Stoking the metabolic fire: does higher meal frequency increase metabolism and enhance fat loss?

Stoking the fire


It has been a long-held belief in bodybuilding and health/fitness circles that eating more frequently throughout the day leads to an increase in metabolic rate and fat-loss. This is colloquially coined, “stoking the metabolic fire.”  In fact, this very concept has been disproved about 15 years ago [1], and still remains accurate to this day, with the most recent research showing no differences in 24hr energy expenditure, respiratory quotient (RQ), or fat oxidation [2]. For those of you who are less attuned to the popular bodybuilding and fitness dogma that I just mentioned, it usually goes something like this:

Gym-goer: “I want to lose weight. What’s the best way to go about doing so?”

Trainer: “Well, first off, you need to eat at least 6 meals per day, spaced 2-3 hours apart. That will ignite the metabolic furnace and enhance fat loss.”

It is here that the person recommending such strict, dogmatic claims shows his lack of knowledge in basic human physiology and biochemistry, not to mention a complete lack of respect for the person’s personal preferences when it comes to dieting.

Breaking it down

There are essentially four factors that affect a person’s overall energy expenditure throughout the course of a day (24EE). Those factors are basal metabolic rate (BMR; also termed resting metabolic rate [RMR]), diet induced thermogenesis of food (DIT; also known as the thermic effect of food [TEF]), exercise thermogenesis (EEx), and spontaneous movement, termed non-exercise activity thermogenesis (NEAT). Mathematically it looks something like this:

24EE = BMR + TEF + EEx + NEAT

Now, if increasing meal frequency in fact does lead to an increase in metabolic rate and fat loss, through whatever means, it would have to affect one of the above factors. Obviously increasing meal frequency will not directly alter EEx or NEAT, so we can cross those off the list immediately, leaving us with BMR and TEF as potential modifiable factors.

Let’s take a step back

However, before we analyze the two remaining variables, let’s consider what energy actually is and what food provides in the context of the body deriving energy from it and using it. Simply put, energy is the capacity to do work. It can neither be created nor destroyed; only transformed. This work can be biological (cellular function, transport of ions, etc.), chemical (breaking or building of bonds between atoms), mechanical (muscle contraction), osmotic, or electrical. Food is essentially potential energy that, when ingested, is oxidized and yields ATP for us to do work. It can also be stored (as glycogen, triacylglyceride, and muscle protein [although not a “true” storage form]) and subsequently “freed” during times when food is not present in order to provide us with an endogenous, readily available fuel source. So the question remains; does a simple manipulation of food intake (frequency of ingesting potential energy) promote a beneficial effect on energy expenditure (our ability to use that food to do work) so that we burn more calories, specifically those derived from our fat stores?

Basal metabolic rate (BMR)

The primary driving force behind 24EE, given that your EEx isn’t through the roof, is fat-free mass (FFM) [3]. Taking this one step further, FFM is the primary driving force behind BMR [4]. Therefore, a majority of the energy expended over the course of a day is dictated by BMR (i.e. how much FFM someone has). Knowing this, how can increasing meal frequency alter someone’s BMR? Plain and simple, it can’t. If anything it would have to indirectly increase BMR through increases in FFM, but this is irrelevant given that there is no indication that eating smaller more frequent meals increases FFM to a greater extent than does eating an isocaloric diet with fewer, larger meals; period. In a related vein, there is some equivocal research suggesting increases in BMR and TEF following exercise [5, 6]. However, most of the research was done in previously untrained men and women. So if anything, the increase in an athletic individual is likely to be negligible at best.  So now all we are left with is the thermic effect of food.

Thermic effect of food (TEF)

Quite simply, TEF is averaged out to ~10% of someone’s total caloric intake. So, if a given person ingests 3,000kcals over the course of the day, ~300kcals will be lost as heat through obligatory processes like absorption, digestion, and storage [3]. Also, as a point of interest, there has been some early research showing that obese individuals actually have reduced values of TEF (i.e. <10%), possibly increasing their risk for weight gain [7].

Nevertheless, will increasing meal frequency have any effect on TEF? Again, the answer is no [8]. In fact, in the acute studies showing non-significant increases in TEF based on meal frequency, it was shown that lower meal frequencies actually yielded the higher values of TEF [1, 9]. This is diametrically opposite of what many bodybuilders and fitness enthusiasts believe! Bottom line: increasing meal frequency doesn’t affect TEF to any significant degree.

Other factors to consider with meal frequency

From a practical standpoint, increasing meal frequency is a great way to increase an athlete’s caloric intake or possibly reducing a dieter’s feelings of hunger on a hypocaloric diet. Furthermore, there is research to suggest that the body anticipates meals based on fixed feeding patterns [10]. This is manifested in ghrelin (a hormone that causes sensations of hunger) signaling the brain that you are hungry because it is ‘expecting’ a meal. Therefore, those who might be considering dropping the number of meals they eat per day may experience an initial increase in hunger due to the ‘entrainment’ of ghrelin on your previous feeding pattern. This will eventually subside after the body adapts your new feeding routine.


In closing, there is no strong evidence to suggest an increase in metabolic rate and body fat oxidation by way of increased meal frequency. So whether you eat three times per day or six or more, the effects on metabolism will essentially be the same. As I mentioned before, BMR is dictated by FFM and TEF is essentially unchanged by when you eat your meals. Therefore, the only two logical modifiable factors when it comes to meal frequency are essentially non-modifiable to any significant degree. On the other side of the coin, things to consider when it comes to meal frequency are increased feelings of hunger with fewer meals during a hypocaloric diet and the possible increase in feelings of hunger with a shift in feeding pattern (from higher frequency to lower). Nevertheless, at the end of the day it comes down to personal preference and the person’s individual fitness/performance goals. If you find that eating more frequently throughout the day is tedious and difficult to follow, perhaps fewer, larger meals may be the way to go. There is no difference.


1. Bellisle F, McDevitt R, Prentice AM. Meal frequency and energy balance. Brit J Nutr. 1997;77(Suppl. 1):S57-S70.

2. Ohkawara K, Cornier M, Kohrt WM, Melanson EL. Effects of increased meal frequency on fat oxidation and perceived hunger. Obesity 2012. Epub ahead of print.

3. Ravussin E, Bogardus C. A brief overview of human energy metabolism and its relationship to essential obesity. Am J Clin Nutr. 1992;55:242S-5S.

4. Bogardus C, Lillioja S, Ravussin E, et al. Familial dependence of the resting metabolic rate. NEJM 1986;315(2):96-100.

5. Osterberg KL, Melby CL. Effect of acute resistance on postexercise oxygen consumption and metabolic rate in young women. Int J Sport Nutr Exerc Metab. 2000;10(1):71-81.

6. Sharhag-Rosenberger F, et al. Effects of one year aerobic endurance training on resting metabolic rate and exercise fat oxidation in previously untrained men and women. Metabolic endurance training. Int J Sports Med. 2010;31(7):498-504.

7. Schutz Y, Bessard T, Jéquier E. Exercise and postprandial thermogenesis in obese women before and after weight loss. Am J Clin Nutr. 1987;45:1424-32.

8. Taylor MA, Garrow JS. Compared with nibbling, neither gorging nor a morning fast affect short-term energy balance in obese patients in a chamber calorimeter. Int J Obes Relat Metab Disord. 2001;25(4):519-28.

9. Munsters MJ, Saris WH. Effects of meal frequency on metabolic profiles and substrate partitioning in lean healthy males. PLOS One 2012;7(6):e38362.

10. Frecka JM, Mattes RD. Possible entrainment of ghrelin to habitual meal patterns in humans. Am J Physiol Gastrointest Liver Physiol. 2008;294:G699-G707.

Posted in Diets | Tagged , , | 10 Comments

An objective look at L-carnitine supplementation for fat-loss and enhanced performance


Opening Comments

Over the past 25-plus years carnitine has received a lot of attention, both from researchers and supplement companies alike. Indeed, both camps are interested in carnitine’s role in fat metabolism; however, it is for two very different reasons. Researchers are primarily interested in the ergogenic capacity that carnitine may have to offer endurance athletes – namely carnitine’s glycogen sparing effect via increased fat oxidation – while supplement companies (and consumers) are mostly interested in carnitine for increased fat oxidation to enhance fat-loss and improve body composition. Being the skeptic that I am, today I will evaluate both sides of the aisle and make some final comments and conclusions about whether or not it’s practical to take carnitine supplements, be it for performance purposes or weight loss endeavors. As always, I will begin with some background information (with a little biochemistry thrown in there), follow it up with the pertinent research, and then end with some closing remarks and applications. Let’s get to it!

Rationale behind carnitine supplementation to improve performance

Before I actually get into the potential benefits of carnitine supplementation, I think it would be best to first cover the rationale behind taking carnitine for performance. In doing so, I will try to keep this as short as possible.

It has been well established that the body can use both carbohydrate and fat (in the form of free fatty acids) for muscular contraction [1]. However, the latter only remains true at low to moderate intensities. Indeed, as exercise intensity is increased (>75-85% VO2 max), the proportion of fat that is and can be used to fuel muscle contraction is decreased – if not completely inhibited – such that carbohydrate oxidation increases (see figure below) [2].

FFA ox

However, as moderate to intense exercise continues (as in a marathon or other endurance-type events) the reliance on FFAs is increased due to lowered glycogen stores and therefore less available glucose to fuel muscle contraction. This is important, because during the final leg of a race, runners, cyclists, etc. tend to speed up and may even sprint to the finish line. This would require additional glucose to fuel the high-intensity (>75% VO2 max) sprint. Depleting ones glycogen stores prior to the final stretch of the race could hinder the racer’s finish and (potentially) placement. It is from this paradigm that the theory of fat adaptation came about. Fat adaptation-ists believe that if one can shift their metabolism during moderate intensity exercise to exclusively rely on FFAs, then that person could potentially conserve glycogen stores for when they are needed most, like during the final stretch of a race (>75% VO2 max). Many dietary manipulations have been undertaken in order to help aid in this adaptation, however I will not cover those here as another entire article could be written on the subject. Rather, we will look at how carnitine may be able to facilitate this need (i.e. increase fat oxidation and spare glycogen) by first looking at some basic biochemistry behind fat metabolism (and thus carnitine’s role therein) that will lay the foundation for our discussion on whether or not carnitine can be used as an effective ergogenic and/or fat-loss aid.

Fat metabolism and carnitine’s role therein   

When talking about fat metabolism, it is important to note that there are various control points at which fat metabolism (in skeletal muscle) can be regulated. A recent review by Lawrence Spriet [3] eloquently states that fat metabolism can be regulated during exercise at six different ‘control points,’ one of which is FFA transport across the mitochondrial membrane (think back to high school biology class). It is at this point that carnitine is almost exclusively involved and where I will pick up the conversation.

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 (the latter I will briefly mention when needed) [4]. 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.

It is at this point that I would like to stop and regroup. The above paragraph is extremely important because it really lays out the basis (theoretically) for carnitine improving both performance and body composition. This however, operates under a couple of assumptions: 1) that carnitine translocation is the rate limiting step in fatty acid oxidation, meaning that; 2) increasing carnitine levels will equate to greater transport of fatty acids into the matrix and greater levels of oxidation; and lastly that, 3) you can indeed increase muscle levels of carnitine in the first place. Granted that all three of these factors are true, than yes, there may be a reasonable case for carnitine supplementation. The real question here is whether or not they hold up under scientific scrutiny.

Research against carnitine supplementation

Above, we just saw that carnitine helps “ship” FFAs into the mitochondria so that they can be oxidized to produce ATP. Therefore, potentially having more carnitine may mean more FFA oxidation and therefore a “sparing effect” on muscle glycogen stores which may lead to increased performance. Indeed, muscle carnitine levels decrease as exercise intensity increases [3]. It would make sense that low muscle carnitine levels would therefore lead to a decrease in FFA usage, given that this effect does hold true under high intensities. However, and counter intuitively, the highest FFA oxidation rates actually occur when carnitine levels are well below resting levels [3]. Furthermore, when fat availability in the blood is artificially increased during exercise (at 80% VO2 max), with no concomitant increases in carnitine, the muscle does indeed oxidize more fat [5]. This suggests that carnitine isn’t the rate limiting step during fat metabolism. Therefore, theoretically increasing muscle carnitine levels may not even amount to further increases in fat oxidation given that maximal rates are already being achieved with reduced levels of muscle carnitine and that artificially high levels of FFA are easily handled in the absence of additional carnitine as it is. Lastly, and most importantly, increasing muscular levels of carnitine has been shown time and time again to be quite futile.

In 1994, Barnett and colleagues showed that 14 days of carnitine supplementation (at 4g/day) did not significantly affect muscle levels of carnitine [6]. Similarly, in the same year, Vukovich et al. investigated the effects of carnitine supplementation on muscle carnitine concentrations and glycogen content during submaximal exercise [7]. Here, subjects ingested 6g/day of carnitine and still did not show any increases in muscular levels of carnitine. And if two weeks isn’t long enough to convince you, Wächter and co. [8] gave subjects 4g of carnitine per day for three months and still saw no increase in muscle levels of carnitine. Moreover, had you even thought about hooking up your at-home IV kit and mainlining your carnitine, you’d still be wasting your time as direct infusion has been shown to be unsuccessful [9, 10]. What’s more is that performance parameters such as perceived exertion, exercise performance, VO2 max, or markers of muscle substrate such as RER, VO2, blood lactate levels, leg FFA turnover, and post-exercise muscle glycogen content were all unaffected by the ingestion of 2-5g of carnitine per day (anywhere from one week up to three months) [11]. Thus, the majority of relevant data looking at the oral ingestion and infusion of carnitine has failed to increase muscular levels leading to a lack of improved performance. Therefore, if we still buy into the hypothesis that fat metabolism can be increased via an increase in muscle levels of carnitine we are sadly left with the realization that this is just not possible. Or is it…

Research supporting carnitine supplementation

Although we just saw that the vast majority of research shows that carnitine supplementation (of up to 3 months) has very little impact – if any – on muscle levels of carnitine, it doesn’t leave out the fact there are some studies that do show an impact of oral ingestion and infusion of carnitine on muscle concentrations. First we will examine the infusion studies.

Effective means of carnitine infusion

As noted earlier, straight infusion of carnitine has little impact on muscle levels of carnitine [9, 10]. However, infusion of carnitine alongside an infusion of insulin actually does have an impact on muscle levels [10]. What researchers saw was ~15% increase in muscle levels of carnitine. Although significant, this is not truly representative of the population taking carnitine because I don’t know about you, but I’m not willing to start injecting myself with physiologically high levels of insulin just to increase my muscle carnitine stores. Nevertheless, for those of you who may be considering this option, there may be an easier way.

Effective means of oral carnitine ingestion  

Indeed, it has been shown that oral ingestion of carnitine, alongside a rather large dose of carbohydrate (~80-94g), is able to effectively stimulate the “uptake” of carnitine as measured indirectly via plasma levels and urinary excretion [12, 13]. This is undoubtedly due to carbohydrates’ insulin stimulatory effect. Although 80-94g of carbohydrate is not unusual for a bodybuilder or weightlifter to consume in one sitting in the offseason or even in the earlier stages of dieting, the dosage may come into conflict during the later stages of prep (when carbs are being reduced) or for those who have lower CHO requirements by default (like the average American). Therefore, some practical limitations may come into play, especially when it means eating relatively high amounts of carbohydrate in order to gain what may be a trivial fat-burning effect from carnitine. What’s more is that although muscle levels of carnitine were indirectly seen to increase, there was absolutely no measure of improved body composition during the studies. However, what they did see was a reduction in glycogen breakdown at low intensity exercise (50% VO2 max), but this was effectively eliminated at intensities around 80% VO2 max. Either way, this does not reveal any convincing evidence that carnitine is a potent fat-burner or ergogenic aid even though major shifts in fuel metabolism can be seen; essentially showing a greater reliance on FFAs as a fuel source. These findings, nevertheless, are limited to conjectures about fat-loss in the long-term and are confounded by methodological issues that do not apply to the normal bodybuilder/fitness population or the endurance athlete – or anyone for that matter.


