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Alan Aragons Research Review November 2013 [Back to Contents] Page 1
Copyright November 1st, 2013 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: [email protected]
2 Has the last decade of nutrient timing research
reached an anti-climax? By Alan Aragon
5 Calcium homeostasis and bone metabolic responses to high-protein diets during energy deficit in healthy young adults: a randomized control trial. Cao JJ, Pasiakos SM, Margolis LM, Sauter ER, Whigham
LD, McClung JP, Young AJ, Combs GF Jr. Am J Clin Nutr.
2013 Nov 27. [Epub ahead of print] [PubMed]
6 Myofibrillar muscle protein synthesis rates subsequent to a meal in response to increasing doses of whey protein at rest and after resistance exercise. Witard OC, Jackman SR, Breen L, Smith K, Selby A,
Tipton KD. Am J Clin Nutr. 2013 Nov 20. [Epub ahead of
print] [PubMed]
7 Leucine supplementation of a low-protein mixed
macronutrient beverage enhances myofibrillar protein synthesis in young men: a double-blind, randomized trial. Churchward-Venne TA, Breen L, Di Donato DM, Hector
AJ, Mitchell CJ, Moore DR, Stellingwerff T, Breuille D,
Offord EA, Baker SK, Phillips SM. Am J Clin Nutr. 2013
Nov 27. [Epub ahead of print] [PubMed]
8 Evaluation of the usefulness of a low-calorie diet
with or without bread in the treatment of overweight/obesity. Loria-Kohen V, Gmez-Candela C, Fernndez-Fernndez
C, Prez-Torres A, Garca-Puig J, Bermejo LM. Clin Nutr.
2012 Aug;31(4):455-61. [PubMed]
10 The Meat and Nuts Breakfast of Champions.
By Matt Jones
13 Jonathan Bailor claims slim is simple but finds many ways to overcomplicate it. By Alan Aragon
17 Martial arts meets academia: an interview with Dr.
Brian Jones. By Alan Aragon
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Alan Aragons Research Review November 2013 [Back to Contents] Page 2
Has the last decade of nutrient timing research reached an anti-climax?
By Alan Aragon
____________________________________________________
Ivy & Portmans big splash in 2004
Ivy and Portmans book Nutrient Timing: The Future of Sports Nutrition
1 hit publication and ushered in one of the biggest
trends in sports nutrition. I own a copy myself, and youd be hard-pressed to find a sports nutrition-oriented practitioner who
hasnt been influenced by the book, which involves detailed prescriptions for pre-, during-, and post-exercise nutrition. As
stated in the first chapter, specific timing of nutrients enables
trainees to avoid the plateau effect and achieve far greater gains in muscle strength and muscle mass. However, while the authors created an awareness of the potential utility of nutrient
timing strategies, the supporting research was comprised largely
of acute (short-term) studies on subjects taken to glycogen
depletion after an overnight fast.
Hit-and-miss after a standout in 2006
Over the course of the next decade, several chronic (long-term)
studies cropped up, and the results have been equivocal. Perhaps
the strongest research supporting nutrient timing was Cribb and
Hayes famous 2006 finding that timing protein, carbohydrate, and creatine immediately sandwiching both sides of the
resistance training bout resulted in significantly greater lean
body mass (LBM) and strength gains than the same nutrients
positioned far from both sides of the bout.2 From that point
onward, chronic timing studies seemed to be hit-and-miss, yet
the conventional wisdom endured over time. This was despite
research like that of Hoffman et al, which was a similar design to
Cribb & Hayes, but failed to observe significant differences
between the treatments.3
Challenging the paradigm
The anabolic window of opportunity concept became virtually a foregone conclusion. It was presumed to be a matter of fact,
and thus was rarely questioned. To my knowledge, the first peer-
reviewed article to challenge the anabolic window concept was the one I co-authored with Brad Schoenfeld.
4 The reach and
impact of this article has been measurably big. Shortly after its
publication in January of this year, it became the number-one
most viewed article in the history of the Journal of the
International Society of Sports Nutrition (JISSN).
Our paper (full text here) contains an in-depth discussion of the
limitations surrounding the traditional nutrient timing paradigm,
focusing on protein and carbohydrate. An examination of the
literature revealed that the prevailing protein timing tenets lack a
consistent evidence basis, especially in chronic trials. In
addition, the carbohydrate timing rules for maximizing the
anabolic response were on questionable ground as well. To the
latter point, the available data have consistently shown the
failure of additional carbohydrate to augment muscle protein
synthesis given an adequate protein dose both at rest5 and post-
exercise.6,7
An important note about our paper is that it never
claims that the longstanding nutrient timing dogma is useless or
invalid. We never claimed that nutrient timing does not matter.
In fact, the practical applications we outlined for the goal of
maximizing the anabolic response involve specific timing except the anabolic window is considerably larger than that of the traditional dogma. We proposed that there is up to a 4 to 6-
hour peri-workout period in which to dose pre- & post-exercise
protein (with each dose being at least 0.4-0.5 g/kg LBM) and
still maximize the anabolic response to resistance training. The
timing of carbohydrate is left largely to personal preference,
with exceptions being endurance applications where glycogen
depletion occurs more than once per day within close proximity
in the same muscle group. The papers final sentence is an eloquent summation (if I may say so myself):
4 Collectively,
these data indicate an increased potential for dietary flexibility
while maintaining the pursuit of optimal timing.
Quantitative evidence further challenges the paradigm
Conducting a meta-analysis of protein timing studies was the
natural progression of investigation after the publication of our
narrative review. Brad Schoenfeld came up with the idea. He
collaborated with myself and James Krieger on the paper.8 To
our delight, it has become JISSNs #2 most-viewed article of the past year within less than a month of its publication, and its already the #6 most-viewed in the history of the journal. The
popularity of this article and its predecessor shows that there are
many folks in both the academic and public domains with an
open mind to the current data, and a healthy skepticism towards
traditional assumptions.
The aim of our meta-analysis (full text here) was to examine the
available protein timing research on strength and hypertrophy in
a systematic, quantitative fashion. Meta-analyses enable an
increase in statistical power by the pooling of data from several
studies. When done correctly, meta-analyses can provide a big-
picture/aerial view of the data and quantitatively uncover the
weight of the evidence (in whatever direction it might lean, if it
leans at all). We used a multi-level meta-regression that
employed a hierarchical/step-wise reduction process designed to
control for covariates (factors aside from timing that might
influence outcomes). Before delving into this any further, it
should be made perfectly clear that we had no agenda and no
pre-conceived hopes or ideas of what the analysis might find.
The whole point of research is to draw tentative conclusions
based on the data. If done backwards, where the data is cherry-
picked or manipulated to support pre-conceived conclusions,
then the entire purpose is completely lost.
The temporal parameters we chose as inclusion criteria are worth
highlighting because theyre critical for properly interpreting the results. We specifically compared studies where protein was
dosed within an hour of either side of the training bout versus
studies where protein was dosed at least 2 hours away from
either side of the training bout. This framework is based largely
on Ivy and Portmans long-standing, highly influential claim that the post-exercise anabolic window is approximately 45 minutes,
after which point the opportunity to capitalize on nutrient-
mediated anabolism significantly diminishes.1
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Alan Aragons Research Review November 2013 [Back to Contents] Page 3
Selected noteworthy details & findings of our meta-analysis
Our analysis had several interesting findings. First of all, there was no significant effect of protein timing on strength or hypertrophy after all covariates were accounted for. This outcome has disturbed and even angered many folks who passionately believe in protein timing near the training bout. However, it must be kept in mind that this result is potentially limited to the parameters we set for comparison, which again, were protein ingested 1 hour pre- and/or post-exercise, versus 2 hours pre- and/or post-exercise. Any effects outside of those parameters were simply not investigated.
Based on the focus of our analysis, we cannot determine whether
or not extended periods of protein neglect beyond 2 hours pre-
and/or post could possibly yield inferior effects on strength
and/or hypertrophy. But once again, our aim was to examine the
proverbial anabolic window of opportunity which is fabled to be a relatively narrow timeframe to slam that shake.
An important finding was that total protein intake (rather than
timing) was the strongest variable associated with hypertrophy.
Average protein intake in the treatment (timed protein) groups
was 1.66 g/kg/day, whereas it was 1.33 g/kg/day in the controls.
Given this, it appears that treatment conditions involved a more
optimized level of protein intake compared to the controls. This
brings us to the issue of the unfair disadvantage of control groups where total protein intake was not matched with that of
the treatment groups. The vast majority of studies simply add a
protein supplement near the training bout and compare that with
a non-protein placebo. We recognized this confounding
imbalance, so we ran a sub-analysis of protein-matched studies,
but still, no significant effect of timing was seen.
It should be noted that of the 23 studies included for analysis,
only 3 of them were protein-matched. This limits the statistical
power of the sub-analysis of true timing studies. Interestingly, 2 of the 3 protein-matched studies did not show a significant
effect of timing. Its also worth mentioning that two frequently cited studies did not meet our inclusion criteria. Esmarck et al
9
didnt make the cut because the protein dose did not contain the minimum of 6 g EAA. Burk et al
10 was excluded because of
insufficient data to calculate effect size. Even if the latter two
studies were included in the analysis, it wouldnt likely alter the outcomes and conclusions, since Esmarck et al saw positive
effects of protein consumed near the end of the training bout
while Burk et al actually saw greater benefits of a protein
supplement timed away from the end of the bout.
