Documenti di Didattica
Documenti di Professioni
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By Dylan Klein
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eating more, and drinking more in the form of sodas and coffee
concoctions. Estimates vary, but it is not controversial that our
average caloric intake has risen substantially since the 1970s,
and this alone is sufficient to explain the obesity epidemic.4
While nutritional researchers sought to identify culprit foods
from an energy standpoint, others sought to identify the reasons
that prompted this uptick in intake. Food addiction came of age.
The most convincing evidence of food that has emerged has to
be the deluge of juxtaposed brain activity scans showing some
known addictive drug alongside sugar. Who isnt convinced by
the brain scans in Figure 1?5 Similar pictures are seen
everywhere these days , offered up as scientific proof that
sugar is addictive. It doesnt hurt that sugar is also a white
powder that it lends itself well to creating images with white
lines, mirrors and drug paraphernalia. In 2013, the biggest
nutrition headline was: Rats find Oreos as addictive as cocaine. 6
But its not just sugar, its seemingly all foods, or at least any
food even the flimsiest case can be made against. Never mind
that the same regions of the brain light up during sex, exercise,
making silly faces at babies and petting puppies. In the 1980s
and 1990s it was fatty foods and McDonalds was a favorite
target. More recently, its sugary foods and carbohydrates in
general, and McDonalds is still a favorite target. Documentaries
and videos, be they mainstream,7,8 lamestream,9 or somewhere in
between,10 and countless media reports have sought to convince
us that certain foods are indeed addictive and the cause of our
battle with the bulge.
The common sense case against food addiction
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Study Two:19 These rats were given the same diet as the
low fat (refined carbohydrate, REF) diet in reference 15
or standard chow (CON) ad libitum for 6 months. The REF
rats gained roughly 20% more body weight CONs. At 6
months the rats were subjected to a lever pressing test to
ascertain motivation. After training to press a lever to
dispense sugar water, the number of lever presses required
for dispensing was progressively increased. The REF rats
demonstrated less motivation by taking longer between
attempts. This was repeated with plain water to the same
result. Nine days after the diet switch, the motivation test
was again conducted. The REF rats remained less motivated
despite consuming the CON diet, and vice versa with the
CON rats suffering no impaired motivation from the REF
diet.
To me, Study Two is one of those accidental gems where the
researchers set out to prove some other beliefs, and never even
realized their results undercut another premise they appear to
hold dear. The REF diet is described as a human junk food diet
(when at such low fat levels it simply is not!) and junk foods are
described as addictive and obesogenic in the discussion of the
paper. Study One employed a more obesogenic human junk
food diet, yet there was no mention of addictive-like
withdrawal behavior. It is conceivable that this was simply
overlooked or not noted in that study, but in Study Two, the test
for motivation involved sugar, a purported addictive agent, as
reward for completing the task. If long term exposure to a
35% sucrose diet caused addiction, one would expect the rats to
be more highly motivated to obtain still more sugar, not less.
Further, when they were withdrawn for a period, one might
expect them to chew through the apparatus to get at the sugar, or
at least try! Instead, they showed less enthusiasm than the
presumably non-addicted rats, could care less if the reward was
water or sugar-water, and demonstrated the same lack of
motivation for the sugar water even after having been deprived
of their fix. This is very compelling evidence against sugar
addiction per se, straight from a study that would otherwise seem
to favor the food addiction paradigm.
So... What exactly does one have to do to evoke addiction-like
behaviors in rats? Intermittent restriction of sugar, fat, or
combinations thereof. These are summarized nicely in a review
article by Avena et.al. entitled Sugar and fat bingeing have
notable differences in addictive-like behavior 20
Intermittent Sugar Water: By alternating access to sugar
water to 12 hours on/off and delaying sugar access several
hours into the circadian feeding cycle, rats increase sugar
intake. They also binge the most in the first hour of access
and engage in larger meals during the access period than
ad libitum fed rats. The rats compensate for the caloric
intake by decreasing chow intake (available ad libitum).
Thus total 24 hour intake remained the same as ad libitum
access rats and they remain normal weight.
Intermittent Fat Access: Rats will binge on shortening
made available for only two hours a day. Interestingly,
restricting access to only 3 times per week leads to a greater
effect. Again, however, the rats compensate with reduced
chow intake and remain normal weight.
Alan Aragons Research Review April 2014
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Study limitations
The effects of 12 weeks of beta-hydroxy-betamethylbutyrate free acid supplementation on muscle
mass, strength, and power in resistance-trained
individuals: a randomized, double-blind, placebocontrolled study.