Although it may be physically possible to increase muscle levels of carnitine using relatively large amounts of carbohydrate repeatedly throughout the day, the fact still remains that there is limited convincing data that shows that carnitine is a potent fat-burner or ergogenic aid. Furthermore, when practical limitations come into play, the usefulness of carnitine as a fat-burner is undoubtedly overshadowed by the well-known effects of a solid caloric deficit in combination with increased physical activity (usually in the form of cardio). I should also note that carnitine has been implicated in aiding recovery from resistance exercise in both young and middle-aged populations [14-16] as well as increasing androgen receptor (AR) synthesis and therefore increasing cellular uptake up testosterone following weight training. This potentially leads to the activation various muscle synthetic pathways [17]. However, despite the potential beneficial basis of carnitine supplementation for muscle recovery and hypertrophy there just isn’t enough convincing data that shows supplemental carnitine will do jack-diddly in terms of sizeable gains in muscle mass accretion. We just don’t have the long-term studies necessary to make that conclusion. Conversely, there is some convincing evidence that transient elevations in anabolic hormones (due to exercise) such as testosterone and growth hormone are not closely associated with increases in muscle mass [18-20]. Therefore, increasing AR synthesis and testosterone uptake may be trivial in the larger scope of things.

The bottom line is that the beneficial role of carnitine for either exercise (be it endurance or resistance) or fat burning in young, healthy populations (especially the athlete) are, at this stage, completely theoretical and, most likely, trivial at best.


1. Asmussen E. Muscle metabolism during exercise in man. A historical survey; in Pernow B, Saltin B (eds): Muscle Metabolism during Exercise. New York, Plenum Press, 1971, pp. 1-11.

2. van Loon LJ, Greenhaff PL, Constantin-Teodosiu D, Saris WH, Wagenmakers AJ. The effects of increasing exercise intensity on muscle fuel utilisation in humans. J Physiol. 2001;536(Pt. 1):295-304.

3. Spriet LL. Metabolic regulation of fat use during exercise and recovery. Nestlé Nutr Inst Workshop Ser. 2011;69:39-53;discussion 53-8.

4. Constantin-Teodosiu D, Carlin JI, Cederblad G, Harris RC, Hultman E. Acetyl group accumulation and pyruvate dehydrogenase activity in human muscle during incremental exercise. Acta Physiol Scand. 1991;143:367-372.

5. Romjin JA, Coyle EF, Sidossis LS, et al. Relationship between fatty acid delivery and fatty acid oxidation during strenuous exercise. J Appl Physiol. 1995;79:1939-1945.

6. Barnett C, Costill DL, Vukovich MD, Cole KJ, Goodpaster BH, Trappe SW, Fink WJ. Effect of L-carnitine supplementation on muscle and blood carnitine content and lactate accumulation during high-intensity sprint cycling. Int J Sport Nutr. 1994;4(3):280-8.

7. Vukovich MD, Costill DL, Fink WJ. Carnitine supplementation: effect on muscle carnitine and glycogen content during exercise. Med Sci Sports Exerc. 1994;26(9):1122-9.

8. Wächter S, Vogt M, Kreis R, Boesch C, Bigler P, Hoppeler H, Krähenbühl S. Long-term administration of L-carnitine to humans: effect on skeletal muscle carnitine content and physical performance. Clin Chim Acta. 2002;318(1-2):51-61.

9. Brass EP, Hoppel CL, Hiatt WR. Effect of intravenous L-carnitine on carnitine homeostasis and fuel metabolism during exercise in humans. Clin Pharmacol Ther. 1994;55(6):681-92.

10. Stephens FB, Constantin-Teodosiu D, Laithwaithe D, Simpson EJ, Greenhaff PL. Insulin stimulates L-carnitine accumulation in human skeletal muscle. FASEB J. 2006; 20:377-379.

11. Stephens FB, Constantin-Teodosiu D, Greenhaff PL. New insights concerning the role of carnitine in the regulation of fuel metabolism in skeletal muscle. J Physiol. 2007;581(2):431-444.

12. Wall BT, et al. Chronic oral ingestion of L-carnitine and carbohydrate increases muscle carnitine content and alters muscle fuel metabolism during exercise in humans. J Physiol. 2011;589(4):963-973.

13. Stephens FB, Evans CE, Constantin-Teodosiu D, Greenhaff PL. Carbohydrate ingestion augments L-carnitine retention in humans. J Appl Physiol.. 2007;102:1065-1070.

14. Volek JS, Kraemer WJ, Rubin MR, et al. L-carnitine L-tartrate supplementation favorably affects markers of recovery from exercise stress. Am J Physiol Endocrinol Metab. 2002;282:E474-E482.

15. Kraemer WJ, Volek JS, French DN, et al. The effects of L-carnitine L-tartrate supplementation on hormonal responses to resistance exercise and recovery. J Strength Cond Res. 2003;17(3):455-62.

16. Ho JY, Kraemer WJ, Volek JS, et al. L-carnitine L-tartrate supplementation favorably effects biochemical markers of recovery and from physical exertion in middle-aged men and women. Metabolism 2010;58(8):1190-9.

17. Kraemer WJ, Spiering BA, Volek JS, et al. Androgenic responses to resistance exercise: effects of feeding and L-carnitine. Med Sci Sports Exerc. 2006;38(7):1288-96.

18. West DW, Phillips SM. Anabolic processes in human skeletal muscle: restoring the identities of growth hormone and testosterone. Phys Sportsmed. 2010;38(3):97-104.

19. West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Apply Physiol. 2012;112:2693-2702.

20. West DW, Burd NA, Staples AW, Phillips SM. Human exercise-mediated skeletal muscle hypertrophy in an intrinsic process. Int J Biochem Cell Biol. 2010;42:1371-1375.

Posted in Reviews, Supplements | 9 Comments

Protein and muscle gain: Are we closer to an optimal dosing strategy? – REVIEW

Daytime pattern of post-exercise protein intake affects whole-body protein turnover in resistance-trained males.

Moore DR, Areta J, Coffey VG, Stellingwerf T, Phillips SM, Burke LM, Cleroux M, Godin JP, Hawley JA.

Nutrition & Metabolism 2012, 16;9(1):91 [Epub ahead of print]



The pattern of protein intake following exercise may impact whole-body protein turnover and net protein retention. We determined the effects of protein feeding strategies on protein metabolism in resistance-trained young men.


Participants were randomly assigned to ingest either 80g of whey protein as 8x10g every 1.5h (PULSE; n=8), 4x20g every 3h (intermediate, INT; n=7), or 2x40g every 6hr (BOLUS; n=8) after an acute bout of bilateral knee extension exercise (4×10 repetitions at 80% maximal strength). Whole-body protein turnover (Q), synthesis (S), breakdown (B), and net balance (NB) were measured throughout 12h of recovery by a bolus ingestion of [15N]glycine with urinary [15N]ammonia enrichment as the collected end-product.


PULSE Q rates were greater than BOLUS (~19%, P<0.05) with a trend towards being greater than INT (~9%, P=0.08). Rates of S were 32% and 19% greater and rates of B were 51% and 57% greater for PULSE as compared to INT and BOLUS, respectively (P<0.05), with no difference between INT and BOLUS. There were no statistical differences in NB between groups (P=0.23); however, magnitude-based inferential statistics revealed likely small (mean effect +/-90%CI; 0.59+/-0.87) and moderate (0.80+/-0.91) increases in NB for PULSE and INT compared to BOLUS and possible small increase (0.42+/-1.00) for INT vs. PULSE.


We conclude that the pattern of ingested protein, and not only the total daily amount, can impact whole-body protein metabolism. Individuals aiming for maximize NB would likely benefit from repeated ingestion of moderate amounts of protein (~20g) at regular intervals (~3h) throughout the day.

Opening Comments

Today’s topic is likely going to gin up strong sentiment from both sides of the meal-frequency aisle when it comes to eating protein and gaining muscle. Indeed, the article above fires a clear shot across the bow at those consuming meals in the lower-frequency-range and thus fewer protein feedings (i.e. potential anabolic muscle-building events) throughout the day. It the literature it has been proposed that multiple (~3-4) protein feedings throughout the day are required in order to optimally gain muscle [1]. For most, this is not an issue given that multiple protein-rich meals are consumed in order to hit daily caloric needs anyway. However, in the past 5-10 years, a new take on dieting has emerged that – at the very least – makes us reconsider how lean mass is gained/preserved. I am of course referring to Intermittent Fasting (IF), a dieting protocol wherein participants fast for a majority of the day (~16-20hrs), complete their workout, and then consume anywhere from 1-3 meals within a short window of time (~4-8hrs on average).

Fewer protein feedings for attenuating muscle loss

Despite its recent surge in popularity, the scientific data behind IF is preliminary at best and includes data that closely characterizes people eating in the lower range of meal frequency (2 meals spread throughout the day) for weight loss as opposed to actual IF protocols (eating within a designated window post-workout). Nevertheless, the data does support at least equal benefits in terms of muscle retention during weight loss/maintenance when consuming fewer, and thus larger protein meals compared to smaller, more frequent ones [2-6]. Moreover, there may even be a slight advantage to doing so under maintenance conditions [4], although any advantages seen in body composition were verified using BIA rather than more accurate measures such as DEXA or MRI. I should also note that most studies were conducted in the absence of a structured training program. All areas for future study!

Optimal protein dosing strategy for muscle gain

On the other side of the coin, research looking at lower meal frequencies (read: fewer protein feedings) compared to higher meal frequencies and subsequent muscle gain have never really been conducted. To my knowledge, the study above is the first one of its kind to look at varying isonitrogenous diets in terms of dosing strategy and whole-body protein balance while not under hypocaloric conditions. Indeed, last month, a 6-week trial did look at varying isonitrogenous diets in terms of dosing strategy on body composition (and therefore muscle mass retention), but did so under hypocaloric conditions and noticed that both groups lost an equal amount of muscle tissue and body fat as measured by DEXA [6]. Unfortunately this does not get us closer to an ‘optimal dosing strategy’ for protein and muscle gain.

So, coming back to today’s study, there are some hefty limitations that do warrant a healthy dose of skepticism and criticism before we go jumping to conclusions about protein dosing and muscle gain. So without further ado, let’s dive right in!

Study strengths

The biggest strength of this study is its innovativeness, as it is – to my knowledge – the first study to look at varying isonitrogenous diets in terms of dosing strategy on whole-body protein retention in humans devoid of a caloric deficit. Other strengths include using resistance-trained males (eliminates “newbie” bias), controlling dietary intake 72h prior to testing (effectively standardizing all the participants), and instructing participants not to engage in any physical activity 72h before testing. I should note that the use of a DEXA to assess body composition was made. However, given the brevity of the study (12h), and no follow-up body composition measures, I see this as neither a strength nor a weakness.

Study limitations

The most glaringly obvious weakness is the acute nature of the study (12h in duration). Any relevant/practical conclusions about smaller, more frequent protein feedings as being optimal for muscle gain are completely speculative and will need longer-term trials in order to verify. Secondly, total protein intakes were 80g over the course of the study period (~0.9g/kg); an intake significantly less than what most trainees consume on a daily basis, and an intake that can be argued to be insufficient for optimal muscle gain [1].

Lastly, the researcher’s use of ammonia end-product to assess whole-body protein balance does not directly measure muscle protein synthesis (MPS); the one factor most people are concerned about when talking about protein ingestion following resistance training. To this end, the authors do cite the limitations of using whole-body tracer methodologies. To quote them;

A limitation of [this methodology] is the inability to delineate tissue-specific changes in protein metabolism.”

Indeed, a much better methodology would have been stable isotope infusion in conjunction with muscle biopsy so that actual MPS could be quantified and analyzed; not just net whole-body retention. Therefore, because they did not use stable isotope infusion, nor did they follow up with biopsy or subsequent body comp measures such as DEXA or MRI, we are left to speculate the true effects of protein dosing strategy on MPS and body composition. Truthfully, all we are left with is data using a poor surrogate for tissue specific muscle gain under insufficient dietary protein intakes.


Given the multitude of limitations contained within the study above, we just can’t say for sure that smaller, more frequent protein feedings are optimal for muscle protein accretion. To be blunt, it wasn’t truly looked at! In reality, all we know is that there was no significant difference between each protocol on whole-body protein balance over a 12h period (although a slight edge was seen in the 20gx4 group). Nevertheless, the overall effect speaks more to the importance of hitting total daily protein intake rather than focusing on dosing strategy when it comes to achieving an anabolic state. Moreover, had optimal protein intakes been achieved (i.e. >0.9g/kg and more in the range of 1.2-1.7g/kg), I believe that any differences – as slight as they were above – would effectively be negated.

So, where does this leave us? What is the take-home message? In a recent article by Alan Aragon on the lower threshold of meal frequency for optimizing muscle gain [7], Alan makes some practical recommendations (that I happen to agree with), based on the evidence to-date. To quote, Alan;

I would error on the safe side and go with three protein-rich meals as an ‘optimal minimum frequency’ for anabolism. It strikes a compromise between conservative practicality [and] exploiting the hypotheticals.”

For now we know that reducing meal frequency, and thus protein feedings, is more than effective when it comes to attenuating muscle loss during weight loss, as long as dietary protein is sufficient. However, we are still in the dark when it comes to optimal meal frequency, and thus protein feedings, when it comes to increasing muscle mass. The study above by no means opens the door to revealing this answer but rather puts it fingers on the handle so that we may start to investigate further. In the end, as long as you are hitting your daily goal of protein intake, I see no need to fret over dosing strategy. On the whole, most people who care about increasing muscle mass are already eating multiple protein-rich meals per day. If this sounds like you, then you are already ahead of the game.


1. Phillips SM, van Loon LJ. Dietary protein for athletes: from requirements to optimum adaptation. J Sports Sci. 2011;29(Suppl 1):S29-38.

2. Arnal MA, Masoni L, Boirie Y, et al. Protein pulse feeding improves protein retention in elderly women. Am J Clin Nutr. 1999;69(6):1202-8.

3. Arnal MA, Masoni L, Boirie Y, et al. Protein feeding pattern does not affect protein retention in young women. J Nutr. 2000;130(7):1700-4.

4. Stote KS, et al. A controlled trial of reduced meal frequency without caloric restriction in healthy, normal-weight, middle-aged adults. Am J Clin Nutr. 2007;85(4):981-8.

5. Soeters MR, et al. Intermittent fasting does not affect whole-body glucose, lipid, or protein metabolism. Am J Clin Nutr. 2009;90(5):1244-51.

6. Adechian S, Balage S, Remond D, et al. Protein feeding patter, casein feeding, or milk-soluble protein feeding did not change the evolution of body composition during a short-term weight loss program. Am J Physiol Endocrinol Metab. 2012;303(8):E973-82.

7. Aragon A. What’s the lower threshold of meal frequency for optimizing muscle gain? AARR 2012 May;2-5.

Posted in Protein, Reviews | Tagged , , , | 1 Comment

Sodas and Childhood Obesity – ARTICLE REVIEW

A Trial of Sugar-free or Sugar-sweetened Beverages and Body Weight in Children

Janne C. de Ruyter, Margreet R. Olthof, Jacob C. Seidell, and Martijn B. Katan

NEJM September 21, 2012

Full Text:


The consumption of beverages that contain sugar is associated with overweight, possibly because liquid sugars do not lead to a sense of satiety, so the consumption of other foods in not reduced. However, data are lacking to show that the replacement of sugar-containing beverages with noncaloric beverages diminishes weight gain.


