11 - Nov - 2012

face
Effects of increased meal frequency on fat

oxidation and perceived hunger.
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. DOI:
10.1002/oby.20032 [Obesity]
11 Sports science professor Tim Noakes goes full

low-carb, part 3.
Copyright November 1st, 2012 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com
By Alan Aragon
14 Nicotine and fat loss.

By Kurtis Frank and Sol Orwell
2
Complex problems, simple solutions.

By Matt Perryman
18 Chronic nutrient timing studies.

By Alan Aragon & Brad Schoenfeld
Timing of food intake predicts weight loss

effectiveness.
Garaulet M, Gmez-Abelln P, Alburquerque-Bjar JJ, Lee
YC, Ordovs JM, Scheer FA. Int J Obes (Lond). 2013 Jan
29. doi: 10.1038/ijo.2012.229. [Epub ahead of print]
[PubMed]
Carbohydrate co-ingestion with protein does not

further augment post-prandial muscle protein
accretion in older men.
Hamer HM, Wall BT, Kiskini A, de Lange A, Groen BB,
Bakker JA, Gijsen AP, Verdijk LB, van Loon LJ. Nutr
Metab (Lond). 2013 Jan 25;10(1):15. [Epub ahead of print]
[PubMed]
Concurrent training in elite male runners: The

influence of strength versus muscular endurance
training on performance outcomes.
Sedano S, Marn PJ, Cuadrado G, Redondo JC. J Strength
Cond Res. 2013 Jan 2. [Epub ahead of print] [PubMed]
No effect of 1 or 7 days green tea extract ingestion

on fat oxidation during exercise.
Randell RK, Hodgson AB, Lotito SB, Jacobs DM, Boon N,
Mela DJ, Jeukendrup AE. Med Sci Sports Exerc. 2012 Dec
14 [PubMed]
Alan Aragons Research Review November 2012
[Back to Contents]
Page 1
Complex problems, simple solutions.

By Matt Perryman
_________________________________________________
Introduction
Let's ask a simple question. When your car breaks down, you
take it to your local mechanic. He knows his way around cars
like I know my way around the liquor store. You know he'll track
down the problem, fix it, and do it so well you won't think twice
about it when you pick your car up.
Are you going to ask him about his graduate degree in
automotive engineering?
My readers, including you AARR regulars, will be aware of my
love for science. I believe that, on balance, scientific research is
the ultimate arbiter of facts about the natural world, including
our bodies.
Over the last few years, however, my interests have zoomed out
to the larger picture. The details of knowledge, and what that "on
balance" implies, rate high on my list. What is a fact? How do
we determine a fact about a living organism? How do we take
those facts and make them relevant to our training and nutrition?
Keeping those questions in mind, are we, as trainers and coaches
and athletes, meant to be engineers, well versed in theory and
engrossed in the deep layers of design, or more like the
mechanic who may not have the first clue about how to design
a car, but is so familiar with how it works that he can tell you
what's wrong by hearing the engine idle?
I'd like to have a look at these two distinct, but related,
questions: what kind of knowledge do we need, and on a deeper
level, what kind of knowledge can we ultimately have about
living organisms in the first place?
A New Biology
A society that permits biology to become an
engineering discipline, that allows that science to slip
into the role of changing the living world without trying
to understand it, is a danger to itself. Modern society
knows that it desperately needs to learn how to live in
harmony with the biosphere. Today more than ever we
are in need of a science of biology that helps us to do
this, shows the way. An engineering biology might still
show us how to get there; it just doesnt know where
"there" is.
Carl Woese recently passed away at the age of 84, and it is to my
regret that I only became aware of his work after his death.
Woese had a long and interesting career, including the discovery
of the "third kingdom" of life, the microbial archaea that may be
the oldest form of life on Earth.
although he would eventually be vindicated. He was nothing if

not a big thinker, and as the quote above, taken from his 2004
paper "A New Biology for a New Century", suggests, he set his
sights on the biggest target of all: the way we think about
biology as a discipline.1
Woese argued that biology needed a guiding vision, and one
distinct from those that drive it in previous centuries. He
identifies a problem near and dear to my interests: how we can
analyze wholes in terms of parts (and vice-versa)? Western
science has long treated life as explainable in terms of the most
fundamental parts atoms and forces a view which leaves the
living world explained away as a "sea of tiny atomic particles".
Woese rejects this picture, calling it the "colorless, reductionist
world of 19th century classical physics", and instead advocates a
richer perspective.
"The time has come," he writes, "to replace the purely
reductionist 'eyes-down' molecular perspective with a new and
genuinely holistic, 'eyes-up,' view of the living world, one whose
primary focus is on evolution, emergence, and biologys innate
complexity." Readers of my blog will find familiar sentiments
there; I find myself captivated by this suggestion and in large
agreement with it.
The conceptual viewpoint is no mere philosophical curiosity.
Woese believed that the reductionist picture creates many
problems, not the least of which being "that the biologists sense
of what is important and what is fundamental was retooled to
conform to the classical physicists perception thereof." From
there, we see the inevitable spillover into the very concept of
organism, of what it means to explain, of what biology itself
really is and how it relates to other sciences. Before you know it,
this understanding has crept into academia and society itself, to
such an extent that it "is impossible to discuss modern biology
without the cacophony of materialistic reductionism
throughout."
For Woese, this biology of materialism and molecules is an
incomplete biology, and we have been looking at the essence of
biology with the wrong lens. Indeed, true complexity, the vast
'nonlinear' world that physics now recognizes to exist, is beyond
the purview of classical physics.
Lets stop looking at the organism purely as a
molecular machine. The machine metaphor certainly
provides insights, but these come at the price of
overlooking much of what biology is. Machines are not
made of parts that continually turn over, renew. The
organism is. Machines are stable and accurate because
they are designed and built to be so. The stability of an
organism lies in resilience, the homeostatic capacity to
reestablish itself.
Woese's work on the evolutionary origins of life via molecular

phylogeny set him apart from the orthodoxy of the time,
Instead of the tired machine imagery, he suggests the metaphor

of an eddy or whirlpool in a stream of water -- one which can
withstand a child poking a stick into it. "Organisms are resilient
patterns in a turbulent flow," he offers. For biology to survive as
a discipline and move forward, it must move away from the
[Back to Contents]
Page 2
focus on parts and pieces. Doing so means "an emphasis on

holistic, 'nonlinear,' emergent biology with understanding
evolution and the nature of biological form as the primary,
defining goals of a new biology."
I'd reiterate that this is no crank at work, but one of the brightest
minds to work in modern biology. I am inclined to agree with his
points; I believe that when speaking of biological organisms, we
are dealing not just with different scales but with a different type
of being from familiar "dead" objects.
And this, of course, has implications for not only biology as a
science but what we (believe we) know about our bodies.
A New Perspective
The reductionism and mechanicism Woese and many
others so deeply abhor may be regarded as the Big
Perspective ("vision") that has guided much of western
science hitherto...All scientific endeavors are 'finite'
because of..our perspectives. But this is no reason for
despair; we can always try to change our
perspectives.
The idea of an objective, God-like point of view, detached from
the observer, is appealing and it has formed the basis of Western
science since the beginning (the blame is typically placed at
Descartes's feet, but the roots go back to Plato). However, it's
also impossible to justify without taking for granted Descartes's
"mind stuff" as distinct from the physical realm of matter and
energy.
The consequence is that there can be no "view from nowhere";
we are limited to an essentially human way of viewing the
world. The idea called perspectivism has its roots in
Nietzsche's writings. Modern philosophers of science have
modernized the idea in the form of "scientific perspectivism",
acknowledging the lack of a privileged, objective point of view
while preserving the useful features of science. For a quick
overview, we can look at a paper by Werner Callebaut.2
Callebaut argues that we may better understand "so-called
universal laws of nature" as "defining highly generalized models
that characterize a scientific perspective." Newton's laws
characterize one point of view, Einstein's another, evolutionary
biology still another. This has a profound implication, namely
that our scientific theories only apply to specific and limited
aspects of the world, and never with any total precision. We're
left with a notion of "science" that leaves theory and observation
closely entangled, far more than the "objective" story leads us to
believe.
otherwise more desirable, perspectives on the world, so

those of us who study science as a human activity can
do the same. It is the best any of us can do.
(Emphasis added).
This is not to deny that there is a real, objective "something"
independent of us, but rather to suggest that our knowledge of
that "something" must depend on a perspective rather than a
God's eye view. What we know, then, is highly dependent on the
specific domain or area under investigation. Move outside of
that and you must adopt a new perspective.
Take, for example, the currently popular belief that you can
understand how muscles grow or fat is mobilized or how
metabolism responds to exercise or diet entirely by analyzing
studies that focus on the networks of biomolecules in single
cells.
Drawing on Pubmed stories about what happens in a living cell
say, the sequence of molecular events that we understand to
trigger protein synthesis in response to weight-training creates
a necessarily incomplete picture; it is a wonderful and rich story
about what goes on there, and it is also entirely dependent on the
tools, methods, and theories which investigate life on that scale.
Move out of that domain, say to an eating-and-exercising athlete,
and you're left no better off. What happens in cells might hint at
why some methods work, but we cannot simply theorize from
specifics about cells to specifics about the how of real life.
What Now?
I left quite a bit out of these papers for brevity's sake as well as
avoiding tiresome technical language, though I'd suggest reading
them in full if you have any interest in these topics.3 It's
important to note the position here; I am not talking about these
papers as factual truths, but rather ideas to consider.
I hope it's apparent that the situation may not be as simple a
story as "science establishes objective facts without fail" (which
usually translates to ripping selected papers out of a brief
Pubmed search to "prove" something or other).
Ronald Giere, who has argued for such a perspectivist model of

science, adds:
That is one possible view, but in light of the discussion above

(and make no mistake, this is a real and on-going debate), I am
not convinced things work that way. We see that biology might
not be what we think and worse yet, neither is science. What
we observe depends, to some extent, on the theories and
concepts by which we filter and give meaning to observations
themselves. And we're stuck using that toolkit to study objects
which may not be playing by the rules we're using to study them.
In biology, what appears simple can be unimaginably complex
and what appears complex beyond comprehension might be
describable with a few simple rules.
Consensus among scientists on a particular scientific

perspective arises out of both social interactions among
members of a scientific community and interactions
with the world, typically mediated by complex
instrumentation. But just as scientists do in this way
succeed in creating more detailed or more general, or
Based on all this, you might wonder if there's a way forward if

we wish to be "evidence based" in our nutrition and exercise.
Aren't we simply paralyzed by the raw complexity, by the
uncertainty of it all? If we can't know facts and truths, how are
we meant to proceed? I'm going to argue that we're in the exact
opposite position: the lack of knowledge and fundamental
[Back to Contents]
Page 3
uncertainty are to our benefit.

First of all, having only few truly "right" answers means it's also
very hard to screw up. There is no optimum that you must strive
to seek; the very idea of "optimum", as you would expect from
an assembly line in a factory, is a phantom. Good enough is not
just "good enough" it's all there is. It's a matter of scale; we
may be ignorant (and ignorant of our ignorance) about biology
in strict analytical terms, but at the top, where we live and play
and eat, the complexity smooths out to simple guidelines.
4.
5.
See Taleb, Nassim. Antifragile: Things That Gain From

Disorder. New York: Random House, 2012. Taleb's
discussion of how we "fragilize" complex systems,
including our own bodies, in our efforts to control and
smooth out volatility including our compulsion to "do
something" is applicable to our efforts in training and
nutrition.
For more on this topic, see: Polanyi, Michael. Personal
Knowledge: Towards a Post-Critical Philosophy. Chicago:
University of Chicago Press, 1974.
This has led me to a position that I might as well call

pragmatism. By this I simply mean that there are no rules, no
strict workouts or dietary plans, no need to obsess about
hypothetical perfection. You don't have to appeal to experts with
special, secret knowledge or worry about all the things you may
love to worry about.
Good enough is all there is. Instead of being driven by factoids
from published research, you work by heuristics (guidelines, or
rules-of-thumb), and you tinker. "Tinkering" is a word I've
picked up from Nassim Taleb, who argues along similar lines:
some phenomena are just not like machines that can be picked
apart and analyzed in fine detail. The best we can do is watch
and experiment.4
You can pick up heuristics by watching people train, by seeing
what has worked and only then see if perhaps there is any
biological explanation to lend support (or not). I would suggest
being a skeptic with regard to any hard "rules" about training or
nutrition, no matter where they come from. The tacit knowledge
of the practitioner, the technician, is what we should see
knowledge driven by observation, not by the abstract theory of
formal science.5
For me, that is the lesson. Do something, do it with an open
mind, and base your knowledge, as a practitioner, on outcomes
rather than abstractions. Evidence comes from many places, and
science itself is not as certain a bedrock as it can seem and
that's okay. We are mechanics, not engineers.
__________________________________________________
EDITORSS NOTE: More of Matts brotacular writings can be
found at Myosynthesis.com.
__________________________________________________
References
1.
2.
3.
Woese, Carl R. A New Biology for a New Century.

