Calories and Energy Balance: How Weight Loss (or Gain) Occurs (Pt. 1)

Image result for balancing act


Having thoroughly covered the difference between weight loss and fat loss and the importance of body composition, I would now like to build upon our discussion and talk about calories and energy balance given that these two topics are 1) widely misinterpreted, and 2) intimately involved in driving changes in body weight/composition—contrary to what some try to argue. Indeed, it is not hard to find claims that calories do not matter when it comes to weight gain or weight loss (and that other things such as hormones or just one single hormone is all that matters). This, however, is simply not an honest interpretation of the literature as will become evident shortly.

Because this is such a hefty topic, I will split it up into two parts (possibly three if needed). In Part 1 (today) I will cover the topic of energy and calories and begin to explain energy balance, at least from the energy intake side of the equation. In Part 2 I will explicitly cover energy expenditure and how measure it, as well as how the energy balance equation changes in response to a variety of conditions (e.g. meal frequency, macronutrient composition, overfeeding and underfeeding) and the implication of such changes—it is here that I may need to break it up into three parts. (TBD!)

The main point in all of this is that calories do matter, energy balance is a thing, and all of it is more complicated than you realized or heard from some Instagram influencer.    

Let us begin with the basics.


Energy is simply the capacity to do something—i.e. work. In your body, that means keeping you alive by maintaining ion gradients, building new macromolecules, allowing for locomotion, and so on and so forth. Should you stop doing any of this, you will die. (The fancy term is thermodynamic equilibrium.) Since energy cannot be created out of thin air, you need to obtain it (i.e. transfer it) from some other source—that source being food. Simply put, food contains energy, so we put that food in our mouths and chemically digest it so that we can transfer the energy it contains (within its molecules) into the bonds of ATP (the universal cellular energy currency) that our cells constantly make that allows us to do work and stay alive.

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Is the Carbohydrate-Insulin Model of obesity over?


Obesity is ultimately the result of excessive body fat accumulation. Given the explosion of obesity rates around the globe, understanding how people become obese has been the center of much scientific investigation. The consensus model that informs most attempts to prevent and treat obesity has to do with energy balance and the mismatch between caloric intake and expenditure [1]. As such, the overconsumption of highly palatable foods coupled with reduced physical activity (termed the ‘obesogenic environment’) leads to increased adiposity and poor health. Despite the wide acceptance of this model (often termed calories in, calories out or CICO), in recent years, a new model of obesity has taken the nutrition research field by storm. This model also aims to explain the obesity epidemic given the lack of successful dietary preventatives and treatments for obesity based on the conventional model. The new model is termed the carbohydrate-insulin model (CIM) of obesity [2]. It posits that dietary carbohydrate, not energy balance, is the primary culprit. The guilt lay in carbohydrate’s ability to robustly increase insulin levels, thereby promoting fat storage and accumulation. This scenario, in turn, promotes increased dietary intake and further weight gain (see image comparing the models below).  

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Weight loss versus fat loss: important difference or pedantic point?


Weight loss, fat loss, who cares? They are essentially the same thing…right? While it might seem pedantic at first, the difference between the two terms is quite important, despite the fact that most people (myself included) tend to use the terms interchangeably—we most likely mean fat loss. If this does not make immediate sense, fear not! My plan today is to illuminate why the idea of weight loss, by itself, is not the entire story, and that fat loss is arguably the more important metric by which we should judge a “weight loss” diet. In doing so, I also aim to show you what the body is comprised of (i.e. body composition); a handful of different ways we can measure it; and, somewhat counterintuitively, why weight by itself actually is an important metric and how you can use it intelligently to achieve your dieting goals. What will become evident, as will be the case in most if not all of my posts, is that things are a little more complicated than they appear.    

First: a simple example

To begin to illustrate a point in the simplest way possible, envision the following scenario: You wake up in the morning, minimal clothing, stumble to the bathroom and weigh yourself on your scale. Let’s just say you weigh 150 lbs. (A weight chosen to equally offend everyone.) You then proceed to “decaffeinate” (as my former PhD advisor would say), as well as take part in the process of egestion. (You guessed it, the exact opposite of ingestion.) You then weigh yourself again: 147.5 lbs. Within minutes no less! Now, obviously you didn’t lose 2.5 lbs. of body fat. If only it were that easy…  

What we just illustrated in that ever-so-relatable example is the concept of body weight and the beginnings of the fact that your body’s weight is made up of more things than just fat. Which brings us to the concept of body composition.   

Body composition: what you are (quite literally) made of 

The absolute “Gold Standard” for evaluating body composition is, well…dissection. Obviously, this is not practical for evaluating the composition of the body in living people, but historically, these types of analyses have been done, and the body compartments have been categorized and inventoried.   

From the most superficial level of analysis, we can categorize your body into two compartments: fat and then everything else. This is literally called a two-compartment model, and many of the techniques used to estimate body composition in living humans are based on this fundamental concept [1].  

Thus, you are made up of fat mass (FM) and everything that is, by definition, not. Everything that is not fat is lumped together and termed fat-free mass (FFM). (How clever.) I should note that you will often hear people use the term lean body mass (LBM) interchangeably with FFM. For the purposes of this piece, I will consider the two equivalent, although, technically, they are not. (We have our pedantic plates full enough as it is!)

To place the two-compartment model in mathematical terms, your total body weight (TBW) is as follows:


Simple enough. Well, sort of. In reality, the FFM portion can be delineated even further into everything that it is comprised of—i.e. body protein that makes up skeletal muscle and your organs; minerals that make up your bone; glycogen (the storage form of carbohydrate); and, as already illuminated at the beginning of this piece, body water. Additionally you have weight that comes from residual, undigested food in the GI tract (i.e. feces), but this is not a part of your body, per se. Thus, our simple two-compartment model can be expanded to incorporate more compartments that are better defined:

TBW = Fat + Protein + Bone + Water + Glycogen

And there you have it, a full breakdown of all the components of your body that contribute your body’s weight. For the average “Reference Man” this amounts to ~15% body fat, ~45% muscle mass, ~15% bone, and ~25% other (i.e. water and glycogen for the most part); and for the average “Reference Woman”, body composition amounts to roughly ~27% body fat, ~36% muscle, ~12% bone, and ~25% other [2]. Obviously, there is wide variation in these averages, but men tend to be bigger and have more lean tissue whereas women are on average smaller and have proportionally more fat tissue.   

Returning to our initial distinction between weight loss and fat loss, it now it obvious that a simple weight change on the scale can indicate a change in any one of these body compartments. Clearly, when people engage in a weight loss diet, their goal isn’t to lose body water—and certainly not muscle mass, organ weight or bone mineral density, despite all compartments decreasing during an energy deficit. Rather, the goal is, implicitly, to lose body fat. That is what people want.   

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Can excess protein get stored as body fat? Pt. 3



Today I (briefly) bring you yet another study looking at the effects of higher protein intakes on body composition. And by higher intakes, I mean consuming protein at levels >3g/kg of bodyweight (1.3g/lb for those not metrically inclined). By most nutrition recommendations this FAR surpasses the requirements of virtually all individuals, be they sedentary (0.8g/kg) or highly trained (~1.7g/kg on average).

If you haven’t yet read my previous articles on the topic, you can read them here and here.

Today’s article is a follow up study to Antonio et al.’s 2014 paper [1] that looked at the effect of high protein intakes (~4.4g/kg), in conjunction with the subject’s normal resistance training routine (RT), on changes in body composition (i.e. fat mass [FM] and fat free mass [FFM]). What they found was that there were virtually no changes in either FM or FFM when consuming a high protein diet (4.4g/kg) for up to 8 weeks, again supporting the contention that excess protein is not converted to fat and stored as such in the human body. However, what Antonio and colleagues failed to do was prescribe an appropriate RT protocol that was standardized and assigned to each participant that ensured progressive overload; in other words constantly increasing the weight lifted and volume performed over the course of the 8-week study-period.

