Tag Archives: health

Should You Hold the Salt? Part II

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,




Haddy FJ1Vanhoutte PMFeletou M. Role of potassium in regulating blood flow and blood pressure. Am J Physiol Regul Integr Comp Physiol. 2006 Mar;290(3):R546-52.

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.

Azak A, et al. Salt intake is associated with inflammation in chronic heart failure. Int Cardiovasc Res J. 2014 Sep;8(3):89-93.

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.

Taylor RS, et al. Reduced dietary salt for the prevention of cardiovascular disease: a meta-analysis of randomized controlled trials (Cochrane review). Am J Hypertens. 2011 Aug;24(8):843-53

He FJ1Li JMacgregor GA. Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials. BMJ. 2013 Apr 3;346:f1325.

Sealey JE, et al. Renin-angiotensin system blockers may create more risk than reward for sodium-depleted cardiovascular patients with high plasma renin levels. Am J Hypertens. 2013 Jun;26(6):727-38.

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

Garg R1Sun B2Williams J2. Effect of Low Salt Diet on Insulin Resistance in Salt-Sensitive Versus Salt-Resistant Hypertension. Hypertension. 2014 Sep 2.

Alderman MH, et al. Plasma renin activity: a risk factor for myocardial infarction in hypertensive patients. Am J Hypertens. 1997 Jan;10(1):1-8.

Laragh JH1Sealey 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.

Houston M. The role of nutrition and nutraceutical supplements in the treatment of hypertension. World J Cardiol. 2014 Feb 26;6(2):38-66.

Garg R1, et al. Low-salt diet increases insulin resistance in healthy subjects. Metabolism. 2011 Jul;60(7):965-8.

O’Donnell M1, et al. Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med. 2014 Aug 14;371(7):612-23.

O’Donnell MJ, et al. Urinary sodium and potassium excretion and risk of cardiovascular events. JAMA. 2011 Nov 23;306(20):2229-38.

O’Donnell MJ1, et al. Salt intake and cardiovascular disease: why are the data inconsistent? Eur Heart J. 2013 Apr;34(14):1034-40.

Atlas SA. The renin-angiotensin aldosterone system: pathophysiological role and pharmacologic inhibition. J Manag Care Pharm. 2007 Oct;13(8 Suppl B):9-20.

Aaron KJ1Sanders PW. Role of dietary salt and potassium intake in cardiovascular health and disease: a review of the evidence. Mayo Clin Proc. 2013 Sep;88(9):987-95.

Perry IJ. Dietary salt intake and cerebrovascular damage. Nutr Metab Cardiovasc Dis. 2000 Aug;10(4):229-35. 

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 NA1Hubeck-Graudal TJürgens 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.

Matthews KA, et al. Blood pressure reactivity to psychological stress predicts hypertension in the CARDIA study. Circulation. 2004 Jul 6;110(1):74-8.

Vrijkotte TG1van Doornen LJde Geus EJ. Effects of work stress on ambulatory blood pressure, heart rate, and heart rate variability. Hypertension. 2000 Apr;35(4):880-6.

Pieper S, et al. Cardiac effects of momentary assessed worry episodes and stressful events. Psychosom Med. 2007 Dec;69(9):901-9.

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.

Vergaro G, et al. Prognostic value of plasma renin activity in heart failure. Am J Cardiol. 2011 Jul 15;108(2):246-51.

Matthews KA, et al. Blood pressure reactivity to psychological stress and coronary calcification in the Coronary Artery Risk Development in Young Adults Study. Hypertension. 2006 Mar;47(3):391-5.

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.

Andraws R1Brown DL. Effect of inhibition of the renin-angiotensin system on development of type 2 diabetes mellitus (meta-analysis of randomized trials). Am J Cardiol. 2007 Apr 1;99(7):1006-12.

Verma S, et al. Plasma renin activity predicts cardiovascular mortality in the Heart Outcomes Prevention Evaluation (HOPE) study. Eur Heart J. 2011 Sep;32(17):2135-42.

de Boer RA, et al. Plasma renin and outcome in the community: data from PREVEND. Eur Heart J. 2012 Sep;33(18):2351-9.

Tomaschitz A, et al. Associations of plasma renin with 10-year cardiovascular mortality, sudden cardiac death, and death due to heart failure. Eur Heart J. 2011 Nov;32(21):2642-9.

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.

Should You Hold the Salt?

The overriding theme of this blog is to provide you, my dear readers, with applicable and cool information about health, fitness, and nutrition. I usually refrain from splitting hairs and will continue to do so. However, this take on salt may be a bit more detailed than what many are comfortable with. However, I feel that salt is a huge health issue that affects all of our lives. If not the health aspect of it, it’s the ability to liberate yourself from a lack of knowledge. Armed with the information here, you can decide for yourself whether you should agonize about including salt in your diet or not. 


Asides from L O V E, it’s another four letter word that evokes all sorts of emotions, especially to those in the nutrition field. Not a day passes by that I don’t get sucked into a conversation about salt.

“Oh, you put salt on your food? That’s bad for your health!”

“But won’t salt raise your blood pressure?”

“Salt hurts your kidneys!”

Along with fat, salt is one of those things that seems to get looked at through the scope of dichotomy. It can’t escape being thrown into one camp or the other. And like fat, salt is one of those things that hit close to home for me, since I also have a family history of high blood pressure, stroke, and heart disease.

My heritage is South Korean. Though I was not born in South Korea, Korean parents gave birth to me, and from a young age I ate somewhat traditional Korean foods. I say somewhat because it was typically poor-class Korean fare reserved mainly for people who have no money but just need to put something in their mouth. As long as I can remember, I usually ate a porridge made of white rice, raw eggs, and soy sauce three times a day.

Now that I am older, I can cook and buy my own food. Korean cuisine is still an intricate part of my life, but I have some variety now, although I am still poor. So how does Korean food relate to what I want to talk about today? My topic today is salt, and if there is one thing food-related that Koreans love, it’s salt. Kimchi, soup, noodle dishes, side dishes, meat dishes… you name it and most likely the dish will have a truckload of salt. It’s not uncommon to see a serving of a certain dish to have over 1g of salt. Even I think it’s crazy how much Koreans love salt.