We conducted an 18-month trial involving 641 primarily normal-weight children from 4 years 10 months to 11 years 11 months of age. Participants were randomly assigned to receive 250ml (8oz.) per day of sugar-free, artificially sweetened beverage (sugar-free group) or a similar sugar-containing beverage that provided 104kcal (sugar group). Beverages were distributed through schools. At 18 months, 26% of the children had stopped consuming the beverages; the data from children who did not complete the study were imputed.


The z score for the body-mass index (BMI, the weight in kilograms divided by the square of the height in meters) increased on average by 0.02 SD units in the sugar-free group and by 0.15 SD units in the sugar group; the 95% confidence interval (CI) of the difference was -0.21 to -0.05. Weight increased 6.35kg in the sugar-free group as compared with 7.37kg in the sugar group (95% CI for the difference -1.54 to -0.48). The skin-fold thickness measurements, waist-to-height ratio, and fat mass also increased significantly less in the sugar-free group. Adverse events were minor. When we combined measurements at 18 months in 136 children who had discontinued the study with those in the 477 who completed the study, the BMI z score increased by 0.06 SD units in the sugar-free group and 0.12 SD units in the sugar group (P=0.06).


Masked replacement of sugar-containing beverages with noncaloric beverages reduced weight gain and fat accumulation in normal-weight children.


Opening comments

Today’s article has a high likelihood of being taken way out of context – something that is not allowed here. Some may argue that this article tries to answer one of the most pressing questions of the 21st century, and that is, “what is the cause of childhood obesity?” However, this article does not due certain methodological weaknesses leaving us wanting for more. Instead, the article shows us exactly what we’ve known all along, and that is, when you eat fewer calories, you gain either less weight or no weight at all. In today’s article, we’re talking about the former. So without further ado, I will show you why this article doesn’t prove that sodas cause obesity before it gets taken way out of context on every news channel around… because it most certainly will.

Introduction & Results

The article begins with acknowledging the concomitant rise in both sugary beverage consumption and obesity in children. The authors postulate this correlation is due to soda’s inability to compensate for calories at subsequent meals – a topic I covered thoroughly back in April. Indeed, the literature to-date suggests that liquid calories do not have the same effect on satiety that solid foods do. Therefore, sodas may promote increased food intake (or lack of calorie displacement) by virtue of sugar’s vehicle (liquid medium) rather than the sugar itself. However, none of this was evaluated in today’s study.

Lastly, the authors note the lack of convincing evidence suggesting sodas’ causational role in obesity due to other collinear factors such as fast food consumption (which usually coincides with soda consumption) and lack of physical activity (or as they put it, increased television watching). Therefore, they sought to examine the effect of replacing soda with a masked, calorie-free soda substitute on weight gain (further adding to the lack of causational data).

In the end, both groups (those who drank the sugar-sweetened soda and those who drank the diet soda) gained weight and fat mass (as expected given their age). However, the group receiving the sugar-sweetened soda gained more weight (16lbs vs. 14lbs) and more fat mass than the sugar-free group (3.5lbs vs. 2.3lbs).

Study Strengths

Strengths of the study include double-blind randomization of participants, an 18 month study duration, large sample size (n = 477), and urinary sucralose measures to assess the sugar-free group’s adherence to the intervention. Other strengths include custom-made sodas which were designed to taste identical (this eliminates subject bias) and teachers’ reminders and physical watching of the children consuming the beverages in school (ensures adherence).

Study Weaknesses

Unfortunately, the study is filled with more weaknesses than strengths. First and foremost, there was no mention of diet or physical activity of any of the 477 participants who completed the study. Secondly, 26% of participants dropped out for unspecified reasons. Thirdly, skinfold measurements and BIA were used to assess body composition, both of which are highly prone to human error. Now don’t get me wrong, I am not naïve enough to think that all 477 kids could have been DXA’d. However, a subset of participants could have been analyzed using DXA to confirm skinfold and BIA measurements. Lastly and most importantly, assuming that the two groups’ diets were identical at baseline, the addition – or in this case the subtraction – of one soda per day (104 kcal) for 18 months resulted in the sugar group potentially receiving over 56,000 kcals MORE than the sugar-free group. All this proves is that if you consume more calories, you gain more weight. WOW, huge shocker there!

Comments and conclusions

It’s not surprising that the sugar-free group gained less weight than their sugary counterparts; the researchers theoretically removed over 56,000 calories from the sugar-free group’s diet over an 18 month period! Furthermore, suspicions of increased food intake caused by soda intake were never even evaluated. In order for that to happen there needed to be some form of assessment of diet over the 18 month period. This, however, was mistakenly left out. On the bright side, this study does lend some credence to efforts to reduce soda intake in children, despite showing no causational effects of soda on obesity whatsoever. Remember, sodas are an easy and readily available source of nutrient-poor calories; that is all. Sodas don’t cause obesity more so than does an extra equi-caloric serving of brown rice each day. If you want to enjoy that can of soda you have to remember to eat less of other things throughout the day (whether or not this is possible in free-living populations is the TRUE question and one that was nowhere close to being answered in this study). Therefore, although the aim was to examine the effects of replacing a chronically consumed sugar-sweetened soda with a diet alternative on weight gain, I would suspect similar findings with ANY food source being substituted with a calorie-free alternative.

Bottom-line: consume fewer calories; you’ll gain less weight if you do.

Posted in Reviews | 2 Comments

Roundtable Interview with Layne Norton PhD, Eric Helms and Alan Aragon


Before I begin I just want to take a minute to thank (for the thousandth time) Layne, Eric and Alan for humbly doing this e-mail interview with me. For those of you who don’t know who these men are, you can skip to the end of the interview (for their website links below) and get educated. For the rest of you, introductions are not necessary. In short, I cannot thank them enough for taking the time to answer my questions. I specifically chose to ask the questions that I did because I noticed that every interview these guys do they pretty much answer the same damn questions over and over. To be quite honest, I find it a waste of their time, and mine, to hear the same responses repeated… and repeated… and repeated. Hopefully you will find today’s interview a little more substantive, meaningful, and fun.

In conclusion, each one of these gentlemen has had a profound impact on me and my life, in more ways than one, and without them I can honestly say that I would not have pursued a degree in nutrition nor would I have had the courage to ever start up Calories in Context; and for that, I can never thank them enough. So, before I get too carried away (because I could write an entire article on how these guys have impacted me), I hope you all enjoy what Layne, Eric and Alan had to say as much as I did. So without further ado, let’s get to it!

Me: What spurred your interest in nutrition/fitness and inevitably made you want to study it in college (be it undergraduate/graduate/doctoral)?

Alan: I think anyone in his right mind has an innate obsession with carbohydrate, protein, and fat :)…  Just kidding, sort of. I originally was a graphic design major in college. Back when I first got into training and nutrition in the late 80’s and early 90’s, personal training wasn’t considered a real job yet, so I was advised against pursuing a fitness-related degree. At a certain point I said, ‘Screw this, I need to go after what I’m genuinely interested in.’ I was torn between going into exercise science or nutrition, but since, at the time, my ambition was to be a trainer, I figured that my certifications would cover the exercise side, so I went for the nutrition degree. I ended up getting my graduate degree in nutrition as sort of an afterthought, but I ended up really enjoying the process of writing and teaching. The rest is bro-history.

Plenty of my colleagues tell me that I should get a doctorate, but I can’t be more satisfied with my current career trajectory, so fixing what ain’t broke isn’t really an option. There was a time that everyone encouraged me to become an RD [Registered Dietitian], but I didn’t feel the strong impetus to do so; same with getting a PhD. Thus far, it hasn’t been a career handicap in the slightest.

Eric: I fell in love, head over heels, absolutely obsessed with bodybuilding, lifting and getting stronger. I tend to get consumed by things I’m passionate about. So really it was hard to see anything else for me as a potential study topic as nothing else held my interest and intrigue in the same way.

Layne: For me it was pretty simple. I started lifting weights in high school to get more attention from girls and try to stop bullies from picking on me. Over time lifting transformed from something I did out of lack of self-esteem to something I did because I loved it. As I read more and more about training and nutrition I realized that there was a huge gap in the advice that every expert in a magazine recommended. I would read one article that said to do one thing, then read another contradicting it. So I decided to start researching for myself. That turned into a passion for research over time.

Me: What aspect(s) about yourself has/have made you as successful as you are today? In essence, what separates you from everyone else out there?

Alan: This is a tremendously tough question to answer. I’m not sure, so I’m just gonna’ ramble. I think part of my success is a result of being as real and honest as possible whenever I try to convey ideas. I’ve been told that I’m good at taking complex information and distilling it into concrete terms that most people can understand. That, plus I’m skeptical as hell, since most information pumped out in this industry is purely crap. I have an impressive list of clients, but a lot of other guys have that too. I guess none of those would separate me from everyone else. So, I really don’t know…

One thing I noticed that might separate me is that I know how to laugh at shit; too many people at the top of their fields are far too wrapped up in appearing polished or being politically correct. It stiffens them up, and their real colors and personality never show, and they end up unnoticed among the hordes of people trying to make names for themselves.  People also tend to be too wrapped up in preserving a god-like aura. We’re all just humans, so we shouldn’t take ourselves so damn seriously every minute we’re in the public eye. One thing I learned early on in the game is that it’s okay to be wrong about stuff, and that it’s actually a sign of diligence and integrity to adjust your position on any given topic depending on how the evidence evolves.

Eric: First of all, I really don’t think I’m separate from everyone else out there. Sure, I’m unique, I’m me. There is only one me, but there is only one everyone for that matter. But, I get what you are trying to ask: “why is it you are interviewing me, why isn’t someone else a relatively well-known name in this field?”

For me, I think it comes down to being genuine. I’m not trying to sell something, I’m not trying to push anything, and I don’t have an agenda. I just want to share my passion and help people. That, coinciding with a relatively extroverted personality and a very dedicated and focused approach to bodybuilding and powerlifting and the science related to it, has put me where I’m at. I also think having grown up immersed in online forums and the internet helped me transfer my information and “get myself out there” during the boom of social media with less of a struggle than some others who might have been less comfortable with this medium.

Layne: To be quite frank, I feel like I just want it more than many other people and worked my butt off over a long period of time.  Even before I was well known in the industry, I would spend tons of time each day answering 60-70 emails from people, asking for nothing in return.  I spent hours each day on bodybuilding forums answering questions and giving out free advice.  I would write articles for free for any website or magazine that would print them.  I was willing to do whatever I possibly could to get my philosophies out there.  On top of that I was taking full time classes, doing research, and of course lifting every day.  But I loved it, so it never felt like work.  But I have always said that I feel like success is a battle of attrition.  Everyone gets discouraged at various points and wants to quit, the difference is who can keep going and putting one foot in front of the other when those rough patches hit.  Anyone can be motivated when things are going well.  What separates people is who can stay motivated when everything is going to crap.

Me: Why do you think people enjoy the information that you put out? What makes it hit home for them? 

Alan: I kind of live a dual life in terms of the information I put out. On one side, I write for various lay publications, where getting all freaky and technical isn’t really gonna’ help anyone. On the other hand, in my monthly research review, I can really slam folks with jargon and complexity when the topic lends itself, knowing that the readership will be familiar with the terms and concepts. I think that it’s important to be sensitive and in-tune with the audience, and this audience varies in my case. I was just on a call today with one of the senior editors of Men’s Health who is putting a story together on various fitness/nutrition myths. I was asked whether or not people “need” a post-exercise shake, like it’s often pushed in the fitness and bodybuilding magazines. I proceeded to explain that there is a continuum of importance for these sorts of tactics, and the vast majority of Men’s Health readers will reap all the benefit they could possibly need by simply nailing their protein target for the day. The rest is just nitpicking toward what might hypothetically clinch that extremely narrow edge, which might be important for elite competitors, but not relevant to weekend warriors.

Eric: You know to be honest, I couldn’t say. I just do my thing. There are billions of people on the planet, and I figure that there are enough people out there that can relate to me that I really don’t have to “do” anything or be anyone besides myself.  I’ve always found that when you are honest, genuine and real, most people can relate to you. And if they have coinciding interests, they are open to what you have to say.

Layne: Probably because I don’t try to BS people with magic tricks.  Anyone who follows me on twitter knows I hate ‘guruism.’ (Term coined by Bret Contreras).  Guruism is when people make up outlandish BS to try to sell people that they have some magic secret that will give people the key to unlocking unbelievable results.  That’s complete crap.  80-90% of this stuff is hard work and dedication.  You can have a terrible approach, but if you work really hard over a really long period of time you will get results. However, this doesn’t mean that they are optimal.  I’m the first to tell people that there are no secrets.  Certainly there are small tweaks to be made to try to optimize things, but if you are looking for some magic ‘secret’, sorry, I don’t have it. 

Me: Where do you see the field of nutrition/exercise science heading in the next 10 years?

Alan: I see it all going to hell in a hand-basket… Hah! Seriously though, I’m excited for what’s to come as research marches on, bringing us closer and closer to understanding how to either simplify or modify training or dietary protocols for the better. The field itself has gradually gained legitimacy (I’m talking about training in particular), and organizations such as the NSCA & NASM have really put their necks out and made strong efforts to raise the barriers toward being considered worthy of being a practitioner in the field. An interesting thing I’ve noticed – but saw coming for quite some time – is the growing interest in solidifying a nutrition certification for those who aren’t interested in standard/traditional collegiate routes governed by the ADA (recently changed to the AND). I think that as much of an eyesore as they may be to the old guard of dietetics administration, newer organizations such as the ISSN are really going to make some deep inroads into the traditional model, as they continue to capture the interest (& preference) of fitness professionals seeking to bolster their credibility in nutritional knowledge.

In general, I see continued growth of the allied health and fitness fields. This is always going to be a double-edged sword, since the fitness field attracts nutcakes and quacks like bees to honey, but at least the nutjobs give me plenty to write about in the spirit of protecting the public from false information.  My hope is that the allied health and fitness professions place a continued emphasis on research-based guidelines, and also an emphasis on critical thinking. I’m not sure if the latter will ever happen to a satisfactory degree, but we can always hope.

Eric: I think the internet becoming more and more involved is a good thing in many ways. It adds speed, transparency and ease of collaboration. I can write a paper with someone I’ve never physically met. I can hook up with a professor at a university on the other side of the planet and discuss research. My thoughts and ideas are open to the criticism of everyone with an internet connection. So I think information will become higher quality slowly but surely through better collaboration and because there will be more people to check the t’s and dot the i’s.

Layne: I honestly am very excited about it.  For decades researchers were just viewed as lab junkies; people who were knowledgeable but had no clue how to apply it.  But right now I know dozens of competitive bodybuilders, lifters, and enthusiasts doing their PhDs or advanced degrees in a relevant field.  I think that the merging of research and practical application is going to provide a lot of the answers we have been searching for.

Me: Similarly, where do you see yourself in the next 10 years?

Alan: If all goes as planned, I see myself doing exactly what I’m doing now. Perhaps the only change would be more volunteer outreaches to younger folks (high school and early college) where I can talk about what it takes to succeed, and how important it is to find out what it is that interests them so they can make a great life of it. It kills me to know that so many students think they have to fit into a conventional/socially expected career mold whether they hate it or not.

Eric: In ten years, I know one thing is for sure. I’ll be happy, pursuing my goals and making awesome human connections. That’s all I know 100% for sure. But, based on my current trajectory, I will have been a PhD for half a decade, and maybe have done some teaching at the university level, published some studies in the field, and possibly gotten bored and started to pursue a second PhD in sports psychology or something.

Also, I will be a veteran competing in the professional ranks in natural bodybuilding, becoming more competitive with each outing. Lastly, I hope to have gotten myself closer to the elite status in raw drug free powerlifting, and maybe I’ll even have put up a respectable total in Olympic weightlifting that I have just started to dabble in. Possibly I’ll be coaching some weightlifters too!