Microbiology and Molecular Biology Reviews 68, no. 2
(2004): 173186. [PubMed]
Callebaut, Werner. Scientific Perspectivism: A Philosopher
of Sciences Response to the Challenge of Big Data
Biology. Studies in History and Philosophy of Science Part
C: Studies in History and Philosophy of Biological and
Biomedical Sciences 43, no. 1 (2012): 69-80. [PubMed]
If you're interested in a more detailed account of
perspectivism, have a look at: Giere, Ronald N. Scientific
Perspectivism. Chicago: University of Chicago Press, 2006.
[Back to Contents]
Page 4
Timing of food intake predicts weight loss

effectiveness.
Garaulet M, Gmez-Abelln P, Alburquerque-Bjar JJ, Lee YC,
Ordovs JM, Scheer FA. Int J Obes (Lond). 2013 Jan 29. doi:
10.1038/ijo.2012.229. [Epub ahead of print] [PubMed]
BACKGROUND: There is emerging literature demonstrating a
relationship between the timing of feeding and weight regulation in
animals. However, whether the timing of food intake influences the
success of a weight-loss diet in humans is unknown. OBJECTIVE:
To evaluate the role of food timing in weight-loss effectiveness in a
sample of 420 individuals who followed a 20-week weight-loss
treatment. METHODS: Participants (49.5% female subjects; age
(means.d.): 4211 years; BMI: 31.45.4kgm(-2)) were grouped in
early eaters and late eaters, according to the timing of the main meal
(lunch in this Mediterranean population). 51% of the subjects were
early eaters and 49% were late eaters (lunch time before and after
1500 hours, respectively), energy intake and expenditure, appetite
hormones, CLOCK genotype, sleep duration and chronotype were
studied. RESULTS: Late lunch eaters lost less weight and
displayed a slower weight-loss rate during the 20 weeks of
treatment than early eaters (P=0.002). Surprisingly, energy intake,
dietary composition, estimated energy expenditure, appetite
hormones and sleep duration was similar between both groups.
Nevertheless, late eaters were more evening types, had less
energetic breakfasts and skipped breakfast more frequently that
early eaters (all; P<0.05). CLOCK rs4580704 single nucleotide
polymorphism (SNP) associated with the timing of the main meal
(P=0.015) with a higher frequency of minor allele (C) carriers
among the late eaters (P=0.041). Neither sleep duration, nor
CLOCK SNPs or morning/evening chronotype was independently
associated with weight loss (all; P>0.05). CONCLUSION: Eating
late may influence the success of weight-loss therapy. Novel
therapeutic strategies should incorporate not only the caloric intake
and macronutrient distribution-as is classically done-but also the
timing of food. SPONSORSHIP: This study was supported by
grants from Tomas Pascual and Pilar Gomez-Cuetara Foundations,
Spanish Government of
Science and Innovation, Seneca
Foundation, NHLBI, NIDDKD, and USDA.
Study strengths
A novel aspect of this study is the reporting of not just
bodyweight, but also energy expenditure, physical activity (in
METs), appetite hormones, and CLOCK genes, whose single
nucleotide polymorphisms (SNPs) have been associated with
weight loss or obesity depending on within-day timing of food
intake. Sample size was relatively large (420 subjects), and trial
duration was long (~20 weeks). Subjects met with a nutritional
professional every 2 weeks, who counseled them on the range of
dietary and behavioral program aspects. Energy and
macronutrient records were software-analyzed.
Study limitations
The authors acknowledged a couple of limitations. First, the
Harris-Benedict equation was used to predict energy
requirements, and they conceded that this ...is not very accurate
to assess energy expenditure, especially during weight loss.
they also admitted that the groups could have had differences in
resting energy expenditure that went undetected. A solution for
this confounder would be the doubly labeled water technique,
which is a more accurate/objective measure of energy
expenditure.1,2 Dietary intake was self-reported, and this

introduces considerable error potential, as opposed to a more
controlled model where food (at least the main meals) are
provided by the lab. Its noteworthy, however, that the
aforementioned measures of control are rare due to their
astronomical expense in long trials with large subject numbers.
Body composition was not measured, and the subjects results
cannot necessarily be generalized to athletic populations.
Comment/application
A quick perusal could lead many to assume that the over-arching
message is that eating later means getting fatter. However, its
important to note that only the timing of lunch (early as opposed
to late) was associated with a significantly greater loss of
bodyweight. The timing of breakfast or dinner was not found to
have any impact on bodyweight change. This finding deserves
emphasis since it runs contrary to the automatic assumption that
people will make namely, that dinner must be consumed early
in order to effectively lose weight. However, taking a look at the
chart above, the mean weight loss between the differing
breakfast and dinner timing was practically identical. Upon
closer examination of what qualified as a statistically significant
difference in weight loss between the late and early lunch eaters
amounted to a difference of 2.2 kg in 5 months hardly anything
to get overly excited about, considering the potential
confounders discussed. The authors found that late eaters
happened to skip breakfast more frequently than early eaters,
which they felt could be a contributing factor to their lesser
weight loss. Curiously, they posited that the late lunch may
prolong a semi-fasted state and induce glucose metabolism
impairments. However, these speculations have questionable
grounds due to the majority of controlled interventions that do
not support them.3-7 The present findings, although interesting,
dont exactly rock the boat of evidence. Replication with tighter
control would be required. Ill conclude by quoting recent work
by Sofer et al, who found opposite & potentially more relevant
outcomes despite concentrating energy intake later in the day:8
...our studies have demonstrated that manipulation of dietary
carbohydrate distribution led to changes in the daily curves of
leptin, ghrelin and adiponectin that coincided with improved
hunger/satiety status, persistence in the weight loss process,
anthropometric outcomes, insulin sensitivity, metabolic
syndrome parameters and inflammatory status.
[Back to Contents]
Page 5
Carbohydrate co-ingestion with protein does not

further augment post-prandial muscle protein
accretion in older men.
Hamer HM, Wall BT, Kiskini A, de Lange A, Groen BB,
Bakker JA, Gijsen AP, Verdijk LB, van Loon LJ. Nutr Metab
(Lond). 2013 Jan 25;10(1):15. [Epub ahead of print] [PubMed]
BACKGROUND: A blunted muscle protein synthetic response
to protein ingestion may contribute to the age related loss of
muscle tissue. We hypothesized that the greater endogenous
insulin release following co-ingestion of carbohydrate facilitates
post-prandial muscle protein accretion after ingesting a meal-like
bolus of protein in older males. METHODS: Twenty-four
healthy older men (75+/-1 y) were randomly assigned to ingest
20 g intrinsically L-[1-13C] phenylalanine-labeled casein protein
with (PRO-CHO) or without (PRO) 40 g carbohydrate. Ingestion
of specifically produced intrinsically L-[1-13C] phenylalanine
labeled protein allowed us to assess post-prandial incorporation
of dietary protein derived amino acids into muscle protein.
Blood samples were collected at regular intervals, with muscle
biopsies being obtained prior to and 2 and 6 h after protein
ingestion. RESULTS: Plasma glucose and insulin
concentrations showed a greater increase in PRO-CHO
compared with PRO (P<0.001). Muscle protein-bound L-[113C] phenylalanine enrichments tended to increase to a greater
extent in PRO-CHO compared with PRO during the first 2 h
after protein ingestion (0.0072+/-0.0013 vs 0.0046+/-0.010
MPE, respectively; P=0.13). However, 6 h after protein
ingestion, differences in muscle protein-bound L-[1-13C]
phenylalanine enrichments were no longer observed between
experiments (0.0213+/-0.0024 vs 0.0185+/-0.0010 MPE,
respectively; P=0.30). CONCLUSION: This study shows that
carbohydrate ingestion may accelerate, but does not further
augment post-prandial incorporation of dietary protein derived
amino acids into muscle protein in healthy elderly men.
SPONSORSHIP: None listed.
Study strengths
According to the US Census Bureau, the older population (65
years) comprises the largest proportion of the total population,
and is also the fastest growing segment.9 This study covers
important ground since the majority of protein research has been
done on younger adults. This is the first study to investigate the
acute anabolic effects of protein and protein/carbohydrate dosing
in older individuals. Subjects consumed a standardized meal the
evening prior to testing, which served to minimize the chance of
confounding differences in circulating substrate levels. After
consumption of the test drinks, blood samples were taken at
frequent intervals (14 samples within a 6-hour period) which
allowed a more accurate picture of the appearance curve.
stock in acute response. The study is otherwise elegant and

tightly controlled. To nit-pick, although it was necessary to
perform the tests on fasted subjects in order to isolate the effect
of the test meal, this of itself is a limitation. The majority of the
day (for people with typical eating patterns) is spent in the fed
state. This limits the applicability of the results to merely the
first meal of the day (or any meal that occurs after a long enough
interval to reach the post-absorptive period). Another limitation
is that the responses seen might only apply to the resting state, as
opposed to the post-exercise state. Another limitation was that
the results might only apply to the type of protein used (casein);
other types need to be investigated in order to get a more
comprehensive data set. A final limitation common to these
types of studies is that they leave unanswered questions about
how the inclusion of fat and/or fiber (common to solid mixed
meals) might influence the muscle protein accretion.
Comment/application
As seen above, the main findings were that despite the caeindextrose treatment causing a greater initial insulin spike which
accelerated amino acid delivery to muscle during the first 90
minutes after ingestion, amino acid delivery overall was not
greater than the casein-only treatment at the 6-hour mark. This
finding is similar to recent work by Staples et al, who found that
an additional 50 g maltodextrin co-ingested with 25 g whey did
not augment muscle protein balance either at rest or postexercise,10 and also work by Moore et al, who found that 20 g
whole egg protein was sufficient to max-out muscle protein
synthesis & albumin protein synthesis after resistance exercise,
whereas a 40 g dose merely increased amino acid oxidation.11
An inherent limitation is the acute nature of the study. Just

because muscle protein synthesis (MPS) is maxed-out in the
short term, this does not necessarily translate to chronic
adaptations, especially those occurring via sufficient total
protein intake as opposed to a particular dose per meal.
Admittedly, this is not what the study was seeking to find, but it
bears mentioning nonetheless, since folks tend to put too much
While the aforementioned work yielded similar results to the

present study, two other recent studies had results that are
potentially at odds with the present study. Yang et al found that
20 g whey protein stimulated myofibrillar muscle protein
synthesis (MPS) above fasting levels in non-frail older adults in
the resting state, while 40 g increased MPS to a greater extent
than 20 g after resistance exercise.12 This could be due to the
difference in protein types; that is, whey could potentially have a
higher ceiling of maximal anabolic effect than casein (in this
population). Pennings et al found that muscle protein accretion
was greater with a 35 g dose of whey than 10 or 20 g in the
resting state.13 Unfortunately, no carbohydrate co-ingestion was
tested in either of these studies. Collectively, roughly 20-40 g
appears to be the sweet spot for maximizing the acute anabolic
response, and older folks are more suited for the higher end.
[Back to Contents]
Study limitations
Page 6
Concurrent training in elite male runners: The