But it’s also not a surprise that Koreans suffer very high rates of high blood pressure (HBP). According to the Korea Centers for Disease Control and Prevention, one in four South Koreans over the age of 30 have high blood pressure. At the moment, it is THE CHAMP for causes of death in South Korea—diabetes trailing behind it. To this day, there are a handful of culprits responsible for giving Koreans HBP, but one thing that authorities, especially health figures, agree on is that high salt consumption is killing Koreans.

Or is it?

Being a maverick, I want to explore the theory that high salt consumption is like digging ourselves an early grave. Salt is like many of the other contentious issues in health and nutrition—there are two sides to the coin. I like to look at both sides to the argument. In this case, I want to get you to know the pros and cons salt consumption, and in specific, what kind of risks high salt consumption carries, as well as the risks of low salt consumption. In this post, I want to go over the perceived benefits of sodium restriction.

Being a South Korean and having a family history of HBP, I have always wanted to talk about salt. It’s another one of those hotly debated topics that no one seems to agree on, yet everyone feels that they have the answers. I, of course, do not have the answers, but I hope to shed some light with this post. And of course, salt is one of those things that are, surprise surprise, context-dependent.

Again, this pesky word, context-dependent. Why can’t we just figure out what nutrients cause what? Because you’re not a cell in a petri dish, I am assuming you are a human being that eats more than just salt. As such, salt will never act in isolation and will influence your health depending on your current health, lifestyle, physical activity levels, genetics, and to a certain degree, gender.

The cure for the world is in this dish. Source


“In the past year, how many times per week did you eat hot dogs, or sausage, or deli meats?”

If you don’t remember, welcome to the club. This type of question is typical when researchers are trying to figure out dietary habits of people in their studies. Do you think it’s accurate to just ask you what you ate for the past year, extrapolate your current nutritional status based on what you thought you ate 3 weeks ago, see that your blood pressure is a bit elevated, and blame it on salt? Well, that’s exactly how many of the current guidelines on salt came to be. On the other hand, better research is coming out using trials and more accurate statistical models. Before we get into the studies and what they show on salt intake, let’s take a cursory tour of salt, your new best friend.

Food Frequency Questionnaire. One tool, but not the end-all-be-all. Source

What is salt?

Chemically, it’s a combo of two elements, Na (sodium) and Cl (chloride), but it’s usually just referred to by authorities as salt, dietary salt, sodium or dietary sodium. And when researchers conduct studies on salt’s health effects, they measure how much sodium you piss out, or urinary sodium excretion. Chlorine also does some stuff in the body; for the most part, however, it’s just attached to the hip of sodium and goes along for the ride.

When you hear the term ‘electrolyte’, you are hearing what we call a group of minerals that carry an electrical charge and are responsible for fluid balance, muscle function, blood pH, and other metabolic processes. Sodium and chloride, along with calcium, potassium, magnesium, and phosphorus, are the more common electrolytes.

Sodium is a necessary component of our physiology and thus, our diet. We need to eat sodium for survival. That’s why we have created intricate sodium regulation processes, such as the Renin-Angiotension Aldosterone System (RAAS), which inhibits urine production during times of salt scarcity. It’s also responsible for maintaining arterial pressure, tissue perfusion, fluid balance inside and outside of cells, and is involved with proper nerve and muscle function (Atlas). In fact, proper functioning of the RAAS is important for heart muscles and just generally keeping you alive.

Additionally, the taste for salt does not get distorted as much as sugar. What I mean by this is that the mechanism for detecting salt in our foods is very precise and accurate. If a food is too salty, most people will notice and may even be turned off by it. This could possibly be an evolutionary mechanism that pressured humans to seek out salt, which is necessary for survival. In contrast, foods that are high in sugar were meant as a reward or treat, thus suggesting they were not necessary to hunt down deer.

Health effects of too much salt

Many, MANY, studies have looked into the health effects of salt. In particular, these studies wanted to study the effects of salt consumption on blood pressure and health since an elevated blood pressure places greater stress on the walls of the blood vessel, damaging them over time. In turn, this places people at a greater risk of heart disease, stroke, and organ failure. Some of the most influential studies were done using observational and epidemiological studies, following hundreds of thousands of people over years and measuring their dietary salt intake through questionnaires, self-reported intake, and observation, although there were quite a few randomized controlled trials, as well.

The latest to have come out was a study that measured the average global consumption of salt and how that translates into cardiovascular deaths. In it, researchers concluded,

“[The] 1.65 million deaths from cardiovascular causes that occurred in 2010 were attributed to sodium consumption above a reference level of 2.0 g per day… These deaths accounted for nearly 1 of every 10 deaths from cardiovascular causes (9.5%)”. (Mozaffarian)

Quite staggering numbers. For reference, 2.0g is actually lower than the 2.3g that we are often told are our daily sodium targets. For people who are over 51 or have hypertension or are diagnosed with kidney, liver, and heart failure, that number drops down to 1.5g.

More than ten years ago, U.S. health authorities devised a plan called DASH (Dietary Approaches to Stop Hypertension) to tackle the ongoing problems of heart disease. Its main premise is to control blood pressure through mainly sodium manipulation. Studies have been done on this diet and they showed promising results. There’s even a DASH-diet book. A meta-analysis done in 2013 pooled together high-quality study designs implementing the DASH program and found this:

“Results showed that a DASH-like diet can significantly protect against CVDs, CHD, stroke, and HF risk by 20%, 21%, 19% and 29%, respectively. Furthermore, there is a significant reverse linear association between DASH diet consumption and CVDs, CHD, stroke, and HF risk”. (Salehi-Abarqouei)

How much difference does all of this make?

Based on these studies, health authorities began to go knife-happy (some encouraging nudges from some pharmaceutical companies may have played a role here) and recommended people slash their sodium consumption. Food corporations began to stick labels on their foods stating “low-sodium”, “no sodium”, “no salt added”, etc. The nutritional bandwagon just got much heavier.

But when looking at these studies, we can’t just take “decreased blood pressure” for an answer… unless of course that’s all you’re looking for. The problem with just walking away with an answer like that is that you’re left asking a looming question:

“Will it be worth it?”


This is absolutely a no-brainer if you’re in critical condition or suffering from an end-stage condition where death is staring you right in the face, such as cirrhosis, end-stage kidney failure, stage five cancers, etc. But at this point, not much will help you in the way of nutrition therapy; dietitians and the rest of the medical team are simply trying to make the passage to the other side of the river as painless as possible.