Layne: I guess that’s a weird question for me.  I don’t necessarily have a 10-year plan.  My approach has always been to keep my head down and keep working hard and the opportunities would take care of themselves.  So far, I have been right, so I plan to stick with the game-plan.  Overall in my life, I want to leave a legacy of someone who worked their tail off, treated people right, and did things with a lot of integrity.  That might sound silly, but integrity and character are things I take extremely seriously.

Me: If there is one piece of wisdom that every beginner weight-lifter out there should absolutely have, what should it be?

Alan: One piece of wisdom? That’s a toughie. If I could pick just one, it would be that achieving big goals takes time – plenty of time. Despite what the multitude of online rip-off ads promise (i.e., “shortcuts” or “secrets”), developing a high level of athletic skill or physique development is a matter of several years of mind-numbingly consistent, hard work. Remember there’s no such thing as a short path to greatness, so enjoy the long haul.  I’ve actually compiled a list of these types of tips, just Google “Wisdom & Wisecracks.”

Eric: Learn from everyone. A smart person who is dedicated to personal growth can find a gem of knowledge or wisdom from literally everyone. As soon as you write someone off, you’ve closed an avenue for growth. Humble yourself, and see everything as an opportunity for growth and learning. Also, patience is the most valuable attribute you can have. My success in lifting and bodybuilding has little to do with my next 3 months of thinking and planning and everything to do with setting myself up for long term goals. I envision where I will be years from now, and then ensure I get there by putting in the work. In less words: humility, openness, patience, hard work.

Layne: Patience.  This is not going to happen overnight.  Please see my comments about success being a battle of attrition.  Success in lifting/bodybuilding is no different. 

Me: Are there any mistakes that you’ve made in the past, specifically with regards to training and nutrition, that you look back on and say, “What the hell was I thinking?!” And if so, what steps did you take to correct those mistakes and learn from your errors?

Alan: Perhaps my biggest training mistake was, as a beginner, following the popular bodybuilding split where each body part is bludgeoned with a high volume once a week. This was straight from the magazines, so how could it be wrong, right? It was blasphemy to train any other way than my idols in the mags. But then I did more reading and experimenting, and although the bro-split worked to a certain degree, cutting volume in half and doubling frequency made a huge difference. I’ve tried increasing frequency further, but cannot maintain it for more than short periods without recovery suffering. Another training mistake I’ve made in more recent times is constantly striving to lift heavier, focusing on the ‘stats’ rather than the feel. That was a good recipe for injury, especially for someone who wasn’t specifically concerned with powerlifting.

Nutrition-wise, perhaps the biggest mistake I made, funny enough, was not having an awareness at all of what might optimize gains in terms of protein and total calories. I knew that nutrition was important, but I never realized just how important it was, and how far off I was missing optimal targets. I just pretty much winged it; figuring things would work themselves out as long as I trained hard. It made a huge difference when I hunkered down and applied research-based findings towards my goals. I’ve mentioned in past interviews that a big mistake I made was being unaware of timing benefits, but eventually came to figure out that the timing had mostly to do with getting the right amount of carbs, protein, and fat within a 24-hour period.

One more mistake I want to add has more to do with philosophy rather than nutrition or exercise per se. I didn’t question enough of the concepts I was taught, either in a formal or informal setting. I often took the words of highly decorated ‘authorities’ as a matter of fact. It turns out that they were not omniscient, and neither is anyone else. Everything is open to dispute, and everything should be questioned. There’s nothing wrong with getting to the origin of any given claim, and seeing if that basis is solid or just pulled out of someone’s hot rear end.

Eric: Oh god, so many. If you aren’t making mistakes you aren’t trying hard enough and you aren’t pushing the envelope enough and you aren’t stretching yourself outside of your comfort zone. But honestly, I wouldn’t go back and change anything. Because I’ve tried every workout program and nutritional concept out there and because I’ve done every exercise, program, and diet on the planet, intelligent and otherwise, I have a vast amount of experience to draw from.

Learning is not accomplished by hoarding information, it only starts there, and that is the tip of the ice berg. Going out and putting all the theories and concepts into play is how you truly learn. We are human adults, we learn by doing. Nearly a decade of reading things, trying things, teaching things to others and coaching others has taught me that action is the way you learn something completely (if there is such a thing) and embody knowledge.

Layne: Sure.  I did all the guru stuff like eating 8 times per day, taking 100g of dextrose after a training session, downing 30g of glutamine per day, doing fasted cardio, etc.  But I would not take it back; those experiences were still valuable.  Mistakes are only bad if you don’t learn from them.

Me: Who has made the biggest impact on you in terms of who you are today, and what about that person sets them apart from anyone else in your life?

Alan: Dude, these questions are intense! I’m used to being asked, “What’s the one carb to avoid in order to not get teh luv handelz

To answer your question, I would have to say that career-wise, there are two people. One of them was one of my graduate professors named Brian Koziol. He was big on picking apart research and digging into the methodological strengths and weaknesses of the various studies that shape our beliefs of what’s what in sports nutrition. He also genuinely seemed to care about whether or not students actually learned anything, in contrast to other professors who appeared to just go through the motions of a job that they weren’t necessarily passionate about.

The other person who heavily influenced my career is a guy named Lyle McDonald. He’s relatively unknown to the general Dr. Oz masses, but very well known to those in the nerdier recesses of the internet (especially Facebook). A debate I had with Lyle on his forum several years back exposed to me the fact that I didn’t know as much as I thought, and that I had grown complacent and casually reliant on my education level at the time. This led me to gather up my balls and get started on my monthly research review, which is a cornerstone of my career to the present day. Lyle is a one-of-a-kind person. More innate brilliance than he knows what to do with. Far too much going on in his mind than formal degrees can contain. I’m not too proud to point out when someone has talent, and as far as the nutrition and dieting stuff goes, Lyle is in a class by himself. His reach of influence has been vast – on not just me, but many others. He’s not the most warmly adored figure in the industry, but I gotta’ give credit where credit is due.

Eric: I wouldn’t be able to list just one person. But I have some members of my family and some close friends who have shown me truly what unconditional love is, what being genuine and authentic means, and I’ve watched people achieve balance and happiness in life through living life authentically and I have emulated this with great success.

I have learned that belief in one’s self is the key to all success. The only true barriers to success are self-imposed. We are the gatekeeper to our own success in life and when we can truly understand that and take control over our own self perceptions and beliefs we can achieve great things. Not that I have mastered this, that never happens! But, because of my family and some of my close friends I at least know what I am attempting to master! A short list would include my fellow coaches at 3DMuscleJourney, and some of my close family.

Layne: Obviously my parents probably had the biggest impact on me.  They taught me a lot of what I know about hard work, how to treat people, and integrity.  Outside of them, definitely my grandfather.  He was my personal hero and the greatest man I have ever met.  If I ended up being half the man he was, I would consider myself an enormous success.

Me: What is your greatest accomplishment to-date, and what makes it so special that it surpasses everything else in your life?

Alan: Oh man, more deep questions… My greatest accomplishment to-date is finding the right girl and marrying her. This was just dumb luck, or extreme fortune, depending on how you look at it. And no, I didn’t just say this so I can show it to her this interview and enjoy the reaction to follow.

Aside from that, I’ve been extremely thrilled to influence the career paths of various individuals. For example, Daniel Yeh and John McMahan of Citadel Nutrition have personally thanked me for helping them make the decision to pour their vital resources into their supplement company. Essentially, they put everything on the line to chase what they believed in (and were passionate about), and now they’re seeing the fruits of their courage and diligence. It’s hugely gratifying to know I played a part in that. Will Citadel Nutrition exist in 10 years? 5 years? Another year? Nothing is certain, especially in the cut-throat industry that sports supplements is. However, my hunch is that they’ll continue to do well, and knowing that I contributed to their sense of integrity is priceless.

Other standout accomplishments were being invited to speak at various conferences including the Fitness Summit and NSCA Personal Trainer’s Summit. The thing about these engagements was that I was invited to speak. I didn’t have to apply to get these opportunities. The fact that they approached me, as opposed to me approaching them, tells me that I’ve reached a certain level of value in the industry that even the big boys notice. Along these lines, one of the most profound events in my career was getting invited onto the staff at Men’s Health magazine as their go-to nutrition guy. Plenty of opportunities flourished as a result of top guys in the publishing industry like Adam Bornstein and Adam Campbell being fans of my work. Men’s Health is the largest magazine of its kind in the world, many times over. For them to recognize me as someone who could fulfill their position of authority in their targeted market (post-college bros and struggling dads) was just tremendous for me.  Being invited to serve on Fitocracy’s advisory board by the founders Dick Talens and Brian Wang was a biggie as well, no pun intended.

Another big milestone for me was getting invited onto the peer review board of the ISSN by the founder himself, Dr. Jose Antonio. If there is any formal “stamp” that I am as nerdy as some folks think I am about criticizing research, then this is definitely it. This also lets me know that the time and effort I’ve spent in fulfilling my interest in the objective study of training and nutrition has not gone unnoticed by the academics in the ivory tower.  Along these lines, I’m collaborating with Eric Helms and Peter Fitschen on a bodybuilding-related article that will be published in a peer-reviewed journal. It’s almost finished; they’re just waiting on me, hahahaha! It will be a kick to finally make it into “The Pubmedz” – especially with an article that isn’t the run of the mill in biomedical circles.

Last but not least, my own accomplishments tend to pale in comparison to what my clients have accomplished – permanent improvements in their habits, and the life-long implementation of sound principles that they were open-minded enough to incorporate into their lifestyles.  To think that I’ve influenced real people’s everyday lives is mind-blowing to me. I know you asked for a single accomplishment, but I couldn’t help but take a trip down memory lane and recall the roses among the thorns in my path.

Eric: I can’t compare apples to oranges in my life, and I’ve done a few things that I’m proud of and happy about up to this point in my life, so I won’t be able to list one thing. I also know that I will continue to do more things that I see as great accomplishments, that’s the purpose of my life in many ways.

But, I would say marrying my wife Barbara is huge, that has brought me so much happiness, enjoyment, fulfillment and a partnership that makes my life amazing. I would also say that I am very proud of finding my way into my graduate work at the Auckland University of Technology. Once I decided I wanted to get my PhD I managed to find a way despite there not being any programs locally that I was qualified for, that sparked my interest or that I could get funding for. I kept hunting, I kept looking, and when an opportunity presented itself I grabbed it and wouldn’t let go. I don’t know how the studies are going to go overseas, but honestly just getting out there and doing it is a huge accomplishment.

Also, getting my natural pro card is a huge accomplishment for me. That has been a goal since I first started lifting, and I think the biggest barrier to achieving it was the self-doubt that I’ve overcome in the process. Convincing myself that I COULD achieve this goal at all was probably the biggest factor in acquiring it. I learned through this process that I could be successful at anything in life even if it required some hard work over a long time period against significant odds.

Layne: Marrying my wife Isabel and staying married.  I see so many phony relationships and people who don’t truly understand what it means to be on the ‘same team.’  My wife and I may fight, but at the end of the day we know that we have each other’s back and we love each other very much.  One of my life long goals is to NEVER be divorced. I met Isabel, fell in love with her, and love her even more today.  But we worked very hard at our relationship, just like everything else, to try to become more in tune with each other and compromise more.  We aren’t perfect by a long shot, but we are always trying.  So having a successful relationship with the love of my life is my greatest accomplishment.  If I do a good job raising kids in the future, then my family will become my greatest accomplishment I think.  As for personal stuff, completing my PhD is what I am most proud of, as it was the ONLY thing in my life I ever wanted to quit at one point. 

Me: We all know that the best ergogenic aid is some kick-ass music. Are there any bands that you just can’t lift without? 

Alan: I actually can’t stand the idea of dealing with any musical delivery implements on me while training. I just get in there and mentally block out whatever music is playing. However, driving to the gym, I have personalized playlists that include the Devin Townsend Project, Strapping Young Lad, Meshuggah, Lamb of God, Pantera, Mastodon, Killswitch Engage, Animals as Leaders, Skyharbor, Solution 45, Timfy James, Hacktivist, and others slipping my mind at the moment. On an amusing note, I occasionally watch Aragorn’s speech at the Black Gate before driving out to the gym.

Eric: What I listen to when I lift it very much depends on my mood. Sometimes it’s play time for me, and while I play hard (very hard), it’s not the same as when I am feeling aggressive in terms of my mood. I like more upbeat, funky music when I’m in this mood. For example, I found myself singing off key really loudly to Journey’s “Don’t Stop Believing” in the middle of a set a week ago, lots of fun.

Other times I go in there andI am hyped up and r eady to kill shit. I get pretty focused sometimes and I definitely relieve tension through training, and something aggressive like Disturbed, Rage Against the Machine, Eminem, Tech n9ne or really anything hard and heavy, rock or hip hop can be appropriate for me.

Lastly, sometimes I like silence when I’m training in a more introspective state; it can almost be a little more of a daily ritual, or practice. In times like these I prefer to train alone, do my thing and I enjoy just the sound of the iron and the plates.

Layne: Absolutely.  Disturbed, Chimaira, 30 Seconds to Mars, Sevendust, Skillet, Papa Roach, Filter, Hatebreed, and Shinedown are some of my favorites. 

Me: What is your favorite nutrition and or exercise-related topic to discuss/debate/write about?  

Alan: I really don’t have a favorite. The more challenging and controversial, the better, because it’s more stimulating.  I have a particular fondness for the macronutrients, since each one of them has its own ongoing war of beliefs in terms of optimal amount, type, timing, and distribution for a number of goals.  As far as training goes, I’m currently interested in the mechanisms of hypertrophy, and thankfully, I have guys like Brad Schoenfeld and Bret Contreras to bounce ideas off of in that department, since they’re deep in the thick, greasy trenches of that line of research. It’s intriguing to think that counter-intuitive aspects like metabolic fatigue could, in concurrence with hormonal factors, contribute to muscle growth (& strength) beyond merely a focus on progressive mechanical/tension-related factors alone. I always anticipate the victory of simplicity (e.g., more weight on the bar = more inches on the gunz), but the odd/esoteric findings can often grab me since they force me to re-think whatever paradigm that’s currently holding me captive.

Eric: My favorite topic changes so often to be honest. I really enjoy the kinesological aspects of movement, why people move certain ways in certain movements, how we can optimize it for specific goals, and how we can improve or correct faulty movement patterns. I also really enjoy the topic of nutritional approaches for both muscle gain and fat loss. Lastly, I’d say I really enjoy the discussion of weight training programming. Periodization, peaking, programming and customizing this to the individual lifter is very fun to talk about.

Layne: Definitely protein.  Did my PhD on protein metabolism and obviously it holds a special place in my heart haha. 

Me: What is one nutritional, physiological, or exercise -based topic that you wished you knew more about? Have you done anything to help expand your knowledge about it?

Alan: Everything…. Seriously, nothing stands out. Well, hold on. I think that I can stand to brush up on biostatistics. It’s not something that excites me (yet), but that’s a sign that I’m behind on it and need to firm up my grip. Time to contact James Krieger and Aaron Fanning (James might see this interview, but Aaron might not).

Eric: There is a whole lot more than just one topic I wish I knew more about! And I continually focus on these things to round out my knowledge. When not studying protein intake in strength athletes (my thesis topic), in my spare time I have been studying substrate utilization, metabolism, exercise endocrinology, in-depth muscle physiology and digestion.

Layne: Definitely would love to learn more about physiological and psychological responses to resistance training and periodization.  I’ve done a ton of reading, but I still feel like the programming aspect of periodization may be where I need more improvement. 

Me: What is your favorite non-exercise/nutrition-related book? What makes it such an excellent read?

Alan: I rarely read anything that isn’t related to nutrition & training. There’s just not enough time in the day. However, I recently got done reading – of all things – a fictional book called The Bronze Bow by Elizabeth Gorge Speare. What makes it an excellent read? Just everything about it kicked my ass. I don’t know how else to describe it.

