11 Lactate, fructose and glucose oxidation profiles in

sports drinks and the effect on exercise

performance.
Azevedo JL, et al. PLoS ONE. 2007 Sep 26;2(9):e927.
[Medline]

13 Reflective re-cap: 7 new things I learned since

January.
By Alan Aragon
Copyright © August 1st, 2008 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com

2 High-fructose calories are still calories.

By Alan Aragon

6 Bottled water is healthier than tap water?

By Jamie Hale

7 Weight loss with a low-carbohydrate,

Mediterranean, or low-fat diet.
Shai I, et al. N Engl J Med. 2008 Jul 17;359(3):229-41.
[Medline]

8 Effect of exercise on 24-month weight loss

maintenance in overweight women.
Jakicic JM, et al. Arch Intern Med. 2008 Jul
28;168(14):1559-60. [Medline]

9 Plasma amino acid response after ingestion of

different whey protein fractions.
Farnfield MM, et al. Int J Food Sci Nutr. 2008 May 8:1-11.
[Medline]

10 Acute and long-term effects of resistance exercise

with or without protein ingestion on muscle
hypertrophy and gene expression.
Hulmi JJ, et al. Amino Acids. 2008 Jul 27. [Epub ahead of
print] [Medline]

Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 1 

High-fructose calories are still calories.
By Alan Aragon
INTRODUCTION
In this article
The inspiration of this article was from a link to an article sent to
me by a friend of mine (a troubleshooting she-guru who I won’t
incriminate by naming). The article was entitled, “The Evils of
Fruit”. The title has since been changed to “The Evils of
Fructose”, presumably because too much of a stink was raised
by the educated crowd. I was originally going to comment on it
in the Lay Press section of this issue, but its misinterpretations
are profound enough to address in a full-length editorial. The
content didn’t completely reflect the sensationalistic title, but the
underlying message was clear that certain circumstances warrant
the limitation of fruit containing higher fructose levels. In the
following article, I’ll take a look at the common
misunderstandings that lead to misconceptions of fruit (and
fructose) pertaining to general health, bodyweight, and body
composition.
Why pick on fruit? It’s the carbs!
Perhaps the root of all the fruit-bashing is the belief that
carbohydrates make you fat, fruits are carbohydrate-rich, and
therefore, fruits make you fat. Not only this, but this line of logic
is compounded with the idea that sugar is the most fattening type
of carbohydrate, and fructose is the most fattening type of sugar.
Since fruits contain fructose, they’re a like a double death
sentence. It’s tempting to be completely facetious throughout
this article, but I’ll keep it under control and objectively attack
the inaccuracies one by one. But first, let’s get some
foundational stuff established.
CALORIES VERSUS CAROHYDRATES
A calorie is a calorie, or is it?
The well known expression “a calorie is a calorie” is misleading,
and easy to argue over depending upon how the it’s interpreted.
Literally speaking, a calorie is a calorie in the sense that a calorie
is static unit of measure, just like a liter is a liter and a gram is a
gram. Nothing can change that. However, people often transpose
their personal values upon that simple statement. The argument
against it is based on the assumption that all of the
macronutrients have equal physiologic effects, when obviously
they don’t. And I don’t think anyone would argue that the
macronutrients have identical effects. But regardless of how
each macronutrient’s role differs within the body, a calorie is
technically still a calorie.
Just a little physics
The First Law of Thermodynamics states that the total mass of a
body in the universe is determined by the energy entering it
minus the energy leaving it. In practical terms, this means that if
you eat more calories than you burn, you’ll gain weight. And
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 2
conversely, if you eat less calories than you burn, you’ll lose
weight. Adjacently, the Law of Conservation of Energy states
that energy can neither be created nor destroyed but may be
transformed from one kind to another. In plain terms, this means
that you can’t create more bodyweight out of thin air, there has
to be an increased intake of calories. Conversely, you can’t
magically lose bodyweight if a surplus of calories is maintained
via that fridge getting raided constantly. Of course, there are
temporary weight gains and losses that can be due to hydration
flux (and thus occur independently of caloric flux), but in the
long-term, basic laws of physics make themselves known,
regardless of macronutrient composition.
Metabolic advantage? Not beyond the short-term
Most of you are aware that the macronutrients have varying
thermic effect (caloric cost of processing). In single-meal studies
comparing their effects, protein causes the highest diet-induced
thermogenesis (DIT), carbohydrate is in the middle, and fat falls
in last place.1-3 The allure of increasing the proportion of dietary
protein at the expense of carbohydrate is the idea that it will
impart a metabolic advantage via increased thermogenesis. This
theoretically should lead to greater weight loss over time.
However, unlike the mixed results seen in self-reported intake or
free-living conditions, rigorously controlled trials comparing
isocaloric treatments differing in macronutrient composition
unanimously show no long-term difference in bodyweight
reduction (body composition effects can vary, we’ll get to that).
In the most tightly controlled long-term trial to date, Das et al
compared 1 year of hypocaloric high- and low-glycemic load
(GL) dieting.4 No significant differences were seen in
bodyweight or bodyfat determined by DEXA, despite 10% less
protein and 20% less carbs in the low-GL group at either the 6th
or 12th month.
In a more disparate comparison, Noakes et al examined the
effects of 3 diets, one with the following macronutrient
proportions (% carb:fat:protein):5
ƒ Very Low Fat = (70:10:20) = 250.8g carb
ƒ High Unsaturated Fat = (50:30:20) = 179.1g carb
ƒ Very Low Carb = (4:61:35) = 14.3g carb
Despite the broadly varying proportions of macronutrients
(particularly fat and carbohydrate), no significant differences
were seen in total weight loss, or loss of bodyfat percent.
Interestingly, the high unsaturated fat diet showed the best
preservation of lean mass.
Duh, getting enough protein matters
A related question is whether or not consuming a suboptimal
amounts of protein can unfavorably impact the thermodynamic
equation. Duh, yes it can, and a sizable amount of the current
research comparing low- and high-carb diets do not match
protein intake. With that fact aside, research specifically
designed to compare varying high- versus low-protein diets have
yielded the predictable answer: getting enough protein matters.
 
For example, Layman et al found that double the RDA (1.6g/kg
instead of 0.8g/kg) caused a greater decrease in bodyfat and less
lean mass loss when compared to administering the RDA for
protein.6 Again, no significant differences in total weight were
observed. A slight amplification in these results came into play
when Layman et al added structured exercise to the protocol, in
which case the higher protein groups lost both more bodyfat and
total bodyweight.7 Dietary intake was self-reported, so it’s
highly probable that the higher-protein groups were better
satiated and thus ate less total calories. Keep in mind, these
results don’t support any metabolic advantage of less
carbohydrates as much as they support consuming sufficient
protein. In a less controlled example, Brehm et al found that an
ad libitum (as desired) diet restricted to 20 g carbohydrate per
day caused more total weight and fat loss than an assigned intake
of 55% carbohydrate, 15% protein, and 30%.8 Again, since
calorie intake was not controlled, a greater satiety factor in the
lower-carb treatment (via increased protein intake) likely curbed
total calorie intake.
Skimping on protein isn’t likely to upset physical laws
Surprisingly, even in the case of what would seem to be a barely
sufficient protein intake compared to a sufficient one, a
metabolic disadvantage isn’t guaranteed to surface. For
example, a trial by Arciero et al found no 12-week difference in
body composition change between isocaloric intakes with
protein at either 25% (110 g) or 40% (187 g).9
In another example, Luscombe-Marsh et al compared a low-fat,
high-protein diet (29% fat, 34% protein) with a high-fat,
standard-protein diet (45% fat, 18% protein) during 12 weeks of
energy restriction (1433 kcal/d) and 4 weeks of energy balance
(1767 kcal/d).10 No differences were seen in both body
composition (via DEXA) or body weight. Interestingly, this was
seen despite one group consuming 64.5 g protein while the other
group consumed 121 g protein during the caloric restriction
period.
In yet another example, Johnstone et al recently compared two
1500 kcal diets; a non-ketogenic (157g carb, 117g prot, 50g fat)
versus a ketogenic diet (33g carb, 125g prot, 100g fat).11 There
was no significant difference in weight loss, and there was an
equal increase in resting energy expenditure. This was somewhat
predictable given that the protein intakes weren’t drastically
different, unlike the previously discussed Layman studies.
Nevertheless, this trial indicates that ketogenic dieting offered no
metabolic advantage over non-ketogenic dieting.
FRUCTOSE: EFFECTS ON HEALTH AND BODY FAT
Meet the “devil”
It’s well known that obesity has increased over the past few
decades and has currently reached epidemic proportions. In the
1980’s, obesity prevalence accelerated. During this same time
period, the beverage industry made the switch from using
sucrose to high-fructose corn syrup (HFCS).12 As a result, HFCS
has gotten tagged as the devil, but this is largely by virtue of
coincidence. During the same time of the switch over to HFCS, a
number of other variables could have contributed to the obesity
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 3
surge. Key factors include competitive increases in food portions
by restaurants and food outlets, the widespread use of labor-
saving devices, personal computers, and the internet. It bears
mentioning that although variations of HFCS can be as high as
90% fructose, the type used for soft drinks is 55% fructose,
making it nearly identical to sucrose. Thus, it’s doubtful that
HFCS per se is inherently any worse than table sugar.
Hypocaloric conditions
Most intuitively realize that the overconsumption of sugar isn’t
wise because it displaces calorie sources in the diet that are more
nutrient-dense and contributory to general health. However,
since sucrose is 50% fructose, some folks will stretch the “sugar
is bad” concept into a matter of “fructose is the most evil type of
sugar, and it will make you fat.” This idea has indeed been
investigated under controlled hypocaloric conditions, and the
results would highly disappoint those passionately against
fructose consumption.
Back in 1988, Grigoresco et al compared various clinical effects
of 30g fructose to an equal amount of starch within a 1400-1600
kcal diet during a 2-month period in type II (non-insulin-
dependent) diabetics.13 No significant difference was seen in
bodyweight weight, HbA1c, fasting glucose, insulin, uric acid,
total cholesterol, high-density lipoprotein cholesterol, and
triglycerides.
In a more poignant example, Surwit et al compared 2 high-
carb/low-fat diets (72% carbs), one with 43% of the total
calories as sucrose, and one with 4% of the total calories as
sucrose.14 This calculates out to 118g sucrose (containing 59g
fructose) versus 46g sucrose (23g fructose). Once again, no
differences were seen in bodyweight and bodyfat reduction
(measured by DEXA) during the 6-week trial. Furthermore, no
adverse effects on blood lipids were seen in the high-sucrose
group.
Hypercaloric conditions
With hypocaloric conditions out of the way, how does fructose
overfeeding compare to that of other carbohydrates? Fructose
overfeeding for both acute and extended periods has adverse
effects various aspects of lipid metabolism, with the most
common effect being raised plasma triacylglycerol.15-17 A recent
focus has been on the fructose’s ability to raise uric acid levels,
which carries negative implications for kidney health.18
Given the adverse effects seen in fructose overfeeding trials, it’s
crucially important to interpret this research within its proper
context. To begin with, fructose is rarely consumed in isolation;
it’s typically within sucrose or HFCS-sweetened products. The
fitness-conscious population tends to be very sparing, and in
many cases, avoidant of added table sugar or non-diet soft
drinks. So for these folks, the risk fructose overconsumption is
virtually nonexistent. The competitive endurance population’s
massive training volume more than offsets their risk of
overconsuming fructose via the sucrose content of common
recovery beverages. Furthermore (and perhaps most importantly)
the fructose doses in the overfeeding studies don’t reflect the
reality of what people are consuming. The average fructose
 