Indeed, we recognized the scarcity of protein-matched studies as
one of the biggest problems with the literature that traditionally
falls under the nutrient timing umbrella. This scarcity of protein-
matched timing studies is also one of the strongest reasons why
vehemence about the timing of protein immediately near training
is not warranted. The limited statistical power of the small
number of protein-matched studies is also a good reason to not
harbor any strong confidence that protein timing is useless.
Another major limitation of the available research is a lack of
studies that use resistance-trained subjects, since this population
would be most likely to expose any potential benefits of protein
timing. Interestingly, no significant influence of training status
was detected in the full meta-regression model that controlled
for all covariates.
Conclusions, for the time being
So, did nearly a decade of nutrient timing research reach an anti-
climax? It depends on how you look at it, since thats quite a broad claim. Protein timing within a narrow anabolic window
relative to the training bout ( 1 hour pre- and/or post-exercise) appears to take a backseat to total daily protein. This finding
seems to reinforce basic logic. Those who consume enough total
daily protein and energy to maximize strength and hypertrophy
are likely to spend the majority of their day in the postprandial
(fed) state. Furthermore, they are also likely to spend the
majority of their day in a state of hyperaminoacidemia resulting
from multiple protein-rich meals. These conditions collectively
would minimize the effects of temporal variations in protein
intake relative to the training bout.
It bears reiterating that theres a lack of protein-matched timing studies. This makes it possible that the null findings we saw
were due to type II error. In other words, false-negative results
could have occurred from insufficient statistical power to detect
significant differences. Another point to consider is that theres no evidence of an ergolytic effect of protein timed near the
training bout, and there is some evidence of positive effects.
Therefore, scooting the dose(s) close to training is generally a
good idea for maximizing all hypothetical routes toward
muscular size and strength. Avoiding lengthy gaps in protein
feeding relative to the training bout (e.g., significantly more than
2 hours) can also hedge your bets toward maximizing anabolic
adaptations. The degree of timing precision is whats debatable.
People mistakenly debate over nutrient timing importance as if
its a black & white issue. This is a false dichotomy, since it should be viewed as a continuum. I created the chart below to
outline the variable importance of nutrient timing.11
Notice how
the span of applications of nutrient timing diminishes alongside
the increase of nutrient timing importance.
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Alan Aragons Research Review November 2013 [Back to Contents] Page 4
References
1. Ivy J, Portman R: Nutrient Timing: The Future of Sports Nutrition. North Bergen, NJ: Basic Health Publications;
2004.
2. Cribb PJ, Hayes A. Effects of supplement timing and resistance exercise on skeletal muscle hypertrophy. Med Sci
Sports Exerc. 2006 Nov;38(11):1918-25. [PubMed]
3. Hoffman JR, Ratamess NA, Tranchina CP, Rashti SL, Kang J, Faigenbaum AD. Effect of protein-supplement timing on
strength, power, and body-composition changes in
resistance-trained men. Int J Sport Nutr Exerc Metab. 2009
Apr;19(2):172-85. [PubMed]
4. Aragon AA, Schoenfeld BJ. Nutrient timing revisited: is there a post-exercise anabolic window? J Int Soc Sports
Nutr. 2013 Jan 29;10(1):5. [PubMed]
5. Hamer HM, Wall BT, Kiskini A, de Lange A, Groen BB, Bakker JA, Gijsen AP, Verdijk LB, van Loon LJ.
Carbohydrate co-ingestion with protein does not further
augment post-prandial muscle protein accretion in older
men. Nutr Metab (Lond). 2013 Jan 25;10(1):15. [PubMed]
6. Staples AW, Burd NA, West DW, Currie KD, Atherton PJ, Moore DR, Rennie MJ, Macdonald MJ, Baker SK, Phillips
SM: Carbohydrate does not augment exercise-induced
protein accretion versus protein alone. Med Sci Sports Exerc
2011, 43(7):1154-1161. [PubMed]
7. Koopman R, Beelen M, Stellingwerff T, Pennings B, Saris WH, Kies AK, Kuipers H, Van Loon LJ: Coingestion of
carbohydrate with protein does not further augment
postexercise muscle protein synthesis. Am J Physiol
Endocrinol Metab 2007, 293(3):E833-842. [PubMed]
8. Schoenfeld BJ, Aragon AA, Krieger JW. The effect of protein timing on muscle strength and hypertrophy: a meta-
analysis. J Int Soc Sports Nutr. 2013 Dec 3;10(1):53. [Epub
ahead of print] [PubMed]
9. Esmarck B, Andersen JL, Olsen S, Richter EA, Mizuno M, Kjaer M. Timing of postexercise protein intake is important
for muscle hypertrophy with resistance training in elderly
humans. J Physiol. 2001 Aug 15;535(Pt 1):301-11.
[PubMed]
10. Burk A, Timpmann S, Medijainen L, Vhi M, Opik V. Time-divided ingestion pattern of casein-based protein
supplement stimulates an increase in fat-free body mass
during resistance training in young untrained men. Nutr Res.
2009 Jun;29(6):405-13. [PubMed]
11. Aragon AA. Continuum of nutrient timing importance (original schematic). NSCA Personal Trainers Conference,
April 2012.
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Alan Aragons Research Review November 2013 [Back to Contents] Page 5
Calcium homeostasis and bone metabolic responses to high-protein diets during energy deficit in healthy young adults: a randomized control trial.
Cao JJ, Pasiakos SM, Margolis LM, Sauter ER, Whigham LD,
McClung JP, Young AJ, Combs GF Jr. Am J Clin Nutr. 2013
Nov 27. [Epub ahead of print] [PubMed]
BACKGROUND: Although consuming dietary protein above current recommendations during energy deficit (ED) preserves lean body mass, concerns have been raised regarding the effects of high-protein diets on bone health. OBJECTIVE: The objective was to determine whether calcium homeostasis and bone turnover are affected by high-protein diets during weight maintenance (WM) and ED. DESIGN: A randomized, parallel-design, controlled trial of 32 men and 7 women were assigned diets providing protein at 0.8 [Recommended Dietary Allowance
(RDA)], 1.6 (2 RDA), or 2.4 (3 RDA) g kg-1 d-1 for 31 d. Ten days of WM preceded 21 d of ED, during which total daily
ED was 40%, achieved by reduced dietary energy intake (30%) and increased physical activity (10%). The macronutrient composition (protein g kg-1 d-1 and % fat) was held constant from WM to ED. Calcium absorption (ratio of
44Ca to
42Ca) and
circulating indices of bone turnover were determined at day 8 (WM) and day 29 (ED). RESULTS: Regardless of energy state, mean (SEM) urinary pH was lower (P < 0.05) at 2 RDA (6.28 0.05) and 3 RDA (6.23 0.06) than at the RDA (6.54 0.06). However, protein had no effect on either urinary calcium excretion (P > 0.05) or the amount of calcium retained (P > 0.05). ED decreased serum insulin-like growth factor I, increased serum tartrate-resistant acid phosphatase, and 25-hydroxyvitamin D concentrations (P < 0.01). Remaining markers of bone turnover and whole-body bone mineral density and content were not affected by either the protein level or ED (P > 0.05). CONCLUSION: These data demonstrate that short-term consumption of high-protein diets does not disrupt calcium homeostasis and is not detrimental to skeletal integrity. This trial was registered at www.clinicaltrials.gov as NCT01292395. SPONSORSHIP: Supported by the US Army Medical Research and Material Command and the USDA Agricultural Research Service program Bone Metabolism in Obesity.
Study strengths
This study is unique in that its the first to examine the important question of how a high protein intake affects calcium
absorption/retention and markers of bone metabolism during
energetic maintenance and deficit conditions. A thorough set of
protein intake conditions was compared (0.8, 1.6, & 2.4 g/kg)
under weight maintenance as well as a 40% deficit condition
comprised of 30% intake reduction combined with 10% increase
in physical activity. Dietary intake was tightly controlled as the
menu was prepared by research dietitians. A similar intake of
calcium among the conditions was enforced via supplementation
to avoid the confounding effects of varying calcium intakes.
Study limitations
Its possible that the study duration (31 days) was not long enough to reveal potential detriments of the higher-protein
conditions on markers of bone health. Also, there was no
progressive resistance training protocol imposed. Resistance
training has a substantive body of evidence supporting its
beneficial effects on bone mineral density.1-3
Higher dietary
protein has recently been shown to reduce bone turnover in the
long-term (24 months) under dieting conditions.4 In this vein,
higher dietary protein (20% as opposed to 10% of energy) has
also been shown to improve calcium absorption from low-
calcium diet, which offsets urinary losses.5 Its plausible that a
high protein intake in combination with progressive resistance
training and sufficient calcium would constitute a potent effect
on increasing or preserving bone mineral density (in addition to
the protective effect on muscle mass). It would have been useful
(and innovative) to investigate a potential dose-response
relationship between graduated protein intakes and bone status
in the presence of a progressive resistance training program. In
this study, exercise was standardized to be low-intensity and
non-progressive.