What if you’re healthy or have room to improve? Do you really need to cut sodium to 2.3g per day? As a frame of reference, ¼ teaspoon of salt is usually about 400mg of sodium, so 1 teaspoon would be about 1600mg of sodium. Per day, you’re looking at 2 tsp of salt.

By following the DASH diet and reducing your sodium intake to 2.3g, you will reduce your systolic blood pressure by 1.3 mmHg if you don’t have clinically diagnosed hypertension. By further reducing sodium to 1.5g per day, you will reduce your systolic blood pressure by an average of 7.1 mmHg (Sacks). Other studies using a low-sodium diet showed average systolic reductions of 1 to 4 mmHg (Taylor).

If you think 1.5g of sodium is an awfully low number, that’s because it is. For some people, the super reduction of sodium only leading to a 7.1 mmHg drop in their blood pressure may not be worth it. Indeed, it may not be if you’re healthy. However, for some people, that level of reduction may be necessary and can actually knock them out of stage 1 or 2 hypertension. Of course, it’s not as if you don’t have to cut salt, but for the sake of discussion, what if you want to?

Just cut sodium?

The ironic thing is that researchers don’t attribute the decrease in blood pressure to sodium alone. In the original DASH studies, the subjects were put into either a control diet (restricted sodium but eating standard American fare) or the DASH diet. Of course, the DASH diet lowered BP a bit more than the control diet, but the DASH-diet also had higher levels of fruits, vegetables, and dairy; not to mention the DASH groups had nutrition education, which is crucial in patient self-efficacy. Also, the DASH-diet recommends limiting alcohol.

By increasing F, V, and dairy, you’re increasing levels of vitamins and minerals. The main minerals that researchers are bringing into the equation of BP reduction are calcium, magnesium, phosphorus, and most importantly, potassium. Potassium acts in opposition of sodium because they carry opposite charges and are found on opposite sides of the cell membrane. Whereas moderate sodium consumption inactivates the RAAS, potassium activates it. However, potassium-induced activation leads to a relaxation of the blood vessels which lead to more elastic blood vessel walls, reducing the force of blood flow (Haddy; Aaron). By having a good balance between the two, you maintain a desirable electrolyte balance. In the DASH-diet guidelines, we’re told to consume 4.7g of potassium per day.

There is one thing that the DASH diet did uncover: sodium can and does fiddle around with blood pressure. As noted above, the control diet ate a reduced-sodium Standard American Diet (SAD), yet still saw BP reductions. So just by reducing how much salt you ate, you can see almost immediate drops in blood pressure. But how beneficial the magnitude of those drops will be really depends on where you currently are with your health.


Before we wrap up this post, let me say a few things that are often overlooked when considering how influential certain nutrients are on your health.

You could do everything right and still be unlucky. In the hospital, awfully bad things can happen to you at the drop of a dime. After a perfect surgery, you may be recovering with the proper nutrition support, but still pass because of an infection that wasn’t seen in the cards. In the same vein, these studies looking at how sodium restriction lowers blood pressure can really only look at one thing. RISK. Lowering blood pressure does not guarantee your safety, but it lowers your risk. Don’t make the mistake that lowering risk means you won’t still escape what Mother Nature has in store for you. If that was a bit morose, I apologize.

Finally, it’s highly unlikely that you are leading a lifestyle exactly similar to the subjects in the studies. If they smoked, drank, or engaged in activities that affected blood pressure (think stress), then they kept smoking, drinking, or engaging in activities that affected blood pressure. Their habits were “adjusted” for by researchers using an algorithm to standardize so their habits do not skew the results of the studies. Let’s remember that research studies shed light on an issue, not stand for a direct translation.

I will close with this quote from an editorial from the Journal of the American Medical Association, which will segue nicely into the next post about the drawbacks of sodium restriction:

Reducing sodium can lower blood pressure in both normotensive and hypertensive patients. There is no direct evidence that it reduces cardiovascular mortality” (JAMA).

Your feedback is always appreciated.

Live life strong,




Shim E1, et al. Dietary sodium intake in young Korean adults and its relationship with eating frequency and taste preference. Nutr Res Pract. 2013 Jun;7(3):192-8.

Atlas SA. The renin-angiotensin aldosterone system: pathophysiological role and pharmacologic inhibition. J Manag Care Pharm. 2007 Oct;13(8 Suppl B):9-20. 

Haddy FJ1Vanhoutte PMFeletou M. Role of potassium in regulating blood flow and blood pressure. Am J Physiol Regul Integr Comp Physiol. 2006 Mar;290(3):R546-52.

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.

Taylor RS, et al. Reduced dietary salt for the prevention of cardiovascular disease: a meta-analysis of randomized controlled trials (Cochrane review). Am J Hypertens. 2011 Aug;24(8):843-53

Aaron KJ1Sanders PW. Role of dietary salt and potassium intake in cardiovascular health and disease: a review of the evidence. Mayo Clin Proc. 2013 Sep;88(9):987-95.

Perry IJ. Dietary salt intake and cerebrovascular damage. Nutr Metab Cardiovasc Dis. 2000 Aug;10(4):229-35.

The Letter. JAMA. 2014 Jun 4; 311(21):2229.

How Often Should You Eat?

How often should I eat?

Another contentious issue that is often challenged in the literature and real-life. You see it all the time… exceptions and generalities. So whenever someone asks me a loaded question like this, my answer is always:

It depends.

That is the honest and simple answer I give to everyone who asks me this question, including clients. Certainly, this is also the answer that most people do not want to hear. But with further explanation, many people’s adverse reactions turn to curiosity, and eventually (hopefully), compliance.

I take pride in providing a no bullsh*t service that doesn’t paint a broad stroke as the “best” or “one and only way” to do things. I instead focus on what’s optimal for people under their unique conditions. Not everyone has the same lifestyle habits, or eat and exercise the same way. That’s precisely why you shouldn’t follow a cookie-cutter meal plan you find on the internet. Why? Simply look at the person who is espousing the diet. They are super-ripped, probably have great genetics, and probably spend a lot more time in the gym than you. Let me not forget to mention that you may not enjoy eating what they eat. And if you are unfamiliar with macronutrient (protein, fats, carbohydrates) content of certain foods, hardly think about swapping foods.