intake in the United States is 9% of total calories (39 g), whereas
fructose overfeeding research showing adverse effects
administers 2-4 times this much.16,19 Fructose is often accused of
being more lipogenic than other carbohydrates. This claim is
simply unfounded. Overfeeding trials comparing an additional
50% of maintenance calories (~135 g) as either sucrose, glucose,
or fructose have not seen any significant difference in de novo
lipogenesis.20,21
Could excess total calories be the culprit? How cutting-edge!
As pointed out in a recent letter by researcher John White to the
editors of the American Journal of Clinical Nutrition, the big
picture comes into clearer focus when examine the latest
relevant large-scale intake survey.22 According to the USDA
Economic Research Service, daily calorie consumption increased
by 24% from 1970-2005. But here’s the clincher: percentage of
daily calories from added sugars decreased 1% during this
period, whereas flours/cereals increased by 3%, and fat
consumption went up by 5%. Given this, it appears that the rise
in obesity is due in large part to a general increase in calories
across the board, rather than an increase in a single
macronutrient subtype. Granted, it would be much more
innovative to have discovered a simple answer; a simple
substance to avoid in the quest to solve the problem of obesity
and its related diseases. Unfortunately, for those seeking a
scapegoat, it all seems to circle right back to general caloric
excess, not fructose in particular.
THE UNFOUNDED FEAR OF FRUIT FOR FAT LOSS
An apple a day keeps the abs away?
Now that the facts and foundations have been laid out, we can
examine the fruit issue for what it really is. At this point I should
clarify that nowhere else but in the semi-crazed
fitness/bodybuilding community is fruit intake ever ill-advised.
Apparently, there’s a certain “hardcore-ness” about being
mortally afraid of an apple while dieting for a photo shoot or a
physique contest. I find this ridiculous from the standpoint of
personal experience supervising competitors’ programs, as well
as from what’s been demonstrated in research.
At the most basic level of reasoning, the typical fruit’s 7-10
grams of fructose is not likely to impede anyone’s fat loss goals.
As a matter of fact, fruits have a number of attributes that make
them an ideal carbohydrate source under hypocaloric conditions.
First of all, fruits are calorically sparse for the amount and
quality of micronutrition they provide. This has obvious
advantages to dieters, particularly dieters who exercise.
Secondly, due to their fiber content and water volume, they
provide more satiety on a per-calorie basis than other
carbohydrate sources. Third, the minor amount of fructose
contained in fruit can contribute to the maintenance of liver
glycogen. The significance here is that glycogen-mediated liver
cell swelling is one of the body’s most potent
anabolic/anticatabolic signals. As such, fruit intake can help
suppress the loss of lean mass under hypocaloric conditions.
Finally, science thus far does not support the idea that fruits are
inherently fattening, or can hinder weight or fat loss. The next
section examines the scant data available on this topic.
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 4
Science the bro’s don’t know about
On obese subjects, Rodriguez et al compared the effect of a low-
versus a high fruit intake (4% of total calories from fructose
versus 13.8%).23 Intake of both groups was roughly 1300 kcal,
so this calculates to about in the 13 g fructose in the low fruit
group and 45 g in the high group. Although serving ranges
weren’t specified in the text, this translates to 0-1 fruit serving in
the low group, and 3-4 servings in the high group. By the end of
the 8-week trial, both groups lost weight and bodyfat but no
significant differences were found between groups. An
interesting outcome was a significantly greater decrease in waist
circumference in the high fruit group.
In a similarly designed trial, Crujeiras et al compared the effect
of a high or low fruit intake under hypocaloric conditions in
obese subjects (same diet setup as the above trial).24 No weight
or fat loss differences were seen between the low and high fruit
group after 8 weeks. However, the high fruit group showed
greater defense against oxidative stress. The authors concluded
that the extra fiber and antixodants provided by the higher fruit
intake would be important assets to a program that focused on
improving cardiovascular risk factors associated with obesity.
These studies indicate that fruit does not hinder weight or fat
loss despite their fructose contribution to the diet. In fact, one
study hints that a higher fruit intake may even enhance fat loss
compared to a calorie-matched low fruit intake. Additionally,
fruit intake may be the “win-win” since it protects against
oxidative stress, which can increase with exercise. Topping
things off, the synergy of nutrients within whole fruit is
cardioprotective. Why not get healthier while getting lean?
SUMMARY POINTS
Calories versus carbohydrates
• A calorie is indeed a calorie, but the confusion over this
statement is rooted in the notion that it’s implying that
macronutrients have identical physiological roles, when
obviously they don’t.
• According to the laws of physics, one must maintain a caloric
deficit to lose weight, and a caloric surplus to gain weight.
[For those who went straight to this summary section, read
the full article; I give important adjacent details to this point].
• In single-meal studies, protein causes the highest diet-
induced thermogenesis (DIT), carbohydrate is in the middle,
and fat falls in last place. This gave rise to the hopes of a
metabolic advantage of high-protein diets.
• Unlike the mixed results seen in self-reported intake trials,
rigorously controlled experiments comparing isocaloric diets
with different macronutrient composition unanimously show
no long-term difference in bodyweight reduction.
• A sizable amount of the current research comparing low- and
high-carb diets do not match protein intake, which can make
a difference in the maintenance of lean mass.
• Surprisingly, even in the case of what would seem to be a
barely sufficient protein intake compared to a sufficient one,
a metabolic disadvantage (indicated by less weight or fat
loss), isn’t guaranteed to occur.
Fructose: effects on health and bodyfat
 
