For results, do something that requires effort

I get into a lot of conversations at the gym about various things, fitness goals being the most popular. One thing I hear ad nauseum is this:

“I need to switch it up”.

Automatically, I ask, “why?”

And likewise automatically, the person will respond, “to shock the system. I have plateaued and my routine isn’t as effective anymore”. Many conversations turn out this way.

A similar remark will be something like, “I don’t understand why I am not seeing results. I’m doing everything right”.

Without getting into further mundane details about this person’s history, I simply ask what they’re doing and make some slight suggestions to help out, which they don’t end up taking seriously anyway.

Here’s a news flash. In order to change, you should do something that requires a bit more effort than what you’re currently doing and you should do it often. It’s not the routine, it’s the level of effort. Consistency may be there, sure, with your 2-hour long gym sessions, but the effort is almost non-existent. Talk is cheap, action speaks. After hearing and seeing what routines people are on, I just want to face palm.

All the time I see people, especially women, doing laterals with 2.5 pounds. This will probably work if they’re a 50 pound 11-year old girl, but if they’re a grown woman looking to build shoulders, they need a better plan. What’s worse, they have no clue how to progress. It just breaks my heart.

So imagine the kind of looks I get when I suggest people to do something that pushes them out of their comfort zone on most days. It’s like they’re speaking to an alien.

If you want to become better at something, you must put effort into it and you must do it consistently. No one who got anything worth writing home about achieved it without a high degree of effort and consistency. Even Donald Trump, who was born with a silver spoon in his mouth, had to fight to keep a top spot. Even Floyd Mayweather, one of the greatest, and richest, boxers of all time, had to fight tooth and nail to harness success.

Now I am no champion. I was not born with great genetics nor was I blessed to have a family who supported athletic endeavors. I was just some average Asian kid who happened to join the military, discovered fitness and nutrition, and decided to help people become healthier and more fit. This is in stark contrast to many fitness professionals who actually do have an athletic background. See, I have something to relate to most people looking to get into better shape: I was once-out-shape and just wanted to be in-shape. This isn’t a story about how I used to be an athlete and fell out of my ways. It is a story about how I was never an athlete and wanted to feel more comfortable in my own clothes. I had massive self-confidence issues. But I didn’t get to where I was by making excuses and partaking in activities that didn’t line up with my goals. I put in the work.

Even now, despite working nearly 90 hours a week, I make time to train. Even though I go to work at 8 and don’t come home until 11 during the weekdays and work 6-8 hours on the weekends, I still make time to train. It’s about doing things that matter (unfortunately, I don’t have enough time to update this blog as much as I’d like). If I find a 30-minute gap between clients, guess what I do? You guessed it, even if you didn’t try. I train. I do some blitz sessions where I would pick a handful of exercises to attack my whole body and a couple of cardio exercises and go to town for those 30-minutes.

But that’s just me. I place my fitness at a higher priority than most people, who prefer to go out and drink and party on weeknights. Nothing against them at all, but that’s them–they do what they do. However, if you’re one of these people yet make excuses as to why you’re not in as good as shape as you want to be, shame on you. This is partly why I get aggravated talking to people about fitness and nutrition: they want to know how to get in shape, but what I say goes in one hear and out the other. Whatevz, yo.

If you can’t do push-ups or pull-ups, yet want to be able to do them one day, what do you think you need to do? You don’t need to be a rocket scientist to figure this one out. Problem is that people act like the answer is so elusive. Practice them or easier variations, and drill the living sh*t out of themDon’t say you want to do something but take no steps toward realizing them.

Many times when my clients feel their progress is slowing, they need to make one change first. Put in a bit more effort to what they’re currently doing. I am proud to say that some of my clients are very strong for only being general fitness folks, but as soon as they add in some more purposeful exercise throughout the day, they see better results.

Here’s my message to you:

Stop making lame excuses.

Start doing something that requires effort, that pushes you out of your comfort zone.

Do those things that push you out of your comfort zone consistently, on most days of the week.

Take blitz sessions as an example. As often as possible throughout the day, do some purposeful exercise. If you’re a desk jockey, take 3 extra minutes on your bathroom (or smoke) break and get out of that sedentary funk. Move around a bit. Here’s what I do on a daily basis:

10 second chest stretch in a doorway
10 high-knee marches each leg
12 bodyweight squats
10 push-ups
10 split squats
10 mountain climbers
30 second side plank each side
30 second jumping jacks

I do this routine in my dress shirt, trousers, and dress shoes and it takes me about 3 minutes. For those 3-minutes, I am out of my comfort zone, which is the chair situated in front of a piece of crap Dell. Then I go to the bathroom to re-adjust my clothes. Not surprisingly, I feel amazing afterward and my productivity sky-rockets.

This isn’t some sort of revolution or amazing discovery. This is simply doing what you’re designed to do. Moving with effort and consistency.

What kind of results are you seeking? What have you been doing? How are you coming along in your goals? As always, I value your feedback and comments. Fire away.

The Best Diet Part III

Welcome to the final installment of the best diet series. If you missed them, read part I and part II before moving onto this part. In this part, I will lay out the most important factors when considering which ‘diet’ to undergo. 

WHAT A SUCCESSFUL DIET REALLY MEANS

As you should know by now, there is no such thing as a ‘perfect’ diet. Not a single eating plan can possibly cover all of the possibilities and preferences of each person. On the other hand, there may be a ‘perfect’ diet for you at a certain time in your life/career. The key is to make sure it works for as long as you want it to. Of course, you will know if a diet works for you based on physiological and psychological assessments. Once you reach a goal, it will be time to either re-evaluate whether you should stick to the said diet or move on to bigger things.

To move towards finding the right eating plan for you there are a few general caveats to know if you want to to translate what the mountain of research has come up with. Each of the below points should be considered guiding principles when evaluating whether you would have success on a specific diet.

  1. It’s healthful. In other words, a good diet will make you look at what you’re eating. Remember the Twinkie Diet above? If your main goal is weight-loss, you can eat 800 calories of junk food per day and lose weight. In the respect, it works. However, it’s not enough to just control calories anymore. You can lose weight eating Twinkies all day, but how sustainable is that for your health? Diet quality matters, especially if you want to promote health and keep off any weight you lost.

 

  1. It’s individualized. A good diet should take into consideration your metabolic condition and lifestyle. In other words, a good diet should take into consideration your diabetes or high-level athletics. Diets should not be cookie-cutter. There is no such thing as a one-size fits all diet, although there may be slight variations between you and the next person. If you’re diabetic, it would make very little sense to eat the same way as a healthy, lean, and active person. Additionally, what type of activity are you doing? Are you an endurance runner, a weight-lifter, a sprinter, a dancer, or a coach potato? Certain sports necessitate more or less of nutrients for optimal performance.

 

  1. It’s fulfilling. A good diet should fulfill your body’s requirements for protein, fats, and carbohydrates without overfeeding you (unless your goal is to become a larger version). By keeping in mind that proteins and fats are more satiating than carbohydrates, you can then construct a weight-loss plan that can control hunger better while improving nutrient intake. In fact, carbohydrates are not technically necessary since the body can create it through an indigenous process, but it’s fulfilling because carbohydrates are required to optimize metabolic function and hedonism. And if you’re an athlete, carbohydrates are indispensable for optimal performance and body composition.

 

  1. It’s sustainable. Research shows that over 90% of people cannot stick to a diet for more than two years. I surmise this is probably because most people don’t know how to choose what diet is best for them and how to adjust a diet based on their preferences. Not knowing how to transition explains in large part why high-level athletes become fat and sick once they become working members of society. This is also a huge problem for high-school athletes going into college — ever heard of the Freshman-15? If Michael Phelps were to stop swimming but maintained his monstrous in-season training caloric intake, his ability to float would surpass his ability to swim in the blink of an Olympic second.

 

This last point is especially important in light of health-promoting diets. If you can’t stick to a diet, then it’s no good. If you go on a diet and lose 10% of your excess fat mass but gain it all back in two years, you’re no better at the finish than you were at the start. Think Biggest Loser. Somewhere there are reports of the contestants developing eating disorders and tipping the scales even more than when they started the show.

Having the “best” diet yet not sticking to it is like having a Bentley collecting dust in your garage. It’s nice to talk about and show people you have this “awesome” thing you can always turn to, but if you’re not going to use it to make yourself a better person, then it’s useless.

Please, don’t let this car collect dust. Source

Mediterranean, Paleo, vegan, Weight Watchers, low-carbohydrate, DASH, or any of the other slick Amazon best-sellers will help you become healthier and leaner. But underneath the veil of the fancy names and acronyms, most successful diets have the above things in common.

SO AGAIN, WHAT IS THE BEST DIET? USE THIS ANSWER.

It depends—whatever is working right now for whatever goals I have, and I should be able to stick to it”. It all boils down to context-dependent effectiveness and preference. Anything outside of that is just minor detail.

The answer probably is not as pretty as a dozen roses, but it’s the truth. You can force-feed yourself a diet you don’t like to lose the extra fat on your left eyelid, but what happens after you meet your goal? Are you going to stick to the diet? Do you know how to eat afterward? Do you know how to eat if you have a medical condition? Do these questions seem like a bunch of pester to you compared to what you should Tweet or tag on Facebook? Making dietary changes is a lifelong process, but it’s one that brings highly coveted awards. Stick with it.