influence of strength versus muscular endurance
training on performance outcomes.
Sedano S, Marn PJ, Cuadrado G, Redondo JC. J Strength Cond
Res. 2013 Jan 2. [Epub ahead of print] [PubMed]
BACKGROUND: Much recent attention has been given to the
compatibility of combined aerobic and anaerobic training
modalities. However few of these studies have reported data
related to well-trained runners, which is a potential limitation.
PURPOSE: Therefore, due to the limited evidence available for
this population, the main aim was to determine which mode of
concurrent strength-endurance training might be the most
effective at improving running performance in highly-trained
runners. METHODS: Eighteen well-trained male runners (age
23.7 1.2 yr) with a maximal oxygen consumption (VO2max)
higher than 65 mLkgmin were randomly assigned into one of
the three groups: Endurance-only Group (EG; n=6), who
continued their usual training, which included general strength
training with Thera-band latex-free exercise bands and
endurance training; Strength Group (SG; n=6) who performed
combined resistance and plyometric exercises and endurance
training; Endurance-Strength Group (ESG; n=6) who performed
endurance-strength training with loads of 40% and endurance
training.. The study comprised 12 weeks of training in which
runners trained 8 times a week (6 endurance sessions and 2
strength sessions) and 5 weeks of detraining. The subjects were
tested on three different occasions (counter movement jump
height, hopping test average height, one-repetition-maximum,
running economy, VO2max, maximal heart rate (HRmax), peak
velocity, rating of perceived exertion and 3-km time trial were
measured). RESULTS: Findings revealed significant time x
group interaction effects for all almost tests (p <0.05).
CONCLUSIONS: We can conclude that concurrent training
(CT) for both SG and ESG groups led to improved maximal
strength, running economy and peak velocity with no significant
effects on the VO2 kinetics pattern. The SG group also seems to
show improvements in 3-km time trial tests. SPONSORSHIP:
None listed.
Study strengths
This study investigated 2 different types (explosive strength or
endurance-strength) of concurrent training (CT) to see which
best improves running performance, and was careful to include a
control group where subjects usual training was continued. A
particular strength of the design was the use of highly
endurance-trained subjects, which is a scarce scenario in the
current literature. Another strength was the examination of the
effects of detraining after the protocols compared (12 weeks of
intervention followed by 5 weeks of detraining). A nice touch
was the assessment of body composition in addition to the
performance measures (which included a track running test,
which has direct relevance, as opposed to strictly lab testing).
Training was supervised by experienced staff.
subjects were instructed to consume the same type of meal.

However, to the authors credit, subjects were instructed to
abstain from caffeine 4 hours prior to testing. Another de facto
limitation (rather than faulty design) is that the results of this
trial might be limited to the design of the training protocols (2
sessions of resistance training and 4 sessions of endurance
training per week), which were as follows:
The endurance-only group (EG) is actually a misnomer
since this groups program included their pre-existent
resistance training, which consisted of a 4-exercise lower
body circuit. External load was via blue Thera-Band

latex-free exercise bands. Each circuit was repeated
3 times with 25 reps per exercise.
The strength group (SG) protocol consisted of lower body
resistance and plyometric exercises. Barbell squats, lying
leg curls, seated calf raises, and leg extensions were doe
with 3 sets of 7 reps at 70% of max intensity. Each
resistance exercise was combined with a plyometric
exercise, with 5 minutes rest between exercises.
The endurance-strength group (ESG) protocol consisted of
the same resistance exercises as SG, but with 20-rep sets
done at 40% of max intensity. Interset rest was 60 seconds,
rest between exercises was 5 minutes.
As seen in these protocols, upper body resistance training was
nonexistent. Optimal implementation of resistance training
aimed at improving running performance would include upper
body exercises to complete the range of stimuli imposed upon
the whole kinetic chain. However, to the authors credit, they
kept the strength training progressive; intensity was adjusted
every 2 weeks in order to accommodate strength increases. A
final limitation is the use of skinfold calipers to assess body
composition instead of another method such as DXA or
hydrodensitiometry, which minimizes technician error.
Comment/application
The main findings were as follows: 1) No significant difference
in body composition across conditions; 2) Maximal strength (1
RM) gains occurred in SG and ESG, but not in EG, and these
gains were maintained despite the detraining period; 3) SG and
ESG improved VO2max at 12 km/h and peak velocity without
significant changes in VO2max or HRmax. SG also improved
running economy at 16 km/h and RPE ratings all of these
improvements were maintained despite the detraining period; 4)
improved track running test performance was seen in SG.
Training studies are notorious for their lack of dietary control,

and this study is no exception. The extent of control was that
Perhaps the most important outcome was the improvement in 3km time trial performance in SG, since this was a field test
directly related to a real-world race. A similar finding was also
seen by Paavolainen et al,14 who found that concurrent explosive
strength & endurance training improved 5-km time trial
performance despite a lack of change in VO2max. They
speculated that performance was enhanced by explosive strength
training causing improved neuromuscular function, which in
turn translated to improved running economy. The practical
application offered by the authors is for coaches to incorporate
explosive strength training in the endurance programs of welltrained endurance athletes. Based on the weight of the current
evidence,14-17 this looks like a sound recommendation.
[Back to Contents]
Study limitations
Page 7
No effect of 1 or 7 days green tea extract ingestion on

fat oxidation during exercise.
Randell RK, Hodgson AB, Lotito SB, Jacobs DM, Boon N,
Mela DJ, Jeukendrup AE. Med Sci Sports Exerc. 2012 Dec 14
[PubMed]
PURPOSE: The aim of this study was to investigate the effects
of 1 day and 7 days ingestion of a green tea extract (GTE) on
whole body fat oxidation during moderate-intensity exercise.
METHODS: Thirty one males completed two exercise trials (60
min cycle 50% Wmax). Following the baseline trial (Day 0)
subjects were randomly assigned to one of three conditions
involving a week supplementation of; 1) 7 days placebo (PLA);
2) 6 days of PLA followed by 1 day of GTE (GTE1); 3) 7 days
of GTE ingestion (GTE7). The morning after the
supplementation week, subjects consumed an additional
supplement and completed a second exercise trial (Day 8). VO2
and VCO2 measurements were taken during exercise to
calculate whole body fat oxidation rates. Blood samples, for
analysis of plasma fatty acids (FAs), glycerol and
epigallocatechin gallate (EGCG), were collected at rest and
during
exercise.
RESULTS: On Day 8 the
plasma
kinetics
and
maximal plasma concentrations of EGCG were
similar in the GTE1 and
GTE7 group (206 28 and
216
25
ngmL-1
respectively). One day of
GTE ingestion did not
affect
markers
of
lipolysis during the exercise
bout. Seven days of GTE
ingestion
significantly
increased plasma glycerol during exercise (P=0.045) and plasma
FAs during exercise (P=0.020) as well as at rest (P= 0.046).
However, fat oxidation did not change in any of the groups.
CONCLUSIONS: There was no effect of 1 day GTE ingestion
on markers of lipolysis or fat oxidation during exercise. Seven
days of GTE ingestion increased lipolysis, indicated by
increased plasma FA and glycerol concentrations, but did not
result in significant changes in fat oxidation. SPONSORSHIP:
This work was supported by a research grant from Unilever Plc.
S.L, D.J and D.M are employees of Unilever. R.R, A.H and A.J
have no professional relationship with the company involved in
this study and have no conflict of interests. N.B was a previous
employee of Unilever however had no conflict of interest at the
time of results interpretation.
subjects to take their supplements, supplement logs were kept

daily as well. Subjects were also required to return all empty
cans when they visited the lab. Inclusion criteria involved
choosing subjects who consumed a maximum of 400 mg
caffeine per day in order to exclude those who might be
desensitized to caffeines effects.
Study limitations
The outcomes might be limited to the short trial duration (7
days). Sample size was small (10-11 subjects per treatment arm).
Moderately trained subjects were chosen, so the results might
not be generalizable to other populations. As acknowledged by
the authors, highly trained endurance athletes have less chance
of showing significant effects on fat oxidation since they have
high pre-existent whole-body fat oxidation rates as a result of
muscular adaptations to their training protocols. A final
limitation is that the results might not be relevant outside of the
exercise testing protocol used, which was 60 minutes of cycling
at 55% VO2max. These findings are not necessarily applicable
to different training modes or to significantly higher or lower
intensities.
Comment/application
The main findings of this study were twofold. There was no

significant difference in circulating EGCG after the 7-day and 1day dosing of GTE/caffeine. Perhaps the most important finding,
depicted above, was the lack of significant difference in fat
oxidation between all three conditions, and this lack of effect on
fat oxidation was seen despite an increase in lipolysis (fat
mobilization, indicated by an increase in plasma fatty acid levels
at rest and during exercise after 7 days of GTE/caffeine
supplementation). The authors speculate that the 7 day trial
period might not have been long enough to form functional
compounds (i.e., proteins and enzymes) involved with
upregulation of fatty acid oxidation.
This study is the first to measure the effect of green tea extract
(GTE) on fat oxidation rates in humans, while also taking into
account plasma catechin levels. Its also the first to directly
compare the effects of 1 & 7 days of GTE ingestion on fat
oxidation during 60 minutes of moderate-intensity exercise. The
lab provided subjects all of their meals the day before the trial.
To bolster compliance, daily text messages were sent to the
The bigger picture of GTEs effectiveness should be taken into

consideration. Human research on the chronic effects of GTE as
a weight loss supplement has shown a consistency of positive
effects on fat oxidation. However, the effects tend to be small.18
To quote the conclusion of a recent systematic review of green
tea catechins (GTC) by Phung et al:19 The administration of
GTCs with caffeine is associated with statistically significant
reductions in BMI, body weight, and [waist circumference];
however, the clinical significance of these reductions is modest
at best. Current data do not suggest that GTCs alone positively
alter anthropometric measurements.
[Back to Contents]
Study strengths
Page 8
Effects of increased meal frequency on fat oxidation

and perceived hunger.
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. DOI: 10.1002/oby.20032
[Obesity]
BACKGROUND: Consuming smaller, more frequent meals is
often advocated as a means of controlling body weight, but
studies demonstrating a mechanistic effect of this practice on
factors associated with body weight regulation are lacking.
METHODS: The purpose of this study was to compare the
effect of consuming 3 (3M) vs. 6 meals (6M) per day on 24-h fat
oxidation and subjective ratings of hunger. Lean (BMI<25
kg/m2) subjects (7M, 8F) were studied in a whole-room
calorimeter on two occasions in a randomized cross-over design.
Subjects were provided isoenergetic, energy balanced diets with
a 1- to 2-week washout between conditions. Hunger, fullness,
and desire to eat ratings were assessed throughout the day
using visual analog scales and quantified as area under the curve
(AUC). RESULTS: There were no differences (P>0.05) in 24 h
EE (8.7 0.3 vs. 8.6 0.3 mj.d-1), 24 h RQ (0.85 0.01 vs. 0.85
0.01) or 24 h fat oxidation (82 6 vs. 80 7 g.day-1) between
3M and6M, respectively. There was no difference in fullness24
h AUC, but hunger AUC (41850 2255 vs. 36612 2556
mm.24 h, P=0.03) and desire to eat AUC (47061 1791 vs.
41170 2574 mm.24 h, P=0.03) were greater during 6M than
3M. CONCLUSION: We conclude that increasing meal
frequency from3 to 6 per day has no significant effect on 24 h fat
oxidation, but may increase hunger and the desire to eat.
SPONSORSHIP: Funding was provided by Research
Fellowships of the Japan Society for the Promotion of Science
for Young Scientists. Research support was provided by the
University of Colorado Clinical and Translational Science
Award and Nutrition and Obesity Research Center.
Study strengths
This study is innovative since surprisingly enough its the
first to ever compare a traditional meal pattern (3 meals) versus
smaller, more frequent meals (6 meals) on 24-hour fat oxidation
and perceived hunger. A 3-day outpatient energy &
macronutrient stabilization period followed each tightly
controlled whole room calorimeter-based test day. All meals
were provided to the subjects during both the lead-in and of
course during calorimeter day. The calorimeter protocol
included 2 bouts of bench-stepping exercise (72 steps per minute
for 20 minutes) in order to mimic free-living activity. Subjects
physical activity was monitored and tracked throughout the
calorimeter period via accelerometer. The inherently
compromised statistical power by the small number of subjects
was alleviated by a crossover design.
relevance of these results to overweight or obese individuals can