• Starting in the 1980’s, obesity prevalence accelerated. During
this same time period, the beverage industry made the switch
from using sucrose to high-fructose corn syrup (HFCS). As a
result, HFCS has gotten tagged as the root of all evil.
• However, a number of other variables (such as days on end
of TV and internet surfing) could have contributed to the
obesity surge, not necessarily the switch to HFCS.
• Fructose overfeeding for both acute and extended periods has
adverse effects various aspects of lipid metabolism, with the
most common effect being raised plasma triacylglycerol.
• However, the average fructose intake in the United States is
9% of total calories (39 g), whereas supplemental fructose
research has administered 2-4 times this much, giving them
limited real-world relevance.
• Overfeeding trials comparing an additional 50% of
maintenance calories as sucrose, glucose, or fructose
(roughly 135 g) have not seen any significant difference in de
novo lipogenesis.
• Daily calorie consumption increased by 24% from 1970-
2005. However, calories from added sugars decreased 1%
during this period, while flours/cereals increased by 3%, and
fat consumption went up by 5%. This points to a general
caloric increase as the obesity culprit, rather than fructose
consumption per se.
• At the most basic level of reasoning, the typical fruit’s 7-10
grams of fructose is not likely to impede anyone’s fat loss
goals. Furthermore, fruit has multiple attributes that make it
an ideal carbohydrate source under dieting conditions.
• Scientific research (rather then unqualified opinion) shows
that fruit does not hinder weight or fat loss despite their
fructose contribution to the diet. Additionally, fruit intake
may be the “win-win” since it protects against oxidative
stress and reduces cardiovascular disease risk.
REFERENCES
1. Karst H, et al. Diet-induced thermogenesis in man: thermic
effects of single proteins, carbohydrates and fats depending on
their energy amount. Ann Nutr Metab. 1984;28(4):245-52.
[Medline]
2. Steiniger J, et al. Diet-induced thermogenesis in man: thermic
effects of single protein and carbohydrate test meals in lean and
obese subjects. Ann Nutr Metab. 1987;31(2):117-25. .
[Medline]
3. Nair Ks, et al. Thermic response to isoenergetic protein,
carbohydrate or fat meals in lean and obese subjects. Clin Sci
(Lond). 1983 Sep;65(3):307-12. [Medline]
4. Das SK, et al. Long-term effects of 2 energy-restricted diets
differing in glycemic load on dietary adherence, body
composition, and metabolism in CALERIE: a 1-y randomized
controlled trial. Am J Clin Nutr. 2007 Apr;85(4):1023-30.
[Medline]
5. Noakes M, et al. Comparison of isocaloric very low
carbohydrate/high saturated fat and high carbohydrate/low
saturated fat diets on body composition and cardiovascular risk.
Nutr Metab (Lond). 2006 Jan 11;3:7. [Medline]
6. Layman DK, et al. A reduced ratio of dietary carbohydrate to
protein improves body composition and blood lipid profiles
during weight loss in adult women. J Nutr. 2003
Feb;133(2):411-7. [Medline]
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 5
7. Layman DK, et al. Dietary protein and exercise have additive
effects on body composition during weight loss in adult
women. J Nutr. 2005 Aug;135(8):1903-10. [Medline]
8. Brehm BJ, et al. The role of energy expenditure in the
differential weight loss in obese women on low-fat and low-
carbohydrate diets. J Clin Endocrinol Metab. 2005
Mar;90(3):1475-82. Epub 2004 Dec 14. [Medline]
9. Arciero PJ, et al. Moderate protein intake improves total and
regional body composition and insulin sensitivity in overweight
adults. Metabolism. 2008 Jun;57(6):757-65. [Medline]
10. Luscome-Marsh ND, et al. Carbohydrate-restricted diets high
in either monounsaturated fat or protein are equally effective at
promoting fat loss and improving blood lipids. Am J Clin Nutr.
2005 Apr;81(4):762-72. [Medline]
11. Johnstone CS, et al. Ketogenic low-carbohydrate diets have no
metabolic advantage over nonketogenic low-carbohydrate
diets. Am J Clin Nutr. 2006 May;83(5):1055-61. [Medline]
12. Saris WH. Sugars, energy metabolism, and body weight
control. Am J Clin Nutr. 2003 Oct;78(4):850S-857S. [Medline]
13. Grigoresco C, et al. Lack of detectable deleterious effects on
metabolic control of daily fructose ingestion for 2 mo in
NIDDM patients. Diabetes Care. 1988 Jul-Aug;11(7):546-50.
[Medline]
14. Surwit RS, et al. Metabolic and behavioral effects of a high-
sucrose diet during weight loss. Am J Clin Nutr. 1997
Apr;65(4):908-15. [Medline]
15. Hollenbeck CB. Dietary fructose effects on lipoprotein
metabolism and risk for coronary artery disease. Am J Clin
Nutr 1993;58(suppl):800S-9S. [Medline]
16. Bantle JP, Raatz SK, Thomas W, Georgopoulos A. Effects of
dietary fructose on plasma lipids in healthy subjects. Am J Clin
Nutr 2000;72:1128–34. [Medline]
17. Teff KL, Elliott SS, Tschöp M, et al. Dietary fructose reduces
circulating insulin and leptin, attenuates postprandial
suppression of ghrelin, and increases triglycerides in women. J
Clin Endocrinol Metab 2004;89:2963–72. [Medline]
18. Johnson RJ, et al. Potential role of sugar (fructose) in the
epidemic of hypertension, obesity and the metabolic syndrome,
diabetes, kidney disease, and cardiovascular disease. Am J Clin
Nutr. 2007 Oct;86(4):899-906. [Medline]
19. McDevitt RM, et al. De novo lipogenesis during controlled
overfeeding with sucrose or glucose in lean and obese women.
Am J Clin Nutr. 2001 Dec;74(6):737-46. [Medline]
20. McDevitt RM, et al. Macronutrient disposal during controlled
overfeeding with glucose, fructose, sucrose, or fat in lean and
obese women. Am J Clin Nutr. 2000 Aug;72(2):369-77.
[Medline]
21. Le KA, et al. A 4-wk high-fructose diet alters lipid metabolism
without affecting insulin sensitivity or ectopic lipids in healthy
humans. Am J Clin Nutr. 2006 Dec;84(6):1374-9. [Medline]
22. White JS. No unique role for fructose sweeteners in obesity or
cardiorenal disease. Am J Clin Nutr. 2008 Apr;87(4):1062-3.
[Medline]
23. Rodriguez MC, et al. Effects of two energy-restricted diets
containing different fruit amounts on body weight loss and
macronutrient oxidation. Plant Foods Hum Nutr. 2005
Dec;60(4):219-24. [Medline]
24. Crujeiras AB, et al. A role for fruit content in energy-restricted
diets in improving antioxidant status in obese women during
weight loss. Nutrition. 2006 Jun;22(6):593-9. [Medline]
 

Bottled water is healthier than tap water? 1
By Jamie Hale
I was watching 60 minutes last night and Andy Rooney came on
and began discussing different types of bottled water. He pointed
out that there were hundreds of different types of bottled water
on the market. Rooney’s questions were was bottled water safer
than tap water and was there a difference in expensive bottled
water versus cheap bottled water? He also spoke to a researcher
whose specialty was investigating water purity and content. The
researcher told Rooney that there was very little difference in the
contents of bottled waters that he had tested. He told Rooney
that he personally drinks tap water.
What’s funny is that we make lemonade, Kool-aid, and coffee
with tap water, but we are afraid to drink plain tap water (at least
some of us who insist on consuming bottled water).
A study conducted by Lalumandier and Ayers looked at the
fluoride level and bacterial content of commercially bottled
waters versus municipal tap water.2 Fifty-seven samples of five
categories of bottled water were purchased from local stores.
Samples of tap water were collected in sterile containers from
the four local water processing plants. Fluoride levels were
determined, and water was cultured quantitatively. Levels of
bacteria were calculated as colony-forming units (CFUs) per
milliliter. Fluoride levels within the range recommended for
drinking water by the Ohio Environmental Protection Agency,
Cincinnati, Ohio—0.80 to 1.30 mg/L—were found in only three
samples of bottled water tested. The fluoride levels of tap water
samples were within 0.04 mg/L of the optimal fluoride level of
1.00 mg/L. The bacterial counts in the bottled water samples
ranged from less than 0.01 CFU/mL to 4900 CFUs/mL. In
contrast, bacterial counts in samples of tap water ranged from
0.2 to 2.7 CFUs/mL. Five percent of the bottled water purchased
in Cleveland fell within the required fluoride range
recommended by the state compared with 100 percent of the tap
water samples, all of which were also within 0.04 mg/L of the
optimal fluoride level of 1.00 mg/L. The researchers concluded
that drinking bottled water based on the assumption of purity can
be misleading.
Americans really love their bottled water, spending
approximately 6.5–7 billion dollars a year on it. Prices of bottled
water range from 75 cents to $6.00 per gallon.
The price of tap water generally runs between 80 cents and
$6.40 per 1000 gallons.
The Natural Resources Defense Council (NRDC) published the
results of a four-year study in which they tested more than 1000
samples of 103 brands of bottled water.3 The study indicated that
approximately 25 percent or more of bottled water is really just
tap water. The NRDC also found that 18 of the 103 brands tested
had more bacteria than allowed under microbiological-purity
guidelines. About one fifth of the waters contained synthetic
organic chemicals, but these were generally at levels below state
and federal standards.
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 6
Bottled water is subject to less rigorous purity standards and less
frequent tests for bacteria and chemical contaminants than those
required for tap water. Bottled water plants test for coliform
bacteria once a week, and city tap water is tested 100 or more
times a month. (These are supposed standards. I’m not sure if we
can always rely on this actually occurring.)
Even if bottled water isn’t safer, at least it tastes better, correct?
Maybe is does, maybe it doesn’t. When blind tests are
conducted, the taste buds really don’t seem to think so. In 2001,
ABC’s Good Morning America conducted a blind water taste
test. The viewers preferences were as follows: 12 percent Evian,
19 percent O-2, 24 percent Poland Spring, and 45 percent New
York City tap. The Yorkshire England water company found
that 60 percent of 2800 people surveyed could not tell the
difference between the local tap water and the UK’s bottled
water.
The hosts of Showtime’s television series Penn & Teller:
Bullshit conducted a blind taste test comparing waters. The test
showed that 75 percent of New Yorkers preferred city tap to
bottled waters. The hosts of the show conducted another test in a
trendy southern California restaurant that featured a water
sommelier who dispensed extravagant water menus to the
patrons. The patrons had no idea that all of the fancy bottles of
water were filled with the same water from a water hose in the
back of the restaurant. Patrons were willing to pay $7.00 a bottle
for L’eau Du Robinet (French for faucet water), Agua de Culo
(Spanish for ass water), and Amazone (filtered through the
Brazilian rainforest’s natural filtration system). I love that
experiment.
Some studies indicate that specific types of bottled water contain
more minerals than tap water. Do these levels of heightened
minerals contribute to your health? Another thing you need to
ask yourself is do I only drink water? Should you count only on
water ingestion to get your minerals? These questions probably
sound ridiculous to you. They are no more ridiculous than
assuming that because a bottled water has more minerals of a
specific type, it will greatly enhance your health.
The biggest advantage of bottled water is the bottle itself. It
makes drinking water more convenient and is easier to carry
than a water spicket or fountain.
In reading through a massive amount of data, I can’t find
anything that would lead me to believe that bottled water is any
safer than tap water.
References
1. Hale J. Knowledge and Nonsense (excerpted with
permission). MaxCondition, 2007. [MaxCondition]
2. Lalumandier JA, Ayers LW. Fluoride and bacterial content of
bottled water vs tap water. Arch Fam Med. 2000
Mar;9(3):246-50. [Medline]
3. Natural Resources Defense Council. Pure drink or pure hype?
1999. [NRDC]
 