Eric: I have to name just one book, seriously? Well, let me start by saying that I’m an avid science fiction and fantasy geek and I play role playing games (and I mean real table top RPGs, not ones on computers) and I probably read a couple books per month that are totally unrelated to fitness. I also have gone through periods where I really enjoyed philosophy, spirituality, and other weird topics. So asking me for one book that stands out is impossible!

Among the books in the philosophy/spirituality/personal-growth realm, I’d say the following books really helped me to grow and to change my perspective: The Way of the Peaceful Warrior by Dan Millman, The Alchemist by Paulo Coelho, The Prophet by Kahlil Gibran and Zen and the Art of Motorcycle Maintenance by Robert Pirsig. Although there are a lot of other books too that stand out.

Among the books in the science fiction/fantasy realm, I’d say the following books really were my favorites and really sucked me in: The Lord of the Rings Trilogy and The Hobbit by JRR Tolkien, The Game of Thrones series by George RR Martin, The Prince of Nothing Trilogy by R Scott Bakker (and the follow up series), The Kingkiller Chronicles by Patrick Rothfuss, The Hyperion Cantos by Dan Simmons, The Ender books by Orson Scott Card, The Dune books by Frank Herbert,  and the Ringworld books by Larry Niven. To be honest though, there are a lot more that stand out; it’s not a comprehensive list.

Layne: Well, it’s a tie.  I loved Dave Ramsey’s book The Total Money Makeover, not so much because I needed a lot of help saving money but because it was motivating to read about how powerful sacrifice can be and it reinforced what my parents taught me about money and success.  I also really enjoyed Tim Tebow’s book Through My Eyes because I love the guy’s work ethic and how he has proved people wrong every step of the way. 

Me: Can we (the readers) expect anything exciting (events, publications, travels, etc.) from you in the upcoming weeks/months/years?

Alan: AARR being posted on the projected date each month (although the universe might actually implode if that happens).  Other than that, I’ll be speaking in at least one of the NSCA conferences in 2013, and of course the Fitness Summit that I’ve been doing each year since 2008.

Eric: I am working on a lit review paper on evidence based approaches to natural bodybuilding with Alan Aragon and Peter Fitschen at the moment that we are just about ready to submit for publication that should be very cool. I’m also going to be involved with a number of projects during my graduate school work over the next 4 years at AUT that will involve a lot of topics, but will mainly involve protein intake in strength athletes during hypocaloric periods. My thesis is looking at this specifically, and I will be attempting to get my findings published and I’ll probably be taking part in publishing a bunch of other sports-science related papers over the course of the of my grad studies.

Also, in November I will be speaking in New Zealand at the Sports Performance Research Institute SPRINZ) conference on protein intake for athletes, and also at the FITex personal training conference on protein supplementation. These conferences are kind of like the equivalent of the NSCA CSCS and CPT conferences here in the states.

Layne: Oh yea, lots of stuff.  I just re-launched my website with a totally new design, more content and way more interaction so I’m updating that several times per week.  I also recently was selected as Dan Soloman’s replacement as the announcer for the Mr. Olympia contest so I’m excited to do that.  I could have never imagined watching the Olympia at home on my TV 11 years ago, that someday I would be calling the play by play… it’s insane.

Me: Where can we (the readers) learn more about what you do, the services you offer, and the information that you put out?



Layne: Definitely through my website as well as Facebook:, Twitter:, and

Me: Thank you all again! It is greatly appreciated.

Alan: Thanks so much for the exceptionally challenging and fun interview, Dylan. I really enjoyed this, and am very thankful that there are folks like yourself to help me carry the torch.

Eric: My pleasure. Thanks, Dylan!

Layne: My pleasure, thanks for the opportunity.

And thank you, the readers, for making this all worthwhile! Look out for a new article in the coming days! Until then…


Posted in Misc. | 16 Comments

Higher Protein Diets: Controversies & Implications

Opening Comments

In the wake of a recent study published in JAMA [1], wherein participants on a low-carbohydrate, higher-protein diet had greater improvements in metabolic syndrome parameters (insulin sensitivity, HDL and triglycerides), I was asked the question, “why would anyone want to consume higher protein given the inherent risks for kidney damage;” and, secondly, “why anyone would want to consume protein over the current RDA (0.8g/kg bodyweight) at all?”

To begin, the RDA is an established minimum for protein intake and does not – in any way, shape or form – correspond to an optimal intake [2]. In all honesty, it may even be sub-optimal in many cases, which I will argue in a little bit. Nevertheless, it is becoming more and more evident that there is still a lingering irrational fear of higher protein diets, if not a complete misunderstanding of the potential benefits from consuming them. Furthermore, as a point of understanding, a high-protein diet does not automatically mean a low-carbohydrate diet, although, as I will allude to throughout, there may be some benefits from altering the ratio of the two macronutrients within either weight loss and/or weight maintenance diets (i.e. replacing carbs with protein). Still, the two are not synonymous as one can easily consume a high-protein AND a moderate- and/or high-carbohydrate diet.

Lastly, I would like to point out the definition of a “high-protein” diet. Most of the literature supports the notion of a high-protein diet being any diet with protein intake contributing ~25-30% of total kcals for a given day (this usually does not go above 40% although 98% protein diets have been studied before). My definition, however, will include any figure over the current RDA of 0.8g/kg bodyweight, as it better addresses the initial questions posed to me earlier. That being said, my goal today is two-fold; 1) to show you that consuming a higher protein diet is not harmful to several health parameters; those being kidney functioning, bone health and cardiovascular disease, and 2) to show you why the current RDA for protein may be insufficient for various conditions in both typical, sedentary populations and healthy, athletic ones; like the elderly who are at greater risk for sarcopenia and strength/power athletes looking to preserve lean body mass.

Are higher protein diets dangerous?

Kidney functioning

Over the years there has been a prevailing notion that higher protein diets can be detrimental to kidney functioning. This seems to stem from the fact that patients with renal disease fare much better on diets with restricted protein intakes [3]. Although lowering and/or restricting protein intake does seem to slow the progression of renal disease due to decreased filtration rates [3], it is grossly inaccurate to state that higher protein intake actually causes kidney damage, especially for healthy persons. In fact, numerous reviews and individual studies on high protein diets have come to the same conclusion that diets higher than the RDA in protein are not detrimental to kidney functioning in otherwise healthy persons [4-7]. Furthermore, there is virtually no evidence (because it doesn’t really exist) to suggest that active individuals (i.e. athletes) are at any risk for kidney damage even though they traditionally consume well over the RDA for protein [8]. For instance, when evaluating dietary nitrogen losses through urine, Poortsmans and Dellalieux [9] compared a habitual, very high-protein diet of bodybuilders to a moderate protein diet (yet still way over the RDA) of other athletes and saw no adverse effects on renal functioning in participants consuming either of the diets, even when intakes reached 2.8g/kg (3.5 times higher than the RDA!). Furthermore, in another acute study looking at 37 male bodybuilders and 20 healthy young males of the same age [10], it was shown that although renal filtration and urinary acid excretion increased as part of a higher protein diet, the capacity for the renal load was far from maxed out. To quote the authors:

“The concomitant increase of renal net acid excretion and maximum renal acid excretion capacity during high periods of high protein intake appears to be a highly effective adaptive response of the kidney to a specific and still physiological pattern of food intake leaving a large renal surplus capacity for an additional renal acid load.”  

Unfortunately, not much else has been done in terms of research on kidney functioning in athletes during periods of high protein intake (probably because there is no need for such studies because protein doesn’t damage the kidneys!) Nevertheless, it is without question that there is a huge lack of convincing evidence that higher protein intakes are harmful to an otherwise healthy person, especially a physically active one.

Bone health

Again, over the years, high protein diets – and even just protein in general – have gotten a bad rap due to their (supposed) deleterious effects on bone health. This usually revolves around the notion that protein promotes and acidic environment in the body, and, in order to correct this pH discrepancy, bone calcium is released in order to neutralize the acidity. This notion is a gross misinterpretation of the facts and some serious homework needs to be done by anyone who thinks that protein is harmful to bones. Let me explain.

Indeed, as urinary net acid excretion (NAE) goes up (due, say, to increased protein), so too does urinary calcium excretion (uCa); no argument there. However, this is not a direct measure of bone calcium balance. Simply put, measuring only urinary calcium is to assume that it’s coming from bone; this just isn’t the case. What people choose to forget – or just flat out don’t know – is that there may be other factors at work that may be contributing to the increase in uCa. In fact, a recent systematic review and meta-analysis shows that there is no evidence to suggest that diets that increase NAE lower overall calcium balance (i.e. deplete bones of calcium) [11]. This is because increased protein in the diet leads to greater intestinal absorption of calcium, which in turns contributes to the increase in uCa [12-15]. For example, in 2005, Kerstetter et al. [14] looked at the impact of a low-, moderate-, and high-protein diet on calcium absorption, urinary calcium excretion, and overall bone turnover using stable isotopes of calcium in healthy subjects. Although uCa was shown to increase as the protein content of the diet got higher, it was shown to be directly caused by the increased intestinal absorption of calcium and not from an increase in bone resorption. Therefore, acutely speaking, a diet high in protein (2.1g/kg) was not shown to affect bone resorption or have any negative affect on overall bone health. Furthermore, diets considered low in protein (0.7g/kg) could have profound effects on bone health due to low protein intake inducing subsequent hyperparathyroidism which leads to reduced calcium absorption in the intestine [16-18]. Low serum calcium (via malabsorption) leads to PTH (a major hormonal regulator of bone) being secreted and causing calcium to be leeched from the bones in order to maintain serum calcium levels. What’s more is that these effects were seen in only a matter of 4 days! Therefore, it might actually be better to consume slightly more protein when it comes to bone health.

Cardiovascular disease

Originally it was thought that diets containing higher amounts of protein may have a negative impact on cardiovascular health [19, 20]. This, more or less, was largely due to protein being so closely associated with saturated fats and cholesterol (think high-fat red meats, milk, dairy, etc.) as well as data showing lower risk of cardiovascular disease (CVD) in vegetarian populations [21]. However, subsequent epidemiological data seems to contradict this premise [22, 23], dismissing at least some of the initial claims about protein increasing risk for cardiovascular outcomes. One must remember that, intakes showing increased red meat being correlated to increased risk of cardiovascular outcomes do not mean that higher protein leads to the same risk. In fact, substituting red meat for other forms of leaner meats has been shown to reduce risk for cardiovascular disease [24]. It is also worth noting that observational data looking at meat intake usually shows that the higher intakes of meat are usually accompanied by lower intakes of fruits and vegetables and higher intakes of fats (i.e. poorer quality diets altogether).

More recently, however, a well-written systematic review [25] of randomized controlled trials using low-carbohydrate, high-protein diets (LCHP) showed that LCHP diets were more effective than traditional diets at 6 months and just as effective, if not more, at reducing weight and cardiovascular disease risk for up to one year. Whether the effects can be attributed to the increased protein or the decrease in carbohydrate is irrelevant. The fact remains that the higher protein content of the diet had no detrimental effect on cardiovascular outcomes as was once thought and even edged out a traditional weight loss diet in terms of CVD management.

Evidence in support of consuming higher-protein diets

Now that we’ve established that it is completely safe to consume higher protein diets – given that the rest of your diet isn’t crap (there’s always the fine print) – let’s try and build a case for why someone would benefit from consuming more protein on a daily basis. In the case of bone health, I mentioned the fact that consuming higher protein – that is, protein intake above the RDA – may work in your favor when it comes to calcium absorption and protecting against hyperparathyroidism. There are, however, some other situations that could, and in all likelihood do, warrant higher protein intakes. Let’s see what they are!

Sarcopenia in the elderly

Over the years much research has gone into preventing sarcopenia (age-related muscle wasting) in the elderly. It is well known that those who are older are at an increased risk for muscle wasting, and this may be due to some refractory effects to muscle protein synthesis that occur as one naturally ages [26]. It has been shown that the elderly do not respond similarly to a given dosage of protein under ~20g when compared to those who are younger [27]. Therefore, the elderly may need considerably more protein (~30g or more/meal spread out over 3 or more meals) in order to stave off muscle loss, regardless of grams per kilogram bodyweight [28]. This may require intakes well above the current RDA for a given person.

Higher protein intakes for athletes

I find it humorous that those who vilify higher protein needs for athletes usually base their argument around the fact that those “needs” were justified using an imperfect method (i.e. nitrogen balance; NBAL). I hate to break it to you, but the RDA you so fervently defend was forged using the same imperfect method. Therefore, the case can be made for athletes to consume higher protein diets. Whether or not they already do is beside the point.

Numerous reviews have covered the subject, all with similar conclusions about protein intakes for both endurance and resistance athletes [29-32], with intakes ranging between 1.2-1.7g/kg for strength/power athletes and 1.2-1.4g/kg for endurance athletes. Furthermore, some unpublished work by Eric Helms [33] thoroughly examines the literature to-date on higher protein needs for athletes who are in caloric deficit and already lean. He makes a convincing case for the increased needs of protein for those types of athletes who still need to perform at a high level but are considerably lean to begin with.

Higher protein for weight loss

Considerable data has also shown us that diets higher in protein compared to ones higher in carbohydrate are as equal if not superior in terms of fat loss and lean mass preservation [25, 34]. In fact, in a recent well-designed 12-month randomized clinical trial (4 months weight loss, 8 months weight maintenance) [35], it was shown that a diet comprised of 1.6g/kg (twice the RDA) protein outperformed a traditional diet using 0.8g/kg protein in terms of percentage of fat mass lost (about the same for both groups) and lean mass preserved (about 10-14% more for the high protein group). Furthermore, in conjunction with a resistance exercise program, the fat-loss and muscle-preservation effects of a higher protein diet are even greater when compared to an isocaloric, traditional, higher carbohydrate diet [36-39]. Simply put, if you want to lose weight, reduce your calories and call it a day, independent of diet strategy. However, if you want to lose more fat and preserve more lean body mass, you may fare better on a diet higher in protein, especially if you’re involved in some sort of resistance training protocol.

Glucose homeostasis

In some instances, weight loss diets comprised of higher protein and lower carbohydrate have been shown to improve glucose homeostasis in overweight and obese people more so than traditional weight loss diets [40, 41].  Furthermore, it has even been shown that higher protein diets improve glucose homeostasis in type 2 diabetics without weight loss [42, 43]. This is important because it illuminates the power of altering the dietary composition of one’s diet. Simply by replacing some carbohydrates with protein can make all the difference.

Protein and satiety

Lastly, from a dieting standpoint and regardless of health parameters, protein and higher protein intakes have been shown time and again to be more satiating than diets comprised of less protein (i.e. higher carbohydrate) [44-46]. Obviously, if you’re a 200lb bodybuilder or football player with high caloric needs, satiety may not be an issue until you get to extreme levels of leanness. Nevertheless, for the average American, higher protein would most likely be beneficial in terms of dietary adherence and satisfaction. Therefore, I see no reason why anyone would want to diet otherwise. And, just to clarify, this does not mean reducing carbohydrate intake to astronomically low levels (<10% of intake). This may, and has been shown, to cause subjects to fall off their diet plan. Rather, simply replace some carbohydrate with an equal amount of protein in order to benefit from increased satiety without depriving yourself of too much carbohydrate.

Conclusions and Comments

In conclusion, it seems evident that higher protein diets are neither harmful nor useless when it comes to health parameters such as kidney, bone, cardiovascular disease, type 2 diabetes, obesity, lean mass preservation and satiety. Obviously, if you have some preexisting medical condition, such as kidney disease, a higher protein intake would not be of benefit. However, this is of triviality because you’re probably already in the hospital (or under some form of medical watch) with strict dietary monitoring anyway.