As always I appreciate feedback, comments, and input. What is your perception of a good diet?

The Best Diet Part II

This is part two of a three part series on what the best diet is. In part I, I briefly went over the major dietary variants found in research and rattled off some of the research in support of them. Despite each diet having their own set of benefits–with many overlapping each other–they’re all running for ‘best diet candidacy’. In this part, I will go over a few general factors that determine whether one diet will work better than another. 

THE OMNIPOTENT CONNECTION—LIFESTYLE AND PREFERENCES

I hope all of this is connecting. If each diet has the potential to be the best, then it doesn’t matter which diet you’re on, right? That’s half true. In each study, you will have people who do not respond as well as others, because of… individual differences. Results of studies are averages and do not explain in full why some people saw better results than others. If that is the case, then it might be better for you to look at these studies, figure out which diet may suit your condition better, and experiment. That is probably the way to go. To boot, there are very smart doctors and researchers who also agree that the best diet for you is the one that fits your lifestyle and metabolic condition.

Yes, in the realm of nutrition, you are a special snowflake. Source

Indeed, large-scale experimental, observational, and free-living studies have been conducted comparing diets with differing macronutrients to each other. Although many of the studies above show that one diet may be superior to another, there also exists research showing that differing macronutrient composition may not matter depending on the situation. One such situation is weight-loss. In light of this statement, it is sound logic to re-consider the previous theory if there is a refuting scientific result.

Back in 2007, Gardner et al published a study that would send ripples through the wide ocean of diet research. They showed that the Atkins (low-carbohydrate) diet resulted in more weight loss and more favorable blood lipids than the Ornish (vegetarian, low-fat), ZONE (balanced, mixed), or LEARN (lifestyle-based, low-fat, mixed) diets. Even at 12 months, the Atkins diet held steady. Two elephants in the room here: 1) mean weight loss between Atkins and the second best diet was 4 pounds (not a whole lot in the grand scheme of things); and 2) at two years, participants in each of the four groups saw non-statistically significant differences. In other words, the Atkins diet was no longer more effective than the other three diets at two years (Gardner, 2007). What does this tell us?

Sustainability is the ultimate trump card. It’s the deciding factor between “(weight) losers” and losers. And it’s also the one thing that will keep the results coming like rain during monsoon season in Thailand. It can be what makes any diet the best.

One of the most cited studies comparing of the effects of different diets on weight loss was published in the New England Journal of Medicine in 2009. They concluded:

Reduced-calorie diets result in clinically meaningful weight loss regardless of which macronutrients they emphasize.” (Sacks, 2009)

Here is another study from the well-known and respected Journal of the American Medical Association. The authors summed up their findings as such:

Significant weight loss was observed with any low-carbohydrate or low-fat dietWeight loss differences between individual named diets were small. This supports the practice of recommending any diet that a patient will adhere to in order to lose weight.” (Johnston, 2014)

And in another study published in PLoS One, Naude et al concluded that:

“Trials show weight loss in the short-term irrespective of whether the diet is low CHO or balanced. There is probably little or no difference in weight loss and changes in cardiovascular risk factors up to two years of follow-up when overweight and obese adults, with or without type 2 diabetes, are randomised to low CHO diets and isoenergetic balanced weight loss diets.” (Naude, 2014)

Finally, Foreyt et al put their conclusion rather nicely:

“Although “a calorie is a calorie” under the controlled conditions of a metabolic unit (i.e., only the level of calorie intake matters and not the source of calories), we conclude that these interrelationships are far more complex in the free-living situation. The different diet-related factors that condition energy balance, including total energy intake, satiety and hunger sensory triggers, and palatability, must be considered when assessing the efficacy of weight-reducing diets of different macronutrient composition.” (Foreyt, 2009)

In terms of weight-loss, the evidence is stacking in favor of a simple message: as long as you stick to a reduced-energy, weight-loss focused diet where you won’t feel like killing yourself, the dietary composition of carbohydrate, protein, or fat really don’t matter.

The above bolded statement literally means you can eat Twinkies all day and lose weight as long as you’re in a calorie deficit. But let’s get a couple of things straight, it doesn’t take a nutrition researcher to know that this won’t do any favors for your health. And if your health begins to decline, then losing weight is nothing but an afterthought in the wake of suboptimal performance in daily life, metabolism decline, and horrible quality of life.

Unless of course you’re like this. Source

What applies to weight-loss also applies to other goals. Subjects in these weight-loss studies volunteered and signed up because their goal was probably to lose weight. What about if you want to gain weight? Same story here—to gain weight, you must be in a caloric surplus regardless of macronutrient composition. For the purpose of this post, this is as simple as it gets.

What about performance? Simply put, it probably doesn’t matter, either… at least not until you become an elite athlete. At that point, you will probably have to fine tune things. No one has done a case study on him, but I highly doubt Michael Phelps eats like a normal human being. He probably eats like ten normal human beings.

After all, eating food does not just serve to keep you alive, but also to make you thrive. Don’t put low-octane gas into a high-octane car.

THE METABOLIC CONDITION CONNECTION

On the other hand, this may not apply if you have a certain medical condition that precludes the weight-loss. Like lifestyle preferences, metabolic, or medical, conditions are something that must be heavily considered when following a diet. Food can be an awfully powerful drug that if abused can lead to undesirable consequences. This is why Hippocrates, the founder of Western medicine, said,

Source

For instance, your risk of becoming diabetic is increased exponentially if you’re obese, and as much as losing weight greatly benefits diabetes management, the effectiveness of the diet can be determined by the macronutrient content. In the particular case of diabetes, losing weight is extremely helpful, but research on this front shows that low-carbohydrate diets outperform all others consistently in terms of glycemic control and lead to better weight loss than low-fat diets because of that glycemic control. Additionally, Feinman et al showed in their massive review that lower-carbohydrate diets are the most effective in terms of rates of diabetes remission and cessation of diabetes medications (Feinman, 2015).

There are other medical conditions that are affected by nutritional modulation. Non-alcoholic fatty liver disease, cardiovascular disease—high triglycerides, hypertension, suboptimal cholesterol levels—renal disease, and inflammatory bowel diseases represent just a small handful of disorders that is influenced by nutrition. Undertaking medical nutrition therapy on your own is ill-advised, so seeking out the help of someone who is licensed to proctor this type of stuff to tailor an eating plan based on lifestyle preferences, goals, and medical conditions is the best bet.

Stay tuned for the next and final installment of this series.

As always, I value your opinion. What kind of diet best suits you? How long have you been on your favorite diet?

The Best Diet Part I

This post will be part one of a three part post series going over the controversy of the ‘best’ diet. 

You make more than 200 decisions in a day—which phone to buy, where to go for vacation, who to date. Obviously these are questions that require tons of deliberation. The general quality of your life is often determined by questions that seemingly have little significance but carry a huge consequence. How about another question that we always ask ourselves, one that has the capability to have an enormous impact or none at all?

“What is the best diet?”

Again, right? Source

Of the hundreds of decisions you make per day, approximately 226 decisions will be about food (Wansink). Due to the propensity of food decisions in your daily lives, it goes to say that such a question is riddled with endless loopholes, criticism, lies, and truth. It’s talked about so commonly that you can just shrug it off, but the importance is scarily deceiving. Most importantly, the significance of this question lies within the context of the person asking it, because certainly, the idea that a perfect diet exists to fit everyone’s wants and needs may be nothing but a false truth.

And if you work in a field that is intricately involved with human health, disease, and nutrition—like a Registered Dietitian (RD)—it’s the worst possible question.  Dealing with a question that is entangled in a web of this and that is difficult enough to write in a blog post, imagine trying to explain it to a person who has no clue. RDs deal with not luxuries people think about once every few years like buying a house or car, but a commodity, and their responses directly affect those 226 daily food decisions people make. And because this question has been asked so many times and approached in so many different ways, the significance of it is slowly beginning to lose out to the myriad of options available in the mainstream.

Wrapped up nicely with the “what is the best diet” are a couple of other multi-faceted questions that you probably want answers for sooner than your birthday.

What are the best foods to eat?”

What’s the best way to do [insert goal here]?”

So on and so forth. The best diet would be the best present ever. Although it makes sense that there is no one best diet and no one best food, these questions cannot be proven through science. If it could, then scientists would still not be spending hundreds of man hours and thousands of research grant dollars trying to figure out what the optimal diet is. Fortunately, science does shed light on the path you should take to achieve good health through diet.

For your next birthday. Source

THE MAZE OF DIETS

Follow any large media outlet and you’ll be sure to read, hear, or smell reports and journalists talking about whether you should “slash carbs to carve a sleek and sexy six-pack” or “drop pounds by dropping fat” or “eat like a caveman and look like one” (uh, do you actually want to look like this?). So much conflicting information, so little time—who to listen to?