Weight loss with a low-carbohydrate, Mediterranean, or
low-fat diet.
Shai I, et al. N Engl J Med. 2008 Jul 17;359(3):229-41.
[Medline]
PURPOSE: To compare the effectiveness and safety of weight-
loss diets over the long-term. METHODS: In this 2-year trial,
we randomly assigned 322 moderately obese subjects (mean age,
52 years; mean body-mass index [the weight in kilograms
divided by the square of the height in meters], 31; male sex,
86%) to one of three diets: low-fat, restricted-calorie;
Mediterranean, restricted-calorie; or low-carbohydrate, non-
restricted-calorie. RESULTS: The rate of adherence to a study
diet was 95.4% at 1 year and 84.6% at 2 years. The
Mediterranean-diet group consumed the largest amounts of
dietary fiber and had the highest ratio of monounsaturated to
saturated fat. The low-carbohydrate group consumed the least
carbohydrates and the most fat, protein, and cholesterol and had
the highest percentage of participants with detectable urinary
ketones. Mean weight loss was 2.9 kg for the low-fat group, 4.4
kg for the Mediterranean-diet group, and 4.7 kg for the low-
carbohydrate group; among the 272 participants who completed
the intervention, the mean weight losses were 3.3 kg, 4.6 kg, and
5.5 kg, respectively. The relative reduction in the ratio of total
cholesterol to HDL-C was 20% in the low-carbohydrate group
and 12% in the low-fat group. Among the 36 subjects with
diabetes, changes in fasting plasma glucose and insulin levels
were more favorable among those assigned to the Mediterranean
diet than among those assigned to the low-fat diet
CONCLUSION: Mediterranean and low-carbohydrate diets
may be effective alternatives to low-fat diets. The more
favorable effects on lipids (with the low-carbohydrate diet) and
on glycemic control (with the Mediterranean diet) suggest that
personal preferences and metabolic considerations might inform
individualized tailoring of dietary interventions.
SPONSORSHIP: Nuclear Research Center Negev (NRCN), the
Dr. Robert C. and Veronica Atkins Research Foundation, and the
S. Daniel Abraham International Center for Health and Nutrition,
Ben-Gurion University, Israel.
Study strengths
The first thing that jumps out is the study length. Non-acute
dietary intervention trials typically fall into 3 categories: barely
long enough (4-6 weeks), just about there (8-12 weeks), nice and
lengthy (6 months-1 year). The 2-year period of the present trial
puts it in the special category, of “exceptionally long for a diet
study”Another strength is the sample size (272 completed the
trial), and relatively low drop-out rate. Although the participants
were in charge of their own intake, dietary control measures
were extensive. Each diet group was assigned a registered
dietitian who met with the group in weeks 1, 3, 5, and 7 and
thereafter at 6-week intervals. Six times during the 2-year trial, a
dietitian conducted 10-to-15-minute motivational phone calls
with struggling participants. Additionally, a group of spouses
received education on how to support the subjects’ dieting
efforts. Finally, the diets were not severely restrictive in terms of
total calories (1800 for men, 1500 for women), and thus were
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 7
more representative of what might apply to real-world, long-
term dieting – as opposed to crash dieting followed by weight
gain rebound, then repeating the cycle.
Study limitations
Off the bat, total bodyweight is a fair indicator of progress in
obese subjects, but its limitations really show up as people get
leaner, and certainly when people get on an exercise program
(that includes resistance training) and start to trade fat for
muscle. Measuring bodyfat % would have provided provide
some valuable data. granted an accurate method such as ADP,
DEXA, or hydrodensitiometry was used. Another limitation, as
mentioned by the authors themselves, was the measurement of
HOMA-IR is not an optimal method to assess insulin resistance
among persons with diabetes.
Comment/application
Certain outcomes of this trial were predictable, such as the
greater improvement in fasting insulin and glucose in the
Mediterranean group compared to the low-fat group, and the
greater improvement in total cholesterol to HDL-C ratio in the
Atkins group compared to the low-fat group. However, certain
outcomes were less predictable, like the greater weight loss with
the Atkins and Mediterranean diets compared to the low-fat diet.
I say this because two previous long-term trials comparing high-
and low-carb intakes showed the superiority of low-carb at the
6th month, but no significant differences in weight loss at the 12th
month.1,2 Other than the length of those previous trials versus the
present one that’s twice as long, there’s no immediately apparent
explanation for the differing outcomes. One could point to the
more extensive measures of dietary control, higher subject
retention, and better adherence in the present study giving it the
advantage. On the flip side, one could also point to a potential
commercial bias of the present study, since it was funded in part
by the Atkins Research Foundation. The other two trials did not
have any such intimate commercial affiliation.
Another aspect about this trial worth pondering is what the
outcomes might have been if formal exercise was structured into
the protocol. My guess is that (with funding bias on hold for a
second) the weight loss differences between treatments would
diminish. Exercise itself improves glucose and insulin
parameters, as well as plasma lipids, so those differences should
diminish as well. Also, the type of exercise would likely have
some influence on the outcome if it had enough volume and/or
intensity to be a better match for the higher-carb diets instead of
the Atkins diet. The latter is rarely used by competitive athletes
outside of maximal strength-focused sports.
An appealing characteristic of Atkins diet was its weight loss
effectiveness despite an unrestricted intake of protein and fat
(carbohydrate was limited to 20 g per day for the 2-month
induction phase with a gradual increase to a maximum of 120 g
per day to maintain the weight loss. Obviously calories still
mater, but apparently, caloric intake was self-regulated probably
due to protein- mediated satiety. Notably, however, the
Mediterranean diet performed on par with the Atkins diet for
weight loss, and actually surpassed it in parameters relevant to
those with glucose control issues. This trial adds evidence
supporting the case of... (drum roll please).... Moderation.
 