The overall message is that high protein diets should no longer be feared based on misinterpreted data and outdated theories. There is no convincing evidence to suggest that high protein diets cause kidney damage, bone resorption or cardiovascular disease in otherwise healthy individuals. Furthermore, there is accumulating evidence for the consumption of more protein, above the RDA, for multiple populations in order to improve health status. So enjoy your protein, especially if it means better glucose homeostasis, lean mass preservation and bone health. Or, at the very least, because it tastes great!


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33. Helms E. The effect of protein intake on fat free mass in lean weight lifters during energy restriction: a case for higher protein intakes. Unpublished, 2012.

34. Layman DK, Bioleau RA, Erickson DJ, et al. A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women. J Nutr. 2003;133:411-417.

35. Evans EM, Mojtahedi MC, Thorpe MP, et al. Effects of protein intake and gender on body composition changes: a randomized clinical weight loss trial. Nutr Metab. 2012;9:55.

36. Wycherley TP, Noakes M, Clifton PM, et al. A high-protein diet with resistance exercise training improves weight loss and body composition in overweight and obese patients with type 2 diabetes. Diabetes Care 2010;33:969-976.

37. Meckling KA, Sherfey R. A randomized trial of a hypocaloric high-protein diet, with and without exercise, on weight loss, fitness, and markers of the metabolic syndrome in overweight and obese women. Apply Physiol Nutr Metab. 2007;32:743-752.

38. Josse AR, Atkinson SA, Tarnopolsky MA, Phillips SM. Increased consumption of dairy foods and protein during diet- and exercise-induced weight loss promotes fat mass loss and lean mass gain in overweight and premenopausal women. J Nutr. 2011;141(9):1626-34.

39. Kerksick C, Thomas A, Campbell B, et al. Effects of a popular exercise and weight loss program on weight loss, body composition, energy expenditure and health in obese women. Nutr Metab. 2009;6:23.

40. Layman DK, Shiue H, Sather C, Erickson DJ, Baum J. Increased dietary protein modifies glucose and insulin homeostasis in adult women during weight loss. J Nutr. 2003;133:405-10.

41. Farnsworth E, Luscombe ND, Noakes M, Wittert G, Argyiou E, Clifton PM. Effect of a high-protein, energy-restricted diet on body composition, glycemic control, and lipid concentrations in overweight and obese hyperinsulinemic men and women. Am J Clin Nutr. 2003;78(1):31-9.

42. Nuttall FQ, Gannon MC. Metabolic response of people with type 2 diabetes to a high protein diet. Nutr Metab. 2004;1(1):6.

43. Gannon MC, Nuttall FQ. Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition. Nutr Metab. 2006;3:16.

44. Keller U. Dietary protein in obesity and in diabetes. Int J Vitam Nutr Res. 2011;81(2-3):125-133.

45. Veldhorst M, Smeets A, Soenen S, et al. Protein-induced satiety: effects and mechanisms of different proteins. Physiol Behav. 2008;94:300-307.

46. Paddon-Jones D, Westman E, Mattes RD, Wolfe RR, Astrup A, Westerterp-Plantenga M. Protein, weight management, and satiety. Am J Clin Nutr. 2008;87(suppl)1558S-61S.

Posted in Diets, Protein | 3 Comments

São Paulo, Brazil: Past and Present

Opening Comments

Best seat in the house

Although my Blog is primarily used for my musings about sports-related nutritionand supplement topics, I would like to take some time and devote a portion of my Blog to something else that has recently become a major interest for me, if not a new found passion. A couple of weeks ago I spent seven days down in São Paulo, Brazil volunteering at a nutrition rehabilitation center along with seven other classmates and our professor. This was actually my second time traveling to this center (my first time was May 2011), so unlike the majority of newcomers in the group, this trip had a significant meaning to me – a meaning that I am still trying to make sense of today. So before I get ahead of myself, let me describe the nature of my trip and then follow up with a couple choice photos of my time spent down there (both last year and present). Hopefully, if anything, you will be able appreciate the amazing work that goes on to help some of the poorest and most nutritionally deprived children this side of the globe. Lastly, in addition to raising awareness, I hope for this to be an enjoyable remembrance – for myself and those – who took a chance to step outside our comfort zones and experience something new and exciting wherein, perhaps, we even learned a little something about ourselves.

Center for Rehabilitation, Education and Nutrition (CREN)

CREN from the street

The center we “volunteered” at – called CREN – was envisioned in the early 1980’s and actually came to fruition by the early 1990’s. The center was established in order to provide nutritional and medical assistance to the most undernourished and impoverished children of São Paulo’s favelas (slums). Today, the center is funded by the Federal University of São Paulo (UNIFESP) and private donations from Italy. All nutritional, psychological, medical and social services are offered, free-of-charge, to the children who attend the center. In essence, CREN operates like a small day-care center (which I will refer to as semi-in-patient care) and health clinic.

The children arrive early in the morning and, after ~10 hours, are picked up in the evening by their parent(s). This facilitates two needs: quality nutrition as well as care for the child and time for the mother and/or father to make an income during the day. There are roughly 70 slots available for the semi-in-patient care at CREN; those children who are not admitted usually have appointments with the nutritionist (and often the psychologist as well) to gauge the growth and development of the child. Ideally this is what should happen; however, this is not always the case. This is because, in order to get to the center, mothers and their child(ren) must take – what could be – a rather long bus ride to the center. Although this may seem trivial to you or I, in actuality this is a fairly substantial added cost for those who live on very little money each day.

Typical bus

My girlfriend Marina and I on the bus last year (2011)

While at CREN, the children are given five meals throughout the day alongside various activities like games, reading, nap-time, etc. Each meal is home-made by the cooks who work at the center. Each meal usually incorporates some form of protein, complex-carbohydrate, vegetables, and fruit or freshly squeezed fruit juice. For instance, a typical lunch would be something like seasoned chicken, rice and beans (pinto or black), collard greens, and fresh-squeezed papaya juice; something we actually ate while down there. This is meant to provide the children with adequate nutrition for proper growth and development during these critical years. Without this intervention, many kids may become stunted (if they are not already) and possibly even cognitively underdeveloped (again, if they aren’t already). Most children, however, are either moderately-severely underweight and/or stunted. This not only puts them at a social disadvantage, but stunting and poor growth throughout childhood predisposes the children to an increased risk for non-communicable diseases like obesity, type 2 diabetes, dyslipidemia, and so on. Regaining ones height, however, is extremely hard to do, especially after the first two years of life. This is why it is so important for these children to come to CREN; that way they may receive the best chance possible to grow and develop properly. You have to remember, not only are they themselves affected, but so too are their children, who will be at even greater risk for being born with low birth weight and becoming stunted; the cycle continues.

“We’re waaaitinggg!”

The children can only take part in the semi-in-patient care from ages 0-5 years. After age five the children must attend the local public schools. However, they may come back for any medical attention that they may need, up until their 19th birthday – again, completely free-of-charge.

Student Involvement

For us – the students – the trip serves as a supplement to a course called Global Nutrition that is taught by an amazing professor – Dr. Daniel Hoffman – whom I call a close friend. Last year I actually took the course and was fortunate enough to become a Teacher’s Assistant for the course this year. I also got to operate as a student chaperone for the incoming group. It was an opportunity that I can never fully express my gratitude towards.

“Shall I lick my plate?”

The trip allows us (the students) to truly experience the nature of undernutrition that we might have otherwise never have seen. Our professor had done – and is still doing – research based out of CREN and, over the years, has managed to form an amazing relationship with the director who was gracious enough to let us come to the center and learn. Over the course of the semester we spent time reading about various micronutrient deficiencies (Fe, I, Zn, Vitamin A, etc.), stunting, the viscous cycle of poverty and health, and the context in which malnutrition manifests itself. Simply reading about malnutrition, stunting and wasting means absolutely nothing until you witness it with your own eyes. That being said, each one of us confronted humanity on a very intimate level and, in the process, discovered parts of ourselves we would have otherwise never have known. It was truly a remarkable experience.

“And we get this FIVE times a day??”

My Experience

“What are you doing here? This is my house. Get out!”

Over the course of the week (both last year and this year) my peers and I got to do a multitude of activities; we saw individual case studies of severely malnourished children and the unique medical, nutritional and social problems that affected each child and how they developed; we got to visit the favelas and the homes (if you can call them that) of patients of the center; we got to sit in on nutrition counseling sessions between the nutritionist and some of the outpatients; and lastly, we got to interact (albeit much less than last year’s trip) with the children. As I already alluded to, I am still trying to wrap my head around everything that I saw and heard during my stay this year. This trip was definitely an emotional one for me, on so many levels. So rather than try to put it into words I have decided to leave many things unsaid until I can figure out how I want to say them. I will, however, leave you all with some choice photos that I think sum up the trip very nicely.

“Did he say more photos? RIGHTEOUSSSS!”

In closing, I have been seduced by a culture and a people that I would have never imagined being a part of. My time spent in São Paulo and at the center – although short – has been a time with life changing implications. I will be returning this winter for a couple of days, and then again next spring for another full week. I urge anyone who reads this to share it with others and to step outside your own comfort zone and experience something that you may have otherwise only read in a book. I know my life has been touched for the better and I can only hope that I made an equally profound impression during my time at CREN; although something tells me that’s wishful thinking. As promised, I leave you all with some pictures (courtesy of my professor and the lovely ladies I traveled with, both this year and last) of my stay in São Paulo, Brazil. I would also like to note that we did manage to have some amazingly fun times while we were down there. A special thanks goes out to last year’s group; Barbara, Marina, Erin, Samantha, Andrea, Tara, Rebecca and Melanie, as well as this year’s group; Thaisa, Janet, Lauren, Alexa, Jessica, Cody, Carolyn, and Eliza. I am honored to have gotten to meet you all and experience this trip with you. I hope I was able to make it as fun for you as you all made it fun for me. Lastly but not least, the biggest thanks goes out to Dr. Dan Hoffman, for without whom this trip and this life-changing experience would have never been possible.

The start of the favela

Plumbing in the favela

Live music one night

Myself dancing with the lovely Thaisa

The Queen

Mandioca frita

The Gang 2011

The Gang 2012

And after a long day…

… we nap.

Cachaça (aka nectar of the Gods)

Perfection (Queen beef, farofa, mushrooms, asparagus, heart of palm, and a Brazilian take on the potato chip) [Not in frame: Xingu beer]

“Até logo!” [From the rooftop bar]


Posted in Misc. | 2 Comments

FDA Flexes Muscle at DMAA – But Should We Even Care?

Opening Comments

Times may be tough, but people still want to get JACKED! That is, not unless the FDA (Food and Drug Administration) has something to say about it. Over the past couple of months things have really heated up over the use of 1,3-dimethylamylamine (commonly known as DMAA) in pre-workout supplements, most notably Jack3d and OxyElite Pro from USPLabs  – the poster boys, if you will, of the DMAA movement. This past April the FDA issued warning letters to ten manufacturers and distributors (USPLabs included) of dietary supplements that contain the “adulterated” ingredient because these companies have not submitted the required evidence to support the safety of their products. To quote Daniel Fabricant, the Director of FDA’s Dietary Supplement Program;

“Before marketing products containing DMAA, manufacturers and distributors have a responsibility under the law to provide evidence of the safety of their products. They haven’t done that and that makes the products adulterated.”

The law that Fabricant speaks of is the Dietary Supplement Health and Education Act of 1994 (DSHEA) which essentially states that, in order for DMAA to be legally sold as a dietary supplement, it must meet one of two requirements; DMAA must either be 1) a naturally occurring substance or 2) have documented history of use prior to 1994. Unfortunately, the evidence to support DMAA as meeting either of these requirements is undeniably scarce. In fact, the entire legitimacy of using DMAA as a dietary supplement hinges on a single study from a Chinese journal that does not exist anymore [1] and whose contents have currently come into question. Because I cannot access this journal article I cannot (and will not) comment on the legitimacy of the issue. Whether or not it’s legal will be left up to the courts to decide.  Rather, I will have to do the next best thing and look at some studies that directly analyze the efficacy and safety of DMAA (as Jack3d and OxyElite Pro) as a dietary supplement.

Unfortunately, all the studies that look at DMAA are from a single group of researchers down at the University of Memphis, TN, whose studies were funded by USPLabs and whose articles (4 out of 5) were published in a second rate journal (1 edition), the reputation of which is tenuous at best. That being said, let’s see if these studies lend any insight whatsoever into to whether or not DMAA is even safe and, more importantly, if Jack3d is even worth spending money on.

DMAA and its Effects on Blood Pressure

In one of the first studies looking at DMAA, researchers had 10 healthy, exercise-trained subjects (5 men, 5 women) ingest either 250 mg caffeine alone, 50mg DMAA alone, 75mg DMAA alone, 250mg caffeine + 50mg DMAA, or 250mg + 75mg DMAA on five different test days [2]. The addition of caffeine is due to the fact that DMAA is usually taken in conjunction with it (like in Jack3d and OxyElite Pro). In the paper there was no specification of a wash-out period between dosages, although the study was considered a randomized, double-blind, cross-over study. Like I said, tenuous.

Subjects ingested the capsules on an empty stomach in the morning following a 10-hour fast – not a likely scenario for most gym-goers, save maybe the few but growing number of intermittent fasters out there. After ingestion, heart rate (HR) and blood pressure (BP) – both systolic (SBP) and diastolic (DBP) – were measured every half hour for two hours, among other parameters that I will not discuss.

After the two hour study period, HR was not seen to be significantly altered by the ingestion of any of the capsules. In fact, HR actually slightly decreased in all protocols, but not enough that it couldn’t have been from procedural error. What was significant was the rise in SBP after the ingestion of 250mg caffeine + 50mg DMAA and 250mg caffeine + 75mg DMAA. SBP rose from ~119mm Hg in both conditions to about 132mm Hg and 141mm Hg, respectively (see table below).

Now, to put this into perspective, the American Heart Association classifies normal BP as being below 120/80 (see table below). Borderline hypertension is above 120/80, and Stage 1 hypertension is above 140/90, and so and so on. As you can see, subjects went from having fairly normal SBP (~119mm Hg) to either becoming Prehypertensive or Stage 1 Hypertensive within an hour!

However, one of the most interesting results of the study is that the effects of DMAA seem to be 1) dose-dependent and 2) exacerbated by caffeine. Therefore, taking greater quantities of both substances, especially in conjunction with one another, will potentially result in even higher levels of BP. The most common consequences of increased BP include stroke and congestive heart failure along with accelerated atherosclerosis, renal artery disease, and a whole laundry list of other comorbidities which can, and often do, result in death.

Conversely, DBP remained within normal ranges despite increasing by about 10mm Hg over the two hour study period. Nevertheless, overall BP was increased to levels deemed unacceptable by any health professional’s standards. What is most interesting is that even though SBP increased, HR did not, which means that either stroke volume or peripheral resistance was increased as a direct effect of DMAA in conjunction with caffeine. This simply means that the arterial walls of the blood vessels were constricted as a result of the supplementation – the exact opposite of what most gym-goers desire. The authors concluded that;

“[T]he vasoconstriction effect of [DMAA] is supported by Eli Lilly’s trademark application for Forthane™, which states “vasoconstrictor preparation.”

This is in reference to 1948 when DMAA was first introduced as an ingredient as part of a nasal inhaler for rhinitis by Eli Lilly & Co. By the 1970s, it had been removed from the market.

If you’re anything like me right now, you’re saying, “so what?” This is a single short-term study with little bearing on realistic, long-term patterns of Jack3d consumption. Moreover, this tells us nothing about the potential ergogenic effects of DMAA on resistance training. I mean, that’s the main reason it’s being sold/purchased!