Image result for caveman

It’s the grass-fed, organic, free-range, non-GMO, pastured limestone that helps him maintain perfect white teeth (source)

Outside of the lab, many camps have laid claim to a best diet, but no one seems to agree with each other fully. One study will come out today that refutes yesterday’s study on the same diet. On the vast intranet, you have various nutrition experts and armchair gurus going to war on their keyboards espousing their preferred diet without tickling the thought that their diet may not actually be the best. The devil is in the details, so asking a layperson to read a full article and understand the meaning of those details is like asking a dolphin to walk on land—it’s not going to happen. That’s why there’s the media to help, except they really don’t. Your best bet is to look for someone who actually reads and keeps up with the literature—say a doctor or an RD. Luckily, I do enjoy a good read and turning the knowledge of science into application is a passion of mine. Very basically, let me answer the almighty question, “which is the best diet”. And it is… <drum roll>

The Mediterranean diet.

A low-carbohydrate diet.

A vegetarian (or vegan) diet.

The Dietary Approaches to Stop Hypertension (DASH) program.

The Paleo diet.

Weight Watchers

… Hold the phone! Didn’t I just say that I would tell you what the best diet is? Why, yes, I did, and I did. I know that best is a term to denote a singular thing that is superior to all others in its respective category, but read on to find out why everything can be the best.

LET THE RESEARCH SPEAK

The topic of what diet is best is probably one of the hottest in nutrition research and a new study (and book) is published just as quickly as a baby is born. According to the research, it’s fine to contradict myself. Why? Because each diet is the best. Before we move onto why each diet can be the best, let’s look at very briefly what some of the recent research actually has to say in favor of the major dietary regimes and their spin-offs:

The Mediterranean Diet—one of the “children” from a combination of research and observation, the Mediterranean diet seeks to reflect the dietary habits of some of the healthiest people in the world. Unlike most dietary programs, the Mediterranean diet is one of the few scientifically studied that attempts to mimic what is actually consumed in observation. Specifically, the Mediterranean diet emphasizes fish, nuts, legumes, fruits, vegetables, and low glycemic carbohydrate sources. In the literature, a Mediterranean diet is similar to a moderate carbohydrate diet, about 40%. Some benefits:

  • Increased life span (Crous-Bou, 2014)
  • Decreased weight and obesity (Sayon-Orea, 2014; Huo 2014; Thomas 2007)
  • Improved non-alcoholic fatty liver disease (Zivkovic, 2007)
  • Improved hemoglobin A1c and other diabetes markers (Carter, 2014; Huo, 2014; Esposito, 2014)
  • Improved blood lipid panel (Huo, 2014; Richard 2014; Thomas, 2007)
  • Decreased risk of certain cancers (Whalen, 2014)

Low-carbohydrate diet—popularized mainstream by Robert Atkins, MD, this dietary protocol has really been in practice throughout mankind’s history. There are various societies that consume low daily carbohydrates, such as the Inuits. Because of carbohydrate’s ability to affect various health markers such as blood sugars, it is being more commonly manipulated, and with good results. Low carbohydrate diets can be characterized in the literature as anything under 40% and as low as 5% of total calories.

  • Improved satiety (Gibson, 2015; Erlanson-Albertsson, 2005)
  • Significant weight loss, even against FDA approved weight loss drugs (Yancy 2010; Yancy, 2004; Sharman, 2004; Bertoli, 2014; Tay 2008)
  • Improved blood lipid panels, especially in those with high triglycerides (Yancy, 2004; Thomson, 2010; Sharman 2004; Volek, 2008)
  • Improved diabetes markers, especially in those with compromised insulin sensitivity (Samaha, 2007; Feinman, 2015; Arora, 2005)
  • Decreased inflammation and tumor growth (especially in response to ketogenic diets)(Ho, 2014; Klement, 2011)

Low-fat diets—programs such as Dietary Approach to Stop Hypertension are those purported to improve blood lipids under the premise that saturated fat and cholesterol increase risk of heart disease and blood pressure. There is extensive evidence that free-living populations do follow a somewhat lower-fat diet and this can also include those who are vegetarian. Asian populations typically consume a diet lower in fat, for example. Fat content is usually below 30% and carbohydrates are higher, above 50%.

  • Decreased weight and obesity (Astrup, 2000; Astrup 2002; Hooper, 2012; Mueller-Cunningham, 2003; Tay, 2008)
  • Improved diabetes markers (Yokoyama, 2014)
  • Improved cardiovascular health, such as blood pressure and blood lipids (Yokoyama, 2014; Shridhar, 2014; Famodu, 1998; Nosova, 2015)
  • Improved inflammatory markers (Turner-McGrievy, 2014; Egert, 2014)
  • Improved non-alcoholic fatty liver disease (Ma, 2015)
  • Decreased risk of certain cancers (Fung, 2010)

Paleolithic diets—the attempt to emulate how our hunter-gatherer ancestors ate. “Paleo” diets have gained an immense surge of popularity since the late 1970’s when a seminal paper was produced citing anthropological data that our hunter-gatherer ancestors ate quite differently than how we are currently eating. Supporters of this program propose that by eating lean meats, vegetables, fruits, nuts, and seeds, and excluding dairy, legumes, wheat, and grains, we will see a boost in our health and performance because we will be eating concomitantly with our genetic makeup. Research does not give a clear macronutrient breakdown of a paleo diet, only that the program fits within the framework of the paleo principles mentioned above.

  • Improves weight loss and obesity (Boers, 2014; Mellberg, 2014)
  • Improves satiety (Jonsson, 2013; Jonsson, 2010)
  • Decreases risk of certain cancers (Whalen, 2014)
  • Improves cardiovascular risk factors (Jonsson, 2009; Klonoff, 2009)
  • Improves diabetes markers (Frassetto, 2009; Klonoff, 2009)
  • Improves metabolic syndrome characteristics (Boers, 2014; Lindeberg, 2012)

“THE RESEARCH HAS SPOKEN… AND I’M STILL CONFUSED”

The above is just a small handful of proposed health benefits of each diet. There are seriously hundreds of thousands of studies on each diet and their derivatives; it’s no wonder the average person has no clue where to start when it comes to which diet they should follow. I also refrained from going into the demerits of each diet because I do not want this post to be the length of half a book. Despite the small list, do you see a pattern? Here is the bottom line and the answer you have been waiting for:

Any diet will work. Any diet has the potential to be the “best diet”. And not surprisingly, each eating pattern overlaps with one another in some aspect of health, whether it’s improving diabetes, cardiovascular disease, or weight. The researchers in each study were looking at a particular end point, because frankly, it will be nearly impossible to study how each food affects each health biomarker, especially in context of individual differences. Nonetheless, each diet possessed the ability to improve health to a statistically significant degree.

Stay tuned to read how to connect the ‘best’ diet to your situation.

REFERENCES

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Arora SK1McFarlane SI. The case for low carbohydrate diets in diabetes management. Nutr Metab (Lond). 2005 Jul 14;2:16.

Astrup A1Astrup ABuemann BFlint ARaben A. Low-fat diets and energy balance: how does the evidence stand in 2002? Proc Nutr Soc. 2002 May;61(2):299-309.

Astrup A1Ryan LGrunwald GKStorgaard MSaris WMelanson EHill JO. The role of dietary fat in body fatness: evidence from a preliminary meta-analysis of ad libitum low-fat dietaryintervention studies. Br J Nutr. 2000 Mar;83 Suppl 1:S25-32.

Bertoli S1Trentani C2Ferraris C2De Giorgis V3Veggiotti P3Tagliabue A4. Long-term effects of a ketogenic diet on body composition and bone mineralization in GLUT-1 deficiency syndrome: a case series. Nutrition. 2014 Jun;30(6):726-8. doi: 10.1016/j.nut.2014.01.005.

Boers I1, Muskiet FA, Berkelaar E, Schut E, Penders R, Hoenderdos K, Wichers HJ, Jong MC. Favourable effects of consuming a Palaeolithic-type diet on characteristics of the metabolic syndrome: a randomized controlled pilot-study. Lipids Health Dis. 2014 Oct 11;13:160. doi: 10.1186/1476-511X-13-160.

Carter P1Achana FTroughton JGray LJKhunti KDavies MJ. A Mediterranean diet improves HbA1c but not fasting blood glucose compared to alternative dietary strategies: a network meta-analysis. J Hum Nutr Diet. 2014 Jun;27(3):280-97. doi: 10.1111/jhn.12138.

Crous-Bou M1Fung TT2Prescott J3Julin B1Du M4Sun Q5Rexrode KM6Hu FB7De Vivo I8. Mediterranean diet and telomere length in Nurses’ Health Study: population based cohort study. BMJ. 2014 Dec 2;349:g6674. doi: 10.1136/bmj.g6674.

de Almeida Ventura Dde Matos Fonseca VRamos EGMarinheiro LPde Souza RAde Miranda Chaves CRPeixoto MV. Association between quality of the diet and cardiometabolic risk factors in postmenopausal women. Nutr J. 2014 Dec 22;13(1):121.

Egert S1Baxheinrich A2Lee-Barkey YH3Tschoepe D3Wahrburg U2Stratmann B3. Effects of an energy-restricted diet rich in plant-derived α-linolenic acid on systemic inflammation and endothelial function in overweight-to-obese patients with metabolic syndrome traits. Br J Nutr. 2014 Oct 28;112(8):1315-22. doi: 10.1017/S0007114514002001.

Erlanson-Albertsson C1Mei J. The effect of low carbohydrate on energy metabolism. Int J Obes (Lond). 2005 Sep;29 Suppl 2:S26-30.