be questioned. Third, the women studied were not all in the same
menstrual phase. Fourth, appetite-related hormones were not
directly measured. a final limitation relayed by the authors is
worth quoting, since they truly seemed to be reaching on this
one (I find this amusing since most authors do whatever possible
to avoid listing limitations): Finally, we performed our studies
under isocaloric conditions to specifically study the effects of
meal frequency, but given the higher ratings of hunger and
lower fullness during 6M, we would expect intake to be
increased during 6M under ad libitum conditions, an effect
which needs to be studied directly.
Comment/application
The main findings were twofold. First off, fat oxidation and
energy were not significantly different between the 3 and 6
meal-per-day treatments. Secondly and perhaps most notably
perceiver hunger and desire to eat were greater in the 6 meal
than the 3 meal condition. The latter results are in line with
recent work by Leidy et al, who compared varying protein levels
consumed within 3 or 6 meals and found that the higher meal
frequency led to lower fullness ratings.20 Leidy et al found that
PYY, a gut peptide associated with appetite reduction, was 9%
lower in the higher meal frequency condition.
The present study adds to a very small body of research
examining the question of meal frequencys effect on 24-hour fat
oxidation. Only two other studies have specifically compared
different meal frequencies on 24-hour fat oxidation, and the
results were inconsistent with each other. Verboeket-van de
Venne and Westerterp found no difference between 2 versus 7
meals per day,21 while Smeets & Westerterp-Plantenga found
that 3 meals resulted in greater fat oxidation than 2 meals.22 The
authors of the present study noted that the results of Smeets &
Westerterp-Plantenga may have been attributable to the
slightly (though non-significantly) lower energy balance in the
3-meal condition. In contrast, the present study achieved nearly
a zero-balance, which was nearly identical between conditions.
As always, its important to consider the evidence of meal
frequency on macro-effects. A comprehensive review of the
research in this area was done in my critique of the ISSN
position stand on meal frequency, and the majority of the
evidence does not support the idea that higher frequency equals
better weight loss or improvements in body composition.7 After I
wrote the latter review in April 2011, more recent meal
frequency research has since been published. A 6-month study
by Bachman and Raynor found no significant differences in
body mass index or energy intake between a 3 meal per day
group and a grazing group that ate at least 100 cal every 2-3
hours.23 In contrast to Leidy et al,20 the grazing group reported a
significant reduction in hunger by the end of the trial.
Several limitations were diligently acknowledged by the authors

(it bears repeating that this is refreshing to see since not all
studies admit potential faults). First off, acute effects were
examined, so long-term effects of this particular design are open
to speculation. Secondly. the subjects were relatively lean, so the
The authors of the present study concluded that, although

popular advice dictates that a grazing pattern is superior to lesser
meal frequency for the goal of weight control, grazing was not
seen to impart any advantages toward this end. In fact, the higher
hunger and lower fullness ratings of the grazing condition render
it a potentially inferior approach for dieters. In my observations,
one size does not fit all, and meal frequency is best optimized
according to individual preference.
[Back to Contents]
Study limitations
Page 9
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
Schoeller DA. Recent advances from application of doubly

labeled water to measurement of human energy expenditure.
J Nutr. 1999 Oct;129(10):1765-8. [PubMed]
Schoeller DA, Schoeller DA. Validation of habitual energy
intake. Public Health Nutr. 2002 Dec;5(6A):883-8.
[PubMed]
Sensi S, Capani F. Chronobiological aspects of weight loss
in obesity: effects of different meal timing regimens.
Chronobiol Int. 1987;4(2):251-61. [PubMed]
Schlundt DG, Hill JO, Sbrocco T, Pope-Cordle J, Sharp T.
The role of breakfast in the treatment of obesity: a
randomized clinical trial. Am J Clin Nutr. 1992
Mar;55(3):645-51. [PubMed]
Keim NL, Van Loan MD, Horn WF, Barbieri TF, Mayclin
PL. Weight loss is greater with consumption of large
morning meals and fat-free mass is preserved with large
evening meals in women on a controlled weight reduction
regimen. J Nutr. 1997 Jan;127(1):75-82. [PubMed]
Sofer S, Eliraz A, Kaplan S, Voet H, Fink G, Kima T,
Madar Z. Greater weight loss and hormonal changes after 6
months diet with carbohydrates eaten mostly at dinner.
Obesity (Silver Spring). 2011 Oct;19(10):2006-14.
[PubMed]
Aragon AA. A critique of the ISSN position stand on meal
frequency. April 4, 2011. [Leangains].
Sofer S, Eliraz A, Kaplan S, Voet H, Fink G, Kima T,
Madar Z. Changes in daily leptin, ghrelin and adiponectin
profiles following a diet with carbohydrates eaten at dinner
in obese subjects. Nutr Metab Cardiovasc Dis. 2012 Aug 14.
[Epub ahead of print] [PubMed]
US Census Bureau, US Dept of Commerce. 2010 Census
shows 65 and older population growing faster than total US
population. Nove 30, 2011. [USCB]
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 Jul;43(7):1154-61. [PubMed]
Moore DR, Robinson MJ, Fry JL, Tang JE, Glover EI,
Wilkinson SB, Prior T, Tarnopolsky MA, Phillips SM.
Ingested protein dose response of muscle and albumin
protein synthesis after resistance exercise in young men. Am
J Clin Nutr. 2009 Jan;89(1):161-8. [PubMed]
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. 2012:1-9.
[PubMed]
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]
Paavolainen L, Hkkinen K, Hmlinen I, Nummela A,
Rusko H. Explosive-strength training improves 5-km
running time by improving running economy and muscle
power. J Appl Physiol. 1999 May;86(5):1527-33. [PubMed]
15. Aagaard P, Andersen JL, Bennekou M, Larsson B, Olesen

JL, Crameri R, Magnusson SP, Kjaer M. Effects of
resistance training on endurance capacity and muscle fiber
composition in young top-level cyclists. Scand J Med Sci
Sports. 2011 Dec;21(6):e298-307. [PubMed]
16. Mikkola J, Vesterinen V, Taipale R, Capostagno B,
Hkkinen K, Nummela A. Effect of resistance training
regimens on treadmill running and neuromuscular
performance in recreational endurance runners. J Sports Sci.
2011 Oct;29(13):1359-71. [PubMed]
17. Aagaard P, Andersen JL. Effects of strength training on
endurance capacity in top-level endurance athletes. Scand J
Med Sci Sports. 2010 Oct;20 Suppl 2:39-47. [PubMed]
18. Hursel R, Viechtbauer W, Dulloo AG, Tremblay A, Tappy
L, Rumpler W, Westerterp-Plantenga MS. The effects of
catechin rich teas and caffeine on energy expenditure and fat
oxidation: a meta-analysis. Obes Rev. 2011 Jul;12(7):e57381. [PubMed]
19. Phung OJ, Baker WL, Matthews LJ, Lanosa M, Thorne A,
Coleman CI. Effect of green tea catechins with or without
caffeine on anthropometric measures: a systematic review
and meta-analysis. Am J Clin Nutr. 2010 Jan;91(1):73-81.
[PubMed]
20. Leidy HJ, Armstrong CL, Tang M, Mattes RD, Campbell
WW. The influence of higher protein intake and greater
eating frequency on appetite control in overweight and
obese men. Obesity (Silver Spring). 2010 Sep;18(9):172532. [PubMed]
21. Verboeket-van de Venne WP, Westerterp KR. Influence of
the feeding frequency on nutrient utilization in man:
consequences for energy metabolism. Eur J Clin Nutr. 1991
Mar;45(3):161-9. [PubMed]
22. Smeets AJ, Westerterp-Plantenga MS. Acute effects on
metabolism and appetite profile of one meal difference in
the lower range of meal frequency. Br J Nutr. 2008
Jun;99(6):1316-21. Epub 2007 Dec 6. [PubMed]
23. Bachman JL, Raynor HA. Effects of manipulating eating
frequency during a behavioral weight loss intervention: a
pilot randomized controlled trial. Obesity (Silver Spring).
2012 May;20(5):985-92. [PubMed]
[Back to Contents]
Page 10
Sports science professor Tim Noakes goes full lowcarb, part 3.

By Alan Aragon
Onward into the sunset

Welcome to the final installment of my critique of Tim Noakes
carbophobic manifesto for the masses.1 As with the previous, Ill
interject my commentary between key sections of Noakes
article. Lets begin where we left off, with Noakes warning that
carbs can be the kiss of death, even for competitive endurance
athletes.
OntheotherhandIhavenoticedthattherearealargenumber
ofslowerfinishersintheArgusCycleTourandintheComrades
Marathon who are, to put it scientifically, either overweight
body mass index (BMI) greater than 25kg/m2 or frankly obese
(BMI greater than 30kg/m2). The point is that the BMI is an
excellent proxy for whether or not one is eating the right
amountofenergyeachday.IftheBMIisgreaterthan25kg/m2
in males (somewhat less for females), one is eating more than
oneshould.
Noakes appears to be reaching for anything he can grasp. So,

there are chunkier competitors who finish slower in marathons?
Stop the presses, how can this be true </sarcasm>? Of course,
its easy to guess the hypothesis hell present (carbohydrate
addiction and carbohydrate resistance, stuff thats been
discussed in the last issue). However, the thing that bugs me in
most in the above section is his passive acceptance of body mass
index (BMI = weight in kg divided by height in meters squared),
particularly within the context of athletic populations. I laughed
out loud at him calling it an excellent proxy for whether one is
eating the right amount of energy each day. Really? Wow...
The NHLBIs BMI guidelines are as follows:2
Underweight: <18.5
Normal weight: 18.5-24.9
Overweight: 25-29.9
Obesity, Class 1: 30-34.9; Class 2: 35-39.9; Class 3: 40
Its important to realize that athletic populations should be

particularly cautious about the application of BMI, since it tends
to overestimate adiposity in those with a high degree of lean

mass. Conversely, it underestimates adiposity in those with a
low degree of lean mass. For example, an athlete whose height is
178 cm (510) would be classified as overweight if he weighed
more than 79 kg (173.8 lb). An athlete of this height and weight
casting negative judgement on himself because hes crossed the
line in terms of BMI is patently ludicrous. Even the clinical
credibility and utility of BMI has been called into question in
relatively recent research. In a systematic review of cohort
studies, Romero-Corral et al found more favorable outcomes for
cardiovascular & total mortality in overweight & mildly obese
groups (feel free to laugh and rub your belly). Importantly, these
results could not be explained even after adjusting for
confounding variables. To quote the authors directly:3 These
findings could be explained by the lack of discriminatory power
of BMI to differentiate between body fat and lean mass.
Subsequent research by Flegal et al found that underweight was
associated with increased mortality from non-cancer, non-CVD
causes, while overweight was associated with decreased
mortality from non-cancer, non-CVD causes.4 Keep in mind that
the aforementioned data is observational, so causal assumptions
cannot be made. However, it does shed some interesting light on
the dubious reliability of BMI standards. A better standard
would account for body composition, but this is inherently
difficult despite its superior theoretical basis. In any case, Kyle
et al recognized the limitations of BMI, and rather courageously
developed a fat-free mass index (FFMI) and corresponding body
fat mass index (BFMI):5
BMI, FFMI, BFMI, and %BF in healthy white Caucasian adults*
2
BMI (kg/m )
FFMI (kg/m )
BFMI (kg/m )
% BF
Men
30.0
27.8
25.0
20.0
18.5
21.7
20.9
19.8
17.5
16.7
8.3
6.9
5.2
2.5
1.8
28.8
25.8
21.7
13.4
10.8
Women
30.0
27.3
25.0
20.0
18.5
18.2
17.5
16.8
15.1
14.6
11.8
9.8
8.2
4.9
3.9
40.0
36.5
33.2
24.6
21.7
*Blue=withinnormal/acceptablelimits
As seen above, the normal/acceptable body fat percent ranges

are 10.8-21.7% for men, and 21.7-33.2% for women. These
ranges are similar to previous healthy standards suggested in
earlier research by Abernathy & Black, listing 12-20% for men
and 20-30% for women.6 Next up, we discuss pediatrics.
The seventh point is that babies particularly should not be
placed on high carbohydrate diets since the proper
developmentoftheirbrains(andfacialstructures)requiresthat
the majority of their calories comes from fat and protein. Yet
many baby formulas are full of sugar and carbohydrate and
cannotprovidethepropernutrientsforoptimumdevelopment
duringchildhood.
[Back to Contents]
Page 11
Similarly children who are obese already at a young age will

most likely have CR and carbohydrate addiction and would
benefitenormouslybybanting.Thereisalsogrowinginterest
that, at the other end of the age spectrum, the elderly brain
(like mine) requires a high fat intake to protect it from the
detrimentaleffectsofaging.
Noakes is essentially recommending that children and babies go