On the other hand, there are some general categories that a majority of people will fall under even if their life stages are different. For example, a student and a working professional are in similar circumstances, as opposed to a student and a competitive bodybuilder. The comparison made here is assuming that the student and business professional do not treat training and eating like it’s their job. In this case, the student and business professional will have training and nutrition protocols that bear more of a resemblance to each other than the student and athlete.

Now, for those of us who have lives outside of the gym, there are a few general guidelines that you should follow if you want to make the most of your nutrition plan.

The importance of keeping a regular meal schedule

This bears repeating. Research has shown over and over again that having a consistent meal pattern gives you better results and health. It is the key factor in making meaningful and lasting progress. There’s not too much debate about this considering how not many follow-up studies are in the literature after a few established this fact. To quote a study done in 2004,

…irregular meal frequency appears to produce a degree of insulin resistance and higher fasting lipid profiles, which may indicate a deleterious effect on these cardiovascular risk factors” (Farshchi, 2004).

What the above essentially means that if you eat with no regularity or your meals are all over the place, you increase your risks of becoming sick or experience more complications if you are sick. When it comes to nutrition, consistency is your trump card for many reasons, which we will discuss below.

But what about eating lots of small meals per day? People say you need to keep ‘stroking’ your metabolism?


This might work if your metabolism works like a dog. Pet your metabolism frequently and it will roll over, pant, and reward you with unconditional love. Except this isn’t really how your metabolism always works.

If you have read any sort of nutrition-related research over the past ten years or read the news or peruse fitness magazines, you have probably heard that you should eat more often to “increase your metabolism”. Researchers have constantly been investigating this idea that a high meal frequency (6+ meals) somehow increases your metabolism. After decades of research and investigation, researchers of high-quality studies came to a general conclusion: for weight loss, it really doesn’t matter how often you eat; it’s the amount of calories that matters at the end of the day. To quote a research study from 2010 about this:

Researchers conclude that “increasing MF [meal frequency] does not promote greater body weight loss under the conditions described in the present study” (Cameron, 2010).

This study was a high-quality study, done for 8 weeks, and both groups ate the same amount of calories. The biggest difference was that one group ate 6 times per day while the other ate 3 times. Additionally, another study in 2012 added to the mounting evidence that a higher meal frequency does not confer extra benefits:

“RMR [resting metabolic rate] and appetite control increased in the LFr [low-frequency] diet, which can be relevant for body weight control on the long term” (Munsters, 2012).

And in one particular study, increasing meal frequency actually led to more hunger. To quote a study done in 2013:

Researchers conclude that “increasing meal frequency from three to six per day has no significant effect on 24-h fat oxidation, but may increase hunger and the desire to eat” (Ohkawara, 2013).

As with any study, you have to keep a couple of things in mind:

  • These studies were done on people who were not terribly active. They might represent the typical gym-goer, but not someone who takes their training seriously, like an athlete. So of course, these findings may not apply to someone competing athletically at a high level.
  • YOU may not like eating 3 meals per day, whether for your own sanity, Obsessive Compulsive Disorder, or because you are an athlete and need to nourish yourself constantly.

What about us regular folk? And yes, this includes me. 

Now let’s see how we can get general fitness folks who have no intention of standing on stage in a banana hammock or running a marathon to look good naked (the below is assuming that you already know your calorie, protein, fat, and carbohydrate needs).

  1. Keep a food journal. You don’t need to get a fancy leather strap and buckle journal for this one. A composition book will do. In it, you will keep track of what, when, how much. A food journal is the simplest yet most effective way to stay accountable. It’s also one of the main things people avoid doing. If it’s so effective, why don’t people do it? If I knew the answer to that question, I wouldn’t even need to look for clients and I would be a financially successful personal trainer.

The reason I believe people don’t keep a food journal is simple: they’re scared of what they may see, lazy, or both. The journal may not be a person, but seeing for your own eyes what you eat on a daily basis may shock you. And no one wants to be told that what they’re doing is wrong, not even by themselves. If you honestly can’t take 30 seconds out of your meal to jot down what you’re eating, you’re lazy—plain and simple. Unless you’re making an insane amount of money, chances are high that you work 8-9 hour days and probably commute. Why not write down what you ate or will eat while commuting? Seriously, how hard is it to write this down?

12pm…5 eggs, 2 cups broccoli, 1 cup berries

You can make time to go out and have a few drinks with your buddies, but can’t keep track of what goes in your mouth? Pssshaw.

  1. Find your preferred eating frequency. If you’re not a competitive athlete or currently in-season for a physique sport, I suggest eating 3-4 meals per day. In the event you want to deviate from my suggestion, make sure you stick with it. If you decide you only want to eat two meals per day, then eat two meals per day.

Just keep in mind that the lesser amount of times you eat, the more likely you will run into vitamin and mineral sufficiency issues. Your margin of error gets increasingly smaller with less meals.

  1. Try to eat at the same time, every day. Find the best times for you to eat and stick with those times. If you can consistently eat a meal between 12-1pm, then do it. Avoid eating two meals, at 10am and 6pm, on one day, then decide to eat 4 meals at 11am, 4pm, 7pm, and 9pm another day. Key word, TRY. Don’t stress out if you can’t keep this schedule.


  1. Try to keep the same nutrient composition at each meal, every day. This does not mean have the same meal composition at each meal, but for a specific meal on different days. For example:

If your plan calls for 160g of protein, 60g of fat, and 100g of carbs per day (1580 kcals), your daily meal plan may look like this:

12pm, meal 1: 40g protein, 15g fat, fibrous vegetables (broccoli, kale, spinach, etc.)
2pm, meal 2: 40g protein, 15g fat, fibrous vegetables
6pm, meal 3: 40g protein, 15g fat, 50g starches (rice, potato, etc.) and some fibrous vegetables
9pm, meal 4: same as above
11pm: sleep

Let’s put the above numbers into example foods:

Meal 1: 1 6oz container of Fage, plain Greek yogurt, 3 whole eggs, scrambled with 1 cup of broccoli, ½ mushrooms, and ½ red peppers
Meal 2: Two scoops of whey protein shake, 1 tablespoon of Chia seeds, 1 tablespoon of maca root powder, 1 tablespoon of raw cacao powder, half a serving of macadamia nuts (1/8 cup)
Meal 3: 8oz chicken thigh (or tofu for vegetarians), 1.5 cups of cooked white rice or 2 medium sweet potatoes, 1 cup of spinach with a teaspoon of butter
Meal 4: Similar to above

The key is to try your best to keep the above meal schedule throughout the week. It’s really that simple.