Enter today’s study: Antonio et al. 2014; A high protein diet (3.4g/kg) combined with a heavy resistance training program improves body composition in healthy trained men and women – a follow up investigation [2].


First the pros of this most recent paper:

  1. It addresses the dearth of research on high protein diets (>3g/kg or 1.36g/lb) in conjunction with a standardized, periodized resistance training program
  1. It uses already resistance-trained subjects (males and females), which eliminates any unusual gains that are typically seen in those who have never or rarely exercised before
  1. Randomization of subjects (ensures both groups are identical [in theory] from the start)
  1. BodPod for body composition (Siri equation; appropriate for study pop.)
  1. Again, training protocol (5 days/week for 8weeks)

– Adequate volume, intensity and frequency of movements (each body part                1-2x per week)

– Periodized (progressively increased weight lifted and volume performed)


Like all research there are methodological drawbacks:

  1. Tenuous control of dietary intakes (MyFitnessPal) that brings into question actual amounts of overall protein and calories consumed
  1. 34% dropout rate (very high)
  1. Average years spent training (5 years in HP group vs. 2.5 years in NP)
  2. No control for hydration status during BodPod measurements; however, hydration status less influential for BodPod measurements than DEXA


In brief:

  1. Both groups gained 1.5kg FFM (on average; some wide variations between individuals).
  1. HP lost more BF (1.6 vs. 0.3kg) despite eating more kcals overall (~400kcals) than NP and being slightly leaner at the beginning of the study

– could potentially be explained by increases in NEAT and TEF in HP

group as protein is more thermogenic

– could be due to lack of accurate dietary recall/recordings

– better compliance of HP with RT protocol than NP group

  1. Both groups gained strength with progressive overload
  1. Blood work was normal for both groups, no adverse effects (for more on the safety of high protein diets see an article I’ve written here)


Protein intakes well above (i.e. 2-4x) RDA (0.8g/kg), in conjunction with periodized RT program that provides systematic progressive overload, can produce significant improvements in body composition (i.e. increase FFM, decrease FM and increase strength/performance). Moreover, and to the point of this article series, extra protein does not get stored as body fat. This is just another study refuting the idea that extra protein over the supposed RDA is converted to fat. While the pathways to convert amino acids to fatty acids DO EXIST, they are virtually irrelevant even in the face of excessively high protein intakes (like the ones seen in this study), especially when combined with a well-designed RT program meant to increase strength and muscle mass. Finally, it could be argued that protein intakes as high as, or even greater than, 3g/kg will not confer any additional benefits over ~2g/kg, as this was the intake seen in the NP group that saw near identical increases in FFM and strength. Thus, high protein diets ~2g/kg or higher can be a safe and valuable part of a structured RT program meant to increase muscle size and strength.


  1. Antonio J, Peacock CA, Ellerbroek A, Fromhoff B, Silver T: The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals. J Int Soc Sports Nutr 2014, 11:19.
  2. Antonio J, Ellerbroek A, Silver T, Orris S, Scheiner M, Gonzalez A, Peacock C: A high protein diet (3.4g/kg/d) combined with a heavy resistance training program improves body composition in healthy trained men and women – a follow-up investigation. Journal of the International Society of Sports Nutrition 2015, 12:39.


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Why weight loss diets work and fail: understanding the energy balance equation



Today I want to talk about weight loss: more specifically, how someone loses weight. Given the recent congressional hearings regarding Dr. Oz and his outrageous weight loss claims – not to mention the myriad other diets and diet books out there claiming miracle-like results – I find that a lesson in the basics of weight loss is in order. And while I hate to be the bearer of bad news, it’s not the carbohydrates, or the high-fructose corn syrup, or animal products, or post-agricultural foods that are making you or anyone else overweight and/or obese. It’s simply too many calories. Similarly, it’s not the elimination of these foods, per se, that promotes weight loss. Rather, it’s a reduction in calories overall (be it through arbitrary dietary avoidances or what have you) that is the final arbiter of how many pounds you lose. End of story.

The premise for this, dare I say it, controversial claim stems from a firm understanding of the energy balance equation and how it operates. Unfortunately, numerous diet gurus have tried to persuade the public (for obvious financial reasons) that calories don’t matter and that the energy balance equation is a farce. Well, I am here to tell you that calories absolutely do matter and that any effective weight loss diet must obey the energy balance equation. Any efforts to circumvent or disregard the energy balance equation will wind up being useless and any hopes at losing those excess pounds will be lost. However, the energy balance equation, otherwise known as ‘calories in and calories out’ it a little more complex than what most believe. Leaving the psychological aspects for another day, today we will take a look at the energy balance equation to see how it operates and where most misunderstandings arise. Moreover, we will apply this knowledge towards seeing why most diets (take your pick), do in fact work (to some limited degree) yet tend to fail over the long-term.

By the end, I hope it becomes clear that whatever weight loss diet you choose to undertake (given that it suits your goals, needs and preferences), the reason that it works is not because of some arbitrary dietary avoidance(s) (or inclusions) but rather through good old caloric restriction.

So without further ado, let’s begin!

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Can excess protein get stored as bodyfat? Pt. 2

ScaleIntroduction & background

Today’s post will be short and sweet.

Previously I covered the topic of excess protein being converted to fatty acids and contributing to fat gain (found here, here and here; this was a rather popular one). In those articles, I concluded by saying that while the metabolic pathways to convert amino acids to fatty acids do indeed exist in humans, the fact of the matter is that the frequency and relevance of such pathways are basically nil. Simply put, protein being converted to and stored as fat doesn’t happen to any appreciable extent in people consuming moderately more protein, even during a caloric surplus. Only until theoretical extremes (both in terms of calories and protein intakes) are reached, for weeks on end (>8 weeks), will you (potentially) see any significant effect of excess protein intakes on fat gain. Yea, a lot of ‘ifs’ and ‘maybes’ in that sentence.

In support of this notion, I looked at a well-controlled study (and I mean well-controlled!) [1] which saw no further increases in fat mass in subjects consuming 140% of their caloric needs alongside higher protein diets (15% or 25%) for 8 weeks compared to individuals consuming similar caloric intakes (i.e. 140% over caloric needs) with lower percentages of calories from protein (5%). Despite being a tightly-controlled metabolic ward study wherein participant’s activity and food intakes (amongst a whole other array of factors) could be monitored, what this study failed to do was look at the effects of a hypercaloric, high-protein diet(s) on bodyweight/composition in conjunction with a structured resistance training program in highly trained individuals; which brings me to today’s study.

Antonio et al. 2014

In this investigation, Antonio et al. [2] took a group of well-trained individuals (almost a decade’s worth of weight-training under their belts; no newbie gains here!) and randomized them to either their normal diet, lower in protein (control; average intake ~1.9g/kg/d or ~150g/d) or their normal diet, higher in protein (HP; 4.4g/kg/d or ~307g/d; achieved via protein supplementation) for 8 weeks. Both groups also maintained their usual training routines/volumes which were not significantly different from each other throughout the study period.

Body composition was measured via BodPod (much better than BIA but not as accurate as DEXA) and food/protein intakes were measured via food diaries (either hard copy or by using the MyFitnessPal© app). Training was also recorded (sets, reps, weight used) throughout the study period. So what did the investigators find?