on the Atkins diet (remember banting is a colloquialism for
the Harvey/Banting diet, which was a forerunner of the Atkins
diet). His claim that many baby formulas are full of sugar and
carbohydrate and cannot provide the proper nutrients for
optimum development is questionable on a couple of counts.
First of all, infant formula composition, unlike most food
products, is actually regulated. The nutrient content of infant
formula sold in the United States is regulated by the FDA, and
these regulations are based on standards set by the American
Academy of Pediatrics (AAP), which is not some rinky-dink
operation that flies by the seat of its pants. The AAP is a
professional/scientific organization that is heavily involved in
research, continuing medical education, and the improvement of
clinical practice guidelines.
Keep in mind that Im not saying that major health organizations
are exempt from critical analysis. However, I would say
that Noakes suggestion that infant diets should consist mostly of
fat and protein is silly, given that mature human breast milk, by
volume, has been reported to consist of 3-5% fat, 0.8-0.9%
protein, 6.9-7.2% carbohydrate (mainly as lactose).7 Further
challenging Noakes protein/fat-centric recommendations for
infants, Koletzko et al reported that protein intake is 5580%
higher in formula-fed babies than in breastfed infants, which has
raised concerns of what the long-term impact might be. Their
research warrants a direct quote (my underlined emphasis
added):8
We randomly assigned healthy infants who were born at
term to receive for the first year infant formula and followon formula with higher or lower protein contents,
respectively. The follow-up data obtained at age 2 y indicate
that feeding formula with reduced protein content
normalizes early growth relative to a breastfed reference
group and the new World Health Organization growth
standard, which may furnish a significant long-term
protection against later obesity.
The final point is how does one determine if one is CR or not.
Firstisthefamilyhistory.Ifthereisaclosefamilymemberwith
adultonsetdiabetes,thenoneismorelikelytobeCR.Secondis
onesweighthistory.Thosewhowereheavy(obese)aschildren
are very likely to be CR. Alternatively a history of progressive
weight gain through adult life or with pregnancy or at the
menopause, and an inability to forestall weight gain when
eatingahighcarbohydratedietisalsoverysuggestive.Frequent
failed attempts to lose weight when following the more usual
calorierestricted but still high carbohydrate diet, is also highly
suggestive.
Finally when the CR is advanced it can be diagnosed with

certainty with a fasting blood sample that shows elevated
fastingglucose,insulinandglycosylatedhaemoglobin
concentrations. If any of these three values is elevated, it is a

sureindicationthatoneisheadingforadultonsetdiabetesand
thequickeroneadoptsapreventive,lowcarbohydratediet,the
better.
What Noakes nebulously labels as carbohydrate resistance is

better referred to as impaired glucose tolerance (IGT), which
presents itself when challenged with an oral glucose load.
Impaired fasting glucose (IFG) may or may not accompany IGT,
but both conditions are associated with pre-diabetes. IGT is
characterized by having a certain degree of insulin resistance, so
these descriptors can be interchanged. The most objective test
for glucose tolerance (which can interchangeably be considered
a test for insulin sensitivity) is the hyperinsulinemic-euglycemic
clamp technique, which requires a steady intravenous infusion of
insulin. Circulating glucose level is then clamped at a normal
fasting concentration, and blood samples are then taken to
monitor serum glucose so that a steady fasting level can be
maintained. The degree of insulin sensitivity is directly
proportional to the glucose uptake by target tissues. In other
words, the less glucose that's taken up by tissues during the
procedure (and the more insulin required to get the job done),
the more insulin resistant/less insulin-sensitive someone is. A
detailed review of these concepts and diagnostic criteria can be
found in peer-reviewed full text here.9
Sonowtomydietarychoices.RecallthatIamprofoundlyCRso
thatImustrestrictcarbohydratesasmuchaspossibletodelay
theonsetofdiabetesforaslongaspossible,hopefullyforever
sothatIwillsuccumbfromsomeother,lessdestructive(but)
terminalillness.SoIrestricttheintakeofthefoodslistedbelow.
Ihavefounditeasiestsimplytoremoveallfrommydiet.Those
withlesserdegreesofCR(andcarbohydrateaddiction)willnot
needtobeasrestrictiveasamI.
Noakes then goes on to list the foods that he completely avoids,

which include sugar, soft drinks, bread, rice, potatoes, porridge,
breakfast cereals, high-energy fruits like bananas, all
confectionary (cakes & sweets), desserts, products containing
artificial sweeteners such as diet sodas, and vegetable oils with a
high omega-6 content. I find this list amusing for many reasons,
but Im still waiting for Noakes to provide some sort of
quantitative allowance for carbohydrates, which he does in the
following passage:
HowevertherealpointisthatifoneisasCRasamI,onehasto
make choices of (i) how much carbohydrate one wants to eat
eachday.Ilimitmyselftobetween5075gramsadayasthatis
the amount that allows me to regulate my body weight
effortlessly without hunger and (ii) which carbohydrate
sourceswillprovidethatscantyamountofcarbohydrate.Ihave
chosen to get my miserly grams of carbohydrate from highly
nutritious vegetables and dairy produce, not from whole grain
cereals.Othersmightbeadvisedtomakeadifferentchoice.
So, there it is. Since Noakes is restricting his carb intake to 5075 grams a day, his diet defaults to the exclusion of the
aforementioned foods. The foods he allows himself are eggs,
fish, organic/grass-fed meat, dairy (I was surprised at this), non[Back to Contents]
Page 12
starchy vegetables, nuts (except for peanuts and cashews, wihch

he considers to be high in carbohyrates), and fruits (only those
with a lower carbohydrate concentration. He allows himself tea
and coffee, but unsweetened of course. One thing Noakes is
careful about doing is not specifically pushing his personal
carbohydrate intake on the reader, although its purported benefit
for everyone across the board is heavily implied.
My opinion? Great, hes restricting carbs and self-righteously
loving it. Good for him, I hope this is his personal long-term
solution to controlling overall caloric intake which is really
the heart of the matter, not carbohydrate per se. An
overconsumption of total calories leading to progressively
excessive body fat was likely the largest contributor to Noakes
diagnosis of pre-diabetic status, which was probably hastened
by his likely neglect for resistance/strength training, which we
now know is potentially the most powerful mode of exercise for
improving glucose tolerance.
I also currently supplement my eating with omega3 fatty acid
capsules(1.62g/day).Thevalueofomega3supplementation
seemstobeuniversallyaccepted.Iamalsoexperimentingwith
supplementationofarangeofvitaminsbutthisisstillaworkin
progress as is my choice of the best vegetables and salads to
limit the CR and two other medical tendencies that genetic
testinghasrevealed.
Apparently, Noakes has an open-minded approach to

supplementation, which can be a double-edged sword. The case
for omega-3 supplementation has been challenged in the peerreviewed literature repeatedly within the past year. A widely
publicized systematic review/meta-analysis by Rizos et al
concluded that omega-3 PUFA supplementation was not
associated with a lower risk of all-cause mortality, cardiac death,
sudden death, myocardial infarction, or stroke.10 Another recent
systematic review/meta-analysis by Kotwal et al is worth
quoting since it nicely sums up the general trend of the
findings:11
Recommendations for the use of fish oil supplements are
included in a number of guidelines, but the neutral
outcomes of recent large trials have served to weaken rather
than strengthen the evidence base. Although it remains
possible that fish oil supplements will produce health
benefits through the prevention of vascular complications,
the size of these gains are probably smaller than previously
believed, and both physician and patient expectations may
need to be reset.
Noakes then recommends that the reader seek counseling from a
registered dietitian (RD), but also acknowledges that not all RDs
will cozy up to the approach of carbohydrate restriction. As a
solution to this, Noakes proposes that consumers should
approach RDs and tell them specifically that they want to bant,
and this in turn might eventually increase the number of RDs
who are willing to engage in it. To me, this sounds like a futile
effort since the majority of RDs will not do a cursory Google
search for the specifics of the Harvey/Banting diet. Rather, a
large segment are more prone to seek information from the
Evidence Analysis Library (EAL) of the Academy of Nutrition
& Dietetics (formerly the American Dietetics Association). The
EAL is a resource designed to assist RDs in clinical judgement.
Much of the ANDs literature (including the EAL) contains

content which in large part is highly critical and cautionary of
low-carb dieting. A prime example is the ANDs most recent
position paper on weight loss, which states the following:12
The EAL also notes that safety has not been evaluated for
long-term, extreme restrictions of carbohydrates 35% of
energy from carbohydrates) and specifically recommends
that practitioners use caution in suggesting a lowcarbohydrate diet for even short-term use in patients with
osteoporosis, kidney disease, or in patients with increased
low-density lipoprotein cholesterol.
The AND has carried on a long-standing tradition of harboring
an anti-low-carb undercurrent. I disagree with the tenacity of
their caution toward the clinical viability of carbohydrate
restriction, since this has been demonstrated as an effective
tactic in a growing body of literature spanning beyond the past
decade.13 At the same time, its unscientific to ignore the full
range of evidence showing the effectiveness of a very wide
range of macronutrient set-ups across a wide range of
populations. This is where individual programming comes in,
rather than assuming that a single dietary approach is the end-all.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
Noakes T. Tim Noakes on Carbohydrates. June 18, 2012. [Health 24]

National Heart, Lung, and Blood Institute. Clinical Guidelines on the
identification, evaluation, and treatment of overweight and obesity in
adults: the evidence report. September, 1998. [NHLBI]
Romero-Corral A, Montori VM, Somers VK, Korinek J, Thomas RJ,
Allison TG, Mookadam F, Lopez-Jimenez F. Association of
bodyweight with total mortality and with cardiovascular events in
coronary artery disease: a systematic review of cohort studies. Lancet.
2006 Aug 19;368(9536):666-78. [PubMed]
Flegal KM, Graubard BI, Williamson DF, Gail MH. Cause-specific
excess deaths associated with underweight, overweight, and obesity.
JAMA. 2007 Nov 7;298(17):2028-37. [PubMed]
Kyle UG, Schutz Y, Dupertuis YM, Pichard C. Body composition
interpretation. Contributions of the fat-free mass index and the body fat
mass index. Nutrition. 2003 Jul-Aug;19(7-8):597-604. [PubMed]
Abernathy RP, Black DR. Healthy body weights: an alternative
perspective. Am J Clin Nutr. 1996 Mar;63(3 Suppl):448S-451S.
[PubMed]
Jenness R. The composition of human milk. Semin Perinatol. 1979
Jul;3(3):225-39. [PubMed]
Koletzko B, von Kries R, Closa R, Escribano J, Scaglioni S,
Giovannini M, Beyer J, Demmelmair H, Anton B, Gruszfeld D,
Dobrzanska A, Sengier A, Langhendries JP, Rolland Cachera MF,
Grote V. Can infant feeding choices modulate later obesity risk? Am J
Clin Nutr. 2009 May;89(5):1502S-1508S. [PubMed]
American Diabetes Association. Diagnosis and classification of
diabetes mellitus. Diabetes Care. 2005 Jan;28 Suppl 1:S37-42.
[PubMed]
Rizos EC, Ntzani EE, Bika E, Kostapanos MS, Elisaf MS. Association
between omega-3 fatty acid supplementation and risk of major
cardiovascular disease events: a systematic review and meta-analysis.
JAMA. 2012 Sep 12;308(10):1024-33. [PubMed]
Kotwal S, Jun M, Sullivan D, Perkovic V, Neal B. Omega 3 Fatty
acids and cardiovascular outcomes: systematic review and metaanalysis. Circ Cardiovasc Qual Outcomes. 2012 Nov;5(6):808-18.
[PubMed]
Seagle HM, Strain GW, Makris A, Reeves RS; American Dietetic
Association. Position of the American Dietetic Association: weight
management. J Am Diet Assoc. 2009 Feb;109(2):330-46. [PubMed]
Hession M, Rolland C, Kulkarni U, Wise A, Broom J. Systematic
review of randomized controlled trials of low-carbohydrate vs. lowfat/low-calorie diets in the management of obesity and its
comorbidities. Obes Rev. 2009 Jan;10(1):36-50. [PubMed]
[Back to Contents]
Page 13
Nicotine and fat loss.

By Kurtis Frank and Sol Orwell
IreadanarticlecalledCanNicotineSafelyBurnFatand
BuildMusclebyKiefer,andIwaswonderingifnicotine
isaseffectiveforfatlossasitsportrayedtobeinthatarticle.
Thanksinadvance.
Nicotine as a fat burner?