Effect of exercise on 24-month weight loss maintenance
in overweight women.
Jakicic JM, et al. Arch Intern Med. 2008 Jul 28;168(14):1559-
60. [Medline]
PURPOSE: To investigate the amount of physical activity that
will facilitate weight loss maintenance. METHODS: Between
December 1, 1999, and January 31, 2003, 201 overweight and
obese women (BMI = 27-40); age range, 21-45 years, with no
contraindications to weight loss or physical activity were
recruited from a hospital-based weight loss research center. They
were randomly assigned to 1 of 4 groups based on physical
activity energy expenditure (1000 vs 2000 kcal/wk) and intensity
(moderate vs vigorous). Participants were told to reduce intake
to 1200 to 1500 kcal/d. RESULTS: Weight loss did not differ
among the randomized groups at 6 months' (8%-10% of initial
body weight) or 24 months' (5% of initial body weight) follow-
up. Post-hoc analysis showed that individuals sustaining a loss
of 10% or more of initial body weight at 24 months reported
performing more physical activity (1835 kcal/wk or 275
min/wk) compared with those sustaining a weight loss of less
than 10% of initial body weight. CONCLUSION: The addition
of 275 mins/wk of physical activity, in combination with a
reduction in energy intake, is important in allowing overweight
women to sustain a weight loss of more than 10%. Interventions
to facilitate this level of physical activity are needed.
SPONSORSHIP: A grant from the National Institutes of Health
and the National Heart, Lung, and Blood Institute.
Study strengths
In a field where it’s nice to see studies in the 3-6 month range, a
study duration of 24 months is more than ample. Another
strength. Attrition (dropout) was low, and the ending sample size
ws large (191 participants). For compliance and educational
purposes, participants attended group meetings weekly during
months 1-6, twice per month during months 7 to 12, and once
per month during months 13 to 18. Subjects received brief calls
from a member of the intervention team, occurring twice per
month during months 7 to 12, once per month during months 13
to 18, and twice per month during months 19 to 24. This added
to the compliance factor.
Study limitations
As is common with large, lengthy trials, only bodyweight was
tested, not body composition. Diet and physical activity were
both self-reported, which is a double-whammy of inaccuracy. To
illustrate the error potential, I regularly refer to a trial by
Lichtman et al, which found that obese subjects who claimed to
be diet-resistant actually overreported their physical activity by
51%, and underreported their caloric intake by 47%.3
Transposing these figures over the the present trial, subjects
reported an intake of roughly 1550 kcal throughout the
intervention period, when in reality they could have been
consuming 47% more, equalling 2278 kcal. As well, reported
exercise output was assigned to be 1000 kcal/week for the
moderate treatment, and 2000 kcal/week fr the vigorous
treatment. Using Lichtman’s data (loosely assuming it’s
applicable to the present sample), these figures would be
reduced to 490 & 980 kcal/week, respectively. If we ignore
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 8
dietary underreporting and assume that only exercise output was
overreported, a minimum loss of about 2.2 kg (1 lb) per week
should have occurred among subjects by the 6 month mark,
totalling 11 kg (24 lb). By the end of the 6 months, weight loss
was 8-10% of total bodyweight, which translates to about 8 kg
(17.6 lb), which is significantly less than the projected figures.
Clearly, the subjects ate nowhere close to what they reported,
and the same misreporting goes for the amount of exercise done.
A significant limitation as far as I’m concerned was the lack of a
non-exercising control group. Recent research by Strasser et al
compared a 400 kcal/day deficit with diet alone with the same
deficit achieved by a combination of diet and exercise.4 No
significant differences in bodyweight or bodyfat reduction
occurred between the groups. The present trial would have been
a perfect opportunity to confirm or refute the results of Strasser’s
work, but alas, a control group was missing.
But even if a control group was included in the design, how
much would misreporting of intake and activity negate its
usefulness? From the standpoint of caloric expenditure, the
vigorous-intensity groups should have should have outperformed
the moderate-intensity groups for weight loss, but they did not.
This could be due to a couple of possibilities – either these
groups underreported their exercise intensity, or they indeed
reached the prescribed intensity, but compensated by eating
more. The latter explanation is supported by research suggesting
a direct relationship between exercise intensity and appetite
exists in women to a greater degree than in men.5
Comment/application
As seen by Shai et al (the other study I reviewed in this section),
weight loss was greatest at the 6 month point, followed by a
regain and plateau. In the present trial, there was a bit more of a
steady regain that persisted until the end of the trial period, by
which point 50% of the subjects’ lost bodyweight was regained.
An interesting question is, what makes the 6-month “sticking
point” so commonly observed? It almost appears that subjects
are pre-programmed to stop losing weight at the 6-month mark,
and slowly regain it. One possibility, which I’ve pointed out in
previous reviews, is the lack of a well-balanced exercise
program; one that includes progressive resistance training, which
undoubtedly would reduce bodyfat percent, support the retention
of lean mass, and possibly keep the participants engaged in the
program for a longer term.
In the present trial, the authors note that of 191 subjects, 47
(24.6%) were able to sustain a weight loss of 10% or more of
their initial body weight by the end of the intervention. This
successful subgroup not only had better dieting behavior, but
were more physically active, exercising approximately 338
minutes per week. This is the equivalent of 68 minutes a day, for
5 days a week. The authors conclude that the level of physical
activity necessary to sustain meaningful weight loss for 24
months is approximately twice the public health
recommendation for physical activity. They forgot to mention
that those who can double the intensity at least periodically
(without getting injured) can reduce that volume by up to 50%.
In the end, it appears that adherence to a diet and exercise
program is the main issue. The best protocol in the world won’t
work without compliance.
 

Plasma amino acid response after ingestion of different
whey protein fractions.
Farnfield MM, et al. Int J Food Sci Nutr. 2008 May 8:1-11.
[Medline]
PURPOSE: to examine the blood amino acid response to whey
protein isolate (WPI), beta-lactoglobulin-enriched WPI (BLG-
WPI), hydrolysed WPI (H-WPI) and a flavor-identical control.
METHODS: Eight healthy adults (four female, four male) were
recruited (age = 27 years; BMI = 23.2) and after an overnight
fast consumed 500 ml of each drink, each containing 25g
protein, in a cross-over design. Blood was taken at rest and then
every 15 minutes for 2 hours post-ingestion. RESULTS:
Ingesting the BLG-WPI drink resulted in significantly greater
plasma leucine concentrations at 45-120 min and significantly
greater branched-chain amino acid concentrations at 60-105 min
post ingestion compared with H-WPI. No differences were
observed between WPI and beta-lactoglobulin-enriched WPI,
and all protein drinks resulted in elevated blood amino acids
compared with flavour-identical control. CONCLUSION:
whole proteins resulted in a more rapid absorption of leucine and
branched-chain amino acid into the blood compared with the
hydrolysed molecular form of whey protein. SPONSORSHIP:
Dairy Farmers, Ltd (Australia).
Study strengths
This is one of those trials whose strength lies more in concept
rather than conclusiveness (since it’s an acute trial). In other
words, comparing the effect of whey protein subtypes is long
overdue. In the word of sports supplementation, claims are made
out the wazoo regarding the superiority of one type over another,
well now we finally have some comparative data to dig into.
This is the first study to date looking at the postprandial plasma
amino acid response after the ingestion of soluble proteins
delivered in different molecular forms. The dose used (25g)
seems sufficient enough to reflect what trainees use in the real
world, although it still might be slightly one lower end,
considering that larger strength athletes may use roughly double
that amount (the equivalent of 2 scoops of powder).
Study limitations
The big limitation here is the acute (short-term) nature of the
study. We’re left with only our imagination to speculate over
whether these results would prove meaningful if carried out over
a period of weeks or months. Also, we’re also left to speculate
over how the trained versus the resting state might affect the
metabolism of the different proteins. Another limitation is the
small sample size (8 participants).
Comment/application
Perhaps if not for the longstanding hype surrounding whey
hydrolysate’s extra-fast, and purportedly more anabolic effect, it
wouldn’t have been so amusing or surprising to see it get
decidedly stomped by the whole-protein isolates. But then again,
there has always been a sort of back-and-forth in the research
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 9
between casein (or casein-dominant protein) versus whey. One
of the more famous “battles” was a trial by Demling and Desanti
comparing Met-Rx (casein-based meal replacement) with Pro-
Score (whey-dominant protein supplement) using overweight
subjects on a resistance training program.6 The Met-Rx group
lost about double the bodyfat and gained double the strength
compared to the Pro-Score group. This was perhaps the first hint
that a casein-dominant protein wasn’t any slouch for
sports/fitness purposes compared to whey. However, I should
mention that as a meal replacer, Met-Rx contained carbohydrates
and the full range of essential vitamins & minerals. And since
the treatments were taken postworkout and again in 8 hours, it
possibly could have imparted a nutrient timing advantage.
Another possible explanation for the superior performance of the
casein-dominant mix is funding bias, but the sponsor of the trial
is not listed in the manuscript.
The unofficial ‘equalizer’ of the Demling trial was a more recent
study by Cribb et al, comparing a humorously high dose
(1.5g/kg/day) of either casein or whey isolate on trained subjects
undergoing a structured strength training program.7 The whey
used in the trial was a product called “VP2” by AST Sport
Science. Lean mass gains were roughly five times greater in the
VP2 group, which also lost a small amount of bodyfat, while the
casein group didn’t lose any. Strength gains were just about
double in the VP2 group. One possible confounder (other than
funding bias) was the VP2 group’s consumption of 250 kcal/day
more than the casein group. Again, funding source isn’t
explicitly listed, but they do disclose the fact that Cribb is a
consultant to AST. On AST’s website, he’s listed as their
director of research.
Back to the present trial... BLG-WPI had the highest leucine
content (13% higher than WPI, and 11% higher than H-WPI).
Total BCAA content in BLG-WPI was 8% higher than WPI and
6% higher than H-WPI. As such, the appearance of plasma
leucine was significantly greater from 45-120 min after ingesting
BLG compared with H-WPI. Also, BLG-WPI showed the
highest absorption of Leucine (and the rest of the BCAAs)
among the treatments. This could hint towards a greater anabolic
potential, but that remains to be tested long-term.
By the end of the 2-hour testing period, the differences between
WPI and BLG-WPI in total plasma amino acid elevations were
not statistically significant. However, both significantly
outperformed H-WPI. Leucine was better absorbed from the
BLG and WPI drink compared with H-WPI. Peak blood BCAA
levels occurred 60-75 minutes after ingestion. Contrary to what
was expected, H-WPI was actually absorbed more slowly than
the native (whole) proteins. In addition, blood amino acid levels
resulting from H-WPI ingestion declined rapidly at the 75
minute mark, while the other treatments kept amino acids
significantly elevated for another 45 minutes.
Since the whole protein isolates were more rapidly and better
absorbed (evidenced by sooner and greater areas of amino acid
appearance), the authors suspect that this may have important
implications for the rates of subsequent muscle protein synthesis.
This trial, like many others, just begs for a long-term version,
with a design perfectly applicable to fitness folks, of course.
 
