesterol and triglycerides. Additionally, too little salt may actually worsen some clinical disorders, such as congestive heart failure (Graudal; Paterna). In a condition such as CHF, you will experience lower extremity edema, which is usually caused by fluid imbalances; but whether this is a problem of too much sodium is unknown, as shown by the lack of evidence for sodium restriction in people with heart failure. Some researchers readily recommend a 3g sodium restriction as opposed to 1.5g and lower (Lennie). There are even some studies suggesting that by inhibiting the RAAS, risk of type 2 diabetes decreases (Andraws).
Ready for some more heat? In some studies, a low-salt diet has been shown to increase insulin resistance, or decrease the body’s ability to use insulin to store energy (Garg). In these studies, despite having a higher blood pressure on the high salt diet (1-3 mmHg), salt sensitive subjects also experienced a decrease in fasting blood sugars, insulin, and homeostasis model assessments. In another study done by the same author, a low-salt diet increased insulin resistance in healthy subjects (Garg). So it seems that salt has an effect on blood sugars, as well.
A suitable cut-off for salt
These types of studies usually set off a firestorm of responses and comments. No surprise there, given how health authorities have so much vested interested in salt. After decades of espousing low-sodium diets, how could they turn back? It’s not like they’re completely wrong, though. Many experts just decide to live in the minutia instead of giving suitable ranges.
We had a few studies come out this year measuring urinary output for thousands of people. Urinary output gives an accurate picture of how much salt someone is consuming. What they found is that sodium intakes below 3g and above 6g were associated with an increased risk of all-cause mortality, meaning you have a higher chance to die from other diseases asides from what they were studying—cardiovascular disease. Investigators from the PURE study measured urinary sodium excretion and came to tentative conclusions regarding optimal salt intake. After an average follow-up time of 3.7 years in 3317 participants, they saw that optimal sodium excretion to be 3-6g per day. Additionally, people with low potassium excretion levels—and thus either low dietary potassium intake or high sodium intake or both—tend to be at a higher risk of CVD independent of dietary salt intake (O’Donnell). What these researchers saw was that people who usually ate high levels of sodium also ate low levels of potassium.
The Cochrane Collaboration, an organization filled with reputable professionals who conduct noteworthy and highly refined reviews on relevant topics, also did their dig on salt. In their report on randomized trials, they measured an average daily salt intake of 9-12g per day. They concluded that a more feasible target is 5-6g per day, and could even make the lower cut-off point 3g… so making it 3-6g per day (He).
By anyone’s standards, 9-12g is high. Unless you’re an athlete competing in ludicrous climates, there’s no reason to eat that much salt. And how can anyone eat all that salt anyway? Ah, but of course, through processed foods. I digress.
With all things being equal, high sodium intake inhibits the action of the RAAS. Increased RAAS activity through low-salt diets or intense hypertensive therapy leads to an increased PRA, which is a risk factor for heart disease, diabetes, and stroke. So why does high sodium intake increase risk of heart disease if it inhibits the RAAS and reduces PRA?
For one, there is the extrapolation that since sodium increases blood pressure and blood pressure places some at an increased risk of heart disease, it stands to reason that high salt intake leads to heart disease. Perhaps people reached this conclusion because despite inhibition of the RAAS through a high-salt intake, people were still suffering from blood pressure disorders. In this study, researchers pointed out that the RAAS can manipulate PRA to manifest hypertension in two ways: the low renin, sodium-volume dependent form and the medium to high hypertension form.
What the question above is considering is that hypertension can happen at both ends of the spectrum, when salt intakes are either too high or too low. If salt intake is too high, body sodium content increases to the point where RAAS is turned off (Laragh). This is probably how high sodium intake can contribute to the development of high blood pressure.
Yet, high salt seems to be just one part of the equation. Eating too much salt leads to increased sodium excretion through inactivation of the RAAS, but high sodium excretion also leads to low potassium excretion, which is probably more important than sodium in terms of regulating blood pressure (Aaron; O’Donnell; O’Donnell). Generally, people who usually have high risk profiles of diseases through a high salt diet are not the healthiest of the bunch—low potassium intake (fruits, vegetables, non-deep fried potatoes), calcium (dairy, vegetables), phosphorus (vegetables), magnesium (cacao, vegetables); smoking; drinking; almost non-existent exercise habits; and a landfill worth of unnecessary stress.