  1. Plan ahead and compensate. This is not something I recommend you do regularly. A prime example of compensating comes in the way of binge drinking. Many people will instinctively hold back on their food during the day in preparation for their booze-fest at night. While this strategy is better than adding booze on top of your current intake, it’s not something you should do all the time, particularly because I don’t recommend you binge drink all the time.
  2. If you screw up, don’t stress. Life goes on, even if you miss a meal.



As always, I approach fitness and nutrition related things with an open mind. I experiment, test, and read to make sure that what I am talking about is as accurate as I can make it. I don’t feign ignorance or arrogance if there is an answer I don’t know. With that said, seriously consider your goals and starting point.

Are you a heavily muscled and chiseled gym-rat? Then you probably won’t do well on a 2-meal a day plan and may instead need to eat north of four.

Are you a heavily fat’ed and plump couch-potato? Then you probably won’t do well on a plan designed for the hunk-o-rama above and may need to eat south of four.

See where I am going? Your eating approach is predicated on your goals, starting point, preference, and lifestyle.

Don’t let any of this confuse you. Once you know how many calories you need, how to read labels, and become familiarized with the foods you eat regularly, this is all a cinch.

As always, I value your feedback. Drop a comment if you have one or shoot me a line.

Live life strong,




Piya, et al. Meal size and frequency influences metabolic endotoxaemia and inflammatory risk but has no effect on diet induced thermogenesis in either lean or obese subjects. Endocrine Abstracts. 2014:34;226.

Munsters MJ1Saris WH. Effects of meal frequency on metabolic profiles and substrate partitioning in lean healthy males. PLoS One. 2012;7(6):e38632.

Ohkawara K, et al. Effects of increased meal frequency on fat oxidation and perceived hunger. Obesity (Silver Spring). 2013 Feb;21(2):336-43.

Cameron JD, Cyr MJ, Doucet E. Increased meal frequency does not promote greater weight loss in subjects who were prescribed an 8-week equi-energetic energy-restricted diet. Br J Nutr. 2010 Apr;103(8):1098-101. Epub 2009 Nov 30.

Farshchi HR, Taylor MA, Macdonald IA. Decreased thermic effect of food after an irregular compared with a regular meal pattern in healthy lean women. Int J Obes Relat Metab Disord. 2004 May;28(5):653-60.

Farshchi HR, Taylor MA, Macdonald IA. Beneficial metabolic effects of regular meal frequency on dietary thermogenesis, insulin sensitivity, and fasting lipid profiles in healthy obese women. Am J Clin Nutr. 2005 Jan;81(1):16-24.

Saturated Fats: Friend, Foe, or Don’t Know?

It usually goes like this…

“But fat and cholesterol increase cholesterol”, my client said.

“So which cholesterol does it increase?” I responded.

“The doctor said the ‘bad one’”.

Without question, this is the most common discussion I get into with anyone who has an inkling of interest in nutrition and taking care of their health. Trying to reverse deeply ingrained beliefs that have the support of governmental agencies and public outlets is a tough nut to crack.

In this article, I want to go briefly into why you should not believe every negative stereotype you have heard about fat, particularly saturated fat, and cholesterol. Now before we move on, let me make it clear that I am not stating fats and cholesterol are not dangerous; they absolutely can be given the right (or wrong) situation—namely genetics, existing physiological stress, and general lifestyle.

A prime example of how saturated fats and fats in general can negatively affect health is a rare genetic disorder people are born with called familial hypercholestermia. In this condition, people lack a gene that allows the body to get rid of LDLc from the bloodstream. Typically, these people will show normal HDL and triglyceride (TG) levels, but their LDLc levels will be through the roof, ranging from 350-1000 mg/dL (a healthy person might exhibit 100 mg/dL). Sometimes, you can’t win against genetics

Also not surprisingly, a high-stress lifestyle puts you at an increased risk of heart disease. The reason is not because you are probably eating a bit too much fat, but because chronic stress puts your body in a state of inflammation, which in turn damages your arteries, increases your blood pressure, and forces your body to go haywire.

My point is that any food can be turned from an angel to a devil. Dietary fats, and cholesterol, have a relative health effect (RHE) on you, just like protein and carbohydrates do. But if you keep a good bill of health, the net effect is a positive one.

What is fat?

Fats, or lipids, belong to one of the three main MACROnutrients, nutrients that supply you with energy, are measured in larger quantities than vitamins and minerals, and play extremely important structural and metabolic roles in the body. Though they top the energy-supply chart by giving you 9 calories per gram, their main job is not to make you fat, but to supply you with long-term energy so you can function and continue plugging away at Facebook.

Since this is not a biochemistry crash course, I will make it as simple as possible so both you and I can understand. Last thing I want to do is confuse myself. Dietary fats are categorized into four groups that have distinct molecular properties and functions. Over the course of a couple of posts, I will go over each fat, but today, we will cover saturated fats.

  1. Saturated fat (SFA)
    1. No double carbon bonds
    2. Solid at below room temperature; spreadable at room; and liquid at above
    3. Stable under high heat (cooking, baking), so makes for suitable cooking oil
    4. Several types of SFA, each with its own effects on health
    5. Since no double bonds, generally does not go rancid and as such, more stable inside the body as well
    6. SFA are required to make sex hormones (testosterone, estrogen); they make up over 70% of the cells in the body; burn in a safer and more efficient manner than glucose
  2. Mono-unsaturated fat (MUFA)
    1. One double carbon bond
    2. Liquid
    3. More stable under high heat, though this depends on the type of plant the oil is from
    4. Since only one double bond, less prone to rancidity, but high heat can damage it
    5. Most make for suitable cooking oil (olive oil excluded)
  3. Poly-unsaturated fat (PUFA)
    1. Two or more double bonds
    2. Liquid
    3. Unstable under high heat, though this depends on how much processing it went through during production
    4. Since it has several double bonds, very prone to rancidity and can cause oxidative damage
    5. Not a suitable cooking oil
    6. PUFA are a function part of the cell membrane, giving cells its fluidity
  4. Trans-fatty acids (TFA)
    1. Originally a saturated fat, but partial hydrogenation modifies the melting point and allows TFA to be solid at room temperature
    2. Products with TFA in them have longer shelf-life
    3. Stable under high heat and long storage
    4. TFA can be found naturally in foods (dairy, meats) and manufactured on a larger scale by food producers (most common source of TFA in current American diets)

Goodie, you know the four main fats. Now what? What about Saturated Fats’ effects on your health?