Comment/application
Note that this study was part of a larger study led by Pasiakos et
al that examined varying protein levels on body composition and
muscle protein synthesis.6 They found that both higher-protein
groups lost a significantly higher proportion of fat mass and
lower proportion of lean mass compared to the RDA group,
without any significant differences between the higher-protein
groups (2x versus 3x the RDA). The main findings of the present
study were that despite increases in urinary acidity, diets that are
2 or 3 times the RDA did not significantly alter urinary calcium
excretion, dietary calcium retention, or markers of bone turnover
and bone mineral density when calcium & vitamin D are
consumed at recommended levels.
In addition, what I found interesting was an outcome that wasnt the specific focus of the present study. There was the lack of
significant difference in total weight loss between the groups
during the 21-day energy deficit period. Weight loss was 3.5 kg
for the RDA group, 2.7 kg for 2x RDA, and 3.3 kg for 3x RDA).
The important detail here is that the increased protein intakes in
the weight maintenance (WM) and energy deficit (ED) phases of
each diet were at the expense of carbohydrate:
What we have is further confirmation that under conditions that
tightly control total energy intake, theres nothing inherently advantageous to weight loss about carbohydrate reduction per
se... The authors ultimately concluded that high-protein diets are
not detrimental to calcium metabolism, but also acknowledge the
need for longer-term studies to render more definitive answers to
the question of bone safety of high protein intake.
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Alan Aragons Research Review November 2013 [Back to Contents] Page 6
Myofibrillar muscle protein synthesis rates subsequent to a meal in response to increasing doses of whey protein at rest and after resistance exercise.
Witard OC, Jackman SR, Breen L, Smith K, Selby A, Tipton
KD. Am J Clin Nutr. 2013 Nov 20. [Epub ahead of print]
[PubMed]
BACKGROUND: The intake of whey, compared with casein and
soy protein intakes, stimulates a greater acute response of muscle
protein synthesis (MPS) to protein ingestion in rested and exercised
muscle. OBJECTIVE: We characterized the dose-response
relation of postabsorptive rates of myofibrillar MPS to increasing
amounts of whey protein at rest and after exercise in resistance-
trained, young men. DESIGN: Volunteers (n = 48) consumed a
standardized, high-protein (0.54 g/kg body mass) breakfast. Three
hours later, a bout of unilateral exercise (8 10 leg presses and leg
extensions; 80% one-repetition maximum) was performed.
Volunteers ingested 0, 10, 20, or 40 g whey protein isolate
immediately (10 min) after exercise. Postabsorptive rates of myofibrillar MPS and whole-body rates of phenylalanine oxidation
and urea production were measured over a 4-h postdrink period by
continuous tracer infusion of labeled [13
C6] phenylalanine and
[15
N2] urea. RESULTS: Myofibrillar MPS (SD) increased (P <
0.05) above 0 g whey protein (0.041 0.015%/h) by 49% and 56%
with the ingestion of 20 and 40 g whey protein, respectively,
whereas no additional stimulation was observed with 10 g whey
protein (P > 0.05). Rates of phenylalanine oxidation and urea
production increased with the ingestion of 40 g whey protein.
CONCLUSIONS: A 20-g dose of whey protein is sufficient for
the maximal stimulation of postabsorptive rates of myofibrillar
MPS in rested and exercised muscle of 80-kg resistance-trained, young men. A dose of whey protein >20 g stimulates amino acid
oxidation and ureagenesis. This trial was registered at
http://www.isrctn.org/ as ISRCTN92528122. SPONSORSHIP:
Supported by GlaxoSmithKline Nutritional Healthcare.
Study strengths
This study breaks new ground by being the first to ever examine
the dose-response relationship of myofibrillar muscle protein
synthesis (MPS) to increasing amounts of whey at rest and after
resistance exercise. Subjects had a minimum of 6 months of
recreational weight-lifting experience. Habitual food intake was
assessed and replicated 48 hours prior to testing. The exercise
protocol was intensive in terms of the work done in the target
muscle group (quads). 16 sets total were done with leg press and
extension at 80% of 1RM with 2-minute rest intervals. A
standout design strength was the assessment of whey-mediated
MPS 3 hours after a standardized high-protein breakfast, in
recognition of the fact that in real world, most people weight-
train in a fed rather than fasted state.
Study limitations
Although the aim of the study was to examine acute response
(which it did a good job of), the very nature of acute response
data is hypothesis-generating in the context of the bigger picture.
Short-term response does not necessarily translate to long-term
adaptation. So, while investigating anabolic response dosing
thresholds provides valuable data, its still preliminary and in need of follow-up by trials examining the influence of these
protocols on endpoints such as hypertrophy and/or strength,
which would require a period of weeks to measure. A final
limitation is a missing intermediate dose between 20 g and 40 g.
It would have been interesting to see the effects of 30 g and 50 g
doses as well, not only to get a finer picture of the response
curve, but also to further exploit where the true plateau is.
Comment/application
The main findings were a lack of significant increase in MPS
with 10 g whey, while MPS significantly increased with 20 g
and 40 g, with a lack of lack of significant difference in MPS
between the latter two doses. However, as seen above, theres an uptrend in MPS that doesnt appear to truly plateau at 40 g, despite the difference between 20 g and 40 g failing to reach
statistical significance. In light of this, the authors diligently
acknowledge the possibility that this small difference could
potentially be meaningful in regards to concrete endpoints in the
long-term:
However, intriguingly, mean postexercise myofibrillar MPS values were ~19% higher in the 20WP than 10WP but only an additional ~10% higher in the 40WP. An additional calculation of the 95% CI for the true difference between the 20WP and 40WP revealed that we could not rule out a 14% increase in the myofibrillar FSR with the ingestion of 40 g whey protein. [...] ...the long-term physiologic impact of a 1014% higher rate of MPS in the 40WP on muscle hypertrophy remains unknown.
The authors astutely mentioned that the dose for maximizing the
anabolic response could potentially vary according to individual
differences in muscle mass. For example, its not known whether someone with 80 kg LBM would have a greater MPS response
to a higher protein dose compared to someone with 50 kg LBM.
Although this hasnt been systematically tested, it intuitively would seem to be true. Knowing that larger individuals require
more total protein, it would be fair to speculate that they also
have a larger capacity for MPS from the constituent doses of
protein that comprise the daily total. In any case, older subjects
have been observed to have a higher protein dosing ceiling for
MPS (35-40 g as opposed to 20 g in younger subjects).7,8
Along
with age comes anabolic resistance. Since most of us dont age in reverse, I would recommend erring toward the higher side of
protein dosing if the main goal is hypertrophy.
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Alan Aragons Research Review November 2013 [Back to Contents] Page 7
Leucine supplementation of a low-protein mixed macronutrient beverage enhances myofibrillar protein synthesis in young men: a double-blind, randomized trial.
Churchward-Venne TA, Breen L, Di Donato DM, Hector AJ,
Mitchell CJ, Moore DR, Stellingwerff T, Breuille D, Offord EA,
Baker SK, Phillips SM. Am J Clin Nutr. 2013 Nov 27. [Epub
ahead of print] [PubMed]
BACKGROUND: Leucine is a key amino acid involved in the regulation of skeletal muscle protein synthesis. OBJECTIVE: We assessed the effect of the supplementation of a lower-protein mixed macronutrient beverage with varying doses of leucine or a mixture of branched chain amino acids (BCAAs) on myofibrillar protein synthesis (MPS) at rest and after exercise. DESIGN: In a parallel group design, 40 men (21 1 y) completed unilateral knee-extensor resistance exercise before the ingestion of 25 g whey protein (W25) (3.0 g leucine), 6.25 g whey protein (W6) (0.75g leucine), 6.25 g whey protein supplemented with leucine to 3.0 g total leucine (W6+Low-Leu), 6.25 g whey protein supplemented with leucine to 5.0 g total leucine (W6+High-Leu), or 6.25 g whey protein supplemented with leucine, isoleucine, and valine to 5.0 g total leucine. A primed continuous infusion of l-[ring-
13C6] phenylalanine with serial muscle
biopsies was used to measure MPS under baseline fasted and postprandial conditions in both a rested (response to feeding) and exercised (response to combined feeding and resistance exercise) leg. RESULTS: The area under the blood leucine curve was greatest for the W6+High-Leu group compared with the W6 and W6+Low-Leu groups (P < 0.001). In the postprandial period, rates of MPS were increased above baseline over 0-1.5 h in all treatments. Over 1.5-4.5 h, MPS remained increased above baseline after all treatments but was greatest after W25 (267%) and W6+High-Leu (220%) treatments (P = 0.002). CONCLUSIONS: A low-protein (6.25 g) mixed macronutrient beverage can be as effective as a high-protein dose (25 g) at stimulating increased MPS rates when supplemented with a high (5.0 g total leucine) amount of leucine. These results have important implications for formulations of protein beverages designed to enhance muscle anabolism. This trial was registered at clinicaltrials.gov as NCT 1530646. SPONSORSHIP: Supported by Nestec Ltd and the Natural Sciences and Engineering Research Council of Canada (postgraduate scholarship to TAC-V). Study strengths
This is the first study to assess the MPS-stimulating capability of
varying doses of leucine added to a sub-optimal protein dose
(within a mixed macronutrient beverage) at rest and after
exercise. Previous research has looked at supplemental leucine
and EAA effects on protein alone,9 so the present study offers
potentially higher practical value. A comprehensive set of
treatments were compared, including two that involved a higher
leucine fortification bringing the total 5 g, whereas previous
research by the same lab totaled 3 g.9 Prepackaged standardized
diets that were consumed during the 2 days immediately
preceding the trials in order to reduce the confounding potential
of dietary variability.