Longer-term Observations using Jack3d

In a follow-up study by the same group, researchers looked at chronic (2-week) consumption of 2 servings per day of Jack3d and OxyElite Pro on the same aforementioned parameters (HR, SBP, DBP) in healthy, exercise-trained subjects [3]. Contrary to their previous study, researchers found that neither Jack3d nor OxyElite Pro significantly increased SBP or DBP over the 2-week study period. This is good news for USPLabs. However, there are some differences in study protocols that can potentially explain the initial results seen in the first study and the null-effects seen in this one.

First off, the dosages of caffeine and DMAA contained within Jack3d and the dosage of DMAA contained within OxyElite Pro are unknown (both list DMAA as part of proprietary blend). Therefore, the levels of DMAA could have been below what was used in the previous study. Furthermore, the caffeine content in OxyElite Pro (100mg) is well below the dosage given in the previous study (250mg), again possibly explaining the differences seen between the two studies. Therefore, the unknown quantities of the compound in question (DMAA) and the lower dosage of caffeine in OxyElite Pro could potentially explain the null-effects seen on SBP and DBP.

Another difference seen between the two studies is that Jack3d contains extra ingredients, like that of arginine, a non-essential amino acid that has been shown to reduce blood pressure (SBP and DBP) [4], at least in subjects with pre-existing clinical manifestations like hypertension. Therefore, the arginine in Jack3d may have helped to counteract the hypertensive effects of DMAA. Although this may seem like a logical justification, it still doesn’t explain why OxyElite Pro had effects similar to Jack3d without the addition of arginine. This, however, could come down to the small n-size used (Jack3d = 7, OxyElite Pro = 6) and the fact that the results may be simply due to chance.

A major limitation of this follow-up study is that compliance of intake was measured via self-reporting and the collection of empty supplement bottles by the researchers at the end of week two. Because there was no strict control over intake, subjects could have potentially A) skipped some dosages (or all, aside from the two study conditions) and thrown out the rest, or B) taken even more than the recommended intake and run out of servings well before the follow-up test therefore eliminating any effects of the supplement by virtue of the “wash-out days” leading up to testing. Given these limitations, in conjunction with a small n-size, the study leaves us questioning the validity of the results.

Nevertheless, despite the various limitations, this study does lend some initial – albeit weak – credence to the argument that normal consumption patterns of either Jack3d or OxyElite Pro (which would be half of what was consumed in this study) are potentially safe when it comes to cardiovascular parameters. Obviously (many) more well-controlled studies are needed to confirm or deny these results.

But What about the Ergogenic Capacity!?!?

Unfortunately, this study tells us nothing about the ergogenic capacity of Jack3d. The researchers didn’t even try to measure it. I mean, sure, we can argue all day that it may be safe to consume, but if it doesn’t actually help with your workout then what the hell is there to argue about?! The simple answer to all of this is that there must be more well-controlled studies looking at realistic, chronic consumption of Jack3d by independent researchers with no financial ties to USPLabs. Unfortunately, these studies do not exist. To my knowledge there are only two other studies that evaluate the safety and efficacy of DMAA as a weight loss supplement [5, 6] and produce equivocal results. Moreover, both studies have limitations worthy of discounting their results altogether, aside from commercial backing; those being no control of dietary intake [5] and no actual measure of weight loss [6]. This essentially leaves us right back at square one.


So, to summarize today’s talking points:

  1. DMAA’s legal marketing and use as a dietary supplement hinges on one study that has (apparently) come into question, the facts of which I cannot comment upon
  2. Jack3d and OxyElite Pro have very few studies evaluating their safety and even fewer studies which effectively provide any insight into whether or not they’re even effective supplements
  3. All of the studies which do evaluate Jack3d and OxyElite Pro are from one group of researchers with direct funding from USPLabs

In the end, like most other hugely-hyped supplements, Jack3d appears to be nothing but another waste of money. You can argue all day that it might be safe, but for what? There’s nothing in Jack3d that can’t be purchased separately and for much less. Until there is compelling data that shows that Jack3d is superior to the individual, well-studied constituents contained within it (creatine monohydrate, beta-alanine, and caffeine) I will gladly sit back while others blindly buy-out what’s left of the, now banned, DMAA products.


1. Ping Z, Jun Q, Qing L. A study on the chemical constituents of geranium oil. J Guizhou Institut Technol. 1996;25(1):82–85.

2. Bloomer RJ, Harvey IC, Farney TM, Bell ZW, Canale RE. Effects of 1,3-dimethylamylamine and caffeine alone or in combination on heart rate and blood pressure in healthy men and women. Phys Sportsmed. 2011;39(3):111-20.

3. Farney TM, McCarthy CG, Canale RE, Alleman RJ, Bloomer RJ. Hemodynamic and hematologic profile of healthy adults ingesting dietary supplements containing 1,3-dimethylamylamine. Nutrition and Metabolic Insights 2012;5:1-12.

4. Dong JY, Qin LQ, Zhang Z, Zhao Y, Wang J, Arigoni F, Zhang W. Effect of oral L-arginine supplementation on blood pressure: a meta-analysis of randomized, double-blind, placebo-controlled trials. Am Heart J. 2011;162(6):959-65.

5. McCarthy CG, Canale RE, Alleman RJ, Reed JP, Bloomer RJ. Biochemical and anthropometric effects of a weight loss dietary supplement in healthy men and women. Nutrition and Metabolic Insights 2012;5:13-22.

6. McCarthy CG, Farney TM, Canale RE, Alleman RJ, Bloomer RJ. A finished dietary supplement stimulates lipolysis and metabolic rate in young men and women. Nutrition and Metabolic Insights 2012;5:23-31.

Posted in Supplements | 6 Comments

Growth Hormone and Nighttime Carbs: Much Ado About Nothing

Opening Comments

Today I want to talk about growth hormone. From what I’ve gathered over the past couple of weeks, there seems to be a prevailing notion that eating carbohydrates at night will somehow prevent natural growth hormone release from occurring and therefore hinder muscle protein synthesis. This is presumably due to carbohydrates causing insulin to be raised and therefore causing growth hormone to be inhibited. As some of you may already be aware, growth hormone secretion is at its maximum during sleep. It makes sense to want to maximize your natural hormonal milieus in order to promote anabolism.  However, what proponents of this misconstrued theory choose to forget – or just flat out don’t know – is that insulin, too, is anabolic. Nonetheless, for argument’s sake, I will solely focus on growth hormone and how a carbohydrate meal at night might – potentially (never?) – lead to less muscle protein synthesis.

For starters, it is true that when insulin is elevated (via ingested carbohydrate), growth hormone is inhibited and therefore low in concentration. However, this hardly deserves much attention given the numerous other factors that go into muscle hypertrophy. Nevertheless, some still translate this single piece of information into meaning that growth hormone will somehow be blunted to the point of no release and therefore inhibiting muscle protein synthesis altogether. This is just plain ridiculous and completely misleading, not to mention that there is not ONE study which even slightly suggests this. Nevertheless, in lieu of today’s topic, I’ll start by describing some of the physiology behind growth hormone and it’s functions and then follow it up with some research studies that will put everything into perspective (hopefully). However, before we begin, be warned, today’s article will be quite lengthy and somewhat sciency.

Growth Hormone Secretion  

Growth hormone (GH) is a peptide hormone secreted from the anterior pituitary of the brain. GH is secreted throughout life but is most important during childhood wherein peak concentrations are the highest they will ever be [1]. For the purposes of today’s article, we will just discuss GH as it pertains to muscle growth and hypertrophy.

In skeletal muscle, GH promotes a positive protein balance by increasing muscle protein uptake/synthesis and by potentially preventing muscle protein breakdown [2]. There are various stimuli which affect the release and inhibition of GH, namely nutrients (such as carbs, protein, and fats), age, stress (exercise), gender, circadian rhythm, and the presence of other, counter-regulatory hormones such as insulin [1, 3]. To say that the regulation of GH is simple is a complete understatement. In fact, the interplay between exercise, diet and GH regulation is not fully understood [3]. It is at this point that I want to discuss what controls GH secretion and inhibition and the relative impacts of the various macronutrients on GH regulation. After all, that’s what you came for, right?

Growth Hormone Regulation

GH is primarily acted on by growth hormone-releasing hormone (GHRH) – aptly named – which signals GH to be released into circulation. In opposition to GHRH is another hormone called somatostatin (SS) which inhibits GHRH and therefore prevents GH to be secreted. Throughout the day both GHRH and SS control the release and inhibition of GH and inevitably dictate the overall magnitude of GH release [3]. This manner of release and inhibition is often termed a pulsatile pattern wherein the largest release happens within the first two hours of sleep (see below). This is thought to be prime time for anabolism.

Like many biochemical and physiological mechanisms GH, too, has feedback inhibition. This simply means that the products of a pathway also turn that pathway off once sufficient levels of product are made. The inhibitory products for GH include, glucose, free fatty acids, IGF-1 and potentially GH itself [3].

IGF-1 (insulin-like growth factor-1) is stimulated when GH is released and acts on the liver and muscle tissue. This causes insulin-like growth factor-1 to be released into circulation where it can act of various tissues such as muscle. It is through IGF-1 that GH indirectly mediates some its anabolic effects. Therefore, it may not be GH per se that causes muscle protein synthesis, but rather IGF-1. However, to date, there is still some controversy as to which one is the primary stimulator of muscle protein synthesis. Nevertheless, as I already mentioned, IGF-1 causes GH to stop being secreted once sufficient levels of IGF-1 have been made. The same applies for glucose and free fatty acids which are also products of GH release. During exercise, GH optimizes the body’s fuel sources by decreasing tissue glucose uptake, stimulating lipolysis, and increasing gluconeogenesis [4]. This makes sure that blood glucose levels are preserved during exercise.

An important thing to keep in mind when talking about GH release and inhibition is that SS causes GH secretion to be inhibited BUT does not cause GH to stop being produced. Therefore, even though GH may not be released into circulation, the pituitary gland is still synthesizing more GH which will inevitably be released once the inhibition is removed. This concept is very important because there seems to be a ‘rebound’ effect for GH secretion after the inhibition is taken away [5].

Therefore the real question is whether or not the initial inhibition presented by a carbohydrate meal will actually reduce the amount of total GH secreted over the course of the day. If this ‘rebound’ effect holds true than GH will just be secreted in higher levels than it would have originally been and therefore reaching its daily quota, so to speak. To my knowledge, there are no studies which directly look at this theory in respect to a nighttime carbohydrate meal and subsequent levels of GH over the course of the night. Moreover, there also needs to be evidence that shows that muscle protein synthesis is somehow reduced because of this inhibition. Because a study like this does not exist, not only is the original argument completely speculative, but it is also founded on very little fact. Nevertheless, let us take a look at some effects of food on GH after a meal and see if we can’t postulate some conclusions about diet and GH.

Post-prandial GH Response to Feeding


It has been shown multiple times that an oral glucose tolerance test results in reduced levels of GH [6-9]. Furthermore, another study demonstrated that carbohydrate alone or in conjunction with protein also caused GH levels to be decreased [10]. However, this study was done in a group of sedentary diabetics who may not serve as the best example for what might occur in a non-sedentary, athletic population. Furthermore, it has also been shown that hypoglycemia is a potent stimulator of GH [7, 11].  Although interesting, this is virtually irrelevant given that hypoglycemia is not something likely to occur in most athletes/bodybuilders who consume anywhere from 4-6 meals a day. Nevertheless, as insulin levels tend to go down, GH levels tend to increase [12].


Next we will consider protein, and more specifically amino acids. Amino acids have come under scrutiny for their potential to increase levels of GH. Although certain amino acids (arginine, ornithine, lysine) taken orally and intravenously in gram doses have been shown to increase levels of GH in sedentary participants, this is not the case in bodybuilders and those who consume high protein diets [13]. Sorry guys.


In 1993, Cappon et al. wanted to test the effects of a high fat drink consumed 45 minutes before a 10 minute bout of intense exercise on subsequent GH levels [14]. Researchers found that, compared to a non-caloric placebo, GH was reduced by 54% and blood concentrations of SS were significantly elevated. The authors postulated a potential link between fat and somatostatin (SS). In fact, in a separate study done a few years earlier, a group of researchers found that both a mixed meal and a fat-rich meal had the greatest effects on elevating SS levels with carbohydrate having the least effects [15].


Obviously keeping SS low and GH high would be the best case scenario in terms of body composition; however, as is life, things are not that simple. The relative impact and relevance of the aforementioned studies on body composition are essentially worthless and at best speculative. They are acute studies which tell us nothing about long-term effects of diet on hormonal responses. Not to mention many of these studies were done with macronutrients in isolation; a situation not relevant to normal eating behaviors to begin with. Finally, there was no direct measurement of lean body mass in any of the studies. Therefore they really tell us little about the potential effects of food on GH in relation to body composition. So where do we go from here?

Well, it just so happens that there is one study which comes close to answering the question at hand, although not entirely. Nevertheless, it draws upon some of the themes I’ve already laid out so far, so let’s see if we can’t inch one step closer to a definitive answer and drive a nail into this coffin.

Effects of Heavy Weightlifting on GH Release at Night

A study done in 2001 looked the effects of heavy resistance exercise on the pulsatile released of GH in humans [16]. At that point, it was well established that exercise was a potent stimulator of GH; however, it was not fully understood on how resistance exercise affected GH throughout the rest of the day, specifically during the nighttime. What the researchers found, contrary to their original hypothesis, was that heavy resistance exercise – completed in the afternoon – actually decreased overnight maximum GH concentrations (see below).

In spite of this overall reduction in maximal GH concentration, they saw that total GH concentration by the end of the night was not significantly reduced when compared to the control. AHA! To put it another way, GH was lower during the first half of sleep (perhaps what might happen if one ate a carbohydrate meal) but remained elevated during the second half of sleep to maintain normal GH concentrations (think about the ‘rebound’ effect I mentioned earlier). As you can see, when faced with lower than normal secretion patterns, most likely due to SS inhibition, GH was released at higher concentrations during the rest of the night in order to meet its ‘quota.’ As I mentioned earlier SS does not affect GH synthesis, only release. In fact, the researchers postulated that the temporal changes in GH over the course of the night were possibly due to the ‘rebound effect’ of SS on GH secretion.

So, if you got nothing from what I just stated, remember this: it appears that GH release has some form of homeostatic mechanism which maintains a certain quota for GH concentrations over the course of the day. Therefore, when something like exercise interacts and alters the normal release pattern of GH, the brain is smart enough to save it and release it later when the inhibition is gone. This presumably keeps GH concentrations unchanged over a 24-hr period. My guess is that this is also true for something as trivial as a carbohydrate meal consumed at night wherein GH might be slightly inhibited by the time you fall asleep. This is probably not something to get worried about at all.

Unfortunately, this study provides very little insight into what would happen with chronic patterns of nightly carbohydrates. What it does do, however, is provide evidence for the ‘rebound’ effect postulated earlier, which seems to be a good model for maintaining normal levels of GH over a 24-hr period. Obviously more studies are needed, especially ones that pertain to nutrition. This also brings me to something I should have mentioned earlier. Had this topic of carbs and GH been such a revelation in the field nutritional science, don’t you think more studies would have been done on it? Usually scientific interest is a good indicator of the importance of a given nutritional topic. Just some food for thought.

Rapid Suppression of GH from Overeating

There is one more study which I would like to cover, and it has to deal with the possibility of GH being completely suppressed by food intake. Obviously this is what nighttime Carbophobics are worried about, so it makes sense to look at the closest study I could find that mimics this question. In a recent study done in 2011, researchers looked to see if GH secretion could be significantly suppressed by the act of overeating [17]. There were essentially three phases of the study; baseline, 3 days post-overeating, and 2 weeks post-overeating. During the entire study period following baseline, researchers had participants consume ~175% of their daily caloric needs while limiting their daily activity to 1500 steps per day (not very active). At baseline GH levels were essentially normal. By day 3, GH levels had significantly dropped by ~80% wherein they remained relatively unchanged during the remaining 2-week period (see below).