Based on the properties of the fats above, if you read between the lines and thought, “saturated fats” don’t seem to be so bad then my job with this article would be done. However, I am sure we all need some clarification.

Over the past fifty years, SFA has gotten a lot of bad press, mainly for its ability to increase cholesterol levels and thereby its theorized ability to increase heart disease risk. Back then, research was not as meticulous, but now we have more and better insight. Studies have been carried out in rodents and humans in randomized trials and researchers kept track of hundreds of thousands of people in cohort studies. In short, there is no good reason to believe that saturated fat is the culprit in heart disease. In fact, much of the hype in the past was not based on studies done on humans, but by speculation and… injecting rabbits with liquid cholesterol. Why do I bring this up? Because a rabbit’s natural diet does not contain cholesterol. They eat plants.

But cholesterol isn’t part of my natural diet!

For one, it’s nearly impossible to isolate one nutrient and study its overall effect on health. Even if all you ate was butter, you wouldn’t be able to measure it. Why? Because eating only butter creates a nutrient imbalance detrimental to health that is independent of saturated fat. To function at peak health, your body also needs protein and carbohydrates.

No matter how many times I state, “saturated fats do not independently increase your risk of heart disease,” it just seems to leave a blank stare on people’s faces. I don’t blame you for reacting the same way. For years, we have been told that saturated fats are bad for health. Most times, if you went to a doctor’s office with high cholesterol, the doctor won’t even ask you about your diet. They may ask you about exercise and what you do.

Doc: “Do you exercise?”

You: “Yes.”

Doc: “Ok.”

Ok, perhaps I should give this doctor a bit more credit.

Doc: “How much?”

You: “I go to the gym 3 times a week.”

Doc: “Ok.”

Next, they will take a quick look at your numbers, probably the LDL cholesterol (LDLc), and if they are not pointed in the right direction, will suggest you either “fix your diet” or try to hand you a prescription for a drug that has side effects. Great!

So what do your lab results mean?

According to the National Cholesterol Education Panel (NCEP), here are ‘normal’ guidelines for lipids:

LDLc: <100 mg/dL
HDLc: > 60 mg/dL
Total Cholesterol: <200 mg/dL
Triglycerides (TG): <150 mg/dL

The LDLc numbers only tell some of the story. Over a decade ago, researchers found out that there are actually two types of LDLc particles—small and large. Small LDLc particles have been shown to be atherogenic—promote heart disease—because they are more likely to get stuck in holes in the arterial wall, whereas large LDLc particles are benign and less likely to get stuck (6). Now the thing to note here is that even if two people had the same concentration of LDLc in their blood, their atherogenic profile will differ. In other words, if one person had an LDLc of 100 mg/dL but it represented large particles, they would be at a reduced risk of heart disease.

Saturated fats have been unjustly vilified and LDLc alone is a poor predictor of heart disease

While I say that saturated fats have been unjustly vilified, that is not permission to go whole-hog on saturated fats. It’s true that research has focused on how saturated fats influence health and found that saturated fats are not the criminals they were thought to be, but it’s also important that you have a balanced intake of fat. According to research and observations, it’s prudent to have most of your fats come from a combination of SFA and MUFA, as this combination has been shown to improve the LDL/HDL ratio, especially in women (9).

But if you turn your attention back to how SFAs negatively affect health, you will see that this theory just does not pan out. In 2010, a meta-review was released in the American Journal of Clinical Nutrition, what dietitians consider to be the holy grail of nutrition research. Here, the study went over 21 prospective epidemiological studies that tracked over 347,000 people. What’s ironic is that one of the researchers of this study, Ronald Krauss, used to be in the anti-fat camp, until he actually looked at the literature and came to his own conclusions. They concluded:

“There is no significant evidence concluding that dietary saturated fat is associated with an increased risk of CHD (coronary heart disease) or CVD (cardiovascular disease)” (1)

Research has also repeatedly shown that SFAs in and of themselves are not harmful to your health. To elucidate this a bit, researchers used 48,000 postmenopausal women from the Women’s Health Initiative program, one of the largest and longest running studies that observed how nutrition, exercise, and lifestyle influenced health, and put them into a modification trial where they can measure how specific parameters influence study primary outcomes. In this case, if decreasing saturated fat over time would decrease CVD risk. Over an average of 8.1 years, total fat intake decreased by 8% and saturated fat by 3%, while consumption of fruits, vegetables, and grains increased. Here is what they had to conclude:

“Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved only modest effects on CVD risk factors” (3).

Ok, “but what about the more specific stuff that saturated fat does, like how experts say that since SFAs increase cholesterol, they also increase your risk of heart disease”?

The above general statement is almost false. SFAs have different chain lengths, and each impart a different effect on health, so to say a blanket statement like above does not take into account the various properties of SFAs. In fact, most of the SFAs have a neutral effect on health, with a few having a positive effect while one having a negative one. SFAs, while they do increase LDL cholesterol, also increase HDL cholesterol, thereby not changing the ratio of total cholesterol to HDL cholesterol, a strong predictor of heart disease risk (2). Additionally, SFA are the strongest at lowering TG levels. From the abstract:

“Lauric acid greatly increased total cholesterol, but much of its effect was on HDL cholesterol. Consequently, oils rich in lauric acid decreased the ratio of total to HDL cholesterol. Myristic and palmitic acids had little effect on the ratio, and stearic acid reduced the ratio slightly. Replacing fats with carbohydrates increased fasting triacylglycerol concentrations.”