Acute and long-term effects of resistance exercise with
or without protein ingestion on muscle hypertrophy and
gene expression.
Hulmi JJ, et al. Amino Acids. 2008 Jul 27. [Epub ahead of print]
[Medline]
PURPOSE: To examine the effects of timed ingestion of high-
quality protein before and after resistance exercise.
METHODS: In this study, young men were randomized to
protein (n = 11), placebo (n = 10) and control (n = 10) groups.
Muscle cross-sectional area by MRI and muscle forces were
analyzed before and after 21 weeks of either heavy resistance
training (RT) or control period. Muscle biopsies were taken
before, and 1 and 48 h after 5 x 10 repetition leg press exercise
(RE) as well as 21 weeks after RT. Protein (15 g of whey both
before and after exercise) or non-energetic placebo were
provided to subjects in the context of both single RE bout (acute
responses) as well as each RE workout twice a week throughout
the 21-week-RT. RESULTS: Protein intake increased (P </=
0.05) RT-induced muscle cross-sectional area enlargement and
cell-cycle kinase cdk2 mRNA expression in the vastus lateralis
muscle suggesting higher proliferating cell activation response
with protein supplementation. Moreover, protein intake seemed
to prevent 1 h post-RE decrease in myostatin and myogenin
mRNA expression but did not affect activin receptor IIb, p21,
FLRG, MAFbx or MyoD expression. CONCLUSION: In
conclusion, protein intake close to resistance exercise workout
may alter mRNA expression in a manner advantageous for
muscle hypertrophy. SPONSORSHIP: The Finnish Ministry of
Education and the Ellen and Artturi Nyysso¨nen Foundation
(Juha Hulmi personal grant).
Study strengths
The concept here is relatively fresh; this is the first study
examine protein supplementation on both acute and long-term
gene expression responses along with cross-sectional area and
maximal force of trained muscles. The 21-week trial duration
was lengthy compared to most trials in this particular area of
research, which typically span 8-12 weeks. Training sessions
were supervised by experienced staff. Cross-sectional area of the
quadriceps femoris was determined via magnetic resonance
imaging (MRI).
Study limitations
None of the subjects had prior heavy resistance training
experience, which can potentially restrict the applicability of the
results to novices. Accordingly, the training regime seemes
rather minimal, consisting of 2 whole-body resistance training
bouts per week. Sets per exercise were 2-3, which graduated up
to 3-5 in a periodized manner. Since the number of exercises per
muscle group were not specified, it’s difficult to speculate over
whether total volume was on the high or low end. Dietary intake
was self-reported, weakening the precision of the protocol. It
would have been ideal for the lab to control dietary intake via
food provision (at least to some capacity), but this is apparently
cost-prohibitive in most studies of this type. As is common
among sports supplemet studies, the sample size was small, with
11 participants in the whey group and 10 in the exercising
control. Finally, bodyfat was assessed via skinfold calipers, a
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 10
notoriously inaccurate means compared to other more “hands-
off” methods such as hydrodensitiometry and DEXA.
Comment/application
15g whey isolate was taken immediately before and immediately
after training. Pre- and postworkout solid meal timing was
purposely minimally restrictive, in order to assess whether or not
the protein supplementation had an additive effect despite
normal temporal meal ingestion. The subjects were instructed
not eat anything 60 minutes before and 30 minutes after training.
I find it difficult to believe that an additional 30g of whey twice
per week, timed around training, could have made any difference
at all, but according to these data, it did. I checked for dietary
imbalance between groups, and there were no significant
differences in the intake of any macronutrient. Protein intake by
both groups was approximately 1.4-1.5g/kg, which should be
sufficient for supporting size and strength gains.8,9 As a personal
field anecdote, I’ve seen the best results for size and strength
gains in client who consume 2-3g/kg. The chances of 30g whey
near training would augment gains at this level of protein intake
are slim, but this obviously has yet to be investigated.
Interestingly, of the 4 muscles comprising the quadriceps, only
the vastus lateralis increased in cross-sectional area by the end of
the trial. This increase was greater in the whey-supplemented
group, but not to a statistically significant degree. The authors
speculate that this is due to the exercise selection, which was
specifically designed to load the vastus lateralis, the muscle from
which biopsies were taken. Additionally, total body mass
increased and bodyfat percent decreased in both exercising
groups, without any significant difference between the groups.
In addition to macrostructural changes, this trial also examined
the microaspects of gene transcripts. Cyclin-dependent kinases,
considered one of the most important regulators of cell
proliferation (and hence tissue growth), increased significantly
after the resistance training only in the whey group. Myogenin is
an important regulator for muscle satellite cell differentiation (an
early point in the process of muscle cell growth). The ingestion
of supplemental whey around training prevented a decrease in
myogenin messenrger RNA. The authors speculated that whey
proteins or particular constituents within whey (such as leucine)
could affect anabolic regulators in muscle when its metabolism
is most active – such as during or immediately after training.
One major caution in accepting these results on face value is the
lack of control of the timing of the meal-based protein
surrounding training. It’s quite possible that a large amount of
meat, milk, or other high-quality protein source consumed near
the 60 minute preworkout and 30 minute postworkout cutoff
points could have negated the effect of the whey supplement.
But with this measure of control plainly missing, we can’t draw
any firm conclusions. If nothing else, whey is inexpensive and
happens to be easy on the stomach when consumed near
training. If it happens to have ‘magical’ hypertrophic effects, all
the better. I’m still skeptical that a small amount of whey can
have additive effects to higher amounts of daily protein (2-
3g/kg), in addition to high amounts of food-based high-quality
protein near training (40-60g pre & postworkout). I’d like to see
some replication, or at least a similar trial on trained subjects.
 

Lactate, fructose and glucose oxidation profiles in
sports drinks and the effect on exercise performance.
Azevedo JL, et al. PLoS ONE. 2007 Sep 26;2(9):e927.
[Medline
[Medline]
PURPOSE: To examine the effect of two sports drinks (one
with a lactate-polymer) on exogenous oxidation profiles and
exercise capacity. METHODS: 6 male Category 1 and 2
cyclists consumed CytoMax (C) or a leading sports drink (G)
before and during continuous exercise (CE). C contained lactate-
polymer, fructose, glucose and glucose polymer, while G
contained fructose and glucose. RESULTS: Peak power output
and VO2 on a cycle ergometer were 408 W and 67.4
mlO2/kg/min, respectively. Subjects performed 3 bouts of CE
with C, and 2 with G at 62% VO2peak for 90 min, followed by
high intensity (HI) exercise (86% VO(2)peak) to volitional
fatigue. Subjects consumed 250 ml fluid immediately before (-2
min) and every 15 min of cycling. Drinks at -2 and 45 min
contained 100 mg of [U-(13)C]-lactate, -glucose or -fructose.
Blood, pulmonary gas samples and 13CO2 excretion were taken
prior to fluid ingestion and at 5,10,15,30,45,60,75, and 90 min of
CE, at the end of HI, and 15 min of recovery. HI after CE was
25% longer with C than G (6.5+/-0.8 vs. 5.2+/-1.0 min). 13CO2
from the -2 min lactate tracer was significantly elevated above
rest at 5 min of exercise, and peaked at 15 min. 13CO2 from the
-2 min glucose tracer peaked at 45 min for C and G. 13CO2
increased rapidly from the 45 min lactate dose, and by 60 min of
exercise was 33% greater than glucose in C or G, and 36%
greater than fructose in G. 13CO2 production following tracer
fructose ingestion was greater than glucose in the first 45
minutes in C and G. Cumulative recoveries of tracer during
exercise were: 92% for lactate in C and 25+/-4.0% for glucose in
C or G. Recoveries for fructose in C and G were 75% and 26%,
respectively. CONCLUSION: Lactate was used more rapidly
and to a greater extent than fructose or glucose. CytoMax
significantly enhanced HI. SPONSORSHIP: CytoSport, Inc.
Study strengths
Participants were fit – not advanced competitors; but at least we
have the newbie factor controlled. In order to bolster the
reliability of sprint performance, subjects were studied twice
with a “popular brand” sports drink and three times with
Cytomax. A rather comprehensive set of parameters were tested,
which helps in the speculation over what mechanisms may have
been responsible for the results. Exercise testing was not a linear
moderate-intensity time-to-exhaustion protocol as traditionally
seen. But rather, it involved a high-intensity bout at the end (to
volitional fatigue), which might mirror actual race competition
more closely, since it typically involves nonlinear efforts,
including bouts of high intensity.
Study Limitations
Although I framed the latter point as a study strength, it’s merely
a single step up from linear, fixed intensity, time-to-fatigue tests,
which have poor reproducibility and reliability. Replacing the
high-intensity test portion (which was judged by maximal time-
to-fatigue) with a time-trial variants would have a more accurate
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 11
translation to race conditions. For example, a fixed-timeframe
wherein total work output is measured may have been even more
closely representative of actual race conditions. Another
alternative would be to measure the time it took to complete a
given workload, which is perhaps the most direct measurement
of performance as it pertains to a race. Finally, the study sample
was tiny (6 subjects), which according to most statistical
standards for adequately ‘powering’ an experiment, is a joke. A
sample this small is sometimes seen with pilot studies, but not
trials considered to be fully fledged.
Comment/application
No nutritional information breakdown was listed for the
“popular brand” sports drink, so I’m forced to assume (without
100% certainty) that it was Gatorade. No nutritional breakdown
was listed for Cytomax either. This is just lazy reporting on the
part of the authors. Funny enough, neither Cytomax nor
Gatorade list their ingredients on their official websites (only the
nutrient stats are listed). The reason for this omission is beyond
me. After some digging, I found both ingredient lists:
GATORADE
water, sucrose syrup, glucose-fructose syrup, citric acid, natural and
artificial flavors, salt, sodium citrate, monopotassium phosphate, ester
gum, sucrose acetate isobutyrate, yellow 5
CYTOMAX
Cytosport's Unique Complex Carbohydrate Blend Including Amylopectin
Starches And, Maltodextrins, Crystalline Fructose, Dextrose, Alpha-L-
Polylactate (Our Patented L-Lactate Formulation Containing Non-Acidic L-
Lactate Ionically Bound To L-Arginine), Citric Acid, Sodium Citrate, Natural
And Artificial Flavor, Malic Acid, Potassium Citrate, Ascorbic Acid, L-
Alanine, Glutamine, Acesulfame Potassium, Guar Gum, Xanthan Gum,
Magnesium Oxide, Caramel Color, Chromium Nicotinate, Monopotassium
Phosphate, Di-Calcium Phosphate, Magnesium Succinate, Potassium
Succinate, Calcium Succinate
To save space, here are the official website links to their other
label information: Gatorade, Cytomax. Sports drinks typically
contain more of the other electrolytes in sweat (potassium,
calcium, and magnesium). However, there’s insufficient
evidence that including electrolytes other than sodium and
chloride (accomplished with salt) is necessary or beneficial,
since the losses of these electrolytes are too small to have any
impact on performance or recovery.12-15
The inclusion of lactate in the sports drinks is not an entirely
novel direction in ergogenic research. As far back as 1991,
Fahey et al compared a the effects of polylactate solution with a
glucose polymer solution and found no differences in perceived
exertion during 180 minutes at 50% VO2 max, but no
performance aspects were measured.16 In 1994, Swensen et al
found that a polylactate solution had no measurable
physiological or performance effects compared to a glucose
polymer solution.17 Notably, polylactate beyond very low
concentrations caused severe gastrointestinal discomfort, a
characteristic also seen in later research by Peronnet et al.18
Based on the scant data available lactate has an unimpressive
50% success rate in research assessing its ability to enhance
endurance. For those who don’t mind betting on half a chance
that Cytomax works better than the “popular brand” according to
the manufacturer, I suppose the product is perfect for you.
 