Results & conclusions

They found that, despite increasing their caloric intakes by ~800kcals/d compared to the control group which actually decreased their caloric intake over the study period, and consuming protein intakes that were 5 times higher than the current RDA (0.8g/kg) and >2 times higher than the control group’s intake (~1.8g/kg), there was no significant difference in body composition between baseline and post-intervention time points, nor were the two groups significantly different in any other respect (Table 2 below; taken from Antonio et al. [2]).

Antonio et al. Table 2In reality, the high-protein group actually increased their lean body mass while slightly decreasing their fat mass (control groups increased both), although to non-significant degrees. In line with the Bray et al. [1] study that I talked about previously (pick your link), it does not appear that high/excessive intakes of protein result in significant fat gain compared to lower, more realistic intakes (in this case, realistic for active, weight-trained individuals, i.e. ~2.0g/kg/d). I should note, however, that the Bray et al. study and the current study do differ in methodology (metabolic ward vs free-living, respectively) and study populations (middle-aged, healthy but sedentary individuals vs. highly-trained individuals, respectively). Nonetheless, the theme remains the same; excess protein under most conditions, even those where protein consumption is increased beyond the theoretical performance benefits while in the face of a mild caloric surplus, does not lead to excess body fat storage/gain. So, while we do possess the metabolic pathways to convert protein to fatty acids, again, this just doesn’t happen in real life situations.

Until next time!


  1. Bray GA, Smith SR, de Jonge L, Xie H, Rood J, Martin CK, Most M, Brock C, Mancuso S, Redman LM: Effect of dietary protein content on weight gain, energy expenditure, and body composition during overeating: a randomized controlled trial. JAMA 2012, 307:47-55.
  2. Antonio J, Peacock C, Ellerbroek A, Fromhoff B, Silver T: The effects of consuming a high protein diet (4.4g/kg/d) on body composition in resistance-trained individuals. JISSN 2014, 11.


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Protein: is it really as bad as they say it is?

red-meat-danger-300x300Introduction & background

Early last March a provocative study published by Levine et al. [1] in the prestigious Cell Metabolism has really shaken up the nutritional science world ever since one of the authors of the study suggested that eating a diet higher in protein is potentially more harmful than smoking cigarettes. Talk about rustling some jimmies!

Now, before we go any farther, let’s keep one thing in mind: this was not a randomized controlled trial wherein participants were randomly assigned to either high or low protein groups and followed for a period of time at which point various health outcomes could be tallied and assessed. No, instead this study was part epidemiological and part rodent research, each of which has their own serious limitations when extrapolating to health policy and human physiology. That being said, Levine et al. reported that in people aged 50-years and over, moderate and high protein intakes were associated with increased type 2 diabetes mortality, but not cardiovascular disease (CVD), cancer, or all-cause mortality. However, when the study population was split into persons aged 50-65 and those 66 and over, high and moderate protein intakes were associated with increased mortality from cancer and all-causes in the 50-65 age group, but not the latter. In addition, when animal protein was accounted for, the harmful associations between protein intake and mortality risks disappeared, suggesting that animal proteins, and not plant-based proteins, are potentially harmful at higher intakes during middle-age. With respect to those over 65, it appears that higher protein intake had a protective effect and was not associated with increased disease mortality risk, save type 2 diabetes. But wait, there’s more!

In subsequent analysis the investigators looked at insulin-like growth factor-1 (IGF-1) and its association with protein intake and mortality risks. In recent years insulin and IGF-1 have been suggested to contribute to the pathogenesis of cancer, due to their similar intracellular signaling pathways and downstream effects on various targets that favor cell survival rather than death [2]. Therefore, cells which should probably die are instead salvaged and are at an increased likelihood of becoming cancerous through various metabolic “reprogramming” mechanisms. This has prompted a recent interest in examining the potential therapeutic effects of low-carbohydrate and/or ketogenic diets in treating cancer due to their ability to drastically reduce serum levels of glucose and insulin [3] – two factors that are predictive of future cancer risk and cancer-related mortality [4-6]. The current study, however, chose to focus only on protein and IGF-1. So, what did the researchers find?

They found that IGF-1 levels were positively associated with protein intakes and that for every 10ng/mL increase in IGF-1 for those ages 50-65, mortality risk of cancer increased by about 9%. No association was observed in those over 65. But that’s not all!

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Can excess protein be stored as body fat?



It’s not uncommon to hear claims that dietary protein eaten in excess of some arbitrary number will be stored as body fat. Even those who are supposed to be reputable sources for nutrition information propagate this dogma. These claims however tend to drastically ignore context. While paging through one of my old nutrition textbooks, I came across a section in the protein chapter regarding amino acids and energy metabolism [1]. To quote the book directly:

“[E]ating extra protein during times of glucose and energy sufficiency generally contributes to more fat storage, not muscle growth. This is because, during times of glucose and energy excess, your body redirects the flow of amino acids away from gluconeogenesis and ATP-producing pathways and instead converts them to lipids […] The resulting lipids can subsequently be stored as body fat for later use.”

(pg. 198)

This is, more or less, supported by another textbook I own [2]:

“In times of excess energy and protein intakes coupled with adequate carbohydrate intake, the carbon skeleton of amino acids may be used to synthesize fatty acids.”

(pg. 213)

While these passages do take into account the metabolic state of the person, I still find these explanations (the first one especially) to be lacking, even borderline misleading. Indeed, more recent evidence is needed when talking about amino acid conversion to fatty acids and subsequent body fat storage. While the metabolic pathways to convert amino acids to fatty acids do in fact exist, the reality of the matter is that under almost no circumstance will this ever happen. In all honesty, I have yet to actually find a convincing scientific example where this happens. So, without much further ado, what is to follow is the long explanation as to why you shouldn’t worry about protein getting stored as body fat.

Protein digestion begins in the stomach and ends in the small intestine

While the physical breakdown of proteins does take place in the mouth, it’s not until the protein reaches the stomach that appreciable chemical breakdown occurs; this is facilitated by hydrochloric acid (HCl) and the enzyme pepsin (converted from its inactive form, pepsinogen). Once the initial protein denaturing and peptide cleaving is complete, the product polypeptides pass through the pyloric sphincter of the stomach and into the proximal small intestine.

The proximal small intestine (the duodenum to be exact) is where most of the digestion of proteins and virtually all of the absorption of amino acids occurs (a very small amount do get excreted in the feces). Here even more digestive enzymes are present to break down the remaining polypeptides into their individual amino acids along with some trace amounts of di- and tri-peptides. Once broken down completely, the free amino acids and di-/tri-peptides can then enter the cells of the small intestine where some (especially glutamine) are used for energy within the intestinal cells, with the remaining passing through into hepatic portal circulation. Those that do pass into circulation are destined for the liver.

Protein absorption claims

Before we head on over to the liver and discuss amino acid metabolism with regards to the initial claims, I would first like to touch upon another related (or variant) claim that some of you may have heard in the lay media or from an uneducated classmate, etc. It usually reads:

“The average person can only absorb 30 grams of protein at one sitting. Anything above that will be stored as fat.”

Unlike the claims in the introduction, this one offers no context whatsoever. Moreover, it’s downright moronic. And while this sounds like straw man argument readily poised for the takedown, I actually got this gem of wisdom from an online article written by a Registered Dietitian. Believe me; I couldn’t make this crap up if I wanted to (note: this is not to slander the RD profession, this is just an example which happened to involve someone who should know better).