Above I mentioned that replacing SFA with MUFA improved LDL/HDL ratios, but it seems that improving, or lowering, your Total Cholesterol/HDL ratio is even better. Also, that last bit is interesting, right? Basically it’s saying that eating carbohydrates instead of fats will increase fasting levels of triglycerides, an independent risk factor for heart disease in both men and women. Another time, another place.

The feverish chase of linking SFA with heart disease has slowed down quite a bit, and I think it’s probably because people have finally come to the realization that not only is it unfair to ostracize SFA, but also because SFAs don’t independently increase the risk of heart disease.  As of this writing, not much more literature on saturated fat and health has been published. Nonetheless, studies continue. One of the few more recent ones I could find was this bit, again from the Journal of Clinical Nutrition. They concluded:

“The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk” (4).

This is Harvard’s way of saying, “we should not implicate only saturated fats as a cause for heart disease, but a variety of factors, including smoking, exercise, genetics, and general dietary habits”. The second one was from the Journal of Clinical Lipidology. Their conclusion was much in line with the above, but there was even more skepticism about the negative health effects of SFA and the beneficial health effects of even MUFA and PUFA.

“High-density lipoprotein (HDL)-C increases with SFA intake… among individuals who are insulin resistant, a low-fat, high-carbohydrate diet typically has an adverse effect on lipid profiles (in addition to decreasing HDL-C, it also increases triglyceride and LDL particle concentrations). Consequently, a moderate fat diet in which unsaturated fatty acids replace SFAs and carbohydrates are not augmented is advised to lower LDL-C”. (5).

The above conclusion should be a bit of a head-scratcher. Why would they advise that people replace SFA with MUFA to decrease LDL when, just a couple lines before, they clearly stated that SFA increases HDL? Based on this, it is prudent to have a good combination of SFA and MUFA, but not to be scared of SFA in the absence of a high carbohydrate diet. More importantly, two of the authors of the above study, Drs. Walter Willet and Alice Lichtenstein, were initially anti-fat and believed SFA to be a culprit in heart disease. Again, I think it is extremely liberating that researchers who once advised against SFA intake are beginning to question their original theories and even do an about-face.

And a review done in 2013 showed that full-fat dairy products had this to conclude:

The observational evidence does not support the hypothesis that dairy fat or high-fat dairy foods contribute to obesity or cardiometabolic risk, and suggests that high-fat dairy consumption within typical dietary patterns is inversely associated with obesity risk” (10).”

Of course, we can’t just accept wholeheartedly that SFA cause no damage. As I mentioned before, they can. But the science is stacking up in favor of exonerating SFA. There is no cold-hard truth, but there hardly ever is in science. If there was, scientists would be out of a job and there would be no more need for ongoing research.

“By the way, I like cheese, yogurt, and butter. What about them?”

Dairy products make up a group of foods that have the highest concentration of saturated fats, collectively. One serving of Camembert cheese has 7g of fat, 4 of it being saturated. One 7 ounce serving of full-fat Greek yogurt has 10-12g of fat, 8 of it being saturated. And one tablespoon of butter has 12g of fat, 8 of it being saturated. They also taste a whole lot better than their chalky non-fat counterparts.

So where am I going with this? In addition to the last study I quoted above, there’s more good news for those of you who like full-fat dairy goodness: a most recent study published online in August 2014 showed that two full servings of full-fat Camembert cheese or yogurt per day over the course of 8 weeks had no negative impact on people with elevated cholesterol and taking no medications (7). This study is followed nicely in the footsteps of a study done earlier in 2014 showing that full-fat dairy reduced the risk or prevented cardiometabolic disorders, even in randomized trials (11).

But this is not news. Studies dating back to the early 2000’s show full-fat dairy products improve health and weight-loss. Whereas cheese improves LDLc more than butter, butter improves HDLc more than any other dairy product (8).

What about eggs?

Ah, the venerable, honorable, and revered egg. There’s nothing quite like it. Indeed, nothing quite like eating nature’s perfect food that comes out of an… anus? Ok, technically, it’s not the anus but a ‘cloaca’. But enough of the technicalities.

Eggs are always a hot topic. Though they are not as high in concentration of saturated fats, they do concern most people when it comes to cholesterol levels. Egg yolks contain nearly all of the nutrition of the egg. It is one of the few natural sources of choline, contains magnesium, vitamin A, and a range of B-vitamins. In essence, whole eggs are one of nature’s perfect food.

In research, there is an ongoing tug-o-war when it comes to egg consumption. On one hand, eggs have been shown to increase HDL levels and converting LDLc into the large particle sizes (12). The mentioned study, done in 2006, showed that eating four eggs per day benefited health in the general population. More studies done later, like these 2010 and 2013 ones, showed that eating three eggs per day improved LDLc and HDL profiles while simultaneously increasing blood antioxidant status, especially during a lower carbohydrate diet (13, 14).

On the other hand, research has shown that eating more than one egg per day has no impact on cardiovascular risk, but may pose a risk to those with type 2 diabetes. At the same time as increasing the risk of heart disease to those with type 2, egg consumption decreases the risk of stroke. Some of these studies were done using egg questionnaires that ask participants to estimate how many eggs they eat per day, over the course of years (15). Can you remember how many eggs you ate last year? Interestingly enough, the study done in 2013 showing beneficial effects touched on how egg consumption can benefit type 2 diabetes.

“Daily intake of 3 whole eggs, as part of a CRD [carbohydrate restricted diet], increased both plasma and lipoprotein lutein and zeaxanthin [antioxidants]. Egg yolk may represent an important food source to improve plasma carotenoid status in a population at high risk for cardiovascular disease and type 2 diabetes (14)”.

 As you can see, the research is not as clear-cut on egg consumption. But by combining both observation and research, I have come to conclusion. Whole egg consumption does not increase your risk for heart disease. In fact, previous clients not only noticed beneficial effects on cholesterol, but also on weight status, blood pressure, and blood sugar control.

Wrap up and we’re not talking about a Big Mac to go

The best way to improve your cardiovascular disease risk and general health seen through lipid test results is to not only decrease and optimize your LDLc, but also to decrease TG. When you turn both of these numbers for the better, your HDLc will naturally go up. How do you achieve these feats? Eat less refined carbohydrates and more SFA and MUFA.