Wilson JM, Lowery RP, Joy JM, Andersen JC, Wilson SM,
Stout JR, Duncan N, Fuller JC, Baier SM, Naimo MA,
Rathmacher J. Eur J Appl Physiol. 2014 Mar 6. [Epub ahead of
print] [PubMed]
INTRODUCTION: Studies utilizing beta-hydroxy-betamethylbutyrate (HMB) supplementation in trained populations
are limited. No long-term studies utilizing HMB free acid
(HMB-FA) have been conducted. Therefore, we investigated the
effects of 12 weeks of HMB-FA supplementation on skeletal
muscle hypertrophy, body composition, strength, and power in
trained individuals. We also determined the effects of HMB-FA
on muscle damage and performance during an overreaching
cycle. DESIGN: A three-phase double-blind, placebo- and dietcontrolled randomized intervention study was conducted. Phase
1 was an 8-week-periodized resistance-training program; Phase
2 was a 2-week overreaching cycle; and Phase 3 was a 2-week
taper. Muscle mass, strength, and power were examined at
weeks 0, 4, 8, and 12 to assess the chronic effects of HMB-FA;
and assessment of these, as well as cortisol, testosterone, and
creatine kinase (CK) was performed at weeks 9 and 10 of the
overreaching cycle. RESULTS: HMB-FA resulted in increased
total strength (bench press, squat, and deadlift combined) over
the 12-week training (77.1 18.4 vs. 25.3 22.0 kg, p < 0.001);
a greater increase in vertical jump power (991 168 vs.
630 167 W, p < 0.001); and increased lean body mass gain
(7.4 4.2 vs. 2.1 6.1 kg, p < 0.001) in HMB-FA- and placebosupplemented groups, respectively. During the overreaching
cycle, HMB-FA attenuated increases in CK (-6 91 vs.
277 229 IU/l, p < 0.001) and cortisol (-0.2 2.9 vs.
4.5 1.7 g/dl, p < 0.003) in the HMB-FA- and placebosupplemented groups, respectively. CONCLUSION: These
results suggest that HMB-FA enhances hypertrophy, strength,
and power following chronic resistance training, and prevents
decrements in performance following the overreaching.
SPONSORSHIP: this research was funded in part through a
grant from Metabolic technologies Inc. JMW, rPl, JMJ, JcA, and
SMcW declare no competing interests. Jr, JF, and SB are
employed by Metabolic technologies, Inc.
Study strengths
This study is innovative since its the first to ever examine the
chronic effects of the free acid form of HMB (HMB-FA) in
trained subjects on a monitored, periodized resistance training
program. Blinding was meticulous on both sides of the
experiment. The design was also unique since its the first to
include an over-reaching period (in addition to the other novel
conditions). The authors provided the details of the training
program in a supplemental document (downloadable here, full
study PDF here). Diet was standardized and designed by a
registered dietitian who counseled the subjects throughout the
study. Compliance with supplementation was over 98%.
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Study strengths
This is the largest analysis of vitamin Ds clinical outcomes ever
done: 107 systematic literature reviews, 74 meta-analyses of
observational studies, and 87 meta-analyses of randomized
controlled trials (RCTs). Its rare to see analyses of this breadth
since, frankly, its a hell of a lot of work. This analysis provides
a relatively comprehensive summary of the existing literature. It
also attempted to account for the extent of bias and
heterogeneity in the observational vitamin D literature.
Study limitations
As acknowledged by the authors, the analysis was unable to
assess the relationship between vitamin D supplementation dose
and effect size in RCTs. Furthermore, the effect of different
choices of comparison groups or of varying vitamin D
distributions and median differences of the observational studies
could not be assessed either. Importantly and as a general
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Comment/application
Variability in muscle size and strength gain after
unilateral resistance training.
Hubal MJ, Gordish-Dressman H, Thompson PD, Price TB,
Hoffman EP, Angelopoulos TJ, Gordon PM, Moyna NM,
Pescatello LS, Visich PS, Zoeller RF, Seip RL, Clarkson PM.
Med Sci Sports Exerc. 2005 Jun;37(6):964-72. [PubMed]
PURPOSE: This study assessed variability in muscle size and
strength changes in a large cohort of men and women after a
unilateral resistance training program in the elbow flexors. A
secondary purpose was to assess sex differences in size and strength
changes after training. METHODS: Five hundred eighty-five
subjects (342 women, 243 men) were tested at one of eight study
centers. Isometric (MVC) and dynamic strength (one-repetition
maximum (1RM)) of the elbow flexor muscles of each arm and
magnetic resonance imaging (MRI) of the biceps brachii (to
determine cross-sectional area (CSA)) were assessed before and
after 12 wk of progressive dynamic resistance training of the
nondominant arm. RESULTS: Size changes ranged from -2 to
+59% (-0.4 to +13.6 cm), 1RM strength gains ranged from 0 to
+250% (0 to +10.2 kg), and MVC changes ranged from -32 to
+149% (-15.9 to +52.6 kg). Coefficients of variation were 0.48 and
0.51 for changes in CSA (P = 0.44), 1.07 and 0.89 for changes in
MVC (P < 0.01), and 0.55 and 0.59 for changes in CSA (P < 0.01)
in men and women, respectively. Men experienced 2.5% greater
gains for CSA (P < 0.01) compared with women. Despite greater
absolute gains in men, relative increases in strength measures were
greater in women versus men (P < 0.05). CONCLUSION: Men and
women exhibit wide ranges of response to resistance training, with
some subjects showing little to no gain, and others showing
profound changes, increasing size by over 10 cm and doubling their
strength. Men had only a slight advantage in relative size gains
compared with women, whereas women outpaced men considerably
in relative gains in strength. SPONSORSHIP: National Institutes of
Health Grant no. 5R01NS040606-03.