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Shridhar K1Dhillon PK1Bowen L2Kinra S2Bharathi AV3Prabhakaran D4Reddy KS5Ebrahim S2Indian Migration Study Group. The association between a vegetarian diet and cardiovascular disease (CVD) risk factors in India: the Indian Migration Study. PLoS One. 2014 Oct 24;9(10):e110586. doi: 10.1371/journal.pone.0110586.

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Slow down on blaming fast food

When we hear ‘fast food’, one of the first things we probably think to ourselves is ‘unhealthy’. Accompanied with the term unhealthy is the unsettling statistics of obesity in the United States—34.9% or 78.6 million. The three terms, ‘fast food’, ‘unhealthy’, and ‘obesity’ do not seem to be mutually exclusive since statistics show that overweight and obese people tend to favor unhealthy food choices, like those at fast food restaurants, more often than healthy people (2, 3). However this social stigma is attached to the population, we cannot escape the ideology that fast food consumption (FCC) is inextricably linked to unhealthiness and obesity, no matter how many times it is replicated in research. The reality is that fast food restaurants are here to stay and as long as there are consumers who prefer taste over function, they will continue to exist.

Although the numbers are frightening, research is beginning to focus more on how public policy can get people to accept fast food consumption rather than ostracizing it, and potentially ostracizing consumers in the process. One such research study is Poti et al’s study on how fast food consumption reflects poor dietary outcomes of children. They sought to evaluate not how FFC may be independently linked with poor health outcomes, but how FFC influences other dietary choices. In other words, they wanted to look at the overall picture of diet. Their introduction stated what previous research has, children who were frequent fast food consumers had higher total energy intake; had lower fiber intake; and consumed diets higher in energy density than their counter-parts. In general, fast food consumers had an overall poorer diet quality compared to non-consumers.

The authors’ hypothesis is in line with previous research done on adults and FFC, and its effects on correlation with other dietary factors. Specifically, they wanted to study this relationship in children since according to them, a study on this has never been done before. They pointed out that previous literature did not control for confounding variables and that “public health efforts targeted at fast food might be overstated as well” (3). As such, their intention is to “determine whether fast food consumers (children) also eat poorly outside of the fast food restaurant and to compared the independent associations of FCC compared with dietary pattern for the remainder of intake with overweight/obesity prevalence and dietary outcomes” (3).

Not surprisingly, the authors found that high-consumers (HC) ate significantly less dairy and more sugar-sweetened beverages, not only while eating at fast food restaurants, but also outside of them compared to non-consumers (NC) and low-consumers (LC). HC also had lower intake of fruits and vegetables, though the between-group differences did not reach statistical significance. In conclusion, the authors’ findings reinforce previous findings that FCC is significantly associated with overweight/obesity. However, the twist here is that once the remainder of diet is factored in, the association disappears and remainder of diet continues to be significantly associated with overweight/obesity.

Study design and research methods

Researchers used a cross-sectional analysis including 4446 US children aged 2-18 years old participating in the 2007-2010 National Health and Nutrition Examination Survey (NHANES) and its dietary interview component. A study of this magnitude is a huge undertaking and whatever relationship they find will surely be significant.

Dietary assessment: Two 24-hour recalls using the United State Department of Agriculture’s (USDA) Automated Multiple-Pass Method by trained interviewers

  • 1st: Day 1 in person
  • 2nd: 3-10 days later by phone

Anthropometric measurements and covariate assessment: In-person interviews collected demographic and socioeconomic data, including sex, age, race-ethnicity, household income, and parenteral education level. Weight, height, and BMI were measured by a physical examination and BMI calculation. BMI classification was defined using the Center for Disease Control’s (CDC) 2000 sex-specific BMI-for-age growth charts, with overweight at or above the 85th percentile but below the 95th percentile, and obesity being at or above the 95th percentile.

Other methods the researchers used were analytic sample; fast food consumption (food from a restaurant without a waiter/waitress and percent classification of FFC—non-consumers (0% of energy), low-consumers (0.1-30%), and high-consumers (>30%); food grouping (using the USDA’s Food and Nutrient Database for Dietary Studies); dietary pattern analysis for the remainder of intake (analysis of remainder of recall to determine diet quality of the stratified groups; and statistical analysis (controlled for sex, age, race-ethnicity, income, parenteral education, total energy intake, and weight status where appropriate)

What was wrong with this study?

One of the most limiting factors of this study is how the information was collected. There is need to extrapolate on how the information is collected, but this is very difficult to practically apply as there are so many food choices available to consumers. The authors attempted to account for variation in food intake for the remainder of diet using cluster analysis and weighted percentages, but I feel this is next to impossible unless the authors collected nutrition labels for everything the children ate during the study.

Additionally, using somewhat subjective assessment methods such as dietary recalls can skew results. The authors admitted that one of the main limitations of their study was the use of self-reported dietary intake. Previous research has shown that people will tend to underreport unhealthy food choices despite being in a study that is meant to report them. This is especially discernible the heavier someone is.

What do I think of this study?

I feel this study was just another drop into an ocean of research showing that what we eat during one meal or day can have an impact on how we eat in general. This study reinforces the hypothesis that low and high FCC can shape how we make food choices outside of the fast food restaurant milieu. This is not surprisingly for health professionals since through education we have intuitively realized that FCC can represent general diet. However, not much concrete evidence exist showing that what we eat outside of fast food restaurants is more strongly associated with adverse health outcomes compared to FCC. A study of this nature can help turn the tide of disfavor towards fast food restaurants.

Of course, I do not feel that this study should be used as exoneration for fast food restaurants, but merely as a way to show that the social stigma and negativity towards fast food restaurants may be unwarranted and overstated when the rest of the diet is not taken into account, which the authors underscore.

How to use this information

In terms of practicality and implementation into public health policy, I feel this study could be a Catch-22. While it does lift some culpability from fast food restaurants, there is a real possibility that the public may misinterpret this study and use it as a ticket to consume fast food without remorse. The key, I believe, is to show that fast food is not the evil we make it out to be if the remainder of the diet is otherwise healthful.

I can see this type of research being properly implemented as a psychological bulwark against guilt-associated food intake. If people are made aware that what they eat 80% of time is what determines the general state of their health, I feel they are more likely to moderate their fast food eating and see it as a treat rather than something they should completely avoid.

References

  1. Ogden CL1Carroll MD1Kit BK2Flegal KM1. Prevalence of childhood and adult obesity in the United States, 2011-2012. 2014 Feb 26;311(8):806-14. doi: 10.1001/jama.2014.732.
  2. Braithwaite I1Stewart AW2Hancox RJ3Beasley R1Murphy R4Mitchell EA5ISAAC Phase Three Study GroupISAAC Phase Three Study Group. Fast-food consumption and body mass index in children and adolescents: an international cross-sectional study. BMJ Open.2014 Dec 8;4(12):e005813. doi: 10.1136/bmjopen-2014-005813.
  3. Poti JM, Duffey KJ, Popkin BM. The association of fast food consumption with poor dietary outcomes and obesity among children: is it the fast food or the remainder of the diet? Am J Clin Nutr 2014;99:162-71.

Carbohydrate Low-down: how many carbohydrates should you eat?

Time to tackle another head of what I consider the 3-headed beast of nutrition: carbohydrates. Especially in the field of dietetics and nutrition, there is a a pseudo-war about whether clients should restrict carbohydrates to see health benefits. And I swear, after this post, I will not be posting monster 3,000 + word posts again.

Every other month, there is a study that either touts or refutes the benefits of either carbohydrate restriction or carbohydrate liberation. Who’s wrong, who’s right?

First, I want to tell you what the other two heads are:

1) Saturated fat and cholesterol
2) Salt

And today, we are going to talk about carbohydrates.

What are carbohydrates (carbs)?

Carbohydrates are energy nutrients, just like protein and fat. They provide the body with substrates to keep it functioning optimally. We are not going to talk about biochemistry here, such as which processes that involved in carbohydrate metabolism, where carbohydrates get absorbed, and the finer details of what happens to carbohydrates after they do get absorbed.

Carbohydrates are made up of three elements: carbon, hydrogen, and oxygen. Through a complex metabolic process, carbohydrate sources like bread, potatoes, and fruit are eaten and subsequently broken down into three simple sugar molecules: fructose, glucose, and galactose. They are the preferred energy source for red blood, brain, and muscle cells, especially during periods of high-intense activities. Carbs are stored in two primary tissues of the body: liver and muscle. The storage capacity of carbs in the liver is ~100g in average humans and 300-500 in muscle, for an average of 400-600g of storage capacity in an average person at any time (Acheson; Jensen).


Mmmm, carbs (source)

Carbohydrates in and of themselves are not evil–far from it. Carbohydrates stimulate the release of insulin, which is an anabolic–building–hormone. Don’t know what insulin is because you’ve been living under a rock? It’s a hormone that acts on your body cells, opening them up like a key and lock, in order to remove sugar from the blood caused by eating carbohydrates. Insulin is a requirement if you want to build muscle. Insulin is also anti-inflammatory, meaning that some carbohydrates are actually required for proper immune function (Hyun).