For instance, let’s take someone who eats, dare I say it, 40 grams of protein in one sitting. If we are to assume only 30g are absorbed at a time, then it’s safe to say that the extra 10g will be excreted in the feces. If this were the case, most people would be egesting tiny sirloin steaks on a daily basis. Nevertheless, based on the initial argument, how are you supposed to store 10g of excess protein as body fat if you can’t even (allegedly) absorb it in the first place? Most people (who I can understand don’t have an advanced degree in nutrition) don’t realize the difference between utilization and absorption and make this fundamental error. I’m not quite sure what this woman’s excuse is, because in order to store or metabolize a nutrient (i.e. utilize it), it must first be absorbed into the body.

The bottom line is that your GI tract will take its sweet time absorbing protein, no matter the amount. Thirty grams is just an arbitrary number that has no roots in scientific evidence. For a more complete and in-depth review of this topic, I suggest reading a rather recent article by my friend and colleague, Alan Aragon.

At this point let us circle back to the initial claim, that excess protein, which has already been absorbed, during times of adequate energy and carbohydrate intake, is converted to fatty acids and stored as body fat.

Liver, the primary site for amino acid metabolism

As we’ve already covered, the amino acids released from the small intestine are destined for the liver. Over half of all the amino acids ingested (in the form of protein) are bound for and taken up by the liver. The liver acts almost as a monitor for absorbed amino acids and adjusts their metabolism (breakdown, synthesis, catabolism, anabolism etc.) according to the body’s metabolic state and needs [2]. It is here the initial claim comes into play. While the pathways for fatty acid synthesis from amino acids do exist, no argument there, the statement that all excess protein, under specified conditions, will be stored as fat ignores recent evidence.

[Enter one of the most tightly controlled studies of our time]

Bray GA, et al. 2012

In 2012, George A. Bray and colleagues [3] sought to examine whether the level of dietary protein affected body composition, weight gain, and/or energy expenditure in subjects randomized to one of three hypercaloric diets: low protein (5%), normal protein (15%), or high protein (25%). Once randomized, subjects were admitted to a metabolic ward and were force fed 140% (+1,000kcals/day) of their maintenance calorie needs for 8 weeks straight. Protein intakes averaged ~47g (0.68g/kg) for the low protein group and 140g (1.79g/kg) and 230g (3.0g/kg) for the normal and high protein groups, respectively.  Carbohydrate was kept constant between groups (41-42%), with dietary fat ranging from 33% in the high protein group to 44% and 52% in the normal and low protein groups, respectively. Lastly, during the course of the 8-week overfeeding period, subjects’ body composition was measured bi-weekly using dual x-ray absorptiometry (DXA; i.e. the “Gold Standard” for measuring body composition).


At the end of the study, all subjects gained weight with near identical increases in body fat between the three groups (in actuality, the higher protein groups actually gained slightly less body fat than the lower protein group, however, this wasn’t significant). The group eating the low protein diet gained the least amount of weight (3.16 kg) with the normal and high protein groups gaining about twice as much weight (6.05 and 6.51 kg, respectively). See the chart below.

Bray Phillips Overfeeding ChartHowever, as you can see, the additional ~3 kg of body weight gained in the higher protein groups (15% and 25%) was due to an increase in lean body mass and not body fat. To quote the conclusions of the authors:

“Calories alone […] contributed to the increase in body fat. In contrast, protein contributed to changes in […] lean body mass, but not to the increase in body fat.”

While we can’t say for sure the exact composition of the lean mass that was gained, we can assuredly say that the extra protein was not primarily used for fat storage. My hunch is that the protein was predominantly converted to glucose (via gluconeogenesis) and stored subsequently as glycogen with the accompanying water weight. Either way, it wasn’t body fat.


So before we continue, let’s just take a second for this sink in. These subjects were literally forced to eat ~1,000kcals more than what they needed to maintain their body weight for 8 full weeks (not an easy task for even the strong willed) and even then it was seen that the protein contributed to increases in lean body mass rather than body fat. Given the initial claim – that once energy, glucose and protein requirements are met all excess amino acids will get converted to fatty acids and stored as body fat – I find it hard to argue that those in the higher protein groups did not meet any of the aforementioned requisites. In reality, they far and away surpassed them, yet still did not gain additional body fat compared to the lower protein group. This is in stark contrast to what is traditionally thought.

In the end, however, we’re still left with the quintessential question underlying the entire concept, and that is: what is the maximal amount of protein (amino acids) that the body can effectively utilize before being converted to fatty acids and stored as body fat? Given the results of this study it appears that; this number is either way higher than three times the current RDA with concomitant hypercaloric intakes for weeks on end, or; it requires a similar overfeeding protocol drawn out over a longer period of time (i.e. greater than 8 weeks) at which point lean mass gains would most likely plateau and fat mass would accrue. Either way, both situations are highly unlikely in the general public and even those consciously trying to gain weight with higher intakes of protein and calories. Moreover, this upper extreme is likely to be highly individual and contingent upon other factors such as genetics, lifestyle, training status (if an athlete), etc. Unfortunately, we just don’t have the answers to these questions right now.


So, while we do biochemically possess the pathways needed to convert amino acids to fatty acids, the chances of that ever happening to a significant degree during higher protein intakes, even in the face of adequate energy and carbohydrates, are irrelevant given what we know about the extreme measures that need to be surpassed in order for any appreciable fat gain from protein to take place.

Indeed, overeating by ~1,000kcals/day for 8 weeks in combination with higher protein intakes did not amount to any additional gains in body fat compared to a lower protein, hypercaloric diet. Rather, excess protein in the face of overfeeding actually contributed to gains in lean body mass (be that what it may); quite the contrary to what textbooks and classrooms teach. In reality, the chances that excess protein contributes to body fat stores are insignificant, and arguably physically impossible under normal and/or reasonable hypercaloric conditions that most people/athletes might face on a daily basis. Only until theoretical extremes, either for protein intakes or calories or both are achieved, will there be any significant contributions to body fat from excess protein intake. This shouldn’t concern most people in the slightest.


1.            McGuire M, Beerman, KA.: Nutritional Sciences: From Fundamentals to Food. 2nd edn. Belmont, CA.: Wadsworth Cengage Learning; 2011.

2.            Gropper S, Smith, JL., Groff, JL.: Advanced Nutrition and Human Metabolism. 5th edn. Belmont, CA.: Wadsworth Cengage Learning; 2009.

3.            Bray GA, Smith SR, de Jonge L, Xie H, Rood J, Martin CK, Most M, Brock C, Mancuso S, Redman LM: Effect of dietary protein content on weight gain, energy expenditure, and body composition during overeating: a randomized controlled trial. JAMA 2012, 307:47-55.

Posted in Diets, Protein, Reviews | Tagged , | 18 Comments

Red meat: back on the chopping block



In a recent article published last week in the prestigious Nature Medicine journal [1], researchers presented novel data on the pathogenesis of cardiovascular disease (CVD), arguing that it’s not the saturated fat (SFA) or cholesterol in your red meat that’s causing your arteries to clog; rather, it’s the carnitine. What’s more is that the media just can’t get enough of it. Indeed, both the New York Times and the Wall Street Journal (just to name a few) jumped on this story and put out articles with quotations from experts warning people against red meat consumption. While this type of alarmism is nothing new, especially with regards to red meat (remember last summer when red meat would just flat out kill you?), this new article is extremely interesting and does offer up a novel explanation for (part of) why red meat is constantly being associated with cardiovascular disease (CVD).

Nevertheless, in spite of the originality of this new paper and its potential implications for future health policy, we should remain critical of the paper’s content and not take giant leaps of faith in accepting new research findings as dogmatic fact (I’m looking at you vegans and vegetarians). Therefore, today’s goal is show you why you should not fear red meat, because it can, like all others foods, fit easily into anyone’s diet and impart beneficial effects on health: even heart-health!