As depicted above, out of the 585 subjects, 232 showed a 1525% increase in CSA, 10 particularly high responders
experienced over a 40% increase in CSA, while on the opposite
end of the spectrum, 36 subjects showed less than a 5% increase
in CSA. The range of size changes was notable due to an actual
decrease in CSA on the low end of the range (-2 to +59%).
Formal examination of individual dietary intake would likely
have explained any drop in CSA, but the range of responses is
strikingly broad nevertheless. Men had 2.5% greater gains in
CSA than women. Next up are the strength effects.
Study strengths
The large number of subjects (585 total) heightened statistical
power and allowed a comparison of gender differences. Crosssectional area (CSA) of the upper arm musculature was
measured via magnetic resonance imaging (MRI), as opposed to
merely circumference, which cannot distinguish between lean
and fat tissue. Training was periodized, with reps beginning at
12 RM and progressing to 6 RM. All of the assessment and
training techniques/protocols were videotaped and shared by all
the sites in order to standardize the methods as much as possible.
Study limitations
Subjects over 40 years-old were excluded from the study,
leaving open questions about the applicability of these outcomes
to older populations. Dietary control was minimal, aside from
the instruction to maintain usual habits. It would have been
helpful to analyze the macronutrient composition of subjects
habitual intake, since variations especially in protein intake
can significantly impact gains in muscle size and strength during
resistance training programs.12,13 Its possible that the results
could be limited to the untrained population, as well as the
training protocol used on the targeted muscles (3 exercises for
the biceps, 2 exercises for the triceps, 3 sets per exercise).
Sessions per week were not specified which is unfortunate
since that leaves us with a very vague idea of total volume.
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In an effort to see just how valid NHANES diet recall data really
is, Archer et al7 analyzed the 39-year history of the multiple
NHANES surveys (from 1971 through 2010) and compared
those intakes to what they estimated to be realistic total daily
energy expenditures for men and women based on the Schofield
predictive equations plus an additional activity factor of 1.35.
Anything reported below this value was deemed not
physiologically credible. So, what did Archer and company
find?
What they found was that during the almost four decades-long
history of the NHANES, the mean reported energy intakes for
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References
1. Levine ME, Suarez JA, Brandhorst S, Balasubramanian P,
Cheng CW, Madia F, Fontana L, Mirisola MG, GuevaraAguirre J, Wan J, et al: Low protein intake is associated with a
major reduction in IGF-1, cancer, and overall mortality in the
65 and younger but not older population. Cell Metab 2014,
19:407-417. [PubMed]
2. Klement RJ, Kammerer U: Is there a role for carbohydrate
restriction in the treatment and prevention of cancer? Nutr
Metab (Lond) 2011, 8:75. [PubMed]
3. Klement RJ, Champ CE: Calories, carbohydrates, and cancer
therapy with radiation: exploiting the five R's through dietary
manipulation. Cancer Metastasis Rev 2014. [PubMed]
4. Goodwin PJ, Ennis M, Pritchard KI, Trudeau ME, Koo J,
Madarnas Y, Hartwick W, Hoffman B, Hood N: Fasting insulin
and outcome in early-stage breast cancer: results of a
prospective cohort study. J Clin Oncol 2002, 20:42-51.