Study limitations
The main limitation was the acute (short-term) nature of the study. While it provides valuable data, it still leaves open question about whether any of these differences in acute response would influence long-term adaptations in strength and/or hypertrophy. Another limitation was that the results may be limited to the exercise protocol, which consisted of only 8 sets of knee extensions at 80% of 1 RM (this was half the volume of work done by Witard et al,
10 which I reviewed on the
previous page). Another limitation was the use of subjects who werent necessarily trained. No training age was specified, nor were any minimums or maximums imposed for training status.
Comment/application
Depicted above are the MPS results in the early and late test periods in the resting (A) and post-exercise condition (B). Below A & B are the combined results of the entire test periods in the resting (C) and post-exercise conditions (D). The notable findings were that MPS increased significantly in all conditions, but MPS in the 25 g whey (W25) and the sub-optimal whey dose plus the higher leucine fortification amounting to 5 g leucine (W6+High-Leu) was greater than the MPS in the other treatments, with no significant differences in MPS between those two treatments. These results are not in full agreement with previous research by the same lab,
9 where 25 g whey was the
most effective treatment for sustaining increased rates of MPS post-exercise even more so than the sub-optimal whey dose fortified with an equivalent leucine dose to 25 g whey. However, the present study included a higher leucine fortification (amounting to 5 g instead of 3 g). Another difference was the inclusion of carbohydrate (35 g) and fat (5.68 g).
Interestingly, there were no significant differences in MPS between the resting and post-exercise conditions. The latter finding does not align with what Yang et al observed in older subjects, who experienced greater MPS post-exercise with 40 g whey than with 20 g,
8 suggesting a saturable response to lower
protein doses in younger subject despite the more sensitized post-exercise conditions.
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Alan Aragons Research Review November 2013 [Back to Contents] Page 8
Evaluation of the usefulness of a low-calorie diet with or without bread in the treatment of overweight/obesity.
Loria-Kohen V, Gmez-Candela C, Fernndez-Fernndez C, Prez-Torres A, Garca-Puig J, Bermejo LM. Clin Nutr. 2012 Aug;31(4):455-61. [PubMed]
BACKGROUND & AIMS: Despite the lack of scientific evidence, bread is one of the most restricted foods in popular hypocaloric diets. The aim of this study was to compare two nutrition strategies (with or without bread) designed to promote weight loss in overweight/obese women. METHODS: A clinical, prospective and randomised study in which 122 women >18 years, BMI 25 < 40 kg/m(2) were divided into two groups: intervention group (BREAD, n = 61) and control group (NO BREAD, n = 61). Both groups received a low-calorie diet (with or without bread), nutrition education and physical activity guidelines, and were monitored for 16 weeks. RESULTS: 104 women completed the study (48.4 9 years, 29.8 3.5 kg/m(2)). Anthropometric and biochemical markers improved after the intervention without significant differences between groups. BREAD group significantly increased total cereal consumption (3.2 1.3 to 3.7 0.5 servings/day, P < 0.05) and the percentage of energy from carbohydrates (41.2 6.4 vs. 45.9 5.0% P < 0.001) and reduced fat (39.0 6.6 vs. 32.7 5.1% P < 0.001). In contrast, NO BREAD group increased the discrepancy with recommended consumption. NO BREAD group had the most dropouts (21.3% vs. 6.6%, P < 0.05). CONCLUSIONS: The bread inclusion in a low-calorie diet designed for weight loss favoured a better evolution of dietetic parameters and greater compliance with the diet with fewer dropouts. Registered under ClinicalTrials.gov Identifier #NCT01223989. SPONSORSHIP: This study was made possible thanks to a research project funded by the Pan cada da (Daily Bread) open call promoted by the Scientific Committee of Bread and by Incerhpan (Interprofessional Agrifoods of the Cereals-Flour-Bread Chain). Study sponsors had no involvement in the study design, in the analysis and interpretation of data, in the writing of the manuscript or submit it.
Study strengths
This study is quite unique and interesting. Its also relevant in light of the recent wave of anti-grain propaganda by various fad
diet authors and their followers. This is the first study to ever
compare the specific inclusion and exclusion of bread in
overweight and obese subjects. The authors make the interesting
point that due to this diet lore, the Spanish population has
decreased its consumption of bread from 368 g/day in 1964 to
134 g/day in 2006,11
yet adult obesity prevalence steadily
increased from 17.4% in the 1990s to 24% in the 2000s.12 Subjects received group counseling/education sessions. Physical
activity was imposed (although rather loosely) to at least 3 times
per week for 30 minutes of moderate to intense physical activity.
Study limitations
I would prefer to have seen dual X-ray absorptiometry (DXA)
instead of bioelectrical impedance analysis (BIA) to assess body
composition. Pimentel et al observed BIA to not only
overestimate percent body fat (%BF) in overweight subjects by
14.2%, but also underestimate %BF in obese subjects by
10.9%.13
Also, LaForgia et al found BIA to have poor individual
accuracy compared to the four compartment model,14
which is
the most comprehensive method of assessing body composition,
accounting for fat mass, bone mineral mass, total body water,
and residual mass. The authors of the present study
acknowledged that its unknown how their results might have panned out beyond the 16 weeks. They also acknowledged that
the results might be limited to the all-female subject sample.
Comment/application
\ The main findings of this study were 3-fold. First, there was a
lack of significant in body composition change between groups.
The bread group lost 4.3 kg while the no-bread group lost 4.0 kg.
As for body fat, the bread group lost 2.5% while the no-bread
group lost 2.1%. Both groups lost muscle mass (0.9 & 0.7 kg in
the bread & no-bread groups, respectively). This shouldnt be a major surprise considering that total energy and macronutrition
was similar between groups. Secondly, there were no significant
between-group differences in blood lipids, glucose control, and
other biochemical measures. Finally, the chart above shows
where the effects of each treatment diverge: program adherence.
A significant increase in transgressions (lapses in dietary
compliance by 150 kcal) was seen in the no-bread group, while
no significant increase in transgressions was seen in the bread
group. Furthermore, in the self-reported adherence ratings, the
bread group scored higher than the no-bread group (64.3%
versus 55.6%), and dropout was markedly lower in the bread
group compared to the no-bread group (6.6% vs 21.3%).
Although the reasons for dropping out varied, exclusion of bread
was found to be a significant factor.
This is one of those studies that strongly challenges the anti-
bread/anti-grain movement, specifically in the important realm
of alleviating obesity. Heres an excerpt from the conclusion, which sums things up well:
This study may be of significant scientific interest since it may represent an advance in understanding nutrition problems in overweight/obese people and provides understanding about how these can influence weight control. It can also help dispel myths about bread being a dangerous or caloric food by highlighting the usefulness of a balanced low-calorie diet within a nutrition education programme as part of patient treatment.
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Alan Aragons Research Review November 2013 [Back to Contents] Page 9
1. Bemben DA, Bemben MG. Dose-response effect of 40 weeks of resistance training on bone mineral density in older adults Osteoporos Int. 2011 Jan;22(1):179-86. [PubMed]
2. Guadalupe-Grau A, Fuentes T, Guerra B, Calbet JA. Exercise and bone mass in adults. Sports Med. 2009;39(6):439-68. [PubMed]
3. Suominen H. Muscle training for bone strength. Aging Clin Exp Res. 2006 Apr;18(2):85-93. [PubMed]
4. Jesudason D, Nordin BC, Keogh J, Clifton P. Comparison of 2 weight-loss diets of different protein content on bone health: a randomized trial. Am J Clin Nutr. 2013 Nov;98(5):1343-52. [PubMed]
5. Hunt JR, Johnson LK, Fariba Roughead ZK. Dietary protein and calcium interact to influence calcium retention: a controlled feeding study. Am J Clin Nutr. 2009 May;89(5):1357-65. [PubMed]
6. Pasiakos SM, Cao JJ, Margolis LM, Sauter ER, Whigham LD, McClung JP, Rood JC, Carbone JW, Combs GF Jr, Young AJ. Effects of high-protein diets on fat-free mass and muscle protein synthesis following weight loss: a randomized controlled trial. FASEB J. 2013 Sep;27(9):3837-47. [PubMed]
7. Pennings B, Groen B, de Lange A, Gijsen AP, Zorenc AH, Senden JM, van Loon LJ. Amino acid absorption and subsequent muscle protein accretion following graded intakes of whey protein in elderly men. Am J Physiol Endocrinol Metab. 2012 Apr 15;302(8):E992-9. [PubMed]
8. Yang Y, Breen L, Burd NA, Hector AJ, Churchward-Venne TA, Josse AR, Tarnopolsky MA, Phillips SM. Resistance exercise enhances myofibrillar protein synthesis with graded intakes of whey protein in older men. Br J Nutr. 2012 Nov 28;108(10):1780-8. [PubMed]
9. Churchward-Venne TA, Burd NA, Mitchell CJ, West DW, Philp A, Marcotte GR, Baker SK, Baar K, Phillips SM. Supplementation of a suboptimal protein dose with leucine or essential amino acids: effects on myofibrillar protein synthesis at rest and following resistance exercise in men. J Physiol. 2012 Jun 1;590(Pt 11):2751-65. [PubMed]
10. Witard OC, Jackman SR, Breen L, Smith K, Selby A, Tipton KD. Myofibrillar muscle protein synthesis rates subsequent to a meal in response to increasing doses of whey protein at rest and after resistance exercise. Am J Clin Nutr. 2013 Nov 20. [Epub ahead of print] [PubMed]
11. Varela-Moreiras G, Avila JM, Cuadrado C, del Pozo S, Ruiz E, Moreiras O. Evaluation of food consumption and dietary patterns in Spain by the food consumption survey: updated information. Eur J Clin Nutr 2010 Nov;64(Suppl. 3):S37e43. [PubMed]
12. Salas-Salvad J, Rubio MA, Barbany M, Moreno B, Grupo Colaborativo de laSEEDO. SEEDO 2007 consensus for the evaluation of overweight and obesityand the establishment of therapeutic intervention criteria. Med Clin (Barc) 2007 Feb 10;128(5):184e96. [PubMed]
13. Pimentel GD, Bernhard AB, Frezza MR, Rinaldi AE, Burini RC. Bioelectric impedance overestimates the body fat in overweight and underestimates in Brazilian obese women: a comparison with Segal equation 1. Nutr Hosp. 2010 Sep-Oct;25(5):741-5. [PubMed]
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Alan Aragons Research Review November 2013 [Back to Contents] Page 10
The Meat and Nuts Breakfast of Champions.