Prevailing paradigm

It’s no news that the prevailing notion about red meat has been that its accompanying SFA and cholesterol are the primary driving forces behind the food’s association with CVD [2-5]. However, a recent meta-analysis refutes this assumption after showing no association between SFA and CVD [6]. While investigation into several other potential disease-causing mediators that commonly accompany red meat, such as salt [7] and heterocyclic compounds (you know, the char on your meat that gives it that “grill taste” you enjoy so much) [8] are proving to be less fruitful in the red meat-CVD debate – albeit salt is generating some interesting data with regards to autoimmune disease progression [9, 10] – today’s article looked at something no one had ever really considered before: carnitine.

Primer on carnitine

In order to save time, I have copied and pasted the following paragraph on carnitine from a previous article wherein I evaluated carnitine’s (null) effects on fat loss and performance. For those interested, you can see the full article here:

“Carnitine – named after the Latin word carnis, meaning ‘flesh’ – is a vitamin-like, water-soluble amine that can be obtained through dietary intake (for example: meat and milk) or by endogenous synthesis via S-adenosyl-methionine (SAM) and lysine in both the liver and kidneys. Almost all (~95-98%) of the bodily stores of carnitine are present in skeletal muscle and in the heart (with the remaining 2-5% in the liver, kidneys and plasma). Carnitine plays a pivotal role in both fat metabolism as well as carbohydrate metabolism […] Throughout most of the day (assuming you don’t sprint everywhere) the human body runs on a mixture of glucose, amino acids, and free fatty acids, with the majority of ATP coming from FFAs. However, in order to oxidize these FFAs (and yield energy in the form of ATP) each fatty acid must undergo a process called beta-oxidation. Beta-oxidation takes place within the matrix of the mitochondria of the cell. In order for the fatty acid to even make it into the matrix, it must rely on the help of carnitine to facilitate its transport in. Once inside, the fatty acids can undergo beta-oxidation and proceed to the Tricarboxylic acid (TCA) cycle and produce ATP.”

Furthermore, carnitine and its derivatives have shown huge promise in various pathological conditions, some of which happen to be to cardiovascular and heart disease [11-14]. While this may seem counterintuitive – even contradictory – to the published Nature Medicine article which argues that carnitine causes CVD, one has to remember that the physiology/biochemistry during a pathological condition is very different from that of a relatively healthy person. Indeed, the benefits of carnitine supplementation for certain cardiovascular and heart pathologies are due to the reduction in heart carnitine levels caused by the condition itself (usually the lack of oxygen to the heart, called ischemia) [13]. Therefore, it would not be wise to say that carnitine is contraindicated for those with heart disease because, in fact, supplementation with carnitine actually improves health under certain cardiovascular conditions. Like all things, nothing is ever black and white. So before I start getting ahead of myself, let’s actually examine the Nature article and see why carnitine might lead, or even (dare I say it) cause, cardiovascular and heart disease.

Biological rationale for carnitine’s role in CVD pathogenesis

The authors, in an attempt to unveil some earth-shattering mechanism for why red meat might be causing CVD, suggest that there could possibly be some type of microbe-dependent, diet-host mechanism that had previously been unexplored. In other words, perhaps the bacteria in our intestines are somehow contributing to CVD. Recent evidence in both human and animal models suggests a role for such a mechanism in a whole host of diseases, such as obesity [15-17] and type II diabetes [18]. Therefore, the idea for a similar rationale in CVD is not so farfetched.

In preliminary research, the authors identified a group of metabolites that were associated with CVD risk [19], wherein, upon further analysis, they found that the metabolite known as trimethylamine N-oxide (TMAO for short) was the primary candidate. Furthermore, the researchers also discovered that this metabolite happens to be a product of gut-dependent-choline metabolism, providing further evidence for a microbial role in CVD progression.

So how does carnitine fit into the picture? Well, carnitine is similar in structure to choline (they’re both trimethylamines) and therefore undergoes the same metabolism as choline (see figure below).

CVD pathogenesis

This in turn produces TMAO and increases plasma levels which could lead to CVD. While carnitine is present in other foods such as fish (a food commonly associated with improving CVD risk [20, 21]), the levels of carnitine are about 10-12 times higher in red meat [22]; potentially letting fish off the proverbial hook, so to speak. However, as it turns out, some types of fish are actually fairly high in TMAO [23]; lending less credence to the notion that only red meat (and not other forms of meat like fish) possibly leads to CVD.

Article findings

To keep things simple (because this article was a beast and I don’t feel like getting into every little methodological detail), I’m going to bullet point the major results. If you REALLY want to read the study, e-mail me and I’ll send it your way. The findings were as follows:

  1. Carnitine was associated with CVD
  2. Human gut microbes are required to form TMAO from carnitine
  3. Vegans and vegetarians produce much less TMAO than non-vegans, and this is primarily due to differences in gut bacteria composition
  4. A dose-dependent relationship between plasma levels of carnitine and CVD exists; however, TMAO was shown to be the driving force behind this association. Therefore, it is not the carnitine, per se, that potentially causes CVD. Rather, it’s TMAO.
  5. ApoE -/- (knockout) mice were shown to have a doubling of CVD progression when supplemented with carnitine or choline.
  6. TMAO inhibits cholesterol removal from peripheral tissues back to the liver in ApoE -/- mice. This, effectively, shifts the net balance towards cholesterol deposition and accumulation, which can progress to atherosclerosis and CVD/heart disease.

So, to briefly summarize, an association (not causation) between carnitine and CVD risk was established in humans, with subsequent rodent data to help provide the mechanistic justification as to why. However, as with all rodent data, there needs to be some reservation when trying to apply the findings to humans (Again, I’m looking at you vegans/vegetarians). ApoE -/- knockout mice have a genetic deletion that specifically causes them to develop dyslipidemia (high blood lipids) and atherosclerosis [24]. Indeed, even in the face of a regular chow, low cholesterol diet, these mice have blood cholesterol levels upwards of 400mg/dL (normal levels ~80mg/dL). This was more than sufficient to induce CVD, showing that plasma lipids do contribute to the pathogenesis of the disease. Therefore, it was shown that, in mice that already had CVD and severe dyslipidemia, a diet with supplemental carnitine exacerbated the disease; it did not cause it. Moreover, the levels of carnitine used to exacerbate the disease were beyond supraphysiological. The mice would have had to consume over 6lbs of red meat per day in order to reach the levels of carnitine they were supplemented with (~2g carnitine/day; the average cut of red meat contains ~70mg/100g [22]). This intake would be even greater for humans. Not realistic by any stretch of the imagination.

In the end, until subsequent research comes out involving more human-derived data, we just can’t translate preliminary and completely unrealistic rodent data into health policy-altering fact. Furthermore, there is substantial data in humans involving realistic intakes red meat that at least makes us think twice about red meat’s role in CVD. Indeed, this research shows actual improvements in traditional risk factors (like someone’s cholesterol levels (LDL and HDL) that do promote CVD) when beef is consumed alongside a reasonable diet (i.e. one with fruits and vegetables, etc.). While these studies do nothing to refute carnitine’s potential role in CVD progression, they do lend credence to the fact that red meat can be incorporated into a traditional heart-healthy diet which actually improves health. Whether or not carnitine/TMAO can exert their potential CVD-causing effects independent of an improved lipid profile and a realistic intake of red meat is far from established, and hard to believe. Obviously future research will need to address this concern.

Evidence to the contrary

Despite the craze after last week’s Nature Medicine article, the fact of the matter is that red meat can be incorporated into a diet that actually lowers one’s risk for CVD and heart disease, based on traditional risk factors, like total, LDL and HDL cholesterol levels. A non-exhaustive list of the research follows.