Whether or not carbohydrates are necessary is something that experts like to debate about. This is where things can get a bit tricky. Notice how I said “preferred”. Some experts like to take it further and suggest that carbohydrates are either not necessary for survival or that you should eat a high-carbohydrate diet.

What is ‘low’?


And it ain’t twerkin’ (source)

Let me just say this: twerking is a menace to our society.

When you look at the research, it’s clear that ‘low-carbohydrate’ does not have a uniform definition. For example, studies done by Volek et al use low-carbohydrate plans that consist of less than 20g of carbohydrates per day. These are also called ‘ketogenic’ diets. Other researchers consider 40% of daily carbohydrate intake low, or 60g or less per day, or 130g or less per day (this 130g figure comes from the idea that the brain requires about 130g of glucose per day to function).

Then you have studies that predominantly use either percentages or absolute numbers. Some studies may use 40% as an arbitrary number for low-carb diets, but researchers of low-carb studies claim that 40% is too high. Whatever the case may be, a low-carb can safely be defined as having an intake of 50-100g. I prefer to use absolute numbers instead of percentages since they give you more solid guidelines. For example, if you used percentages, you would get different numbers depending on how many calories one eats.

For the sake of discussion, let’s say you want to get into a ketogenic state by eating 50g of carbs per day.

If you were a 2000-calorie diet, 10% would be 50g of carbs (50 * 4 = 200 kcals; 2000/200 = 10%)

But if you were on a 4000-calorie diet, 10% would be 100g of carbs, enough to knock you out of ketosis.

Instead, you can just say you want to eat 50g of carbs, regardless of what your calorie intake may be to get into ketosis.

Breakdown of carbohydrate intake:

  • 0% or 0: no carb
  • 20-50g: very-low carb (if high-fat, this is considered a ketogenic diet)
  • 50-75g: low carb
  • 75-150: moderate carb
  • 150-225: moderate to high carb
  • 225+: high carb

Before we move on, let me make clear that I am a fan of lower-carbohydrate intakes. But what I mean by lower is that my plans are lower than what public health agencies and authorities suggest. The United States Department of Agriculture (USDA) nutrition guidelines suggest up 45-65% of daily calories to be in the form of carbohydrates. Of course, this highly depends on the individual, but suffice it to say that a vast majority of people would benefit from a lower carb intake than what they’re currently eating.

Source 

Benefits of lower-carb plans

This part is going to be short. I cannot help but be a bit biased toward carb intake on the lower side, and as such I realize that there are more benefits to lower-carb diets than consequences for a vast majority of people. When I refer to lower-carbs, I mean anything under 45%, which is the minimal that health authorities recommend.

In the literature,  lower-carb plans have been shown to:

  • Improve fat-loss at a quicker rate than low-fat/high-carb diets (Shai; Yancy; Gow; Gardner)
    • Some studies show that low-carb diets induce almost double the amount of weight loss as high-carb diets in the same time frame
  • Retention of lean body mass (muscle) better than conventional diets (Volek, 2002; Volek 2004; Miyashita)
  • Decrease risk factors and improve health biomarkers of certain cancers (Sedlacek; Ho)
  • Improve blood levels of inflammatory markers and endothelial/vascular function (Rajaje; Mah)
  • Improve insulin sensitivity (Blouet; Volek) and decreases levels of circulating insulin, which reduces risk of diabetes (Kodama; Demol)
  • Improve lipid profile (LDL, HDL, TG, total cholesterol ratio) thereby improving Metabolic Syndrome risk factors (Hu; LeCheminant; Sharman) compared to high-carb diets, which worsen diabetic complications and cardiovascular risk (Chen)
  • Superior glycaemic control compared to a low-fat/high-carb diet (Guldbrand)
  • More favorable impact on low-grade (chronic) inflammation compared to a low-fat diet (Jonasson)
  • Improves levels of leptin, which is considered the fat-burning hormone (Llanos)
  • In terms of athletic performance, too high of carb (above 5g per pound of bodyweight) intakes do not seem to confer additional benefits compared to moderate carb intake (Sherman)
  • Naturally lowers overall daily caloric intake by improving satiety (Wycherley; Bravata)

The last point is probably the most important point in this whole low-carb paradigm. Although many studies show that low-carb diets reduce weight, over half of them actually admitted that subjects lost more weight because they ate less due to satiety, which leads to less food intake. Translation: lower total calorie intake.

When talking about low-carbohydrate diets, you can’t ignore the impact that carbohydrates have on athletic performance. Most of the literature shows, without a shadow of a doubt, that high-carb diets outperform low-carb diets when it comes to athletic performance. But in the past ten years or so, low-carb gurus such as Mark Sisson, Robb Wolff, Stephen Phinney, and Jeff Volek have been proposing that a low-carb diet with high fat not only as effective as higher carb plans, but they also improve longevity, health, and body composition. If you need proof, look no further than some elite level athletes:

  • Professional cyclist, Dave Zabriskie
  • Ultramarathon runner, Timothy Olson
  • Triathlete Simon Whitfield
  • Winter Olympics pursuit event winner, Bjoern Ferry

Compared to high-carb plan athletes, low-carb athletes are much fewer in numbers. Whether their success is due to their diet or their insane genetics and training routine is still up for debate. One thing for sure is that low-carb diets DO work for some elite level athletes.

People who may benefit from low-carb plans:

  • Sedentary to moderately active people
  • Those with Metabolic Syndrome (overweight or obese; high lipids; impaired insulin sensitivity; high fasting blood sugars; high blood pressure)
  • Those with a history of high-carb plans
  • Those who are pre-contest (need to decrease carbs to improve appearance)

*** A little aside about fructose

Fructose, which is the sugar found in abundance in fruits, is primarily metabolized in the liver. The enzyme which catalyzes fructose metabolism is made in the liver. People say that fructose is an unnecessary component of an eating plan. Sure, it may be unnecessary… if you want to live like a zombie. Fructose is preferentially converted to glycogen in the liver so it can be used later, namely to keep your blood sugars under control. When you’re low-carbin’ it, this is important. Additionally, fructose is more efficient at supplying a constant stream of sugar to working muscles during exercise (Rizakalla).

After you eat fructose, it gets shuttled to the liver for processing. Unlike fructose, glucose and galactose act quicker, 30-45 minutes after ingestion. This is why all the holy Godmothers praise fructose as the next sweet savior, since it doesn’t increase blood sugar and keeps insulin levels down. Agave nectar, anyone? Now a low-carb plan will naturally dictate a decrease in fructose consumption because it decreases overall carbohydrate sources. Why is fructose consumption an important topic?

On average, the liver can only process 50g of fructose per day (Sun). This is equivalent to 24 ounces of high-fructose corn syrup sweetened soda, or 4 fruits per day. And what happens after you eat more fructose than your liver can handle? Since fructose is a nutrient just like many of the other things we eat, it’s quite plausible to theorize that bad things happen if you eat too much fructose. In 2002, a study released in the American Journal of Clinical Nutrition sent ripples through the nutrition world and raised a serious handful of eyebrows. In it, they concluded this:

“Fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models” (Elliott).

However, in this particular study, the researchers were focusing on the additional sugars and sugar derivatives, like high-fructose corn syrup, and not the fructose found in plant foods. On top of that, they used animal models and used non-physiological doses, or doses that are unrealistic to humans in terms of their bodyweight. Later research come out trying to figure out if fructose consumption really was linked to insulin resistance and all that jazz. While the above study used animal models, studies refuting negative consequences of normal fructose consumption were based on epidemiological data. These data support that fructose levels 100g per day had no negative effect on bodyweight (Rizkalla).

Unfortunately, many people who were ill-informed and with bad intentions took this fructose conjecture and ran with it. Even to this day, people run with it. While I don’t believe fructose is something you should be alarmed about if you don’t drink sodas and eat sh*t, you shouldn’t necessarily go hog-wild on it, either. Moderation, folks.

Not the same as…

Back to our main program…

Drawbacks of low-carb plans

Let’s preface this portion with me stating that low-carb plans, in my eyes, are plans that state you should eat less than 75g of carbs per day. 

Although low-carb diets have been shown to improve glycemic control, weight-loss, and lipid profile in the short-term (within a couple of weeks), most of the benefits diminish after a year and the diet is quite comparable to its higher carb counterpart when controlled for calories. A massive review and meta-analysis published this year looked at how well low-carbohydrates fared against balanced diets matched for calories. They found that over time, balanced diets (40% carbs, 30% protein, 30% fat) were almost as effective as low-carb diets in almost all parameters, although low carb diets were more effective at reducing triglycerides, improving lipid panels, and improving insulin concentrations (Naude, 2014).

Carbohydrates are required for intense activity. If you have ever tried to train on a low-carb diet, then you don’t even need to defer to scientific studies. For example, I will use the Paleo framework as an example here. Paleo does a good job at being extremely vague at how many carbohydrates you should consume per day. However, over time, the more fanatical and active Paleo-ites, Crossfitters, began to recognize the benefits of carbohydrates for athletic performance. From the Crossfit website:

Carbohydrates should be predominantly low-glycemic and account for about 40% of your total caloric load” (Crossfit.com). I don’t recall where I saw this–it was a few years ago–but someone interviewed competitors from the CrossFit games, asking them about their diet and whether they adhered to a Paleo diet. If my memory serves me correctly, not a single one of the top competitors adhered to a strict Paleo diet: they drank buku amounts of milk. 