[PubMed]
5. Stattin P, Bjor O, Ferrari P, Lukanova A, Lenner P, Lindahl B,
Hallmans G, Kaaks R: Prospective study of hyperglycemia and
cancer risk. Diabetes Care 2007, 30:561-567. [PubMed]
6. Weiser MA, Cabanillas ME, Konopleva M, Thomas DA,
Pierce SA, Escalante CP, Kantarjian HM, O'Brien SM:
Relation between the duration of remission and hyperglycemia
during induction chemotherapy for acute lymphocytic leukemia
with a hyperfractionated cyclophosphamide, vincristine,
doxorubicin, and dexamethasone/methotrexate-cytarabine
regimen. Cancer 2004, 100:1179-1185. [PubMed]
7. Archer E, Hand GA, Blair SN: Validity of U.S. nutritional
surveillance:National Health and Nutrition Examination Survey
caloric energy intake data, 1971-2010. PLoS One 2013,
8:e76632. [PLoS ONE]
8. Hill RJ, Davies PS: The validity of self-reported energy intake
as determined using the doubly labelled water technique. Br J
Nutr 2001, 85:415-430. [PubMed]
9. Lissner L, Troiano RP, Midthune D, Heitmann BL, Kipnis V,
Subar AF, Potischman N: OPEN about obesity: recovery
biomarkers, dietary reporting errors and BMI. Int J Obes
(Lond) 2007, 31:956-961. [PubMed]
10. Heerstrass DW, Ocke MC, Bueno-de-Mesquita HB, Peeters
PH, Seidell JC: Underreporting of energy, protein and
potassium intake in relation to body mass index. Int J
Epidemiol 1998, 27:186-193. [PubMed]
11. Subar AF, Kipnis V, Troiano RP, Midthune D, Schoeller DA,
Bingham S, Sharbaugh CO, Trabulsi J, Runswick S, BallardBarbash R, et al: Using intake biomarkers to evaluate the extent
of dietary misreporting in a large sample of adults: the OPEN
study. Am J Epidemiol 2003, 158:1-13. [PubMed]
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As far as contradictory evidence that suggests that lowcarbohydrate and/or high total/animal protein diets might
increase the risk of type 2 diabetes, all such studies are
observational in methodology and do not indicate cause and
effect.34-38 We do know, however, that diets higher in
total/animal protein tend to be associated with lower fruit and
vegetable intake and higher intakes of processed foods and
sugars (i.e. all the makings of a crappy diet). Indeed, in a recent
meta-analysis looking that the link between dietary patterns and
type 2 diabetes risk,39 it was shown that diets that conformed
more to what would be considered a healthy diet (i.e. less
processed grains and more fruits and vegetables) was associated
with reduced risk of type 2 diabetes while diets that were
considered unhealthy (i.e. higher in processed grains/meats
and refined sugars) were associated with increased risk of type 2
diabetes. What this goes to show is that having a well-balanced
diet is probably more important than limiting or increasing a
single macronutrient without regard to the rest of your daily
intake. In the end, a crappy diet is a crappy diet. I dont care how
much protein you are or arent eating.
Wrapping up
In the end, it doesnt look like the recent Cell Metabolism study
is anything to lose sleep over. Horrible study methodology
paired with biased statistics and a body of shabby inconclusive
and/or contradictory observational research suggests that
reducing your protein intake should be the last thing on your list
of dietary amendments (no comment about Alans PAP!).
And with that I will leave you with the concluding remarks from
the aforementioned unpublished letter-to-the-editor, written by
Layman et al:
Our overall assessment of [the Cell Metabolism] paper is that
the conclusions and analyses are biased and flawed. While there
is growing consensus that a moderate protein intake between 1.0
and 1.5 g/kg/d may confer health benefits beyond those afforded
by the current RDA for protein, we also recognize there are gaps
in the current knowledge base and encourage discussion of
important contradictory evidence/data. Future research must be
well designed, rigorously reviewed, and credibility
communicated. Unfortunately, the article by Levine et al.
presents conclusions not supported by their own analyses or the
greater literature.
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First off, congrats on the publication of the paper, which
breaks ground since its the first to compare a volumeequated strength-type versus a hypertrophy-type program
on trained subjects. What was the spark that inspired this
investigation? Id like some insight on the inception of the
idea and initial motivation to carry this out.
The genesis of this study actually dates back well over a decade.
As a former competitive bodybuilder, the subject of maximizing
hypertrophy has always been a big interest. It was perplexing to
me that the vast majority of studies on hypertrophy 1) used
untrained subjects and, 2) were carried out using routines that
werent very practical to how lifters actually train. So when I
decided to pursue an academic career, I set my focus on carrying
out a study that addressed these issues and thus had real practical
implications for hard-training lifters. I actually proposed a
variation of the study I eventually conducted during my masters
degree work at the University of Texas but ultimately decided to
do a project rather than a thesis (which incidentally was
published as a review paper called The mechanisms of muscle
hypertrophy and their application to resistance training in the
JSCR) and save the study for my PhD dissertation. It turned out
to be a big plus in that I hit the ground running once I began my
doctoral work; all my scholarly efforts were directed to making
the study happen. On that note, I need to give a big shout out to
my dissertation committee here: Dr. Brent Alvar, Dr. Nick
Ratamess, and Dr. Mark Peterson. We had numerous strategy
sessions about every aspect of the study and they all were a huge
help in fine-tuning the methodology so it had maximum impact.
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