Recently, nicotine (primary stimulatory compound found in
cigarettes, also used as a means in isolation to reduce cravings
for cigarettes) has become more commonly used for fat burning
purposes. The link between weight loss and nicotine initially
comes from epidemiological research, where a consistent
correlation between less weight and nicotine usage exists
(mostly attributed to less food intake secondary to both social
factors and appetite suppression), but a recent surge of
popularity has occurred with athletes and lay persons looking to
lose weight.
A good deal of the popularity can be traced back to an article
titled, Can Nicotine Safely Burn Fat and Build Muscle? The
Surprising Facts1 by the author John Kiefer, best known for
developing a popular dietary method called Carb Back-Loading.
Independent of whether or not nicotine can be used as a fat
burner and muscle building agent, the article itself does not
constitute sufficient evidence to recommend nicotine, and its use
of references warrants critique.
Adrenaline Diabetes
Adrenaline Diabetes was the term used by the author to define
a state where the body becomes resistant to the effects of
catecholamines and catecholamine mimetics which is
supposedly similar in phenotype to true type II diabetes,
specifically insulin resistance. This phrase was used in regards to
the supposed decreased efficacy of classical fat burners such as
ephedrine or clenbuterol, as these compounds target and interact
with the same receptors as adrenaline. As any new phrase or
phenomena, it needs to be proven to actually exist.
He supports the existence of this phenomenon (that the body can
become insensitive to catecholamines such as adrenaline) with
four citations: the last three of which are review articles which
can be found by merely doing a Pubmed search for Betaadrenergic (the receptor in question) and desensitization and
the first is an acute experiment.2 This study was in vitro (outside
of the body), and saturated a cell to acutely induce betaadrenergic insensitivity in order to assess how the cell responds
to it. This study does not support the claim of adrenaline
diabetes, which would be characterized by chronic insensitivity
in a living model rather than an acute study. All receptors can be
desensitized pretty effectively if we override them acutely in
vitro.
longer periods of time) have more potential for desensitization

while shorter agonists, like catecholamines themselves should be
(fight or flight response should be short in nature) either inert or
potentiated. This is normally seen in studies on asthmatics as
long-term bronchodilators (typically acting on the same
receptors) tend to induce some degree of insensitivity while
ephedrine, a short acting one, seems to be potentiated in vivo.3
This is because when the agonist is removed of culture, the
receptor gets resensitized within hours if not minutes.4 Quick to
be insensitive, quick to be sensitive; this makes the claim of
adrenaline diabetes very inaccurate if not operationalized further.
Much of the article supporting Nicotine as the next best fat
burner was built on this notion that catecholamine mimetics are
subpar since you can become resistant to them. This is an
unsubstantiated claim, as it was not supported in the article and
no currently accepted disease state is characterized by a chronic
state of adrenaline insensitivity at the receptor level.
But wait, there's more? Not really.
To follow up the supposed hit to catecholamine/catecholamine
mimetic's efficacy, Nicotine was supported as a great option due
to being a muscle builder (via mTOR activation) and a fat burner
(via AMPK activation). Both are proteins in the cytoplasm of a
cell, and are central points of metabolism sort of like
crossroads or junction points; they seem to regulate many
mechanisms in the body. mTOR is characterized as the cell
protecting and growth mediator (alongside some other ones) and
AMPK acts as a nutrient sensor protein, activated during energy
deficits to increase glucose and fat uptake into cells and their
subsequent catabolism into ATP.
The claim of nicotine activating mTOR was drawn from an
article noting that nicotine was the main ingredient in cigarette
secondhand smoke that may cause insulin resistance, and that
this was tied into mTOR activation which was shown in vitro.5
For those unaware, although mTOR itself is activated by the
insulin receptor it sends a signal back to the first post-receptor
substrate, IRS-1, to desensitize the receptor. This is a
homeostatic mechanism in the cell and a nice example of
regulation, and how mTOR activation can cause insulin
resistance.
The fact that, by this same mechanism, nicotine induces insulin
resistance was not mentioned. The closest mention was citation
15, where it was said that carbs alongside nicotine increases fat
storage in a cell relative to carbohydrate along; this is
theoretically plausible assuming the mTOR link, it is just
unfortunate that the citation is wholly irrelevant and does not
actually say anything about pairing carbohydrates with nicotine
nor an increase in fatty acid accumulation.6 The aforementioned
mTOR study was also cited for nicotine can induce insulin
resistance in the morning, with no actual evidence of the
morning being relevant (beyond a reference to the authors diet
plan, which uses a circadian rhythm and insulin sensitivity
manipulation).
Oddly, the actual desensitization response to anything that acts

on this receptor class is not too straight forward and it seems
longer lasting ligands (things that circulate in the blood for
That being said, mTOR in that one study was induced in vitro so
there does appear to be a degree of activation there. Whether or
not this is even relevant practically is not known, it is currently
the only study that exists on the topic and at best is preliminary
[Back to Contents]
Page 14
evidence.
The second claim of AMPK activation causing nutrient uptake
was also an in vitro study, where an increase in nitric oxide
caused an increase in peroxynitrate (a free radical) which then
induced AMPK. The study was conducted in immortalized fat
cells, which is again a preliminary study (a nicely conducted one
at that) which needs replication.
The problem here is that mTOR and AMPK have a yin-yang
relationship in all cell lines, when one gets activated it
suppresses the other.7 Reliance on in vitro studies to support
claims made it seem like you can have your cake and eat it too,
but unless a novel pathway suddenly appears in the future that
can prevent crosstalk it seems likely that both of the above are
active. Either one of them will overcome the other, or they will
negate.
No evidence exists to support a localized mTOR in skeletal
muscle and AMPK in adipose either (this is a currently unknown
but theoretically plausible nutrient partitioning effect) so touting
these two mechanisms of action for nicotine is, at best, an
unfortunate result of relying too much on in vitro evidence and
not accounting for cellular crosstalk (when one protein or
receptor interacts with another). At worst, its a hasty misuse of
science, resulting in largely irrelevant supporting data.
On the topic of nicotine as a fat burner
There is a lot of research on nicotine that can be found currently,
which dwindles in amount when you control for nicotine per se
(excluding cigarettes) and when you look at studies that induce
weight loss rather than those that prevent weight regain after
smoking cessation the latter of which are fairly common. We
have one (cited by the aforementioned article) that shows an
acute increase in metabolic rate following usage of up to 2 mg
nicotine gum paired with caffeine in otherwise healthy men,8 and
one in otherwise healthy smokers only reporting a thermogenic
response in men,9 and we have one study that noted in nonsmoking using a 15mg patch that 1.6 kg was lost over 91 days,
although after 6 months the difference was no longer apparent.10
The former two studies support the notion that a fat burning
effect may exist (which appears to be mediated via an
acetylcholine-induced release of catecholamines as per the first
study, so I guess it is a good thing that 'adrenaline diabetes'
doesn't exist) and the latter supports the notion of appetite
suppression causing a reduction in weight even when blinded.
Animal studies suggest that the mechanisms of weight loss are
mediated via acetylcholine receptors (as blocking these receptors
block the weight loss), although this implicates both increased
catecholamines as well as appetite suppression.
That is basically it. For the purposes that many people are using
it for (anti-smoking aids ingested with exercise and diet for the
purpose of body fat loss) it is a very underresearched topic.
Misinterpretation of science
At several points in this article, references were cited in support
of the claims. 26 in total, all conveniently hidden behind a Like
this on social media form of pseudo-paywall (where the benefit
is in exposure rather than finances). All citations and their
respective claims are analyzed as follows:

Citations 1-4 were collectively in support of adrenaline
diabetes, with three being reviews on desensitization of the
beta-adrenergic receptors11 on adverse effects of these
agonists12 and one on the receptor category (GPRC) in
general13 with the last one being the acute study mentioned
previously.14 None of these citations mention nor support
the notion of chronic catecholamine insensitivity nor the
concept of adrenaline diabetes.
Citation 5 was used in support of Nicotine, like other
stimulants, raises lipoprotein lipase in muscle tissue but
lowers it in fat cells; Translation: your muscles can absorb
and burn triglycerides easily, but your fat cells cant store it.
In short, nicotine makes it harder to get fat., the article in
question15 assessed cardiac muscle tissue rather than skeletal
muscle tissue, which are markedly different metabolically.
Citation 6 was used to mention how nicotine can locally act
via a different receptor class as do catecholamine mimetics;
this one appears to be a correct citation to an intervention.16
Citation 7 is the mTOR study17 which itself is a good
preliminary study. The following claims were derived from
this article; What makes nicotine so effective for cutting
and general fat loss is the fact that its also an effective
stimulator of the mTOR pathway, When youre cutting,
youre in a state of calorie deprivation, which automatically
decreases TOR. Nicotine, however, turns it back on, and
Nicotine is a prime regulator of TOR. A single in vitro
study does not constitute such a claim.
Related, Citation 26 is also the exact same study, and was
used to support ingesting nicotine earlier in the day can
cause transient insulin resistance despite the time of day
not being relevant in this study. The former part was used to
mention Carb-Back Loading, the author's diet program.
Citation 8 is a link to AMPK activation in fat cells via
oxidant stress.18 This is a pretty good study mechanistically,
but the claims it was in support of were First, free-radical
accumulation during training can ignite muscle growth, but
its a hermetic response. Elevating it for a while is good, but
elevating it for too long is bad which aside from the
religious typo of 'hormetic', this study was conducted in fat
cells which are not muscle cells and the claim AMPK
activation also prevents fat cellsonce againfrom storing
fat is an absolute, which is false. AMPK is activated by
literally hundreds of phytonutrients to varying degrees, and
Nicotine barely activates AMPK relative to the reference
drugs of Curcumin, Metformin, or Berberine all of which do
not abolish fat gain.
Citation 9 claims that Nicotine stimulates one of these
myostatin-bashing pathways (in reference to novel
pathways to downregulate Myostatin) and can be found
here.19 The study compared a high myostatin active bull
genotype against a low active and noted a correlation
between the expression of the nicotinic acetylcholine
recepetor (what nicotine acts upon) and noted an inverse
correlation with myostatin enhanced genotype and nicotinic
receptor expression. There was not even an in vitro study
[Back to Contents]
Page 15
conducted to assess how nicotine influences myostatin; this