Rich Froning: not getting by eating 2-3 sweet potatoes a day. Source

The example above is Rich Froning, one of the best CrossFit athletes to have ever competed and is a genetic beast. He didn’t start his career in CrossFit, either; it was in powerlifting. I will admit that this guy kicks ass and takes names, but don’t think for a second that all he eats per day are a couple of sweet potatoes. To build a physique and acquire conditioning like him takes years of hard, consistent work, not the fly-by-night plan that promises a six-pack in 4 weeks. By eating a diet with reduced carbs, you may be able to work towards his physique, but his athletic performance is a whole different matter.

Now in the literature, research shows that too little carbohydrates depletes liver glycogen, which can lead to hypoglycemia (low blood sugar) and subsequent decline in athletic performance (Costill; ADA). With too little carbohydrates, you may ‘bonk’, which is the term described when the liver cannot maintain blood sugar at the pace that sugar is being used during exercise. This is especially true in endurance sports such as marathon running and cycling, where you are working at above 75% of your maximum heart rate for hours and your body relies on carbohydrates for fuel. Plus, good luck finding many low-carb Olympic athletes standing on the podium. I listed a few athletes up top, but they are far from the rule.

Another major potential issue of going too low in carbs for too long is the dysregulation of thyroid hormones. The thyroid gland produces hormones that are specially responsible for regulating metabolic rate. Carbohydrates are known to induce increases in metabolic rate because they stimulate the increase of thyroid hormones. Connecting the dots, we see that if you restrict carbs for too long, you run the risk of decreasing metabolic rate via decrease in thyroid hormones (Muller; Danforth). There is even some talk on low-carb forums where people have unexpectedly get diagnosed with hypothyroidism.

The last drawback of low-carb diets I will talk about in this post is the ability of long-term low-carb diets to increase levels of cortisol and decrease levels of testosterone. Some of the literature has shown that staying low-carb for too long throws the balance of androgens and cortisol off-balance, especially in those who are participating in high-intense activities, such as ice hockey (Anderson; Tegelman). For men, this could pose a problem.

Carbohydrates trigger the release of insulin from the pancreas in healthy and most sick individuals (unless you’re type 1 diabetic, in which you lack insulin). Common sense dictates that insulin is a requirement for survival. This is pretty much a fact and not many people argue about it, even the low-carb gurus. But what many people overlook is that insulin is also anti-inflammatory. Low-carb experts often claim that insulin is the reason that people get fat. No, I argue, that is not true. Eating too much is the main reason people get fat. Insulin is just there to clear sugar from the blood, which is toxic if levels get and stay high (of course, a carb-based diet will drive up insulin levels in the absence of intense physical activity). Having high blood sugars is indicative of a state of inflammation and without insulin to clear it, you will heal slower, get infected easier, and die quicker. In short, you need insulin. So although eating less carbohydrates decrease insulin production, chronic use of low-carb plans may delay wound healing and increase risk of infection (Hyun).

Carbs, in the form of starch, is necessary for optimal health and gut function. Your microbiota, or the gut living in your gastrointestinal tract, require starch and fiber to survive and grow, and in return, giving you  health (Chassard; Sonnenburg).

People who should be more cautious of low-carb plans:

  • Very active athletes
  • Athletes with high muscle mass
  • Those with a history of very-low carbohydrate diets
  • Those who have terrible control over their sweet tooth

Although the above are drawbacks of low-carb plans, especially the last two, don’t be deterred from undertaking low-carb diets in a sensible way. One study is not enough to prove a causal relationship. Also keep in mind that the short-term decreases in thyroid hormone and increases in cortisol may not translate to you and do not mean that low-carb diets are inherently bad . Remember that low-carb diets have been and continue to be used with great success to get sick people healthier. It’s just that for athletic performance, you want to be more cautious.

Should you get low?


Your carbs probably shouldn’t be as low as this car (source)

Low-carb and high-carb plans definitely have their place. They are each part of the continuum and depending on your circumstances, each can be warranted. For example, low-carb plans may be more suitable if you have a severely deranged metabolism, such as high trigs, abnormal lipid panels, and God knows what else. If you’re looking for a quick and safe way to get your health back in line, low-carb plans can be highly effective.

But as stated above, low-carb diets work their weight-loss magic because they are better at keeping you full, which leads to early satiety. For example, in a conference in Atlanta in 2013, researchers presented a study that measured appetite and hunger ratings after two isocaloric breakfasts: one rich in protein/low in carbs and one with low protein/high carbs. A breakfast with 30-39g of protein and low in carbs was better at curbing hunger than a high carb breakfast, despite being the same number of calories.

Better hunger stomping means less appetite which means less calories. In spite of that, low-carb plans are not all that much better for absolute weight-loss compared to higher-carb diets as long as energy intake is accounted for. Essentially, if you eat less than you need to maintain your body weight, you will lose some weight regardless of how many carbs you eat. This was sufficiently demonstrated by a professor from an Iowa university a few years where he ate a diet consisting mainly of donuts, cakes, and cookies. However, low-carb diets have been shown to be superior in terms of health biomarkers and the aforementioned hunger control. Better hunger control probably means better dietary adherence, which is an all-important factor determining efficacy of diets.

Low-carb plans are not without their consequences. The key in all of this is making smart food decisions and engaging in a good exercise program, not your typical broscience bull crap.

How I do things

Liebman’s review on optimal intake ranges for carbs is a very good starting place for many people, and is the range I stick to for most of my and my clients’ activities. Unless you are an uber-active endurance athlete or blessed with God-like genetics, then you are probably better off wading in the swamp of 26-44% of carbohydrates per day. We can turn those figures to 20-40% to make things a bit easier. Having carbs at these numbers eliminates the risk of running into low thyroid, leptin, and energy issues over the long haul.

Eating 20-40% of your carbs also regulate the necessity to meet  exercise needs. This is especially important if you want to build more muscle, since the insulin released from eating carbohydrates is potent anabolic stuff (and that’s why constantly high insulin levels lead to fat gain, since fat storage and creation is an anabolic process). If you want to look at this in terms of numbers, then I suggest staying in the range of 75-150g of carbs per day. You can run the lower number on your non-training days and closer to 150g on your training days if you’re fat and/or sick. This number may register higher if you engage in more physical activity.

If you want to do a low or very-low carb diet, be my guest. I am not here to discourage you from doing so. You may very well be someone who responds positively to a lower-carb diet. It’s quite true that many people have anecdotal accounts of low-carb plans doing wonders for them. When I reached 5% bodyfat, I was on a low-carb/moderate fat/high protein diet. When my wife and I were preparing for our two previous powerlifting competitions, we used low-carb plans to decrease body fat while making sure we don’t lose strength and muscle. For people who are trying to lose fat and lose it fast, short-term stints with a low-carb plan might be the ticket that gets you to paradise.

Since adherence is usually the thing that separates champions from losers, you want to make sure you pick a plan, stick with it, and make modifications later when you are done. Low-carb adherence is no exception; sticking to it may not be any easier than sticking to a high-carb plan, though it may depending on your disposition towards food. If you are on a low-carb diet and want to increase your carbohydrates, whether it’s after a powerlifting competition or a photo shoot, then start by slowing adding 20g or so of carbs per day until you reach a level where your mood, performance, and body composition either stabilizes or improves.

Setting up an efficient plan:

  • Carbohydrates: 20-40% or 75-150g per day
  • Fat: 30-40% or 0.5g of your target bodyweight per day
  • Protein: 30-40% or 1.0g of your target bodyweight per day

Bottom line

Calories are your main priority. In a vast majority of the studies mentioned in this article, the researchers mentioned whether or not the diets were matched in calories. And in all of the studies matching calories but differing macronutrient composition, weight-loss was almost identical. If they were different, we are looking at 2-4 pound difference in a span of 12 weeks. Nothing to really split hairs about.

The shining light about low-carb plans is their ability to improve satiety, leading to possible better adherence to eating plans and moods. Lower-carb diets are also superior to high carb diets in terms of health improvements, especially in the short-term (6-12 months). Effects persist as long as people stay on the diet.

A low-carb plan cannot suit everyone’s needs and goals. Start with those numbers based off of the evidence and modify them to suit your lifestyle.

As always, your feedback is appreciated.

Live life strong,

David

REFERENCES

Hyun E, et al. Mechanisms behind the anti-inflammatory actions of insulinCrit Rev Immunol. 2011;31(4):307-40.

Acheson KJ, et al. Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. Am J Clin Nutr. 1988. 48:240-7.

Jensen J, et al. The role of skeletal muscle glycogen breakdown for regulation of insulin sensitivity by exercise.Front Physiol. 2011 Dec 30;2:112.
Shai I, et al. Weight loss with a Low-carbohydrate, Mediterranean, or Low-fat diet. N Engl J Med. 2008. 359:229-241.

Yancy WS Jr, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med. 2004 May 18;140(10):769-77.

Gow ML, et al. Impact of dietary macronutrient distribution on BMI and cardiometabolic outcomes in overweight and obese children and adolescents: a systematic review. Nutr Rev. 2014 Jul;72(7):453-70.

Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. JAMA. 2007 Mar 7;297(9):969-77.

Volek JS, et al.  Body composition and hormonal responses to a carbohydrate-restricted diet. Metabolism. 2002 Jul;51(7):864-70.
Volek J, et al. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body compositionin overweight men and womenNutr Metab (Lond). 2004 Nov 8;1(1):13.
Miyashita Y, et al. Beneficial effect of low carbohydrate in low calorie diets on visceral fat reduction in type 2 diabetic patients with obesity. Diabetes Res Clin Pract. 2004 Sep;65(3):235-41.

Sedlacek SM, et al. Effect of a low fat versus a low carbohydrate weight loss dietary intervention on biomarkers of long term survival in breast cancer patients (‘CHOICE’): study protocol. BMC Cancer. 2011 Jul 6;11:287.

Ho VW, et al. A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation. Cancer Res. 2011;71(13):4484-4493.

Rajaie S, et al. Comparative effects of carbohydrate versus fat restriction on serum levels of adipocytokines, markers of inflammation, and endothelial function among women with the metabolic syndrome: a randomized cross-over clinical trial. Ann Nutr Metab. 2013;63(1-2):159-67.

Mah E, et al. Postprandial hyperglycemia impairs vascular endothelial function in healthy men by inducing lipid peroxidation and increasing asymmetric dimethylarginine:arginine. J Nutr. 2011 Nov;141(11):1961-8.

Blouet C, et al. The Reduced Energy Intake of Fats Fed a High-Protein Low-Carbohydrate Diet Explains the Lower Fat Deposition, but Macronutrient Substitution Accounts for the Improved Glycemic Control. J Nutr. 2006;136:1849-1854.

Volek JS, et al. Comparison of a very low-carbohydrate and low-fat diet on fasting lipids, LDL subclasses, insulin resistance, and postprandial lipemic responses in overweight women. J Am Coll Nutr. 2004 Apr;23(2):177-84.

Kodama S, et al. Influence of fat and carbohydrate proportions on the metabolic profile in patients with type 2 diabetes: a meta-analysis. Diabetes Care. 2009 May;32(5):959-65.
Demol S, et al. Lowcarbohydrate (low & high-fat) versus high-carbohydrate low-fat diets in the treatment of obesity in adolescents. Acta Paediatr. 2009 Feb;98(2):346-51.
Chen YD, et al. Why do low-fat high-carbohydrate diets accentuate postprandial lipemia in patients with NIDDM? Diabetes Care. 1995 Jan;18(1):10-6.

Hu T, et al. Effects of low-carbohydrate diets versus low-fat diets on metabolic risk factors: a meta-analysis of randomized controlled clinical trials. Am J Epidemiol. 2012 Oct 1;176 Suppl 7:S44-54.

LeCheminant JD, et al. Comparison of a reduced carbohydrate and reduced fat diet for LDL, HDL, and VLDL subclasses during 9-months of weight maintenance subsequent to weight loss. Lipids Health Dis. 2010 Jun 1;9:54.

Sharman MJ, et al. Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men. J Nutr. 2004 Apr;134(4):880-5.

Guldbrand H, et al. In type 2 diabetes, randomisation to advice to follow a low-carbohydrate diet transiently improves glycaemic control compared with advice to follow a low-fat diet producing a similar weight loss. Diabetologia. 2012;55:2118-2127.

Jonasson L, et al. Advice to follow a low-carbohydrate diet has a favourable impact on low-grade inflammation in type 2 diabetes compared with advice to follow a low-fat diet. Annals of Medicine. 2014;1-6.

Llanos AA, et al. Favorable effects of low-fat and low-carbohydrate dietary patterns on serum leptin, but not adiponectin, among overweight and obese premenopausal women: a randomized trial. Springerplus. 2014 Apr 4;3:175.

Sherman WM, et al. Dietary carbohydrates, muscle glycogen, and exercise performance during 7 d of training. Am J Clin Nutr. 1993;57(1):27-31.

Wycherley TP, et al. Effects of energy-restricted high-protein, low-fat compared with standard-protein, low-fat diets: a meta-analysis of randomized controlled trials. Am J Clin Nutr. 2012 Dec;96(6):1281-98.

Bravata DM, et al. Efficacy and safety of low-carbohydrate diets: a systematic review. JAMA. 2003 Apr 9;289(14):1837-50.

Elliott S. Fructose, weight gain, and the insulin resistance syndrome. Am J Clin Nutr. 2002;76(5):911-922.

Rizkalla SW. Health implications of fructose consumption: a review of recent data. Nutrition & Metabolism. 2010;7:82.

Naude CE, et al.  Low carbohydrate versus isoenergetic balanced diets for reducing weight and cardiovascular risk: a systematic review and meta-analysis. PLoS One. 2014 Jul 9;9(7):e100652.

Costill DL. Carbohydrate for athletic training and performance. Bol Asoc Med P R. 1991 Aug;83(8):350-3.

American Dietetic Association, et al. American College of Sports Medicine position stand. Nutrition and athletic performance. Med Sci Sports Exerc. 2009 Mar;41(3):709-31.

Chassard C1, Lacroix CCarbohydrates and the human gut microbiotaCurr Opin Clin Nutr Metab Care. 2013 Jul;16(4):453-60.
Sonnenburg ED1, Sonnenburg JL2. Starving our Microbial Self: The Deleterious Consequences of a Diet Deficient in Microbiota-AccessibleCarbohydratesCell Metab. 2014 Aug 21. pii: S1550-4131(14)00311-8.
Mullur R, et al. Thyroid hormone regulation of metabolismPhysiol Rev. 2014 Apr;94(2):355-82. doi: 10.1152/physrev.00030.2013.
Danforth E Jr, Burger A. The role of thyroid hormones in the control of energy expenditure. Clin Endocrinol Metab. 1984 Nov;13(3):581-95.
Anderson KE, et al. Diet-hormone interactions: protein/carbohydrate ratio alters reciprocally the plasma levels of testosterone and cortisol and their respective binding globulins in man. Life Sci. 1987 May 4;40(18):1761-8.
Tegelman R, et al. Effects of a diet regimen on pituitary and steroid hormones in male ice hockey players. Int J Sports Med. 1992 Jul;13(5):424-30.

Meal timing: do you need to watch when you eat?

“They say I’ll get fat if I eat carbohydrates at night.”

“People say to eat oatmeal and fruits in the morning because they’ll give me more energy throughout the day.”

“You need to eat lots of carbohydrates during the day so you don’t lose muscle.”

Again, more conventional wisdom. But like most of the questions I address on here, it’s another contentious issue. Meal timing is one of those things that people feel intelligent talking about but rarely get right. Hell, I am not one to talk, but at least I know one thing:

Meal timing probably doesn’t really matter for a vast majority of people. What matters is how much you eat per day, what you put in your mouth, and whether you’re meeting macro- and micronutrient needs. If you’re not paying attention to these things, then don’t worry about when to eat carbohydrates and if you should avoid combining fats with carbs, yadda yadda yadda.

Now…

On the other hand, meal timing can be appropriate for some of you. If you fall within one of these categories below, you may benefit from a more detailed meal timing approach.

  1. You are a high level and elite athlete.
  2. You train more than once a day. This is fundamentally different than doing cardio in the morning and doing lifting in the evening, and is usually reserved for those wanting to compete in a sport.
  3. You are beyond the ‘general fitness’ recommendations and are looking for an edge. You have decent body composition and want to increase the pace at which you progress. For example, if you are below 15% bodyfat, you may benefit from a more detailed approach.

 

Just because there are 6 donuts don’t mean you get 6 meals. Source

My nutrition philosophy is a three-pronged. However, I am not trying to re-invent the wheel; merely sending the message through a different perspective and medium. Before we move into meal timing, let’s cover what the other two points of the triangle are:

  1. Clean up the quality of your food. Strive to make the best possible food choices by eating single ingredient foods most of the time.
  2. Eat for your activity levels. Frequency, type, and goals often determine diet composition. Endurance runners will not eat the same as general fitness folks.

What about those who are not elite but want to be better than average?

Let’s get one main thing straight. Dieting and eating should not be complicated. After all, you eat to survive (or to perform, your choice) so something instinctive and required should not be as complicated as rocket science. And even if you want to be above average, nutrition and meal timing still doesn’t have to be needlessly complicated. The key thing to keep in mind in regards to meal timing is that you want to make sure you time your meals appropriately in accordance with the length, time, and intensity of your activity.

This is the face of awesome. Source

 In order to be like a superhero, you must first get down the basics, which are figuring out what to eat and why to eat. To be average and not become a slouch like over 30% of Americans, focus on single ingredient foods and eat less junk. For example, eat more vegetables and non-bastardized meats and less soda. If you’ve never touched a weight in your life (I mean a real weight–not the 5 pound dumbbells that you use for your overhead presses), your conditioning sucks, and you’re one French fry away from breaking your scale, then these two changes will go pretty damn far. At this point, you don’t need to worry about meal timing.

If you workout like an average person, maybe do the treadmill 2 times a week and some weight lifting that wouldn’t make my grandmother sweat, you will probably eat anywhere between 75-150g of carbohydrates. That’s about it. But we are not here to be average.   I generally focus on two things for those looking to become better than average. Even for those at a higher level, these methods work well. These are not listed in priority.