In 1994, Scott et al. [25] saw that, in free living subjects, a 5-week diet containing red meat had similar effects on lowering plasma total and LDL cholesterol when compared to a similar diet containing chicken. Five years later in 1999, Davidson and co. [26] also showed that, in free-living subjects consuming lean red meat, subjects lowered total and LDL cholesterol, as well as, raised HDL cholesterol to the same degree as those on a white meat diet. Fast forward to 2003, to quote the concluding remarks of Beauchesne-Rondeau et al. who examined the effects of beef, lean fish and poultry on lipoprotein profiles in hypercholesterolemic men (important line bolded) [27]:

[W]ith respect to [heart disease] risk, an AHA diet with a high [polyunsaturated to saturated fat ratio]  and high fiber content, regardless of the protein source, induced numerous favorable changes such as reductions in plasma total and LDL cholesterol and apo B, total and VLDL triacyl-glycerols, and total:HDL cholesterol in hypercholesterolemic men, and it overlapped the effects of protein sources on LDL apo B pre-viously observed in normocholesterolemic subjects.”

Finally, in a well-controlled study conducted last year, Roussell et al. [28] showed that, when incorporated into a well-balanced diet (again, plenty of fruits and vegetables) red meat can actually improve one’s heart health. This was evidenced by improvements in total and LDL cholesterol, as well as, plasma triglycerides. To quote the authors directly;

[These] results […] provide convincing evidence that lean beef can be included in a heart-healthy diet that meets current dietary recommendations and reduces CVD risk.”

Concluding remarks

So, even with the incorporation of red meat into someone’s diet, one can definitely improve their lipid profile and reduce their risk for CVD and heart disease, as long as that diet is sensible and contains reasonable amounts of fruits and vegetables, etc. The big thing to keep in mind is that, while new research like this may seem compelling and interesting, it’s often wrought with the media’s biased, sensationalist coverage. It’s important to keep in mind the overall context of one’s diet when evaluating the individual food constituents and their effects on someone’s health. Red meat should not be feared or vilified. Rather, it should be eaten and enjoyed, in moderation, like all other foods.

There is still a lot to be learned about carnitine and its role in CVD. As we have seen, under certain pathological conditions supplemental carnitine and its derivatives can be beneficial to patients with previous heart complications. Furthermore, it has yet to be shown why foods like fish, which have been shown to have the detrimental metabolite TMAO, are not usually associated with CVD. Lastly, I want to also point out that physical activity and life style modifications have yet to be mentioned in this discussion. Given my fitness-oriented readership, I feel the need to at least briefly mention that weight-loss and physical activity both affect the composition of one’s gut microbiota. Indeed, a couple of the strains of bacteria that were shown to be associated with carnitine metabolism in the Nature article were actually shown to be reduced in another study which observed overweight individuals who lost weight and increased their physical activity [29].

So, while the masses may buy into the media’s frenzy about red meat being evil, I’ll be firing up the grill this weekend and enjoying a nice steak.


1.            Koeth RA, Wang Z, Levison BS, Buffa JA, Org E, Sheehy BT, Britt EB, Fu X, Wu Y, Li L, et al: Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat Med 2013.

2.            Wilson PW, Kannel WB, Silbershatz H, D’Agostino RB: Clustering of metabolic factors and coronary heart disease. Arch Intern Med 1999, 159:1104-1109.

3.            Keys A: Coronary heart disease, serum cholesterol, and the diet. Acta Med Scand 1980, 207:153-160.

4.            Micha R, Wallace SK, Mozaffarian D: Red and processed meat consumption and risk of incident coronary heart disease, stroke, and diabetes mellitus: a systematic review and meta-analysis. Circulation 2010, 121:2271-2283.

5.            Bernstein AM, Sun Q, Hu FB, Stampfer MJ, Manson JE, Willett WC: Major dietary protein sources and risk of coronary heart disease in women. Circulation 2010, 122:876-883.

6.            Siri-Tarino PW, Sun Q, Hu FB, Krauss RM: Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr 2010, 91:535-546.

7.            Bibbins-Domingo K, Chertow GM, Coxson PG, Moran A, Lightwood JM, Pletcher MJ, Goldman L: Projected effect of dietary salt reductions on future cardiovascular disease. N Engl J Med 2010, 362:590-599.

8.            Hansen ES: International Commission for Protection Against Environmental Mutagens and Carcinogens. ICPEMC Working Paper 7/1/2. Shared risk factors for cancer and atherosclerosis–a review of the epidemiological evidence. Mutat Res 1990, 239:163-179.

9.            Wu C, Yosef N, Thalhamer T, Zhu C, Xiao S, Kishi Y, Regev A, Kuchroo VK: Induction of pathogenic T17 cells by inducible salt-sensing kinase SGK1. Nature 2013.

10.          Kleinewietfeld M, Manzel A, Titze J, Kvakan H, Yosef N, Linker RA, Muller DN, Hafler DA: Sodium chloride drives autoimmune disease by the induction of pathogenic T17 cells. Nature 2013.

11.          Malaguarnera M: Carnitine derivatives: clinical usefulness. Curr Opin Gastroenterol 2012, 28:166-176.

12.          Pauly DF, Pepine CJ: The role of carnitine in myocardial dysfunction. Am J Kidney Dis 2003, 41:S35-43.

13.          Mingorance C, Rodriguez-Rodriguez R, Justo ML, Alvarez de Sotomayor M, Herrera MD: Critical update for the clinical use of L-carnitine analogs in cardiometabolic disorders. Vasc Health Risk Manag 2011, 7:169-176.

14.          Serati AR, Motamedi MR, Emami S, Varedi P, Movahed MR: L-carnitine treatment in patients with mild diastolic heart failure is associated with improvement in diastolic function and symptoms. Cardiology 2010, 116:178-182.

15.          Backhed F, Manchester JK, Semenkovich CF, Gordon JI: Mechanisms underlying the resistance to diet-induced obesity in germ-free mice. Proc Natl Acad Sci U S A 2007, 104:979-984.

16.          Turnbaugh PJ, Gordon JI: The core gut microbiome, energy balance and obesity. J Physiol 2009, 587:4153-4158.

17.          Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, Ley RE, Sogin ML, Jones WJ, Roe BA, Affourtit JP, et al: A core gut microbiome in obese and lean twins. Nature 2009, 457:480-484.

18.          Greiner T, Backhed F: Effects of the gut microbiota on obesity and glucose homeostasis. Trends Endocrinol Metab 2011, 22:117-123.

19.          Wang Z, Klipfell E, Bennett BJ, Koeth R, Levison BS, Dugar B, Feldstein AE, Britt EB, Fu X, Chung YM, et al: Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature 2011, 472:57-63.

20.          He K, Song Y, Daviglus ML, Liu K, Van Horn L, Dyer AR, Greenland P: Accumulated evidence on fish consumption and coronary heart disease mortality: a meta-analysis of cohort studies. Circulation 2004, 109:2705-2711.

21.          Whelton SP, He J, Whelton PK, Muntner P: Meta-analysis of observational studies on fish intake and coronary heart disease. Am J Cardiol 2004, 93:1119-1123.

22.          Rigault C, Mazue F, Bernard A, Demarquoy J, Le Borgne F: Changes in l-carnitine content of fish and meat during domestic cooking. Meat Sci 2008, 78:331-335.

23.          Yancey PH: Organic osmolytes as compatible, metabolic and counteracting cytoprotectants in high osmolarity and other stresses. J Exp Biol 2005, 208:2819-2830.