By Matt Jones
____________________________________________________
Introduction
The suggestion made by Charles Poliquin within the articles and
multimedia section of the Poliquin Groups website reads as follows: rotating meat and nuts breakfast increased mental acuity and focused energy allows for a slow and steady rise in blood sugar to remain stable for an extended period of time what you eat for breakfast sets up your entire neurotransmitter
production for the day.
All of these suggestions are made relative to popular breakfast
choices that are generally higher in carbohydrate, including oats,
cereal, and bread.
For those unaware, Charles Poliquin is a well-respected, highly
successful strength and conditioning coach. But as is known
globally, a good strength coach does not necessarily make a
good nutritionist. It is not the aim of this article to openly
criticise Poliquins practices or question his motives or intentions, nor will I launch an outright tirade on him. That
would be too easy. However, it is necessary to discuss the
application of this much-famed breakfast.
As with all AARR articles, the extravagant claims will be
examined meticulously, and honestly with frequent reference to
the existing evidence base. In this case, Ill examine the claims of optimised neurotransmission and neurotransmitter production
for the day.
Neurotransmitter basics
A neurotransmitter is a chemical signal that allows for
transmission of signals from one neuron to another, across a
synapse. Neurotransmission allows for, and control muscle fiber
contraction, bodily actions, emotions and feelings. The most
significant neurotransmitters in the human body are
acetylcholine, norepinephrine, dopamine, Gamma Amino
Butyric Acid (GABA), glutamate, serotonin and endorphins.
There is a substantial body of evidence to support the notion that
nutrition has a significant influence on the appearance of blood
and brain neurotransmitters.1-3
Neurotransmitters and cognitive function
Research has demonstrated that serotonin is a known sleep-
inducing agent,4 with human research indicating that serotonin
reduces subjective alertness, objective performance, and
increases feelings of relaxation and lethargy.5 The
neurotransmitter dopamine on the other hand is associated with
pleasurable reward, behavior, cognition, mood, memory,
movement, attention and learning. Interestingly, dopamine is
critically involved in the drug addiction process by inducing
pleasant states or by relieving distress.6 Acetylcholine has a
number of physiological functions; it is a widely distributed
excitatory neurotransmitter that in the central nervous system
and is involved in wakefulness, attentiveness and memory.
Interestingly, Alzheimers disease is characterized by a significant reduction in acetylcholine concentration and
function,7 highlighting its importance in human health
performance.
Neurotransmitters and nutrition
Neurotransmitters are primarily synthesized from amino acids,
particularly the branched chain amino acids (BCAAs), tyrosine and tryptophan. The rates at which neurotransmitters are
synthesized depends upon the availability of the amino acid
precursor. Research from rodent studies in the 70s and early 80s demonstrated that increased concentrations of tryptophan resulted in an elevation in serotonin synthesis, and increasing
concentrations of tyrosine resulted in elevations in dopamine and
certain catecholamines.8
This was supported by earlier research indicating that the
administration of a single dose of tryptophan elevated brain
tryptophan levels, and thus the levels of serotonin and its major
metabolite 5-hydroxyindole acetic acid (5-HTP). The
administration of tyrosine, elevated brain tyrosine levels, and
thus catecholamine increased in the central nervous system
(CNS), while the consumption of lecithin or choline (found in
fat) increased brain choline levels and neuronal acetylcholine
synthesis.9 Ultimately concluding that tryptophan was the
precursor for serotonin, tyrosine was the precursor for dopamine
and choline the precursor for acetylcholine.
All of these early studies utilised both observational and knock-
out rodent models, using a single dose of the precursor, although
similar effects have been seen following the consumption of
dietary sources, real-food. Again using a rodent model, Wurtman
& Fernstrom9 demonstrated that the consumption of a single
protein-free high-carbohydrate meal elevated brain tryptophan
levels. Similarly, the consumption of a single 40% protein meal
accelerated brain catecholamine synthesis through increased
availability of tyrosine. Fernstrom10
concluded that a minimal
change of delta 0.07 in the tryptophan to large neutral amino
acid ratio is required to influence mood following protein
consumption, so a considerable shift in the ratio is required to
have an effect on subsequent cognition.
These data clearly demonstrate that the neurotransmitters
serotonin, dopamine and the catecholamines are under specific dietary control. Essentially this is the data Poliquin has built his
meat and nut breakfast on, and in that regard he is correct. The
acute effects of a high-carbohydrate protein-free meal, atypical
of a modern Western diet breakfast (think oatmeal and cereals)
does induce marked increases in serotonin synthesis, and thus
may result in increased feelings of lethargy.
However, is the absolute avoidance of carbohydrate justifiable
based on the current evidence? Is the process irreversible as
Poliquin suggests, does breakfast dictate the neurotransmitters
for the entire day? If Poliquin had read a little further instead of
cherry-picking the juiciest data, he would have realized that this
is not the case.
Interestingly, in the same research by Wurtman & Fernstrom9
found that the addition of protein to an otherwise protein-free
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Alan Aragons Research Review November 2013 [Back to Contents] Page 11
high-carbohydrate meal suppressed the increases in brain
tryptophan and serotonin synthesis, because protein contributes
to the blood plasma considerably larger amounts of the other
neutral amino acids (e.g., BCAAs, phenylalanine) than of tryptophan. Tryptophan and other large neutral amino acids,
most notably the BCAAs leucine, isoleucine and valine share the same specific transporter across the blood-brain barrier and
thus compete for uptake.11
Therefore, brain 5-HTP synthesis will
increase when there is an increase in the ratio of free tryptophan
to BCAAs in the blood. This explains why the addition of protein to an otherwise protein-free high-carbohydrate meal can
suppress serotonin synthesis.
This theory has also been confirmed in humans. Using 20 men,
Lieberman et al13
administered single oral doses of tryptophan
(50 mg/kg) and tyrosine (100 mg/kg) in a double-blind,
crossover study. Tryptophan increased subjective fatigue and
decreased self-ratings of vigor and alertness, but did not impair
performance on any of the tests. Compared to placebo there was
no difference in performance with tyrosine, although tyrosine
administration did reduce reaction time relative to tryptophan.
Lieberman et al concluded that tryptophan has significant
sedative-like properties, but unlike other sedatives this may not
impair performance in a series of cognitive tests. However, it is
extremely unlikely probably impossible in fact that a human would ever consume 50 mg/kg tryptophan in a single dose from
a dietary source, and thus would not necessarily have to worry
about the negative mental effects of isolated tryptophan
consumption.
Poliquins strong recommendation to avoid carbohydrate at breakfast, in fear of neurotransmitter malfunction, mental
breakdown and impaired performance has only a handful of
cherry-picked studies to support it. In reality, the brain
neurotransmitters are influenced by the ratio of free tryptophan
to large neutral BCAAs,14 so a mixed meal that is able to maintain a balance in that ratio is more likely to optimize
neurotransmitter synthesis. Furthermore, an increase in the ratio
of free tryptophan to large neutral amino acids following a high-
carbohydrate protein-free meal is reversible through the addition
of protein to that meal, ultimately balancing the ratio again. This
invalidates Poliquins suggestion that the first meal of the day dictates brain neurotransmitter production for that entire day.
Worth mentioning is an intricate study by Fischer et al.14
They
examined the cognitive effects of isoenergetic meals consisting
of three carbohydrate ratios, a carbohydrate-rich meal (4:1), a
balanced meal (1:1), and a protein-rich meal (1:4) in 15 healthy
subjects, in an attempt to elucidate which breakfast combination
is most suitable in a school environment. Unsurprisingly,
attention and decision times were improved in the first hour with
the high carbohydrate meal, due to the provision of and greater
rise in glucose metabolism. However, during the first hour it was
both the balanced and higher protein meals that resulted in
improved performance. In addition, overall reaction times in a
central task were fastest after both the balanced and high-protein
meal, thus suggesting a high-protein meal or a balanced meal
appear to result in better overall cognitive performance. The
results also revealed participants subjective measures of tasty and pleasant were greater in the balanced meal than in the
high-protein meal, which suggests this would be the most
effective in a practical/dietary adherence sense.