What does all this mean?
If all of this flew over your head, don’t worry. No one really knows how much sodium each person should eat and there is no crystal clear answer. I may be painting a picture showing that sodium restriction is not necessary, but that’s not it, either. I will constantly remind you that context matters. But in the face of conflicting research and the inability to precisely control for non-dietary behaviors, I can’t help but question the validity of much of this salt research.
Outside factors, like genetics, dietary and lifestyle habits, and physiological responses of a low-salt diet, definitely goof around with BP. For example, the Koreas Center for Disease Control and Prevention didn’t even state that high sodium consumption was a primary cause for HBP. They listed alcohol, smoking, and stress. I will even go so far as to say that the three mentioned factors contribute to increased blood pressure more than sodium.
I am not going to talk about alcohol and smoking here, since most of us know that too much drinking and smoking don’t do any favors for your health. By the way, according to the World Health Organization, South Korea is #6 in the world in terms of units of alcohol sold per capita.
Sodium is not the only thing to look at
I think it’s quite amazing how often salt gets thrown under the bus, and we’re not talking about to make the road less slippery, although talking about salt can certainly be a slipper slope. Wow, quite a few puns for one sentence. To just look at sodium as the culprit in health decline is not truly looking at the whole picture.
Many mass-produced books released today are not truly nutrition books, but books on how to give your whole lifestyle an overhaul. Although their main focus is nutrition, they take a multi-pronged approach to your health. Books are not alone in this regard, either. Organizations such as the American Heart Association consider other factors when it comes to heart dysfunctions. The primary example I am going to use here is stress.
Stress is a true killer
Based on physiological responses, stress is involved intimately with every preventable disease out there. Studies have repeatedly shown that stress elevates blood pressure immediately by stimulating the nervous system to release hormones that constrict blood vessels, thus increasing force of blood flow (Kulkarni). This part of the nervous system is called the ‘sympathetic nervous system’ and is involved in responding as the ‘fight or flight’ mechanism. Most importantly, your body doesn’t know how to differentiate between a small stress such as a traffic jam and a major stress such as hanging off of a cliff. Running from a bear or preparing for a throw down behind the local pub can be considered major stresses that were present throughout human history, leading to the development of this crucial system.
As much as I dislike running… Source
The problems arise when small stresses accumulate in our daily lives, whether it’s through work, toxic relationships, or having a generally pessimistic view on life. This puts our bodies in a constant state of alertness and steadfastness. And to test whether lesser stressors lead to hypertension, researchers conducted studies measuring how work and psychological stress predicts CVD. They found that it did; just worrying about work increases heart rate by almost 10 beats per minute (Matthews; Vrijkotte; Pieper). Things like a broken copier machine, getting packed like sardines in the subway, and watching Kim Kardashian cry over her man on this month’s tabloids all add to the little stresses that cause chronic and sustained elevations in blood pressure. Seriously, researchers used video games to measure increases in blood pressure (Matthews). Compared to how long humans have been around, none of these were present until recently, when society got bored and desperate for money that they had to create reality TV shows and follow people who contribute to the endless yo-yo dieting paradigm (/end rant). So although stress does not directly lead to hypertension, it sets off a cascade of reactions that eventually do.
“Kanye said I couldn’t go to the nightclub with my other spoiled friends!” Source
**Research studies aside, is it not surprising that despite the myriad of pharmaceutical drugs that the rates of high blood pressure, stroke, heart disease and other diseases are not decreasing at the same rate that medications are being prescribed? In the future, I will touch on the pros and cons of taking blood pressure lowering medications. Interestingly enough, some of these medications actually increase the risk of diseases that they are marketed to prevent.
So are you saying that sodium should be ignored?