24.          Pendse AA, Arbones-Mainar JM, Johnson LA, Altenburg MK, Maeda N: Apolipoprotein E knock-out and knock-in mice: atherosclerosis, metabolic syndrome, and beyond. J Lipid Res 2009, 50 Suppl:S178-182.

25.          Scott LW, Dunn JK, Pownall HJ, Brauchi DJ, McMann MC, Herd JA, Harris KB, Savell JW, Cross HR, Gotto AM, Jr.: Effects of beef and chicken consumption on plasma lipid levels in hypercholesterolemic men. Arch Intern Med 1994, 154:1261-1267.

26.          Davidson MH, Hunninghake D, Maki KC, Kwiterovich PO, Jr., Kafonek S: Comparison of the effects of lean red meat vs lean white meat on serum lipid levels among free-living persons with hypercholesterolemia: a long-term, randomized clinical trial. Arch Intern Med 1999, 159:1331-1338.

27.          Beauchesne-Rondeau E, Gascon A, Bergeron J, Jacques H: Plasma lipids and lipoproteins in hypercholesterolemic men fed a lipid-lowering diet containing lean beef, lean fish, or poultry. Am J Clin Nutr 2003, 77:587-593.

28.          Roussell MA, Hill AM, Gaugler TL, West SG, Heuvel JP, Alaupovic P, Gillies PJ, Kris-Etherton PM: Beef in an Optimal Lean Diet study: effects on lipids, lipoproteins, and apolipoproteins. Am J Clin Nutr 2012, 95:9-16.

29.          Santacruz A, Marcos A, Warnberg J, Marti A, Martin-Matillas M, Campoy C, Moreno LA, Veiga O, Redondo-Figuero C, Garagorri JM, et al: Interplay between weight loss and gut microbiota composition in overweight adolescents. Obesity (Silver Spring) 2009, 17:1906-1915.

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Protein supplementation and resistance training: worthwhile or worthless? – ARTICLE REVIEW


Muscle performance, size, and safety responses after eight weeks of resistance training and protein supplementation: a randomized, double-blinded, placebo-controlled clinical trial

Walter AA, Herda TJ, Costa PB, Ryan ED, Stout JR, Cramer JT.

Journal of Strength and Conditioning Research 2013, 25 February [Epub ahead of print]


ABSTRACT: The purpose of this study was to examine the effects of two different types of protein supplementation on thigh muscle cross-sectional area, blood markers, muscular strength, endurance, and body composition after eight weeks of low- or moderate-volume resistance training in healthy, recreationally trained, college-aged men. One hundred and six men were randomized into five groups: low-volume resistance training with bio-enhanced whey protein (BWPLV; n=22), moderate-volume resistance training with BWP (BWPMV; n=20), moderate-volume resistance training with standard whey protein (SWPMV; n=22), moderate-volume resistance training with a placebo (PLA; n=21), or moderate-volume resistance training with no supplementation (CON; n=21). Except for CON, all groups consumed one shake before and after each exercise session and one each non-training day. The BWPLV, BWPMV, and SWPMV groups received approximately 20g of whey protein per shake, while the BWP groups received 5g additional polyethylene glycosylated (PEG) leucine. Resistance training sessions were performed three times per week for eight weeks. There were no interactions (p>0.05) for muscle strength and endurance variables, body composition, muscle cross-sectional area, and safety blood markers, but main effects for training were observed (p≤0.05). However, Albumin:Globulin ratio for SWPMV was lower (p=0.037) than BWPLV and BWPMV. Relative protein intake (PROREL) indicated a significant interaction (p<0.001) with no differences across groups at pre, however, BWPLV, BWPMV, and SWPMV had a greater intake than PLA or CON at post (p<0.001). The present study indicated that eight weeks of resistance training improved muscle performance and size similarly among groups regardless of supplementation.

Opening Comments

It’s common practice for many strength athletes and bodybuilders to consume protein supplements around and even during training. This practice is more or less supported by a growing body of literature over the past 10-15 years that suggests the ingestion of protein both before and after weight training for the purposes of maximizing muscle gain [1, 2]. Today’s article adds to the ever-growing compendium of research on protein supplementation, its safety, and its purported beneficial effects on body composition, muscular hypertrophy, strength, and endurance when added to a structured resistance training (RT) program. This study is conceptually novel in that it also tries to address the issue of optimal training volume alongside supplementation for RT gains.

With regards to protein supplement safety, the researchers site some weak data supporting a possible contraindication for supplement usage [3-5]. For those of you who have been following me for the past year know that I have already covered this topic before (i.e. the safety of higher protein diets). For those of you who are newcomers, I suggest you read my thorough examination of higher protein diets from last July. While my article doesn’t address protein supplementation, per se, it does address the majority of safety concerns of higher protein diets on a myriad of health topics. That being said, higher protein intakes are completely harmless unless you already have some preexisting kidney condition. For today, I will limit my analysis to the findings on protein supplementation, protein type, and its effects on body composition, muscular hypertrophy, strength and endurance. I will also briefly touch upon some of the observations on training volume and its effects on strength and muscle size given that it too is a hot topic in exercise science research.

In the end, the researchers saw no difference between the three supplement groups or between the supplement groups and the placebo (PLA)/control (CON) groups on improvements in body composition, muscle hypertrophy, strength or endurance. Moreover, they did not see any difference between training volumes on any of the muscular outcomes (i.e. they all got stronger and gained muscle to a similar degree in spite of overall training volume as well as supplement status). It can also be inferred from the study that protein timing, that is, consuming protein immediately after training (as was seen in the intervention groups) offered no further benefit over consuming protein – if at all – at some later point in time (as can be inferred by the lack of immediate protein ingestion after training for the PLA and CON groups). This, however, was not a primary goal of the study and will not be a point of focus in today’s review. Nevertheless, for those interested in the topic of nutrient timing, I would suggest accessing a recent, well-written comprehensive review by friend and colleague, Alan Aragon along with exercise science stud, Brad Schoenfled [6].

Moreover, despite what we already know about higher protein diets and their safety (ala my previous coverage), I should note that the researchers saw no adverse health outcomes (as assessed by various blood bio-markers) associated with the introduction of protein supplementation in conjunction with RT. Go figure.

As I’ve already alluded to, the authors wrap up their discussion by stating that, regardless of supplementation status and training volume, all groups showed significant improvements in all muscular outcomes. They also go on to suggest that lower training volume alongside protein supplementation may promote similar outcomes as training with higher volume; something that may be of interest to athletes who are recovering from an injury. I will respond to their conclusions later.

Study strengths

This study’s strengths include its rather large sample size (n=106), randomization, the blinding of subjects and researchers, study duration (8-weeks), and concept. In addition, supplementation adherence was tightly regulated, with subjects consuming the protein and PLA supplement in the lab, under the observation of the researchers, 30-minutes before, as well as, immediately following the RT bout. On non-training days, the treatment and PLA subjects were advised to consume 1 packet of the supplement in the morning, in the same manner as they had done in the lab. They were also instructed to return the empty packets in order to ensure compliance (which was, on avg., about 95%). I should also note that the supplementation dosage of 20g of whey protein is highly supported in the literature [2, 7, 8], with estimates ranging from 20-30g of high quality protein as being the “sweet spot,” as it were, for muscle protein synthesis (MPS). The additional leucine (5g) in the “bio-enhanced” groups seems like an exercise in idiocy more than anything else. Despite leucine being the primary dietary stimulus for MPS [9, 10], to my knowledge there is no strong data supporting the addition of leucine to an already adequate amount of protein for the enhancement of MPS. In fact, there is compelling data to the contrary [11, 12]. Either way, each group was receiving an adequate bolus of protein following training.