Mechanisms
Fischer et als research14 might lead one to presume carbohydrate-rich foods contain significant amounts of
tryptophan, thus increase free tryptophan concentrations after
ingestion, elevating tryptophan uptake and stimulating serotonin
synthesis. However, this is not the case. A bowl of oats for
example porridge or oatmeal depending which side of the pond you are a common staple of many a Western breakfast, vilified by Poliquin for the potential negative effects on
neurotransmission and mental performance. Well, the amino
acid profile of 100g oats indicates a tryptophan concentration of
234 mg, compared to 694 mg isoleucine, 1284 mg leucine, and
937 mg valine, which collectively make up the BCAAs.15
So, a
high-carbohydrate breakfast does not contain that much
tryptophan, although it accelerates serotonin synthesis through
an increase in tryptophan uptake by the brain.
It would appear that although the carbohydrate meal alone does
not contain much tryptophan, the insulin secreted following the
carbohydrate meal results in a rapid removal and significant
decrease in plasma levels of the large neutral amino acids
(tyrosine, phenylalanine, BCAAs and methionine) that would ordinarily compete with tryptophan for uptake by the brain.
Tryptophan then crosses the blood-brain barrier and is converted
to serotonin.5 It thus appears that it is not actually the
carbohydrate that causes the problem; it is the insulin response
to that carbohydrate that drives the large neutral amino acids out
of the bloodstream, leaving tryptophan free to pass the blood
brain barrier, with no competition.
Logic
The insulin index formulated by Holt et al15
clearly demonstrates
that beef, the food favored by Poliquin in his infamous meat and
nut breakfast, elicits an insulin response of 7910 2193
pmol/min/L (expressed as area under the curve, or AUC). Grain
bread, a food demonized by Poliquin in fear of it frying all brain
cells has an insulin AUC of 6659 837 pmol/min/L. The insulin
index clearly indicates beef is more insulinogenic than many of
the carbohydrate-rich foods tested. This suggests that the net
effect in regards neurotransmitter synthesis of a high-protein
carbohydrate-free meal may be similar to that of a mixed meal.
The greater insulin response to beef consumption will lead to a
reduction in the BCAAs and other neutral amino acids, leaving free tryptophan to be taken up by the brain. Interestingly, 100 g
steak contains more tryptophan than the same portion of oats
(288 mg versus 234 mg).16
Logic, intuition and a basic understanding of the insulin index
suggests this could be true, although a number of rodent studies
have disproved the hypothesis, where Rouch et al17
revealed a
high-protein diet significantly reduced serotonin concentrations
for 2-hours, and Wurtman & Fernstrom9 reported similar
findings. Interestingly, the reduction in serotonin following
protein feeding is thought to be among the reasons why protein
is more satiating that carbohydrate.
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Alan Aragons Research Review November 2013 [Back to Contents] Page 12
As discussed previously, research has demonstrated that
Poliquins suggestion that the first meal of the day dictates that whole days brain neurotransmitter activity is false. The process is reversible and easily altered. Looking at more of the evidence
to disprove this claim, Fernstrom and Fernstrom analyzed the
brain tryptophan concentrations and rates of serotonin synthesis
in fasted rats fed a high-carbohydrate meal followed 2-hours
later by a protein-containing meal.18
They demonstrated that
when the high-carbohydrate meal was fed first, brain tryptophan
concentrations increased as did serotonin synthesis, and these
changes were reversed at 4 hours if the second meal contained
protein. Interestingly the authors went on to conclude, quote:
brain tryptophan concentrations and serotonin synthesis are thus responsive to the sequential ingestion of protein and
carbohydrate meals if there is a sufficient interval between
meals.
Rouch et al19
reported the plasma ratio of free tryptophan to
large neutral amino acids was increased by a carbohydrate meal,
and remained high for 2-hours, a subsequent casein (protein)
meal reversed this change. In an intriguing twist, a first casein
meal reduced the ratio, and was not increased again by a
subsequent carbohydrate meal. This finding actually supports
Poliquins claims in that an initial high-protein carbohydrate-free meal is more favorable than a high-carbohydrate protein-free
meal in regards neurotransmitter synthesis.
The reversible nature of neurotransmitter synthesis is supported
by the central fatigue hypothesis in humans, which predicts that
the ingestion of BCAAs during exercise will raise plasma BCAA concentration and hence reduce transport of free
tryptophan into the brain; subsequently reducing the formation
of serotonin and alleviating sensations of fatigue and therefore
improve endurance performance.20
To-date, this hypothesis is
still controversial despite many years of research. Nevertheless,
it highlights the reversible nature of neurotransmitter synthesis.
Conclusion and recommendations
My recommendation based on this evidence is that a single
macronutrient meal can have a significant impact on the brain
neurotransmitters. A protein-free high-carbohydrate meal typical
of the meals consumed at breakfast by many Westerners think oatmeal, etc can increase serotonin synthesis, and thus increase feelings of fatigue as Poliquin claims. However, a high-protein
high-fat carbohydrate-free meal can increase dopamine and
catecholamine synthesis. The latter can be favorable, but with
your daily macronutrient requirements in mind, combined with
the fact that eating single-macronutrient meals would be
extremely tasteless and boring, it would be more appropriate for
most to consume mixed meals than to focus on meals free from
certain macronutrients in fear of a surge of sleep-inducing
neurotransmitters. Furthermore, the current evidence does not
consistently indicate decrements in mood, cognitive
performance, or alertness from a protein-rich meal that also
includes carbohydrate.
In conclusion, the exclusive promotion of low-carbohydrate,
high-protein, high-fat meat and nut breakfast is largely
unsubstantiated, but has minimal support by a few cherry-picked
studies. A mixed meal consisting of protein, carbohydrate and
fat is adequate, and in a practical sense is likely to be optimal.
______________________________________________________________________________
Matt is the lead performance nutritionist at Nutrition Condition. He holds an MSc in Nutrition Science, and a BSc in Sports Science. Matt coaches world-class athletes, large corporations and personal clients. Matt employs strong scientific principles within his practices and has is a great proponent of the evidence-based approach. Matt can be contacted at [email protected] or on twitter @MattJonesNC
References
1. Wurtman, R., & Fernstrom, J. (1974). Nutrition and the Brain. Scientific American, 230, 84- 91. [The Wurtman Lab]
2. Growdon, J., Cohen, E., & Wurtman, R., (1977). Treatment of brain diseases with dietary precursors of neurotransmitters. Annals of Internal Medicine, 86, 337 339. [PubMed]
3. Gelenberg, A., & Gibson, C., (1984). Tyrosine for the treatment of depression. Nutrition & Health, 3, 163 173. [PubMed]
4. Hartman, E., & Spinweber, C., (1979). Sleep induced by L-tryptophan. Effect of dosages within the normal dietary intake. The Journal of Nervous and Mental Disease, 167, 497 499. [PubMed]
5. Spring, B., (1984). Recent research on the behavioural effects of tryptophan and carbohydrate. Nutrition & Health, 3, 55 67. [PubMed]
6. Le Foll, B., Gallo, A., Le Strat, Y., Lu, L., & Gorwood, P., (2009). Genetics of dopamine receptors and drug addiction: a comprehensive review. Behavioural Pharmacology, 20, 1 17. [PubMed]
7. Francis, P., (2005). The interplay of neurotransmitters in Alzheimers disease. Central Nervous Systems Spectrums, 10, 6 9. [PubMed]
8. Wurtman, R., Hefti, F., & Melamed, E., (1980). Precursor control of neurotransmitter synthesis. Pharmacological Reviews, 32, 315 335. [PubMed]
9. Wurtman, R., & Fernstrom, J., (1975). Control of brain monoamine synthesis by diet and plasma amino acids. The American Journal of Clinical Nutrition, 28, 638 647. [PubMed]
10. Fernstrom, J., (1994). Dietary amino acids and brain function. Journal of the American Dietetic Association, 94, 71 77. [PubMed]
11. Maughan, R., (2000). Nutrition in sport. Blackwell Science, United Kingdom
12. Chaouloff, F., Kennett, G., Serrurrier, B., Merino, D., & Curzon, G. (1986). Amino acid analysis demonstrates that increased plasma free tryptophan causes the increase of brain tryptophan during exercise in the rat. Journal of Neurochemistry, 46, 1647 1650. [PubMed]
13. Lieberman, H., Corkin, S., Spring, B., Wurtman, R., & Growdon, J., (1985). The effects of dietary neurotransmitter precursors on human behaviour. American Journal or Clinical Nutrition, 42, 366 370. [PubMed]
14. Fischer, K., Colombani, P., Langhans, W., & Wenk, C. (2002). Carbohydrate to protein ratio in food and cognitive performance in the morning, Physiology & Behaviour, 75, 411 423. [PubMed]
15. Holt, S., Miller, J., & Petocz, P., (1997). An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods. American Journal of Clinical Nutrition, 66, 1264 1276. [PubMed]
16. http://nutritiondata.self.com/ 17. Rouch, C., Nicolaidis, S., & Orosco, M., (1998). Determination, using
microdialysis, of hypothalamic serotonin variations in response to different macronutrients. Physiology & Behaviour, 65, 653 657. [PubMed]
18. Fernstrom, M., & Fernstrom, J. (1995). Brain tryptophan concentrations and serotonin synthesis remain responsive to food consumption after the ingestion of sequential meals, The American Journal of Clinical Nutrition, 61, 312 319. [PubMed]
19. Rouch, C., Meile, M., & Orosco, M., (2003). Extracellular hypothalamic serotonin and plasma amino acids in response to sequential carbohydrate and protein meals. Nutritional Neuroscience, 6, 117 124. [PubMed]
20. Gleeson, M., (2005). Interrelationship between physical activity and branched-chain amino acids. The Journal of Nutrition, 135, 1591 1595. [PubMed]
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Alan Aragons Research Review November 2013 [Back to Contents] Page 13
Jonathan Bailor claims slim is simple but finds many ways to overcomplicate it.