Again, this article’s purpose is not to get you to eat more saturated fat, although it’s definitely not deterring you so. If your preference is to stay away from saturated fat, that’s your decision. The goal of this article is to enlighten you, stating that there’s no reason to be scared of saturated fat in the presence of a whole foods diet. If you’re eating a Standard American Diet that consists of Oscar-Meyer bacon, cheese so processed it can only be called ‘cheez’, and freezer-burned French fries, then adding saturated fat will do more harm than good. But let’s make it known that it’s not the saturated fat that’s doing the damage, it’s the diet.

Can you see yourself having good health after eating like this?

Perhaps you want to start replacing your rancid and unhealthy polyunsaturated fats—cottonseed, peanut, canola, corn, soybean, safflower, and sunflower—with saturated fats and reap the benefits. Here are some sources. Take note how these sources are also whole foods that taste good, unlike the PUFAs that we are all commonly told to consume.

  • Egg yolks
  • Fattier cuts of animal meat
  • Greek yogurt, kefir, cottage cheese, milk (not a huge fan of milk for reasons outside the scope of this article), cheese
  • Coconut products (especially extra virgin coconut oil)
  • Grass-fed, organic cow, goat, sheep butter
  • Beef tallow and pork lard (though the fatty acid composition of these two are highly dependent on how the animals were raised)

And in case you are wondering…

I will include my n=1. I try to refrain from doing this too much because I apparently lack age. And many people will be quick to point out that, “I am young and active” and that I “will soon see the negative effects of eating the way I do”.

Except, I won’t. Stop to take a look at all of the sick and obese teenagers. More than 60% of these kids will develop type 2 diabetes later in life and will probably die of heart disease; but not before going blind or losing their hands and feet. I am 28, so unless I come down with an unavoidable genetic disorder, chances are extremely low that I will succumb to heart disease based on the research and my lab results.

I have a family history of high cholesterol, high blood pressure, peptic ulcers, and stroke. Both of my grandfathers died in their early 60’s of a stroke, my aunt had half of her stomach resected, and my mother is currently on blood pressure, cholesterol, ulcer, and arthritis meds. The most ironic thing about my mother’s diet is that she eats hardly any saturated fats yet has high cholesterol. She doesn’t drink, smoke, doesn’t even work part-time, but she is currently eating the very same “heart healthy” vegetable oils peddled by our government agencies. If only she would listen to what I say to her.

My diet mainly consists of whole fat Greek yogurt, kefir, grass-fed butter, coconut oil, chicken thighs, salmon, beef stew, whole eggs, loads of vegetables, and berries. I eat most of my calories at night, especially my carbohydrates, I fast 12-hours a day, and I exercise three times a week. Much less than your normal gym-rat who believes fat and cholesterol are bad for you. So my last blood work showed some peculiar yet predictable results.

Total cholesterol: 179
LDL: 101
HDL: 67
TG: 60
Fasting blood sugar: 90 mg/dL

Not too bad coming from a person born into a sick family.

Your main takeaway from this article is this:

Unless you have a genetic disorder or just flat out don’t like saturated fats, there’s no need to fear saturated fats. Like proteins and carbohydrates, they have an RHE, which can either be made better or worse depending on your circumstances. In the presence of a high carbohydrate diet, especially one composed of refined carbohydrates, SFA can do damage. But in the absence of a high carbohydrate diet, SFA not only improve HDL, triglyceride, and blood sugar levels, but they also provide you with a clean burning energy source.

As always, I appreciate your feedback.

Live life strong,




  1. Siri-Tarino PW1,Sun Q,Hu FBKrauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):535-46.
  2. Mensink RP1,Zock PL,Kester ADKatan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipidsand apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr. 2003 May;77(5):1146-55.
  3. Howard BV1,Van Horn L,Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006 Feb 8;295(6):655-66.
  4. Astrup A1,Dyerberg J,Elwood P, et al. The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? Am J Clin Nutr. 2011 Apr;93(4):684-8.
  5. Baum SJ1,Kris-Etherton PM,Willett WC, et al. Fatty acids in cardiovascular health and disease: a comprehensive update. J Clin Lipidol. 2012 May-Jun;6(3):216-34.
  6. Cromwell WC1,Otvos JD. Low-density lipoproteinparticle number and risk for cardiovascular disease. Curr Atheroscler Rep. 2004 Sep;6(5):381-7.
  7. Schlienger JL1,Paillard F,Lecerf JM. Effect on blood lipids of two daily servings of Camembert cheese. An intervention trial in mildly hypercholesterolemic subjects. Int J Food Sci Nutr. 2014 Aug 6:1-6
  8. Nestel PJ1,Chronopulos A,Cehun M. Dairy fat in cheese raises LDL cholesterol less than that in butter in mildly hypercholesterolaemic subjects. Eur J Clin Nutr. 2005 Sep;59(9):1059-63.
  9. Müller H1,Lindman AS,Brantsaeter ALPedersen JI. The serum LDL/HDL cholesterol ratio is influenced more favorably by exchanging saturated with unsaturated fat than by reducing saturated fat in the diet of women. J Nutr. 2003 Jan;133(1):78-83.
  10. Kratz M1,Baars T,Guyenet S. The relationship between high-fat dairy consumption and obesity, cardiovascular, and metabolic disease. Eur J Nutr. 2013 Feb;52(1):1-24.
  11. Astrup A. Yogurt anddairyproduct consumption to prevent cardiometabolic diseases: epidemiologic and experimental studies. Am J Clin Nutr. 2014 May;99(5 Suppl):1235S-42S.
  12. Fernandez ML. Dietary cholesterol provided byeggsand plasma lipoproteins in healthy populations. Curr Opin Clin Nutr Metab Care. 2006 Jan;9(1):8-12.
  13. Mutungi G1,et al. Eggsdistinctly modulate plasma carotenoid and lipoprotein subclasses in adult men following a carbohydrate-restricted diet. J Nutr Biochem. 2010 Apr;21(4):261-7.
  14. Blesso CN1,Andersen CJ,Bolling BWFernandez ML. Egg intake improves carotenoid status by increasing plasma HDL cholesterol in adults with metabolic syndrome. Food Funct. 2013 Feb;4(2):213-21.
  15. Rong Y1,Chen L,Zhu T, et al. Egg consumption and risk of coronary heart disease and stroke: dose-response meta-analysis of prospective cohort studies. BMJ. 2013 Jan 7;346:e8539.