Three-day dietary recalls were also used to evaluate the diets between the groups, although no additional dietary instructions were given to the subjects besides to continue their usual dietary habits. Body composition was measured via hydrostatic weighing (aka underwater weighing), once considered the “Gold Standard” for body composition measurements. Despite more accurate methods out there (most notably DEXA and MRI), there are more error-prone methods (BOPPOD, BIA, skinfolds) that could make this study much worse. Muscle cross-sectional area (CSA) was also ascertained – albeit by a quite novel method that I was unaware of, called peripheral quantitative computerized tomography (pQCT). Based on the literature, pQCT is primarily used for supplemental measurements of bone mineral density alongside DEXA, although it has been recently validated for measurements of muscle CSA and proves to be quite reliable [13].

Study limitations

Unfortunately, the study’s limitations far outweigh its strengths. Firstly, despite the authors’ attempt at recruiting “recreationally trained males,” they fall short of eliminating “newbie” gains that may mask any effects of supplementation. For example, it was reported that half of the subjects participated in about 4 hours of aerobic exercise per week, while less than half of the subjects reported participating in about 3 hours of weightlifting per week. Anyone who is familiar with weight lifting knows that these subjects are neither athletes nor intermediate to advanced lifters. At the very best they’re entry-level beginners (more like untrained weightlifters), something even the authors saliently note in their discussion:

“Since the sample in the present study consisted of untrained or recreationally-trained healthy young men, it is possible that the profound effects of the resistance training alone… may overshadow any additional, smaller benefits of whey protein supplementation.”

Therefore, given the training status – or lack thereof – of the subjects, any results can only be applied to healthy, young, untrained and/or entry-level weightlifters. This is contrary to how the authors try to extrapolate their findings with regards to recommendations for athletes (tisk tisk).

Another disparaging limitation of the study was the failure to control for dietary/protein intakes. Case in point, failing to control for overall protein intakes led to a wide range of intakes between the groups (0.69-2.86g/kg bodyweight), with the PLA and CON groups leaning more towards the lower end of the range (0.69-1.96g/kg) and the supplement groups comprising the upper end (1.04-2.86g/kg). Nevertheless, given the subject’s baseline weights (ballpark avg. of 78kg or ~172lbs), the supplement groups were taking anywhere from ~80-225g of protein and the PLA and CON groups were slightly worse off with intakes ranging from 53-152g/day. So in other words, the researchers were looking at a clusterf***k of overlapping protein intakes, ranging from terrible to more-than-adequate, both inter- and intra-group-wise. Basically, some subjects that were receiving the supplement were getting less protein per day than some subjects not receiving the supplement at all. This could be another reason why no differences were seen between supplement and non-supplement groups.

Comments & Conclusions

Given the totality of information from the present study, most notably the untrained status of the subjects and the failure to control for protein intakes, we just can’t conclude that protein supplementation is worthless in the context of a sufficient, high-quality protein diet along with a structured RT program for intermediate to highly trained athletes/weightlifters. Probably the closest thing we have to an answer is a recent meta-analysis looking at protein supplementation and increases in muscle accretion and strength in a wide range of lifting populations [14]. In the end, however, protein supplementation’s beneficial effects may only apply to those hitting the lower end (1.2g/kg) of the recommended protein intake for strength/power athletes. This, however, probably has more to do with increasing overall intake rather than supplementation, per se.

In regards to protein type, I’m also not quite sure what the researchers were hoping to find by using leucine-enriched whey as the secondary supplement. The subjects were already receiving a bolus of whey protein which is to be considered adequate for muscle protein synthesis. Indeed, in 2009, Moore et al. [7] found that muscle protein synthesis displayed a dose response relationship to dietary protein ingestion, topping out at around 20g, while multiple studies by Koopman et al. have shown no benefit of additional supplemental free leucine when a sufficient amount of casein-hydrolysate was ingested post-workout [11, 12]. So, despite hopes of seeing differences in protein type, the results were doomed from the start. Instead, I would like to have seen a whole food source or something else vs. whey that might be of real-life significance and applicability. My hunch, however, is that it won’t matter in the long run as long as the whole food source is of high-quality protein (i.e. high in leucine and EAAs). This may be of some concern to those who are vegetarian and tend to be lacking in high-quality protein sources. In this case, whey would be a great addition to cover all their bases.

As far as training volume and strength/hypertrophy is concerned, it would be presumptuous to argue that, based on this study, increased training volume has little to no benefit on muscular outcomes when compared to fewer sets and therefore lower overall volume. In probably the most well-controlled study of its kind, Marshall et al. reported greater increases in 1RM strength on the squat in an 8-set/exercise group compared to a 1-set/exercise and 4-set/exercise group after 10 weeks of squat training [15]. What’s even more compelling about this study is that the 8-set/exercise group started out stronger than the 1-set and 4-set/exercise group yet still increased their 1RM by MORE than the 1-set and 4-set group. Let that sink in for a second… Despite being stronger from the start, the 8-set group got stronger, relatively, than the people who started out weaker. Usually, those who are weaker and less trained have the most to gain and, relatively, gain more strength than those who are already strong to begin with. In addition, only the 8-set group got significantly stronger in the squat after 3 weeks, showing an immediate effect of volume on strength gains. This has implications for those athletes trying to get stronger within a finite period of time. Either way, a growing body of evidence suggests that if you want to get bigger and stronger, you should increase your volume (i.e. do more sets) [16-21].

In the end, this study tells us nothing that we don’t already know; put novice trainees on a structured RT program and they’ll get bigger and stronger and improve their body composition. Shocker! Unfortunately, a poor research design made this study virtually useless to examine the practical effects of protein supplementation on muscular outcomes in athletes and weightlifters. Nevertheless, regardless of this study, logic dictates that protein supplementation will never be necessary in the face of already sufficient protein intakes (assuming there is an emphasis on high quality proteins, rich in leucine and EAAs); an assumption this is supported by a recent meta-analysis [14].

As it stands, current recommendations for protein intake for strength and power athletes range from 1.2-2.2g/kg of bodyweight [22-26]. Furthermore, in a well-written review by Kevin Tipton and Robert Wolfe [22], the authors note that protein intakes as high as 3.0g/kg aren’t harmful and may even be of some benefit to the athlete, while a more recent study showed that, in Korean bodybuilders, habitual intakes of ~4.3g/kg had no adverse health effects [27]. Nevertheless, regardless of overall intake, the most salient point Tipton and Wolfe make, and one that I happen to agree with above all else, is that, as long as protein intake doesn’t hinder the intake of other macronutrients (carbs/fats), there’s no reason not to consume higher amounts of protein (even up to 3-4g/kg although this is not necessary by any stretch) given that there is no inherent harm, even at the more “extreme” intakes. So, in the end, if you’re already taking in adequate, or even more than adequate amounts of protein on daily basis, without extra protein supplements, don’t waste your money. I am unaware of any studies comparing chronic whole food vs. protein powder consumption in conjunction with a training regimen.

Moral of the story: if you find that whey protein (or whatever powder you choose) is easier and more convenient than firing up the grill or slaving over a hot stove pre- and post-workout, than by all means, hit the powder. Personally, I enjoy the taste and love portability of whey protein powder (just shake and drink). Preferences aside, the key thing to remember is that there is nothing magical about protein supplementation, despite what the supplement companies are telling you. As of now, all it is is a way to further augment your total dietary protein intake, which, in the end, is all that matters.

To quote my friend and colleague, Alan Aragon:

“If this daily target [read: total] is achieved with both whole foods and supplements, then great – but supplementation should not be viewed as necessary or optimal.”


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