By Alan Aragon
Background
According to his LinkedIn profile, Jonathan Bailor is a self-
proclaimed nutrition and exercise expert and former personal trainer who specializes in using high-quality food and exercise
to simplify wellness. However, his profile reveals that his main day-job since 2005 is at Microsoft. His current position is Senior
Program Manager. This immediately reminds me of Dave
Asprey, a computer programmer-turned-health guru with a
pseudoscientific slant and a flair for gimmickry. Bailors book is called The Calorie Myth, which Im assuming has gotten a healthy amount of publicity through the marketing might of
publishing giant HarperCollins. Heres his promotional video thats making the social media rounds. In the clip, Bailor delivers a summary of the obesity problem, as well as his
solution. Thus far, I havent seen any research-based critiques of it, and boy, is it begging for one. My commentary will follow
key excerpts from the video, and end off with discussion of his
questionable training methods.
Today more of us are dieting and exercising than ever, and yet more of us are overweight and diabetic than ever.
While the second part is true, the first part is false. We are not
dieting and exercising more than ever. The latest data shows that
were consuming about a full meals worth of calories (445 kcal) more than we did in 1970,
1 while reducing our energy
expenditure by the equivalent of 30 minutes of walking (142
kcal) since 1960.2 So, contrary to Bailors claim, were actually
eating more and moving less.
Its been proven that on average we are consuming about 300 more calories per person per day than we were in the late 70s. Between then and now, that adds up to well over 3 million more calories per person, which if the starvation is healthy, count your calories, and metabolism works like math premise were true, means the average American today should weigh well over 1000 pounds.
The above statement makes no sense at all. If the typical adult
consuming 2500 kcal/day added 300 kcal/day to that, he or she
would eventually plateau at a bodyweight whose maintenance
requirement is 2800 kcal and this is certainly not going to be what sustains a 1000-lb person. Who knows where Bailor got
that figure from (Im assuming he did some wonky math on progressively increasing intake by 300 kcal each day), but it
makes a good attention-grabber for audiences with zero
knowledge in this area.
Just like no quantity of clean water will ever clog a sink, no quantity of the high-quality, clean foods we were designed to eat will ever clog our body. Eat smarter, not less, problem solved.
Here Bailor is claiming that reducing calories-in is not the
solution to weight loss. This is another oversimplification, since
for many folks who are overweight or obese from overeating, a
caloric deficit (via reduction of calories-in and/or increase of
calories-out) is precisely what needs to be sustained in order to
reverse the condition. Intake reduction can be achieved a number
of ways. You can reduce the portion size of the foods you
currently consume. Or, you can eat more energy-sparse foods
that end up displacing the amount of energy-dense foods (which
is what Bailor is recommending). Or, you can do a combination
of both. The thing is, all of those options are paths toward
reducing the intake of metabolizable energy. So, its utterly misleading to say that eating less is not the solution when thats exactly what ends up happening terms of energy intake when
these tactics are employed.
Compounding the falsehoods, he also claims that increasing
intake will not cause weight gain if its comprised of high-quality foods. According to Bailor, food quality is determined by
4 factors: 1) satiating capacity, 2) aggression, or how likely
those foods are to be stored as body fat, 3) nutrient density, and
4) efficiency, or how many calories can be stored as body fat.
The latter factor is a reiteration of #2, but then you wouldnt be able to build a catchy acronym (SANE). He then goes on to
outline 3 factors that determine the sanity of foods: 1) water, 2) fiber, and 3) protein. Whats already apparent is that in Bailors attempt to simplify getting slim, he stacks sets of rules that complicate and cloud the real objective, which again is to
impose and sustain a caloric deficit. This can and should be
achieved on an individual basis that respects personal preference
and tolerance (and athletic goals when applicable). But lets go on to see Bailors justification of the latter set of rules.
Water, protein, and fiber-rich foods are sane. On the other hand, dry, relatively low-fiber and low-protein foods are insane. Starches and sweets such as cookies and bread, pasta and potatoes are some of the insane foods that will contribute to a hormonally clogged sink.
This leaves a huge gray area of unaddressed permutations. There
are plenty of high-protein, low-fiber foods like meats. What
about protein powders, which are water-free and low-fiber?
Bailor is just fine with protein powder despite its failure to meet
2 of the 3 criteria for sane foods. There are also plenty of low-protein, high-water, high-fiber foods. According to Bailor,
combining the latter two makes it okay in some cases. To quote
him in the Frequently Asked Questions page of his website,
When it comes to achieving optimal athletic performance, right before, during, and right after the event, we need to quickly get
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Alan Aragons Research Review November 2013 [Back to Contents] Page 14
our muscles glucose and amino acids. The most SANE option
Ive found for doing this is blending fruits with whey protein powder and consuming these shakes before, during, and after
the event. For on-the-go protein he approves of protein bars, as long as they contain a minimum of 4 times more protein than
sugar. Nevermind that protein bars, like protein powders, are
typically low in fiber, and of course water-free. Along these
lines of irony, Bailor says that the more natural a food is, the
more sane it is. Yet, he recommends consuming low-fat or fat-
free versions of dairy products, as well as consuming egg whites
mixed with whole eggs in order to increase the proportion of
protein and decrease fat intake. Harp on insanity but give a free pass to logical incoherence... Got it.
Bailor calls for the avoidance of starches including potatoes. He apparently is in denial that potatoes are rich in
micronutrition, water, and fiber. A recent scientific review by
Weaver and Matt describes the misunderstanding and injustice
leveled at potatoes:3
Potatoes are often left out of the vegetable category in food guidance because of their purported association with higher fat diets. Yet white potatoes are a good source of several shortfall nutrientspotassium, magnesium, fiber, and vitamin B-6, and as consumed, provide 3%-4% of total energy. [...] Potatoes should be counted as a vegetable in food guidance systems. In fact, they had their own category in the 1933 USDA food guidance system because of their important contribution to nutrient intake.
Its also ironic that Bailor bashes potatoes while harping on the importance of satiety. Holt et al found that potatoes were far
more satiating than all 38 common foods tested, including
protein-dominant foods.4 Its tough to talk about potatoes
without mentioning Chris Voigt, the head of the Washington
State Potato Commission. This brave man went on a 60-day
potato-only diet and lost 21 lbs while improving his blood lipid
profile and reducing his fasting glucose levels.5
Another fun factoid challenging Bailors stance is that the top 10 countries with the lowest obesity rates unanimously consume a
starch-dominant diet.4 In light of this, its amusing how Bailor
advises to skip the rice when eating Asian dishes, since 8 of the
top 10 countries that lead the world in low obesity rates are
Asian.6 Its given that correlation does not automatically equal
causation, so observational evidence should be viewed with
caution. However, the fact that a low-carb diet is not the
common thread among the leanest (or the healthiest) populations
on the planet strongly suggests that starch avoidance is likely to
be a trivial factor at best in the war against obesity.
As for the controlled interventions, research comparing high
versus low-carb diets rarely matches protein intakes between
groups. Therefore, the higher-protein condition typically yields
more favorable results. This isnt surprising considering the positive effects of protein on satiety, thermogenesis, and lean
mass preservation. However, studies that do match adequate
protein intake fail to show a weight loss or fat loss advantage of
the low-carb condition.7,8
Eat way more non-starchy vegetables, way more sea food and nutritious meats, more low-sugar fruit, and more nuts and
seeds. Get so full and satisfied from eating as many sane foods as you want, whenever you want, that youre too full for dessert. So go ahead, double the portion of your nutritious high-protein main dish, triple that side of non-starchy veggies.
These are the words of someone without a lot of dietary
counseling experience. Granted, you cant really expect that from someone whose formal background involves computer
software development and management. Heres the problem. Any push towards filling up on a strict set of foods and strictly
avoiding another set of foods is at best, a short-term solution. At
worst, it can backfire and lead to excessive fat gain and all of the
accompanying problems.
Bailor repeatedly mentions that we need to repair our broken
hormonal systems in order to lower our bodyweight set-points.
Im wondering how he plans to achieve that with dietary recommendations which combine a fiber fetish with fat-phobia
and carbo-phobia. This is an ideal recipe for decreasing
testosterone9,10
and triiodothyronine (T3) production.11,12
Thats a double-whammy for compromising muscle gain and fat loss
efforts.