1. Foster GD, et al. A randomized trial of a low-carbohydrate
diet for obesity. N Engl J Med. 2003 May 22;348(21):2082-
90. [Medline]
2. Stern L, et al. The effects of low-carbohydrate versus
conventional weight loss diets in severely obese adults: one-
year follow-up of a randomized trial. Ann Intern Med. 2004
May 18;140(10):778-85. [Medline]
3. Lichtman SW, et al. Discrepancy between self-reported and
actual caloric intake and exercise in obese subjects. N Engl J
Med. 1992 Dec 31;327(27):1893-8. [Medline]
4. Strasser B, et al. Fat loss depends on energy deficit only,
independently of the method for weight loss. Ann Nutr
Metab. 2007;51(5):428-32. [Medline]
5. Pomerleau M, et al. Effects of exercise intensity on food
intake and appetite in women. Am J Clin Nutr. 2004
Nov;80(5):1230-6. [Medline]
6. Demling RH, Desanti L. Effect of a hypocaloric diet,
increased protein intake and resistance training on lean mass
gains and fat mass loss in overweight police officers. Ann
Nutr Metab. 2000;44(1):21-9. [Medline]
7. Cribb PJ, et al. The effect of whey isolate and resistance
training on strength, body composition, and plasma
glutamine. Int J Sport Nutr Exerc Metab. 2006
Oct;16(5):494-509. [Medline]
8. Campbell B, et al. International Society of Sports Nutrition
position stand: protein and exercise. J Int Soc Sports Nutr.
2007 Sep 26;4:8. [Medline]
9. Tipton KD, Wolfe RR. Protein and amino acids for athletes.
J Sports Sci. 2004 Jan;22(1):65-79. [Medline]
10. Jeukendrup A, et al. A new validated endurance
performance test. Med Sci Sports Exerc. 1996
Feb;28(2):266-70. [Medline]
11. Schabort EJ, et al. A new reliable laboratory test of
endurance performance for road cyclists. Med Sci Sports
Exerc. 1998 Dec;30(12):1744-50. [Medline]
12. Coyle EF. Fluid and fuel intake during exercise. J Sports
Sci. 2004 Jan;22(1):39-55. [Medline]
13. Jeukendrup AE, et al. Nutritional considerations in triathlon.
Sports Med. 2005;35(2):163-81. [Medline]
14. Deuster PA, Singh A. Responses of plasma magnesium and
other cations to fluid replacement during exercise. J Am
Coll Nutr. 1993 Jun;12(3):286-93. [Medline]
15. Montain SJ, et al. Sweat mineral-element responses during 7
h of exercise-heat stress. Int J Sport Nutr Exerc Metab. 2007
Dec;17(6):574-82. [Medline]
16. Fahey TD, et al. The effects of ingesting polylactate or
glucose polymer drinks during prolonged exercise. Int J
Sports Nutr. 1991;1:249–256. [Medline]
17. Swensen T, et al. Adding polylactate to a glucose polymer
solution does not improve endurance. Int J Sports Med.
1994 Oct;15(7):430-4. [Medline]
18. Peronnet F, et al. Respective oxidation of 13C-labeled
lactate and glucose ingested simultaneously during exercise.
J Appl Physiol. 1997 Feb;82(2):440-6. [Medline]

Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 12 

Reflective re-cap: 7 new things I learned since January.
By Alan Aragon
Post-exercise insulin spiking isn’t necessary for most.
Post-exercise “insulin spiking” has become standard practice in
bodybuilding and fitness circles. Many people believe that
unless you consume a fast-acting liquid mix of amino acids or
protein hydrolysate plus quickly absorbed carbohydrate, you
won’t achieve the walloping insulin spike supposedly necessary
for recovery and growth. However, the insulin elevation required
to max out net anabolism is relatively minor, and what was news
to me was just how minor it is. One study showed that insulin’s
ability to prevent muscle protein breakdown (even in the midst
of ample amino acid availability via continuous infusion) was
maximal at about 2-3 times the normal fasting level of insulin.1
But to put things into perspective, a moderate-size mixed meal
can elevate insulin anywhere from 4-8 times fasting levels. The
researchers thus concluded that no rise in insulin availability is
necessary for amino acids to stimulate protein synthesis, and that
insulin’s suppression of protein breakdown is maximal with
modest elevations - less than seen during normal feeding. As a
matter of fact, a properly placed pre-exercise meal will keep
insulin sufficiently elevated even after your training bout is over.
As little as 6 g of essential amino acids plus 35 g sucrose taken
immediately pre-exercise kept insulin elevated to roughly 4
times fasting levels 1-hour after 40-50 minutes of resistance
training.2
Even doubling your daily fat requirement won’t hinder next-day
glycogen storage.
The reason folks are afraid of post-exercise fat intake is because
they’ve been told it will slow down muscle refuelling. However,
much of the principles of nutrient timing that the fitness
population clings to are only fit for a narrow range of endurance
sports. Nevertheless, silly tactics are used such as the avoidance
of postworkout fat for the goal of hurrying up glycogenesis.
What people don’t realize is that typical training for general
fitness, or strength and power sports is not glycogen-depleting.
Another thing that many don’t realize is that even in the event of
complete glycogen depletion, the presence of other
macronutrients has no bearing on the replenishment of glycogen
24 hours later.3 News to me was that as much as an additional
165g fat (55 g in the 3 meals postworkout) failed to reduce the
amount of glycogen resynthesis 24 hours after complete
depletion.4 This is the equivalent of adding 2 avocados, 6 tbsp
peanutbutter, or 4 tbsp oil to the 3 meals following your
workout. So much for worrying about post-exercise fat slowing
down recovery.
Postworkout caffeine can benefit the extreme endurance athlete.
Endurance athletes who train to glycogen depletion (which
involves 90-120 minutes of continuous work on a single muscle
group), and must use those same muscles competitively within
the same day need to worry about maximal speed of glycogen
restoration. Lucky for this population, the record for the highest
rate of glycogen synthesis thus seen in orally administered
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 13
conditions was recently set.5 This was achieved by ingesting
carbohydrate at roughly 1g/kg/hr for a total of 4g/kg by the end
of the 4 hr test period. For an average person weighting 74 kg
(162.8 lbs), this is 74 g carbs per hour, for 4 hours. This is the
equivalent of having 2 cups of rice or pasta per hour. For you
convenience freaks, a gel packets (or half a Clif bar) plus a 20 oz
bottle of Gatorade per hour for 4 hours post-exercise will do the
trick. In this study, no special designer carbs were used; just a
typical assortment of sports drinks, gels, and bars. In addition,
taking caffeine in two equal doses immediately post exercise and
after 2 hours of recovery for a total dose of 8 mg/kg increased
the rate of glycogen synthesis 66% higher than the non-
caffeinated group. So for example, a 74 kg (162.8 lb) person
would take 296 mg immediately after training, and then another
296 mg two hours later. Each 296 mg dose is the equivalent of
2-3 cups of coffee, or one and a half No Doz pills. I’d caution
that caffeine virgins should use half of this dose for a couple of
weeks before taking the full amount in order to minimize
stomach upset, jitters, and insomnia.
Supposedly “cutting-edge” forms of creatine are actually
inferior to the economical, widely available original.
Creatine monohydrate (CM) has established its legitimacy as an
ergogenic aid for repeated short bouts of high-intensity exercise.
So, why not forge ahead and attempt to improve it? Two of the
more publicized forms of creatine are Kre-alkalyn (KA), touted
for its resistance to acid degradation in the stomach, and creatine
ethyl-ester (CEE), claiming improved absorption into cells
which lowers the effective dose and causes less bloat. However,
these claims turn out to be meaningless, since these forms of
creatine are vulnerable to stomach acid breaking them down into
the inactive waste product, creatinine. This means that taking
KA or CEE results in significantly less of the active agent
reaching the final destination – muscle tissue. In recent research
by Tallon et al, the rate of creatinine formation from CM was
less than 1%, while KA supplementation resulted in 35% greater
conversion of creatine to creatinine in stomach acid.6 The same
researchers showed that CEE also rapidly degrades into
creatinine in stomach acid, while commercially available CM
remains virtually unaffected.7 So, not only are these products
over-hyped, they are actually inferior to the old standby. To
ensure you’re getting a high-quality creatine, check for the
CreaPure® seal on the label.
Whey protein hydrolysate is not superior to other forms.
In the world of protein supplementation (especially pre- and
post-exercise), the faster-acting protein is generally regarded as
superior for furthering net anabolism. The latter idea is debatable
given the current state of the evidence, but that’s another topic.
It’s logical to assume that protein hydrolysates, already pre-
digested into peptide fragments, would raise blood levels of
amino acids faster than whole proteins. However, Farnfield et al
recently found that both regular whey protein isolate and a beta-
lactoglobulin-enriched version of whey isolate caused a more
rapid absorption of amino acids into the blood than hydrolyzed
whey isolate.8 Not only that, but blood amino acid levels also
declined most rapidly in the hydrolyzed whey, giving it by far
the lowest plasma amino acid “area under the curve”. The two
whole proteins outperformed the hydrolyzed protein on both
 