I am saying that sodium is not the nutritional villain everyone thinks it to be. Again, remember that context is your friend here. Like saturated fats, sodium is another nutrient that is guilty by association. Have you ever seen someone who has high blood pressure? Next time, if you care to, take note of their lifestyle and diet. Nine times out of ten, they will be leading a lifestyle conducive to high blood pressure and health disorders. We’re talking about diets high in processed foods, getting hung up over every little and big thing—traffic, phone calls, nagging kids, etc.—to smoking, drinking, and plopping their lazy behinds on the couch to watch Djokovic get buried by Nishikori in the 2014 U.S. Open… while eating ice cream. This is not an exaggeration. I can’t count on one hand the number of people I have counseled who led this exact lifestyle. And when I go to the supermarket, I notice that the people who get winded walking through the produce section are sprinting to the cookies and crackers aisle after picking up their hypertensive medications… without skipping a beat. To these people, sodium is just one of those things that tend to be high because their lifestyles are in the gutters.
Nishikori probably doesn’t have a problem with his BP. Source
In short, the issue with sodium is overblown. It’s also misconstrued. People read research and automatically think, “oh, if the New York Times says this, it must be true”. Go a step further and those who are more enlightened will read research and think, “oh, if this paper says this, it must be true”. Except, research is not always black and white—it’s more of a yellow light that points at an issue to be explored. In this case, it’s salt—and there is no shortage of research either supporting or refuting drastic salt consumption reductions.
I’m in neither camp exclusively, though I tend to lean towards the refutation camp. This is not because I like to try to antagonize the issues I grew up with and the authors championing them. It’s because I am both genuinely curious to see what the research really says and how that can affect the service I provide in the future. For instance, if I can get you the same results with either a low or moderate sodium diet, which one would you prefer?
On the other hand, I do feel that salt can be overdone, just like saturated fats. Unless you have no problem with it, I feel the 1.5-2.4g restriction of sodium is unnecessarily too low. Actually, I wouldn’t take issue with it if research actually showed that these levels were unquestionably better than 3-6g.
Here is what I see based off the research:
- Going above 6g of sodium per day affects blood pressure in a negative way
- Low-salt (1.5-2.4g per day) can drop BP by up to 11 mmHg in salt-sensitive people
- Low-salt overactivates the RAAS, which is a risk factor for heart disease
- Work-related stress affects blood pressure
- Worrying affects blood pressure
- Video games and other acute episodes that flip on the sympathetic nervous system increase blood pressure
- Rather than decreasing sodium (unless it’s at 9-12g per day), increase potassium
As always, your feedback is appreciated.
Live life strong,
Sacks FM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med. 2001 Jan 4;344(1):3-10.
Salt intake of high group was 8.53g, way too high by anyone’s standards. Interestingly, blood pressure did not differ between the two groups.
Center for Disease Control and Prevention. Get the Facts: Sodium and the Dietary Guidelines. 2012 Jun. http://www.cdc.gov/salt/pdfs/sodium_dietary_guidelines.pdf
Laragh JH1, Sealey JE. The plasma renin test reveals the contribution of body sodium-volume content (V) and renin-angiotensin (R) vasoconstriction to long-term blood pressure. Am J Hypertens. 2011 Nov;24(11):1164-80.
Atlas SA. The renin-angiotensin aldosterone system: pathophysiological role and pharmacologic inhibition. J Manag Care Pharm. 2007 Oct;13(8 Suppl B):9-20.
Paterna S, et al. Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend? Clin Sci (Lond). 2008 Feb;114(3):221-30.
Graudal NA1, Hubeck-Graudal T, Jürgens G. Effects of low-sodium diet vs. high-sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride (Cochrane Review). Am J Hypertens. 2012 Jan;25(1):1-15.
Kulkarni S, et al. Stress and hypertension. WMJ. 1998 Dec;97(11):34-8.
Muhlestein JB, et al. Relation of elevated plasma renin activity at baseline to cardiac events in patients with angiographically proven coronary artery disease. Am J Cardiol. 2010 Sep 15;106(6):764-9.
Shao W, et al. Activation of the renin-angiotensin system by a low-salt diet does not augment intratubular angiotensinogen and angiotensin II in rats. Am J Physiol Renal Physiol. 2013 Mar 1;304(5):F505-14.
Tomaschitz A, et al. Association of plasma aldosterone with cardiovascular mortality in patients with low estimated GFR: the Ludwigshafen Risk and Cardiovascular Health (LURIC) Study. Am J Kidney Dis. 2011 Mar;57(3):403-14.