And yet again, we see how Bailor complicates a simple concept
like eating more fruit by setting rules about the type of fruit
allowed. Demonizing certain foods while deifying others is a
false perceptual framework that can lead to adverse
psychological effects. Hes also putting the evil/off-limits stamp on dessert, thereby creating a platform for obsessiveness and
food neuroticism. An all-or-nothing, rigid approach to dieting
has actually been associated with overeating, increased
bodyweight, and eating disorder symptoms, while flexible
dieting has shown a stronger association with lower bodyweight
and the absence of depression and anxiety.13,14
Its clear that Bailors simplifications are anything but simple. Neither are they logical or grounded in science.
Bailors eccentricity doesnt end with diet
Bailor is strongly enamored with eccentric resistance training
(focusing on the negative phase of the repetition) to the point of claiming its the best way to train. In fairness, theres an interesting body of research on the benefits of eccentric training
on strength and hypertrophy. A relatively recent meta-analysis
by Roig et al15
found that eccentric training is more effective at
increasing total and eccentric strength than concentric training.
However, a subgroup analysis of 3 studies that equated intensity
as a percentage of 1RM showed no major differences between
eccentric and concentric training in promoting strength gains.
The authors repeatedly stress that strength gains from eccentric
exercise are highly specific to the mode of contraction and
velocity of movement. One of their caveats is worth quoting
directly:
Because total strength was calculated as the average of eccentric, concentric and isometric strength gains, we must consider that excessively weighted gains in eccentric strength could have influenced the measure of total strength.
Now, heres where things go awry. Bailor claims that the eccentric phase should last 10 seconds. His reasoning is to
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Alan Aragons Research Review November 2013 [Back to Contents] Page 15
maximally stimulate the type IIB fibers, and thus evoke the most
profound hormonal response possible in terms of making inroads
into fat loss and setpoint-lowering. I sent this video of Bailor
coaching a bodyweight squat to my friend and colleague Brad
Schoenfeld, who I consider to be one of the top researchers in
area of exercise science. Heres his feedback:
1. From a strength perspective, there is certainly a transfer from eccentric training to concentric training, but optimal concentric strength is achieved through training concentrically.
2. Eccentric seems to be at least as effective as concentric exercise for hypertrophy. But optimal hypertrophy would seem to require that both modes of action be included. There is some evidence that eccentric training has a preferential effect on fast twitch fibers and thus the slow-twitch fibers would not be adequately stimulated. What's more, there appear to be different "types" of hypertrophy associated with each action: eccentric training has an effect on "in series" hypertrophy while concentric has more of an effect on 'in parallel' hypertrophy. It's a highly complex topic that requires more research (limitations are in the training experience of subjects, time course of study, and others). Bottom line is that there current evidence indicates that both modes of actions are important.
3. Humans don't possess type IIb fibers--these are exclusive to rodents; we possess the IIx isoform.
4. There is no evidence that a 10-second slow eccentric is optimal for hypertrophy. In fact, there is evidence that faster eccentrics are actually more hypertrophic than very slow eccentrics (although there are some methodological issues with this research as well).
5. The knees-over-toes myth of squats is something I've covered extensively. His point should have been that you should not force the knees into forward translation but rather sit back into the squat; whether the knee goes past the toes or not is irrelevant.
On the note of Brads final point, Fry et als examination of the knees-over-toes issue warrants mention.
16 They found that
although restricting forward movement of the knee past the toes
(as Bailor recommends) decreases stress on the knees, it also can
transfers stress to the hips and lower back. This picture from
their paper is worth a thousand words:
Fry et al concluded that allowing the knees to go beyond the toes
may be necessary to optimally distribute forces on all of the
joints involved with the squat. Bailors claim that the knee should never pass the toe is thus a load of grass-fed baloney.
Concluding thoughts
Im not quick to criticize anyone who makes a diligent effort to disseminate high-quality information that considers the full
range of scientific evidence. There is a growing number of folks
in this industry who indeed produce excellent, research-based
work. In contrast, Bailors relatively short video clip is just so crammed with misleading and plain-false information, that it
quickly rustled me into myth-slaying mode. The clip is so well-
produced, that its immediately intriguing and engaging to those without any solid understanding of physiology. Sure, there are
moments of good information, but those moments are
consistently interspersed with hogwash. For example, many
people do need to eat more vegetables, but then he imposes the
non-starchy vegetable rule. Also, many do need to eat more
fruits, but then he imposes the low-sugar fruit rule. On a final
note, its difficult to tell who is lucidly sheisting the public, and who sincerely believes their own fairy tales with the best of
intentions. Bailor appears to lean toward the latter, but that
doesnt exempt his material from meeting my red pen.
References
1. United States Department of Agriculture. Food Availability (Per Capita) Data System. Summary Findings: Food Patter Equivalents and Dietary Trends. Updated Sep 16, 2013. [ERS/USDA]
2. Church TS, Thomas DM, Tudor-Locke C, Katzmarzyk PT, Earnest CP, Rodarte RQ, Martin CK, Blair SN, Bouchard C. Trends over 5 decades in U.S. occupation-related physical activity and their associations with obesity. PLoS One. 2011;6(5):e19657. [PubMed]
3. Weaver C, Marr ET. White vegetables: a forgotten source of nutrients: Purdue roundtable executive summary. Adv Nutr. 2013 May 1;4(3):318S-26S. [PubMed]
4. Holt SH, Miller JC, Petocz P, Farmakalidis E. A satiety index of common foods. Eur J Clin Nutr. 1995 Sep;49(9):675-90. [PubMed]
5. http://20potatoesaday.com/ 6. Central Intelligence Agency. A Spotlight on World Obesity
Rates. Updated Apr 30, 2013. [CIA] 7. Soenen S, Bonomi AG, Lemmens SG, Scholte J, Thijssen
MA, van Berkum F, Westerterp-Plantenga MS. Relatively high-protein or 'low-carb' energy-restricted diets for body weight loss and body weight maintenance? Physiol Behav. 2012 Oct 10;107(3):374-80. [PubMed]
8. Johnston CS, Tjonn SL, Swan PD, White A, Hutchins H, Sears B. Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets. Am J Clin Nutr. 2006 May;83(5):1055-61. [PubMed]
9. Anderson KE, Rosner W, Khan MS, New MI, Pang SY, Wissel PS, Kappas A. Diet-hormone interactions: protein/carbohydrate ratio alters reciprocally the plasma levels of testosterone and cortisol and their respective binding globulins in man. Life Sci. 1987 May 4;40(18):1761-8. [PubMed]
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Alan Aragons Research Review November 2013 [Back to Contents] Page 16
10. Volek JS, Kraemer WJ, Bush JA, Incledon T, Boetes M. Testosterone and cortisol in relationship to dietary nutrients
and resistance exercise. J Appl Physiol (1985). 1997
Jan;82(1):49-54. [PubMed]
11. Mathieson RA, Walberg JL, Gwazdauskas FC, Hinkle DE, Gregg JM. The effect of varying carbohydrate content of a
very-low-caloric diet on resting metabolic rate and thyroid
hormones. Metabolism. 1986 May;35(5):394-8. [PubMed]
12. Pasquali R, Parenti M, Mattioli L, Capelli M, Cavazzini G, Baraldi G, Sorrenti G, De Benedettis G, Biso P, Melchionda
N. Effect of dietary carbohydrates during hypocaloric
treatment of obesity on peripheral thyroid hormone
metabolism. J Endocrinol Invest. 1982 Jan-Feb;5(1):47-52.
[PubMed]
13. Stewart TM, Williamson DA, White MA. Rigid vs. flexible dieting: association with eating disorder symptoms in
nonobese women. Appetite. 2002 Feb;38(1):39-44.
[PubMed]
14. Smith CF, Williamson DA, Bray GA, Ryan DH. Flexible vs. Rigid dieting strategies: relationship with adverse
behavioral outcomes. Appetite. 1999 Jun;32(3):295-305.
[PubMed]
15. Roig M, O'Brien K, Kirk G, Murray R, McKinnon P, Shadgan B, Reid WD. The effects of eccentric versus
concentric resistance training on muscle strength and mass
in healthy adults: a systematic review with meta-analysis. Br
J Sports Med. 2009 Aug;43(8):556-68. [PubMed]
16. Fry AC, Smith JC, Schilling BK. Effect of knee position on hip and knee torques during the barbell squat. J Strength
Cond Res. 2003 Nov;17(4):629-33. [PubMed]
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Alan Aragons Research Review November 2013 [Back to Contents] Page 17
Martial arts meets academia: an interview with Dr. Brian Jones. By Alan Aragon
____________________________________________________
____________________________________________________
Dr. Brian Jones has a PhD in exercise science and is currently a
full time faculty member at Georgetown College in Kentucky. He
teaches courses in anatomy and physiology, exercise physiology,
and research methods among others. Dr. Jones has written three
books, authored two textbook chapters, and has written for
numerous print and online periodicals. He has extensive
experience in strength and conditioning/personal training with
clients ranging from professional athletes to clinical special
populations. Dr. Jones is the current state director of the NSCA
and holds the CSCS certification. He is a fellow and faculty
member in the Institute of Marti