study being even more preliminary than the previous in vitro
studies.
Citations 10 and 11 were used to support nicotine enhancing
working memory. They are correct translations of what the
studies claim (one review20, one rat intervention21).
Citation 12 was used to support the statement that working
memory is your ability to reason correctly, succinctly, and
efficiently rather than the currently accepted definition of
(give or take a few words) the system that actively holds
multiple pieces of transitory information in the mind. The
study noted correlations with working memory and other
aspects of cognition, and hypothesized that working
memory could consist of more.22 The article uses it, either
intentionally or accidentally, to try and make the
aforementioned citations 10 and 11 more vast in their
implications, to then say nicotine can make you smarter. I
won't debate as to whether nicotine can or cannot make you
smarter, but the above citation was used to misinterpret the
aforementioned two.
Three citations support the claim Nicotine, because of its
unique receptor stimulation on fat cells, causes them to
dump fat like a drunk sorority girl puking her guts out after
a party. We have already discussed citation 6 (making a
reappearance), which simply discusses which receptors
nicotine acts on. Citation 13 is the aforementioned citation 5
(duplicated), which assessed cardiac muscle tissue, not
skeletal tissue. Citation 14 is a review on brain energy
homeostasis,23 discussing how nicotine interacts with
appetite. This literally has nothing to do with dumping fat
either technically (lipolysis) or for long term fat-burning
effects; it supports somebody eating less.
To defend the notion that nicotine is not suited to a high
carbohydrate diet and that fat cells exposed to nicotine and
insulin simultaneously can actually increase the rate of fat
storage in fat cells, the following Citation 15 was made
note of.24 Insulin and Dexamethasone were incubated in
cells, and then nicotine was added; there was no nicotineonly cell, only an insulin+dex control cell (which actually
increases LPL, adding nicotine increased it further). There is
absolutely no way this study can at all support the claims
made.
Citation 16 was used to support The fat-dumping potential
of nicotine also increases with physical activity. The study
never measured serum free fatty acids, NEFAs, nor
triglycerides; only metabolic rate (which appeared to be
slightly but synergistically increased).25 This is a poor way
to phrase the benefits seen in the study.
Uncoupling protein 1 (UCP1) is a protein in mitochondria
that regulates uncoupling, a release of potential energy as
heat in response to a variety of stimuli; activation of UCP1
might cause weight loss as it wastes energy for heat.
Anyways, this was a topic mentioned in the article (Citation
17) as caloric restriction was said to reduce UCP1 activity;
the study noted a decrease at 48 hours of starvation, yet a
spike at 56 hours that was unexplained.26 This is hardly
conclusive of the claim.
Citation 18 and 19 do not support the claim of Nicotine restimulates UCP1...so you keep burning fat even if you drop
calories. as neither induced caloric restriction previous to
the experiment.27,28
Citations 20-22 were used to support the appetitesuppressive effect of nicotine, and these citations appear to
be legitimate.29-31
Citation 23 was mentioned as mTOR may also augment
tumor cell growth (context dependent) and the author made
note that Curcumin could negate this effect. It is again an in
vitro study,32 but Curcumin does appear to antagonize the
proliferative effects of nicotine in this cell line (via inhibitin
mTOR activation and the subsequent genomic signalling).
Citation 24 was mentioned in support of how nicotine clears
slower in the evening (despite taking 24 hours to clear the
body, which will always cross over into one evening at
least). The study merely made not of several issues that
could alter the pharmacokinetics of nicotine patches.33
Citation 25 was used in the middle of a paragraph talking
about nicotine dosing, and is a study noting synergism
between nicotine and caffeine.34 It seems out of place here
(possibly being used to recommend 1mg given what the
study and article says), but reappears in the section saying to
stack with caffeine where it makes more sense. There does
appear to be some slight synergy with caffeine and nicotine
in a dose-dependent manner, as assessed by this study using
doses up to a 2mg/200mg nicotine/caffeine combination on
acute thermogenic response. No clue where the claim about
for fat loss and mobilization during training came in,
since there was no training in this study.
Overall, this article offers a number of interesting speculations,
but its also a good example of how citations do not necessarily
mean that the topic on hand is scientific. References in blog
posts are just links, and these links can be poorly directed and
misinterpreted.
Summation
In sum, Nicotine is a promising anti-obesity drug, and the antiinflammatory effects of it can theoretically confer more benefit
to obese persons than classical stimulants. The aforementioned
claim needs to be studied though, as studies on nicotine and
inducing weight loss are surprisingly scarce. There is no
evidence to currently support nicotine as a muscle building agent
beyond a single in vitro study of questionable practical
significance, and the fat burning effects of nicotine do not appear
to be greater than that of classical stimulants such as ephedrine
or caffeine. The concept of adrenaline diabetes most likely
does not exist, and especially not the same degree as chronic
insulin resistance, and as such nicotine is unlikely to exert more
weight loss to athletes than classical stimulants (mentioned
before).
Nicotine is another possible option to add to a supplement
regimen or to throw into your minds database; it does not
currently revolutionize anything pertaining to fat loss or musclebuilding.
[Back to Contents]
Page 16
Kurtis Frank and Sol Orwell are the co-founders of

Examine.com, a compendium of available scientific research on
supplementation and nutrition. In my opinion, its the most
diligent resource of its kind. The sites nicotine page is currently
in progress and can be seen here.
__________________________________________________
18.
19.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
Kiefer J. Can Nicotine Safely Burn Fat and Build Muscle? The
Surprising Facts. Accessed November 21, 2012. [Dangerously
Hardcore]
Bawa-Khalfe T, Altememi GF, Mandyam CD, Schwarz LA,
Eikenburg DC, Standifer KM. The presence of beta2adrenoceptors sensitizes alpha2A-adrenoceptors to desensitization
after chronic epinephrine treatment. BMC Pharmacol. 2007 Dec
20;7:16. [PubMed]
Astrup A, Lundsgaard C, Madsen J, Christensen NJ. Enhanced
thermogenic responsiveness during chronic ephedrine treatment in
man. Am J Clin Nutr. 1985 Jul;42(1):83-94. [PubMed]
Tran TM, Friedman J, Baameur F, Knoll BJ, Moore RH, Clark RB.
Characterization of beta2-adrenergic receptor dephosphorylation:
Comparison with the rate of resensitization. Mol Pharmacol. 2007
Jan;71(1):47-60. [PubMed]
Bergman BC, Perreault L, Hunerdosse D, Kerege A, Playdon M,
Samek AM, Eckel RH. Novel and reversible mechanisms of
smoking-induced insulin resistance in humans. Diabetes. 2012
Dec;61(12):3156-66. [PubMed]
Chajek-Shaul T, Scherer G, Barash V, Shiloni E, Caine Y, Stein O,
Stein Y. Metabolic effects of nicotine on human adipose tissue in
organ culture. Clin Investig. 1994 Jan;72(2):94-9. [PubMed]
Xu J, Ji J, Yan XH. Cross-talk between AMPK and mTOR in
regulating energy balance. Crit Rev Food Sci Nutr.
2012;52(5):373-81. [PubMed]
Jessen AB, Toubro S, Astrup A. Effect of chewing gum containing
nicotine and caffeine on energy expenditure and substrate
utilization in men. Am J Clin Nutr. 2003 Jun;77(6):1442-7.
[PubMed]
Perkins KA, Sexton JE, DiMarco A. Acute thermogenic effects of
nicotine and alcohol in healthy male and female smokers. Physiol
Behav. 1996 Jul;60(1):305-9. [PubMed]
Newhouse P, Kellar K, Aisen P, White H, Wesnes K, Coderre E,
Pfaff A, Wilkins H, Howard D, Levin ED. Neurology. 2012 Jan
10;78(2):91-101. [PubMed]
Lefkowitz RJ, Pitcher J, Krueger K, Daaka Y. Mechanisms of betaadrenergic receptor desensitization and resensitization. Adv
Pharmacol.1998;42:416-20. [PubMed]
Sears MR. Adverse effects of beta-agonists. J Allergy Clin
Immunol. 2002 Dec;110(6 Suppl):S322-8. [PubMed]
Premont RT.Once and future signaling: G protein-coupled receptor
kinase control of neuronal sensitivity. Neuromolecular Med.
2005;7(1-2):129-47. [PubMed]
Bawa-Khalfe T, Altememi GF, Mandyam CD, Schwarz LA,
Eikenburg DC, Standifer KM.
The presence of beta2adrenoceptors sensitizes alpha2A-adrenoceptors to desensitization
after chronic epinephrine treatment. BMC Pharmacol. 2007 Dec
20;7:16. [PubMed]
Sztalryd C, Hamilton J, Horwitz BA, Johnson P, Kraemer FB.
terations of lipolysis and lipoprotein lipase in chronically nicotinetreated rats. Am J Physiol. 1996 Feb;270(2 Pt 1):E215-23.
Andersson K, Arner P. Systemic nicotine stimulates human adipose
tissue lipolysis through local cholinergic and catecholaminergic
receptors. Int J Obes Relat Metab Disord. 2001 Aug;25(8):122532. [PubMed]
Bergman BC, Perreault L, Hunerdosse D, Kerege A, Playdon M,
Samek AM, Eckel RH. Novel and reversible mechanisms of
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
smoking-induced insulin resistance in humans. Diabetes. 2012

Dec;61(12):3156-66. [PubMed]
An Z, Wang H, Song P, Zhang M, Geng X, Zou MH. Nicotineinduced activation of AMP-activated protein kinase inhibits fatty
acid synthase in 3T3L1 adipocytes: a role for oxidant stress. J Biol
Chem. 2007 Sep 14;282(37):26793-801. [PubMed]
Sadkowski T, Jank M, Zwierzchowski L, Siadkowska E, Oprzadek
J, Motyl T. Gene expression profiling in skeletal muscle of
Holstein-Friesian bulls with single-nucleotide polymorphism in the
myostatin gene 5'-flanking region. J Appl Genet. 2008;49(3):23750. [PubMed]
Levin ED. Nicotinic receptor subtypes and cognitive function. J
Neurobiol. 2002 Dec;53(4):633-40. [PubMed]
Levin ED, Torry D. Acute and chronic nicotine effects on working
memory in aged rats. Psychopharmacology (Berl). 1996
Jan;123(1):88-97. [PubMed]
Kyllonen PC. Reasoning ability is (little more than) workingmemory capacity?! Intelligence. 1990;14(4): 389-43. [Elsevier]
Chen H, Saad S, Sandow SL, Bertrand PP. Cigarette smoking and
brain regulation of energy homeostasis. Front Pharmacol.
2012;3:147. [PubMed]
Chajek-Shaul T, Scherer G, Barash V, Shiloni E, Caine Y, Stein O,
Stein Y. Metabolic effects of nicotine on human adipose tissue in
organ culture. Clin Investig. 1994 Jan;72(2):94-9. [PubMed]
Perkins KA, Sexton JE, Epstein LH, DiMarco A, Fonte C, Stiller
RL, Scierka A, Jacob RG. Acute thermogenic effects of nicotine
combined with caffeine during light physical activity in male and
female smokers. Am J Clin Nutr. 1994 Sep;60(3):312-9. [PubMed]
Champigny O, Ricquier D. Effects of fasting and refeeding on the
level of uncoupling protein mRNA in rat brown adipose tissue:
evidence for diet-induced and cold-induced responses. J Nutr. 1990
Dec;120(12):1730-6. [PubMed]
Yoshida T, Sakane N, Umekawa T, Kogure A, Kondo M,
Kumamoto K, Kawada T, Nagase I, Saito M. Nicotine induces
uncoupling protein 1 in white adipose tissue of obese mice. Int J
Obes Relat Metab Disord. 1999 Jun;23(6):570-5. [PubMed]
Arai K, Kim K, Kaneko K, Iketani M, Otagiri A, Yamauchi N,
Shibasaki T. Nicotine infusion alters leptin and uncoupling protein
1 mRNA expression in adipose tissues of rats. Am J Physiol
Endocrinol Metab. 2001 Jun;280(6):E867-76. [PubMed]
Fulkerson JA, French SA. Cigarette smoking for weight loss or
control among adolescents: gender and racial/ethnic differences. J
Adolesc Health. 2003 Apr;32(4):306-13. [PubMed]
Grunberg NE, Bowen DJ, Winders SE. Effects of nicotine on body
weight and food consumption in female rats. Psychopharmacology
(Berl). 1986;90(1):101-5. [PubMed]
Fulkerson JA, French SA. Cigarette smoking for weight loss or
control among adolescents: gender and racial/ethnic differences. J
Adolesc Health. 2003 Apr;32(4):306-13. [PubMed]
Clark CA, McEachern MD, Shah SH, Rong Y, Rong X, Smelley
CL, Caldito GC, Abreo FW, Nathan CO. Curcumin inhibits
carcinogen and nicotine-induced Mammalian target of rapamycin
pathway activation in head and neck squamous cell carcinoma.
Cancer Prev Res (Phila). 2010 Dec;3(12):1586-95. [PubMed]
Gries JM, Benowitz N, Verotta D. Importance of
chronopharmacokinetics in design and evaluation of transdermal
drug delivery systems. J Pharmacol Exp Ther. 1998
May;285(2):457-63. [PubMed]
Jessen AB, Toubro S, Astrup A. Effect of chewing gum containing
nicotine and caffeine on energy expenditure and substrate
utilization in men. Am J Clin Nutr. 2003 Jun;77(6):1442-7.
[PubMed]
[Back to Contents]
Page 17
Muscle Strength & Hypertrophy in Chronic Nutrient Timing Studies Compiled by Brad Schoenfeld & Alan Aragon
What follows is an update of the collection of chronic nutrient timing studies first presented in the September 2012 issue of AARR. Two
studies are added, and the chart is not a pasted image file like the previous (its now intrinsically part of this document), so it should be
more clearly visible.
_____________________________________________________________________________________________________
KEY: yellow = significant benefits from timing nutrients near training; no background color = no significant benefits from timing nutrients near training;
blue = total protein (including supplementation) was matched between experimental & placebo/control conditions. Note that the baseline/habitual
protein amounts listed are the average of the groups compared.
Total Protein
intake
habitual or
baseline vs
with supp
Protein
Matched
with
Control?
10 g milk/soy protein
combo consumed
either immediately or 2
hours after exercise
1.05 g/kg
(supplement
increased this
to 1.18 g/kg)
32
untrained
young
men
6% CHO solution, 6 g
EAA mixture, combined
CHO + EAA
supplement or placebo
consumed during
exercise
Cribb and
Hayes,
2006
23 young
recreation
al male
bodybuilders
Willoughby
19
untrained
young
males
Study
Subjects
Supplementation
Esmarck
et al, 2001
13
untrained
elderly
males
Bird et al,
2006
et al, 2007
Measurement
Method
Training Protocol
Strength Results
Body
composition
Results
Yes
MRI and
muscle
biopsy
Progressive resistance
training consisting of
multiple sets of lat
pulldown, leg press
and knee extension
performed 3 days/wk
for 12 wks
Significant
increase in
muscle CSA with
immediate vs.
delayed
supplementation
Not specified,
but a range
was
listed:15% of
9.8-13.7 MJ;
87.8-122.7g.
No
DXA
training consisting of 3
sets of 8-10 repetitions
for all the major
muscles performed 2
days/wk for 12 wks
Immediate intake
increased both
dynamic and
isokinetic
Strength, whereas
delayed intake only
improved
dynamic strength.
Immediate pre-post
supplementation
caused greater
increases in 1RM in 2
out of 3 exercises
1 g/kg of a supplement
containing 40 g whey
isolate, 43 g glucose,
and 7 g creatine
monohydrate
consumed either
immediately before and
after exercise, or early
morning & late evening
20 g whey-dominant
protein or 20 g
dextrose consumed 1
hour before and after
exercise
1.01 g/kg
(supplement
increased this
to 2.01 g/kg)
Yes
DXA and
muscle
biopsy
exercises for the major
muscle groups
performed 3 days/wk
for 10 wks
Immediate pre-post
supplementation
caused greater
increases in 1RM in 2
out of 3 exercises
2.27 g/kg
(supplement
increased this
to 2.76 g/kg)
No
Hydrostatic
weighing,
muscle
biopsy,
surface
measurements
DXA, CT,
and
muscle
biopsy
training consisting of 3
sets of 6-8 repetitions
for all the major
muscles performed 4
days/wk for 10 wks
Protein
supplementation
caused greater
increases in relative
strength (maximal
strength corrected for
bodyweight) in bench
press & leg press
1RM leg press & leg
extension strength
increased, with no
significant difference
between groups
No significant
differences in
muscle CSA
increase
between groups
1RM & 5 RM bench