speed of absorption and extent of amino acid elevation – so
much for the pricey hype of hydrolysates. The next step would
be to compare the anabolic effect of these treatments over a
period of months using a relevant study design. My guess is that
the differences would be close to nil, with a slight advantage to
whatever product is tied to the sponsor.
Fish oil is not the potent fat loss supplement it’s hyped to be
Fish oil is touted for a number of health benefits that are fairly
well supported, but when I kept reading about bold fat loss
claims, I had to take a closer look. Upon reviewing the literature,
I found that fish oil’s history as a fat loss aid is far from a slam
dunk; in fact it’s very hit-and-miss. The latest study by Hill et al
has potential application to athletes and active folks, since it’s
the first to examine the effects of fish oil supplementation with
aerobic exercise.9 The exercising fish oil-supplemented group’s
weight/fat loss is 2 kg more than the control group, which is
relatively modest but qualified as statistically significant.
However, it’s crucial to note that the daily intake of the
exercising fish oil group averaged 143.4 kcals less than the
exercising control group. This caloric difference would allow the
fish oil group to accumulate a 12,906 caloric deficit, which
would lead to 1.68 kg (3.7 lb) loss by the end of the trial.
According to the data table, the exercising fish oil group lost 2
kg (4.4 lb) more than the control group. So, factoring in the
reduced calories of the fish oil group, we’re now looking at a
difference of 0.32 kg (0.7 lb) – less than a pound in the span of
12 weeks. Talk about fishy claims. So, since you can’t put all
your stock in fish oil for fat loss, I have a secret for you:
decrease your caloric intake and/or increase your exercise for a
period of months. It works like magic.
Glycemic index: still useless after all these years
Ongoing attempts in the commercial and even the scientific
domain are made to justify the use of the glycemic index (GI)
for a number of interventions, including weight loss. Most you
reading are aware that GI is a measure of a food’s ability to raise
raise blood sugar, so it plays nicely into the (unfounded)
carbohydrate/insulin/obesity hypothesis. One of the many
problems with GI is that it’s calculated by measuring the blood
glucose area under the curve for only a 2-hour period. The
differences in GI between many foods would greatly diminish or
disappear if a reasonable post-ingestion timeframe like 4 hours
was observed. Yet based on this small duration, the entire worth
of a food often gets pre-judged. Furthermore, GI is calculated
after consuming an isolated food in an overnight fasted state. So
it doesn’t necessarily apply to any other meal in the day which
will have some degree of absorption overlap from the previous
meal. The glycemic response to a particular food can vary
considerably. Between and even within individuals, the response
can vary 23–54%.10 Even isolated glucose, the easiest
carbohydrate to accurately measure for glycemic effect, has
shown a 25% variation in the published reports.11
Since GI doesn’t account for the amount of carbohydrate in a
given serving of food, another metric has been developed called
glycemic load (GL), which factors in not only GI, but also the
amount of carbs in a given serving. In theory, GL should
represent a step forward in our carb judging criteria. However, in
Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 14
the one of the most meticulously controlled trials in the history
of diet research, investigators at Tufts University compared one
year of high- and low-glycemic load (GL) dieting.12 No
significant differences were seen in bodyweight or bodyfat
reduction despite 10% more protein & 20% less carbs in the
low-GL group. Unlike previous trials, this one used doubly
labeled water, a highly sophisticated means to track all of the
calories expended. It also used DEXA, the gold standard of
measuring body composition. And unlike other trials, food for
the first 6 months was prepared and administered by the lab,
leaving zero room for self-reporting error. The second 6 months
was designed to more closely mimic free-living, self-selected
eating conditions, and still no difference was found in body
composition between high and low GL diets. And no, this is not
an isolated outcome I cherry-picked to illustrate my point. The
majority of long-term studies (6 months or longer) in fact show
no benefit of a lower-GI diet for weight control.13-16
References
1. Greenaff PL, et al. Dose-response relationship during
hyperaminoacidaemia between insulin and leg protein
turnover in healthy young men studied by tracer amino acid
exchange. J Physiol. 2004;558P [J Physiol]
2. Tipton KD, et al. Timing of amino acid-carbohydrate
ingestion alters anabolic response of muscle to resistance
exercise. Am J Physiol Endocrinol Metab. 2001
Aug;281(2):E197-206. [Medline]
3. Roy BD, Tarnopolsky MA. Influence of differing
macronutrient intakes on muscle glycogen resynthesis after
resistance exercise. J Appl Physiol. 1998 Mar;84(3):890-6.
[Medline]
4. Fox AK, et al. Adding fat calories to meals after exercise
does not alter glucose tolerance. J Appl Physiol. 2004
Jul;97(1):11-6. [Medline]
5. Pedersen DJ, et al. High rates of muscle glycogen resynthesis
after exhaustive exercise when carbohydrate is coingested
with caffeine. J Appl Physiol. 2008 Jul;105(1):7-13. Epub
2008 May 8. [Medline]
6. Tallon MJ, Child R. Kre-alkalyn® supplementation has no
beneficial effect on creatine-to-creatinine conversion rates.
Presented at the 4th International Society of Sports Nutrition
(ISSN) annual meeting. [CR Technologies]
7. Child R, Tallon MJ. Creatine ethyl ester rapidly degrades to
creatinine in stomach acid. Presented at the 4th International
Society of Sports Nutrition (ISSN) annual meeting. [CR
Technologies]
8. Farnfield MM, et al. Plasma amino acid response after
ingestion of different whey protein fractions. Int J Food Sci
Nutr. 2008 May 8:1-11. [Medline]
9. Hill AM, et al. Combining fish-oil supplements with regular
aerobic exercise improves body composition and
cardiovascular disease risk factors. Am J Clin Nutr. 2007
May;85(5):1267-74. [Medline]
10. Sheard NF, et al. Dietary carbohydrate (amount and type) in
the prevention and management of diabetes: a statement by
the american diabetes association. Diabetes Care. 2004
Sep;27(9):2266-71. Review. [Medline]
 
11. Pi-Sunyer FX. Glycemic index and disease. Am J Clin Nutr.
2002 Jul;76(1):290S-8S. [Medline]
12. Das SK, et al. Long-term effects of 2 energy-restricted diets
differing in glycemic load on dietary adherence, body
composition, and metabolism in CALERIE: a 1-y
randomized controlled trial. Am J Clin Nutr. 2007
Apr;85(4):1023-30. [Medline]
13. Aston LM, et al. No effect of a diet with a reduced
glycaemic index on satiety, energy intake and body weight
in overweight and obese women. Int J Obes (Lond). 2008
Jan;32(1):160-5. [Medline]
14. Sichieri R, et al. An 18-mo randomized trial of a low-
glycemic-index diet and weight change in Brazilian women.
Am J Clin Nutr. 2007 Sep;86(3):707-13. [Medline]
15. Raatz SK et al. Reduced glycemic index and glycemic load
diets do not increase the effects of energy restriction on
weight loss and insulin sensitivity in obese men and women.
J Nutr. 2005 Oct;135(10):2387-91. [Medline]
16. Raben A. Should obese patients be counselled to follow a
low-glycaemic index diet? No. Obes Rev. 2002
Nov;3(4):245-56. [Medline]

Layne Norton is a friend of mine, so I may come off as biased by

recommending his DVD. However, you will be astounded that a
bodybuilder can string several coherent sentences together in
between sets. It’s worth seeing just for that. And I’m sure even
the advanced guys will get a few good ideas from this video, and
most of us will get a good motivational kick either way. Here’s
the trailer, more details can be found at his website.

Thanks once again for getting your wits filled with another
AARR issue. If you have any questions, comments, suggestions,
bones of contention, cheers, jeers, any feedback at all, send it
over to aarrsupport@gmail.com. All suggestions are taken very
seriously. I want to make sure this publication continues to stand
alone in its excellence.

Alan Aragon’s Research Review – August, 2008                                    [Back to Contents]                  Page 15