  1. Meal timing
  2. Daily carbohydrate timing
  3. Peri-workout nutrition (future post)

Meal Timing

This is the most general of the three and probably makes the most sense if you really think about it. Let me pose a question to you: if you are on a diet of 1800 kcals, do you think eating 1800 kcals at one sitting will have the same effect on you as eating 1800 kcals spread over several meals? Don’t fail on me.   In terms of effects, the answer is no and I hope this is what you answered. Now, there are instances in which people can get away with eating 1800 kcals at one sitting (Ori Hofmekler’s The Warrior Diet), but I don’t see this as sustainable, and for hormonal purposes, not ideal.

This is Ori. Great shape for his age; but not everyone should eat like him. Source

In contrast to what I said above, a study just came out this year that showed two meals to be superior to six for type 2 diabetics. The difference wasn’t huge–2-3 pound difference, but it was significant enough. The two-meal-a-day group also experienced other beneficial health effects–lower fat mass, blood glucose, blood glucagon, and C-peptide (6). For some, two meals is a bit on a low side, but it is also the lowest I will go. Six meals, on the other hand, I feel is unnecessary, unless you are a competitive athlete and have inordinate caloric needs (north of 4000 kcals) and find it extremely difficult to fit in all of your calories in 3 or 4 meals.

Spreading out your meals provides a steadier stream of nutrients for your body, especially on a training day. As much as I advocate extending fasting, I am wholeheartedly against evening fasted training. There is never a time when you should fast for the whole day then go train. Ever.   That segues well into the next point.

Fasting

I am a huge proponent of short, daily intermittent fasting and have been for years. Fasting has been around for a very long time. Fasting is associated with cleansing both spiritually and physically (think religious and cultural practices, like Ramadan). Biochemically, though, fasting is linked to longer life, better brain function, and better lean mass retention in primates. Studies done in humans show that fasting and restricting carbohydrates intermittently throughout the week yield better insulin sensitivity and body fat loss than traditional caloric restriction in the short-term (1). Now, Ramadan is very similar to the Warrior Diet discussed above in that Muslims eat one time per day, in the evening, within a very small time frame. However, Ramadan happens once a year for a month, so Muslims are not really doing this type of fasting all year around. Not surprisingly, my clients who practice Ramadan drop anywhere from 8-15 pounds in a month.

Want to know something more fascinating? My Muslim clients who come back from fasting and resistance train along with a sensible diet see some of their best gains in strength, fat-loss, and muscle mass.

(This is called reverse dieting in the flexible dieting world, which I will discuss in the future).

Unlike normal fasting practices and those found in mainstream (cayenne pepper and lemonade diet? No thanks), I advocate shorter daily fasts. For most people, I lay out a plan of 12-16 hour fasts for 5 days and 16-18 hour fasts for 2 days. Meal composition should not really differ between the days; only the amount of calories. I will start talking about intermittent fasting (IF) in the future, since there is so much controversy surrounding it. (I will leave this piece about IF: I am about 8% bodyfat and my wife is about 15% bodyfat while on an IF plan, all while experiencing no negative side-effects. We have been IF’ing for about two years).

Avoid extended fasting on training days.

So my philosophy for meal timing is thus:

1. 2-5 meals per day, depending on your schedule.
2. Fast for 12-16 hours 5 days out of the week and 16-18 hours 2 days out of the week

Daily Carbohydrate Timing

The same way that eating manipulating calories throughout the day has different effects on the body, so does carbohydrate timing. I am always for unconventional wisdom, because frankly, conventional wisdom fails the person looking to become better miserably. You need something more than cereal, fruits, and a couple slices of deli meats. You need carbs (the right sources, obviously) and you need to time them right.   Now when it comes to carbohydrate timing, you want to eat the bulk of your carbohydrates in the evening.

Yes, you heard that right, in the evening.

 

IMG_0925

IMG_0926

 

An example of a lovely dinner. Pork belly, white rice, pickled radish, kimchi, red leaf lettuce… don’t forget the beer.

***I hope my bold statement up there was a bit liberating for you to know that you will not get fat if you eat carbs in the evening as long as you control for total calories. Remember that this is not a ticket to currently eat what you are eating and then add carbs at night. This is especially true if you got fat or getting fatter with the way you are eating right now.

Why in the evening? Well, the research is new and is just starting to come out, but it is promising nonetheless. Some studies show that participants on equal caloric diets but differing meal compositions experienced different results. Those who ate most of their carbohydrates in the evening lost more weight, body fat, retained more lean muscle mass, and decreased their waist circumference (2). The same author did another study that showed that a low-calorie diet with carbohydrates eaten at dinner time prevented mid-day hunger and improved hormonal profiles compared to a traditional low-calorie diet (3).

Unfortunately, Dos Equis is a terrible beer and you shouldn’t drink it, regardless of time of day. Source

 

What should you eat for breakfast?

What’s left, are the other two nutrients: protein and fats. I have especially found that a high-protein breakfast with a moderate amount of fat holds me over very nicely for several hours. Many of my clients feel the same way. And if you ever heard me recommend bacon and eggs for breakfast, it is for good reason.

One particular study showed that postmenopausal women who choose to avoid carbs in the morning have better control over their hunger (4). For those who want to lose weight, better hunger control equals better results (though I wouldn’t recommend eating bacon and eggs day-in and day-out–don’t forget the vegetables and quality starches). This study is certainly applicable as postmenopause is a condition that throws female sex hormones into disarray and makes losing weight, especially the belly fat, more difficult.

Another study showed that adding two eggs to breakfast 5 days a week for 14 weeks led to a reduction in daily carbohydrate intake, which can be beneficial if you are a controlled carbohydrate intake. The kicker to this mentioned study is that those who ate eggs experienced no adverse change to their blood lipids (7).

Training, of course, confounds how you should time carbohydrates. Research by Dr. John Ivy, author of Nutrient Timing, ushered in a whole new era of nutrient timing research in the early 2000’s, showing that carbohydrate consumption around exercise, especially post, was much more effective than consuming all of your carbohydrates in the meals before exercise (8). With this in mind, you would consume most of your carbohydrates after training. We will go more in-depth with carbohydrate timing in the future.

So my philosophy of carb timing is thus:

  1. Eat most of your carbs at night, preferably after training.
  2. If you train in the morning or day, then eat carbs after training.

Here is how I do it. Remember that my goal is to slowly gain some size while keeping body fat the same.

Example 

8AM: Wake
10AM, meal 1: 50g whey protein shake with a serving of kelp, 1 tbsp chia seeds, 1 tbsp maca root powder in 16oz unsweetened, plain almond milk, 1 tbsp fish oil, small handful of macadamia nuts
1PM, meal 2: 40g of protein through turkey bacon with handful of mix nuts; 5 soft-boiled eggs and 3 cups of broccoli florets in lemon juice, parsley, salt, pepper, and red pepper flakes
4PM, meal 3: 50g whey protein shake with 1 tbsp. fish oil, handful of carrots
7PM, meal 4: 7oz canned, bone-in salmon, lemon juice, chopped spinach, 1 cup of oatmeal , and all-purpose tomato sauce
10PM, meal 5: Half a rotisserie chicken with stone ground mustard, kimchi, 2 cups or white rice or 3 baked potatoes
12AM: sleep

Comments? Questions? Drop a line.

REFERENCES

1. Harvie M, et al. The effect of intermittent energy and carbohydrate restriction v. daily energy restriction on weight loss and metabolic disease risk markers in overweight women. Br J Nutr. 2013 Oct;110(8):1534-47.

2. Sofer S, et al. Greater weight loss and hormonal changes after 6 months diet with carbohydrates eaten mostly at dinner. Obesity, 2011 Apr 7.

3. Sofer S, et al. Changes in daily leptin, ghrelin and adiponectin profiles following a diet with carbohydrates eaten at dinner in obese subjects. Nutr Metab Cardiovasc Dis. 2013 Aug;23(8):744-50.

4. Acute Satiety Effects of Sausage/Egg-based Convenience Breakfast Meals in Premenopausal Women

5. Brennan IM, et al. Effects of fat, protein, and carbohydrate and protein load on appetite, plasma cholecystokinin, peptide YY, and ghrelin, and energy intake in lean and obese men. Am J Physiol Gastrointest Liver Physiol. 2012 Jul;303(1):G129-40.
6. Kahleova H, et al. Eating two larger meals a day (breakfast and lunch) is more effective than six smaller meals in a reduced-energy regimen for patients with type 2 diabetes: a randomised crossover study.Diabetologia. 2014 Aug;57(8):1552-60.

7. Rueda JMKhosla P1.Impact of breakfasts (with or without eggs) on body weight regulation and blood lipids in university students over a 14-week semester. Nutrients. 2013 Dec 16;5(12):5097-113.
8. Ivy JL. Regulation of muscle glycogen repletion, muscle protein synthesis and repair following exercise. J Sports Sci Med. 2004 Sep 1;3(3):131-8.

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?

Nope.

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

Wrap-up

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,

David

 

REFERENCES

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. 

Salt.

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?”

Source

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.

Wrap-up

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,

David

 

REFERENCES

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.

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