press & squat
strength increased,
with no significant
difference between
groups
No significant
differences in
total body mass
or lean body
mass between
groups.
Training produced a
significant increase in
1RM strength both in
the bench press &
squat, no differences
between groups.
Significant
increase in fatfree mass
occurred with
the time-divided
regimen,
whereas no
change was
evident with the
time-focused
regimen.
Verdijk et
al, 2009
28
untrained
elderly
males
10 g casein hydrolysate
or placebo consumed
after exercise
1.1 g/kg
(supplement
increased this
to 1.2 g/kg)
No
Hoffman
et al, 2009
33 welltrained
young
males
1.60 g/kg
(supplement
increased this
to 2.22 g/kg)
Yes
DXA
Burk et al,
2009
13
untrained
young
males
Supplement containing
42 g protein
(milk/collagen blend)
and 2 g carbohydrate
consumed either
after exercise, or early
morning & late evening
Two casein-dominant
protein doses (35 g
each) consumed either
in the morning &
evening away from the
afternoon training bout
- or - consumed in the
morning, and then
again immediately prior
to the resistance
training bout
Placebo
condition
consumed
1.05 g/kg,
protein
condition
consumed
1.37 g/kg
Yes
DXA
multiple sets of leg
press and knee
extension performed 3
days/wk for 12 wks
3-4 sets of 6-10
repetitions of multiple
exercises for the entire
body peformed 4
days/wk for 10 wks.
3-4 sets of 6-10
exercises, each
muscle group trained
2x/wk, totaling 4
days/wk for 8 wks
[Back to Contents]
CHO + EAA
caused the
greatest gains in
fat-free mass
and muscle fiber
CSA relative to
placebo
Significant
increases in lean
body mass and
muscle CSA of
type II fibers in
immediate vs.
delayed
supplementation
Significant
increase in total
body mass, fatfree mass, and
thigh mass with
protein vs. carb
supplementation
Page 18
Hulmi et
al, 2009
31
untrained
young
males
15 g whey isolate or
placebo consumed
after exercise
1.43 g/kg
(supplement
increased this
to 1.53 g/kg)
No
MRI,
muscle
biopsy
Progressive,
periodized total body
resistance training
consisting of 2-5 sets
of 5-20 repetitions
performed 2 days/wk
for 21 wks
Strength increased
similarly in the protein
& placebo group, but
only the protein group
increased isometric
leg extension strength
vs the control group
Wycherly
et al, 2010
34
untrained,
older men
& women
w/type 2
diabetes
21 g protein, 0.7 g fat,

29.6 g carbohydrate
consumed either
immediately prior to, or
at least 2 h following
exercise
1.11 g/kg (no

habitual vs
treatment
information
given)
Yes
DXA,
waist girth
training 8-12
exercises, total
sessions 3 days/wk
for 16 wks
Not measured
Erskine et
al, 2012
33
untrained
young
males
20 g whey protein or
placebo consumed
after exercise
1.35 g/kg
(supplement
increased this
to 1.56 g/kg)
No
MRI
4-6 sets of elbow

flexion (8-10 reps)
performed 3 days/wk
for 12 weeks
Weisgarber
9
untrained
young
adults (5
men, 4
women)
Whey protein (0.3 g/kg)

or placebo consumed
during exercise.
1.35 g/kg
(supplement
increased this
to 1.56 g/kg)
No
DXA,
ultrasound
3 sets of 6-10 reps of

multiple exercises for
the entire body
performed 4 days/wk
for 8 weeks
No significant
differences in maximal
isometric voluntary
force or 1 RM strength
between groups
No significant
differences in 1 RM
strength increase
between conditions
et al, 2012
Significant
increase in CSA
of the vastus
lateralis but not
of the other
quadriceps
muscles in the
protein group vs
placebo
Fat mass, fatfree mass, and
waist
circumference
decreased with
no significant
differences
between groups
No significant
differences in
muscle CSA
between groups
No significant
differences in
muscle size or
lean mass
increase
References in the order they appear on the chart:

1.
2.
3.
4.
5.
6.
7.
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]
Bird SP, Tarpenning KM, Marino FE. Independent and
combined effects of liquid carbohydrate/essential amino
acid ingestion on hormonal and muscular adaptations
following resistance training in untrained men. Eur J Appl
Physiol. 2006 May;97(2):225-38. [PubMed]
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. resistance exercise
does not enhance postexercise muscle protein synthesis. J
Appl Physiol. 2009 May;106(5):1730-9. [PubMed]
Willoughby DS, Stout JR, Wilborn CD. Effects of
resistance training and protein plus amino acid
supplementation on muscle anabolism, mass, and strength.
Amino Acids. 2007;32(4):467-77. [PubMed]
Verdijk LB, Jonkers RA, Gleeson BG, Beelen M, Meijer K,
Savelberg HH, Wodzig WK, Dendale P, van Loon LJ.
Protein supplementation before and after exercise does not
further augment skeletal muscle hypertrophy after resistance
training in elderly men. Am J Clin Nutr. 2009
Feb;89(2):608-16. [PubMed]
Hoffman JR, Ratamess NA, Tranchina CP, Rashti SL, Kang
J, Faigenbaum AD. Effect of protein supplement timing on
strength, power and body compositional changes in
experienced resistance trained men. Int J Sport Nutr Exerc
Metab. 2009 Apr;19(2):172-85. [PubMed]
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]
8.
Hulmi JJ, Kovanen V, Selnne H, Kraemer WJ, Hkkinen

K, Mero AA. Acute and long-term effects of resistance
exercise with or without protein ingestion on muscle
hypertrophy and gene expression. Amino Acids. 2009
Jul;37(2):297-308. [PubMed]
9. Wycherley TP, Noakes M, Clifton PM, Cleanthous X,
Keogh JB, Brinkworth GD. Timing of protein ingestion
relative to resistance exercise training does not influence
body composition, energy expenditure, glycaemic control or
cardiometabolic risk factors in a hypocaloric, high protein
diet in patients with type 2 diabetes. Diabetes Obes Metab.
2010 Dec;12(12):1097-105. [PubMed]
10. Erskine RM, Fletcher G, Hanson B, Folland JP. Whey
protein does not enhance the adaptations to elbow flexor
resistance training. Med Sci Sports Exerc. 2012
Sep;44(9):1791-800. [PubMed]
11. Weisgarber KD, Candow DG, Vogt E SM. Whey protein
before and during resistance exercise has no effect on
muscle mass and strength in untrained young adults. Int J
Sport Nutr Exerc Metab. 2012 Dec;22(6):463-9. [PubMed]
Here is a full-length PDF version of the book of the above title,

which is a highly digestible read on understanding health
statistics. It was sent to me by a friend (and AARR contributor)
James Heathers.
If you have any questions, comments, suggestions, bones of

contention, cheers, jeers, guest articles youd like to submit, or
any feedback at all, send it over to aarrsupport@gmail.com.
[Back to Contents]
Page 19

11 - Nov - 2012

Hochgeladen von

Dokumentinformationen

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

11 - Nov - 2012

Hochgeladen von

Copyright:

Verfügbare Formate

face

Effects of increased meal frequency on fat

11 Sports science professor Tim Noakes goes full

14 Nicotine and fat loss.

Complex problems, simple solutions.

18 Chronic nutrient timing studies.

Timing of food intake predicts weight loss

Carbohydrate co-ingestion with protein does not

Concurrent training in elite male runners: The

No effect of 1 or 7 days green tea extract ingestion

Alan Aragons Research Review November 2012

Complex problems, simple solutions.

although he would eventually be vindicated. He was nothing if

Woese's work on the evolutionary origins of life via molecular

Instead of the tired machine imagery, he suggests the metaphor

Alan Aragons Research Review November 2012

focus on parts and pieces. Doing so means "an emphasis on

otherwise more desirable, perspectives on the world, so

Ronald Giere, who has argued for such a perspectivist model of

That is one possible view, but in light of the discussion above

Consensus among scientists on a particular scientific

Based on all this, you might wonder if there's a way forward if

Alan Aragons Research Review November 2012

uncertainty are to our benefit.

See Taleb, Nassim. Antifragile: Things That Gain From

This has led me to a position that I might as well call

Woese, Carl R. A New Biology for a New Century.

Alan Aragons Research Review November 2012

Timing of food intake predicts weight loss

expenditure.1,2 Dietary intake was self-reported, and this

Carbohydrate co-ingestion with protein does not

stock in acute response. The study is otherwise elegant and

An inherent limitation is the acute nature of the study. Just

While the aforementioned work yielded similar results to the

Alan Aragons Research Review November 2012

Concurrent training in elite male runners: The

subjects were instructed to consume the same type of meal.

body circuit. External load was via blue Thera-Band

Training studies are notorious for their lack of dietary control,

Alan Aragons Research Review November 2012

No effect of 1 or 7 days green tea extract ingestion on

subjects to take their supplements, supplement logs were kept

The main findings of this study were twofold. There was no

The bigger picture of GTEs effectiveness should be taken into

Alan Aragons Research Review November 2012

Effects of increased meal frequency on fat oxidation

relevance of these results to overweight or obese individuals can

Several limitations were diligently acknowledged by the authors

The authors of the present study concluded that, although

Alan Aragons Research Review November 2012

Schoeller DA. Recent advances from application of doubly

Alan Aragons Research Review November 2012

15. Aagaard P, Andersen JL, Bennekou M, Larsson B, Olesen

Sports science professor Tim Noakes goes full lowcarb, part 3.

Onward into the sunset

Noakes appears to be reaching for anything he can grasp. So,

Its important to realize that athletic populations should be

to overestimate adiposity in those with a high degree of lean

As seen above, the normal/acceptable body fat percent ranges

Similarly children who are obese already at a young age will

Noakes is essentially recommending that children and babies go

Finally when the CR is advanced it can be diagnosed with

concentrations. If any of these three values is elevated, it is a

What Noakes nebulously labels as carbohydrate resistance is