Obviously these conditions are not relevant to normal consumption patterns, even among those who are bulking. However, as you can see, GH can be suppressed, although this relates little to our argument because I doubt a single carbohydrate meal at night will reproduce anything like what was seen during this study, even under chronic conditions of nighttime carb meals.

Nevertheless, the question remains; will this negatively affect gains in lean body mass? Well, here’s the kicker! Even with GH being suppressed by up to 80%, participants actually increased their lean body mass (~2lb increase)! Let me repeat that; they actually increased their lean body mass. Now, I will admit that it wasn’t statistically significant, although it was bordering significant, and that the LBM gains could have been tissue other than skeletal muscle. Nonetheless, the fact still remains that protein synthesis wasn’t completely inhibited, even in the face of dramatically low GH levels and almost complete inactivity. Would greater gains in LBM have been seen if GH wasn’t reduced as much? Would activity have nullified the results and attenuated the drop in GH levels? Who knows? The key thing to keep in mind is that muscle protein synthesis is a complex system that involves multiple players. Singling out two factors amongst a host of others is flat out ridiculous.

Concluding Remarks

The fact of the matter is that those who fear carbs at night are basing their fear off of one piece of information that holds little scientific backing. Hopefully by now I’ve convinced you that GH regulation is a complex system with many factors that each plays a role. To say that carbs at night will reduce the capacity to build muscle is completely ludacris and unfounded – that is unless that meal is part of a diet which comprises 175% of your daily needs. So, in the end, there is no scientific evidence whatsoever to suggest that carbs consumed at night will reduce one’s goal of gaining muscle, and I doubt there ever will be. The main thing to keep in mind is that there is much more to building muscle than splitting-hairs. The people who care the most about this stuff are the ones who should care the least, and those who capitulate to stupid misinformation like that are worse off than they were when they knew nothing at all. If you learned nothing, remember this:

Lift heavy, eat right, rest up, and most importantly don’t concern yourself with trivial aspects of dieting that are at best speculative and at worst completely false. Dichotomous thinking never did anyone any good. Ever.


1. Silverthorn DU. Endocrine control of growth and metabolism. In: Human physiology: an integrated approach, 5th ed. Pearson Education, Inc.: San Francisco, CA, 2010.

2. Rooyackers OE, Nair KS. Hormonal regulation of human muscle protein metabolism. Annu Rev Nutr. 1997;17:457-85.

3. Kraemer WJ, Nindl BC, Gordon SE. Resistance exercise: acute and chronic changes in growth hormone concentrations. In: The endocrine system in sports and exercise. Blackwell Publishing: Malden, MA, 2005.

4. McArdle WD, Katch FI, Katch VL. The endocrine system: organization and acute and chronic responses to exercise. In: Exercise physiology: energy, nutrition, and human performance, 6th ed. Lippincott, Williams and Wilkins: Baltimore, MD, 2007.

5. Giustina A, Veldhuis JD. Pathophysiology and neuroregulation of growth hormone secretion in experimental animals and the human. Endocrine Reviews 1998;19(6):717-797.

6. Bernardi F, Petraglia F, Seppala M, et al. GH, IGFBP-1, and IGFBP-3 response to oral glucose tolerance test in perimenopausal women: no influence of body mass index. Maturitas 1999;33:163-179.

7. Frystyk J, Grofte T, Skjaerbaek C, Orskov H. The effect of oral glucose on serum free insulin-like growth factor-I and –II in healthy adults. J Clin Endocrinol Metab. 1997;82:3124-3127.

8. Hjalmarsen A, Aasebo U, Aakvaag A, Jorde R. Sex hormone responses in healthy men and male patients with chronic obstructive pulmonary disease during an oral glucose load. Scand J Clin Lab Invest. 1996;56:635-640.

9. Nakagawa E, Nagaya N, Okumura H, et al. Hyperglycaemia suppresses the secretion of ghrelin, a novel growth hormone-releasing peptide: responses to the intravenous and oral administration of glucose. Clin Science 2002;103:325-328.

10. van Loon LJ, Saris WH, Verhagen H, Wagenmakers AJ. Plasma insulin responses after ingestion of different amino acid or protein mixtures with carbohydrates. Am J Clin Nutr. 2000;72:96-105.

11. Roth et al. 1963.

12. Volek JS, Sharman MJ. Diet and hormonal responses: potential impact on body composition. In: The endocrine system in sports and exercise. Blackwell Publishing: Malden, MA, 2005.

13. Chromiak JA, Antonio J. Use of amino acids as growth hormone-releasing agents by athletes. Nutrition 2002;18:657-661.

14. Cappon JP, Ipp E, Brasel JA, Cooper DM. Acute effects of high-fat and high-glucose meals on the growth hormone response to exercise. J Clin Endocrinol Metab. 1993;76-1418-1422.

15. Ensinck JW, Vogel RE, Laschansky EC, Francis BH. Effect of ingested carbohydrate, fat, and protein on the release of somatostatin-28 in humans. Gastroenterology 1990;98(3):633-638.

16. Nindl BC, Hymer WC, Deaver DR, Kraemer WJ. Growth hormone pulsatility profile characteristics following acute heavy resistance exercise. J Appl Physiol. 2001;91:163-172.

17. Cornford AS, Barkan AL, Horowitz JF. Rapid suppression of growth hormone concentration by overeating: potential mediation by hyperinsulinemia. J Clin Endocrinol Metab. 2011;96(3):824-830.

Posted in Carbohydrate | 10 Comments

Anabolic Arachidonic Acid: Mass-builder or Massive Waste of Money? – ARTICLE REVIEW

Effects of arachidonic acid supplementation on training adaptations in resistance-trained males

Roberts MD, Iosia M, Kerksick CM, Taylor LW, Campbell B, Wilborn CD, Harvey T, Cooke M, Rasmussen C, Greenwood M, Wilson R, Jitomir J, Willoughby D, Kreider RB.

J Int Soc Sports Nutr. 2007;4:21.



To determine the impact of AA supplementation during resistance training on body composition, training adaptations, and markers of muscle hypertrophy in resistance-trained males.


In a randomized and double blind manner, 31 resistance-trained male subjects (22.1 +/- 5.0 years, 180 +/- 0.1 cm, 86.1 +/- 13.0 kg, 18.1 +/- 6.4% body fat) ingested either a placebo (PLA: 1 corn oil, n = 16) or AA (AA: 1 AA, n = 15) while participating in a standardized 4 day.week-1 resistance training regimen. Fasting blood samples, body composition, bench press one-repetition maximum (1RM), leg press 1RM and Wingate anaerobic capacity sprint tests were completed after 0, 25, and 50 days of supplementation. Percutaneous muscle biopsies were taken from the vastus lateralis on days 0 and 50.


Wingate relative peak power was significantly greater after 50 days of supplementation while the inflammatory cytokine IL-6 was significantly lower after 25 days of supplementation in the AA group. PGE2 levels tended to be greater in the AA group. However, no statistically significant differences were observed between groups in body composition, strength, anabolic and catabolic hormones, or markers of muscle hypertrophy (i.e. total protein content or MHC type I, IIa, and IIx protein content) and other intramuscular markers (i.e. FP and EP3 receptor density or MHC type I, IIa, and IIx mRNA expression).


AA supplementation during resistance-training may enhance anaerobic capacity and lessen the inflammatory response to training. However, AA supplementation did not promote statistically greater gains in strength, muscle mass, or influence markers of muscle hypertrophy.

Opening Comments

The other day I got a request to do an article on arachidonic acid (AA) supplementation. Now, to be completely honest, I haven’t heard much about arachidonic acid in terms of supplementation for muscle and strength gains, although I am familiar with the lipid and its role within the inflammatory response. So, I figured why not, could be interesting. As it turns out, arachidonic acid research, in terms of supplementing for muscle hypertrophy, strength, etc. in humans, is quite scarce. To my knowledge this is the only study to look at arachidonic acid supplementation on muscle protein synthesis – contrary to what some supplement companies may have you think.  Furthermore, this study attempts to look AA’s effects on body composition and strength, two factors I’m sure many of you are interested in improving. I will first start with a short history of the literature surrounding AA – as it pertains to weightlifting – and then jump right into the above study wherein I will touch upon the strengths and weaknesses of the study and my views on/potential implications for AA supplementation.

Arachidonic Acid: A Quick Review of the Literature

Arachidonic acid (AA) is an omega-6 polyunsaturated fatty acid (PUFA) – denoted 20:4 ω-6 – found naturally in foods and in membrane phospholipids of humans. Contrary to what some people think, AA is not an essential fatty acid. The human body can effectively make enough AA through various enzymatic pathways which I will not get into. AA is converted into a group of eicosanoids known as prostaglandins (PGs). PGs play an important role in regulating the inflammatory response as well as other immune responses in the human body. It is estimated that the average 70kg man (~154lbs) contains about 50-100g AA spread throughout various tissues and membranes [1], although it is thought that the AA status of the body is dependent upon dietary intake [1] as well as activity level [2-3]. An interesting study from 2000 saw that the fatty acid profile of skeletal muscle differed between endurance-trained and sedentary individuals – with less AA and in the trained group – even though the fatty acid composition of the diet was similar [3]. This implies that physical activity may play a more important role than diet in terms of the fatty acid composition of cell membranes.

Early in vitro and animals studies demonstrated that PGs (and therefore AA) are implicated in the inflammatory response of muscles after mechanical stimulation (comparable to that of resistance exercise) as well as the rates of protein synthesis and degradation in both skeletal and cardiac muscle [4-7]. Because AA is converted to prostaglandins (PGs) via the COX-2 pathway – the same pathway inhibited by non-steroidal anti-inflammatory drugs (i.e. Ibuprofen, acetaminophen) – it is thought that commonly used pain killers (Advil, Tylenol, etc.) could potentially inhibit the necessary myogenic inflammatory response needed for muscle protein synthesis. Reaffirming this notion, a study done by Trappe et al. showed that subjects supplemented with normal doses of NSAIDs prior to resistance training completely eliminated PG synthesis of the inflammatory response as well as muscle protein synthesis following the exercise protocol [8]. Paired to together with research showing that 1.5g of AA/day for a month and half significantly increased PG synthesis [9], AA has now been implicated as a mass-building supplement for weightlifters and gym-rats alike. Today’s study gets at the crux of this argument, so without much further ado, let’s dissect this paper!

The Study

Study Strengths

Because you have the abstract above (and have the ability to read), I’ll start off by listing the study’s strengths, which to my surprise were a whole bunch. First off, big points to any study which uses healthy, resistance-trained subjects. This eliminates any effects that could be confounded by what are called, “beginner gains.” This study was also a randomized, double-blind, placebo-controlled study, which ensures that both groups are identical (aside from the experimental protocol) and that any biases from both researchers and subjects which might affect the results are eliminated. Body composition was measured using dual-energy x-ray absorptiometry (DXA), otherwise known as the “Gold Standard” for body comp measures. Another awesome feature of this study was the use of muscle biopsies. Not too often do people agree to donate a chunk of their own muscle tissue (nor is it permitted often). Biopsies were taken before strength testing to eliminate any effects that might occur due to exercise. You can’t get more accurate than actually looking at someone’s muscle tissue!

Nutritionally speaking, recommended calorie and protein intakes were well-above adequate (+500kcals/day above baseline needs and 2g/kg BW, respectively), although this was merely recommended and not tightly controlled. Nevertheless, a dietary supplement was given out (290kcals, 24g CHO/45g PRO/1g Fat) in order to reach the additional calorie and protein requirements needed to promote muscle gains. Subjects were also told to avoid foods high in omega-3 fatty acids as well as commonly used NSAIDS which might interfere with the inflammatory response of exercise.

Study Weaknesses

The fact that dietary intake was self-reported this potentially confounds the results, even though 4-day dietary records were used to validate intakes. Another potential weakness of the study was that the placebo group was given a corn-oil supplement which can be converted to AA (from linoleic acid) using various enzymatic pathways in the body. Dietary analysis, however, revealed similar levels of linoleic acid in the diets. This, however, is only as valid as the diet records. All in all, this was a well carried-out study with very few weaknesses.


The researchers found that there were no significant differences between the two groups in terms of body mass, fat free mass, fat mass, percent body fat, 1RM bench press, or 1RM leg press. Pity. However, anaerobic peak power was significantly different between the two groups, with the higher peak power coming from the AA group on days 25 and 50. This comes on the heels of previous research which showed that, 10 days of a soybean derivative – that naturally contains AA – increased time to fatigue in active males during a cycling test at 85% VO2 max [10] as well as in soccer players performing exhaustive, intermittent sprints [11]. Nevertheless, the major finding of this study was that AA supplementation did not lead to greater gains in strength, muscle hypertrophy or body composition when compared to a placebo, which, let’s be honest, is the main goal of most of the readers of this Blog.

Summary & Finals Comments

In the end, it appears that AA supplementation may be more of a waste of money rather than a muscle-building fatty acid (especially when AA supplements range from $50-60 a pop!). However, this is only one study. Obviously more studies need to be done in order to confirm or refute the findings presented here. Given that it’s been 5 years since this study was done, without any corresponding follow-up whatsoever, this tells me that AA supplementation doesn’t appear to be the “next big thing;” at least not now. There may be some potential benefits if you’re an endurance athlete, but right now, it’s still speculative and the results are more relevant to phosphatidylserine (the soybean derivative I mentioned earlier). So next time you hear outrageous claims about arachidonic acid providing awesome muscle and strength gains, just remember that it’s probably based off of speculation rather than sound scientific research.


1. Zhou L, Nilsson Å. Sources of eicosanoid precursor fatty acid pools in tissue. J Lipid Res. 2001;42(10):1521-42.

2. Helge JW, Wu BJ, Willer M, Daugaard JR, Storlien LH, Kiens B. Training affects muscle phospholipid fatty acid composition in humans. J Appl Pysiol. 2001;90(2):670-7.

3. Andersson A, Sjödin A, Hedman A, Olsson R, Vessby B. Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men. Am J Physiol Endocrinol Metab. 2000;279(4):E744-51.

4. Vandenburgh HH, Shansky J, Karlisch P, Solerssi RL. Mechanical stimulation of skeletal muscle generates lipid-related second messengers by phospholipase activation. J Cell Physiol. 1993;155(1):63-71.

5. Vandenburgh HH, Shansky J, Solerssi RL, Chromiak J. Mechanical stimulation of skeletal muscle increases prostaglandin F2 alpha production, cyclooxygenase activity, and cell growth by a pertussis toxin sensitive mechanism. J Cell Physiol. 1995;163(2):285-94.

6. Rodemann HP, Goldberg AL. Arachidonic acid, prostaglandin E2, and F2 alpha influence rates of protein turnover in skeletal and cardiac muscle. J Biol Chem. 1982;257(4):1632-8.

7. Palmer RM. Prostaglandins and the control of muscle protein synthesis and degradation. Prostaglandins Leukot Essent Fatty Acids 1990;39(2):95-104.

8. Trappe TA, White F, Lambert CP, Cesar D, Hellerstein M, Evans WJ. Effect of ibuprofen and acetaminophen on postexercise muscle protein synthesis. Am J Physiol Endocrinol Metab. 2002;282:E551-556.  

9. Kelley DS, Taylor PC, Nelson GJ, Mackey BE. Arachidonic acid supplementation enhances synthesis of eicosanoids without suppressing immune functions in young healthy men. Lipids 1998;33:125-130.

10. Kingsley MI, Miller M, Kilduff LP, McEneny J, Benton D. Effects of phosphatidylserine on exercise capacity during cycling in active males. Med Sci Sports Exerc. 2006;38:64-71.

11. Kingsley MI, Wadsworth D, Kilduff LP, McEneny J, Benton D. Effects of phosphatidylserine on oxidative stress following intermittent running. Med Sci Sports Exerc. 2005;37(8):1300-6.

Posted in Fats, Reviews | 8 Comments