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ERD

Examine.com

Research Digest

Greg Nuckols

5 Year Anniversary Edition


1

From the Editor


First, we want to thank you for taking the time to check out the
Examine.com Research Digest (ERD). We feel a connection to those
who love to get their hands dirty, wading through interesting and
complex topics in nutrition and supplementation.
Examine.com was founded five years ago to help cut through the
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We responded with ERD, which covers new research in depth,
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Greg has always been a big supporter of ERD, so
we made this special anniversary issue for his
readers, containing five ERD articles he thought

The Examine.com
Research Digest is
my go-to resource for
nutrition information.
It helps keep up
up to date on the
latest studies that
are relevant to my
clients and I, and its
presentation and
readability make it
beneficial for both the
seasoned researcher
and the layman.
- Greg Nuckols

you would find interesting.


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2

Table of Contents
05

Beyond eat less, move more: treating obesity in 2016

11

High versus low fat diets for insulin sensitivity

19

Root rage: The impact of ashwagandha on muscle

28

Not-so-safe supplements

35

Throwdown: plant vs animal protein for metabolic syndrome

By Spencer Nadolsky, DO

More body weight means more risk for metabolic syndrome. But the question of
whether more fat (and especially saturated fat) impacts insulin sensitivity hasnt
been adequately addressed until now.

So called adaptogens like ashwagandha are typically studied for stress-easing


potential. A randomized trial looked into this popular herb for a different purpose:
bolstering adaptations to weight training.

Studies have shown that supplement buyers generally trust the supplements
they buy. That might not be the safest assumption, as dietary supplements that
are presumed helpful or neutral may sometimes cause serious side effects, as
quantified by this study.

The DASH diet is frequently tested in clinical trials, and often performs well. But the
diets formulation includes strong limitations on red meat, which may be based on
outdated evidence. This study compared animal-protein rich diets with a typical
DASH diet.

Contributors
Researchers

Margaret Wertheim
M.S., RD

Alex Leaf
M.S(c)

Courtney Silverthorn Zach Bohannan


Ph.D.
M.S.

Anders Nedergaard
Ph.D.

Jeff Rothschild
M.Sc., RD

Katherine Rizzone
M.D.

Spencer Nadolsky
D.O.

Greg Palcziewski
Ph.D. (c)

Editors

Gregory Lopez
Pharm.D.

Reviewers

Pablo Sanchez Soria Kamal Patel


Ph.D.
M.B.A., M.P.H.,
Ph.D(c)

Arya Sharma
Ph.D., M.D.

Natalie Muth
M.D., M.P.H., RD

Stephan Guyenet
Ph.D.

Mark Kern
Ph.D., RD

Gillian Mandich
Ph.D(c)

Adel Moussa
Ph.D(c)

Sarah Ballantyne
Ph.D.

Beyond eat less,


move more:
treating obesity
in 2016
By Spencer Nadolsky, DO

The mainstay therapy for obesity management among

ing point to getting a deeper understanding of obesity.

clinicians and researchers that dont specialize in obesity treatment is providing advice along the lines of
eating fewer calories and/or burning more calories.
Obesity is not thought of as a disease, but as a sequelae of laziness and lack of willpower. Many people say
put the fork down or push yourself away from the
table, implying that these are ways to manage obesity. Unfortunately, following this advice has a very low
success rate, which is why we need to shift the way we
think about obesity management.
To shift our perception of how to manage obesity, we
must first change our views of obesity itself. Instead of
being a result of sheer laziness, the pathophysiology
of obesity is actually quite complex. Sure, there is an
energy imbalance, leading to more energy stored as
opposed to burned, but the complexities go much deeper than this. Why does this happen? Does it happen the
same way in every person? Why cant people just lose
weight and keep it off? These questions are a good start-

Obesity as a disease
There was an uproar in the fitness community in 2013,
when the American Medical Association declared obesity a disease. Many people questioned why someone
who eats too much and moves too little should be classified as having a disease. I can understand where this
sentiment comes from, when it is said by someone that
does not understand obesity. However, the term disease
describes obesity very well.
A disease is defined as a condition of the living animal
or plant body or of one of its parts that impairs normal
functioning and is typically manifested by distinguishing signs and symptoms. In what ways does obesity not
fit this? How do other chronic diseases like hypertension and type 2 diabetes differ from obesity? You dont
die from hypertension, you die from the end result
of hypertension (e.g. myocardial infarction (MI) or a
cerebrovascular accident). Same with type 2 diabetes.

Many people say put the fork


down or push yourself away from the
table, implying that these are ways
to manage obesity. Unfortunately,
following this advice has a very low
success rate, which is why we need to
shift the way we think about obesity
management.
6

Obesity doesnt kill us through excess adipose tissue.


We die from the sequelae: obesity leads to hypertension,
which ends with an MI. If we arent looking at mortality, but instead quality of life, then think about type
2 diabetes leading to neuropathy, which causes awful
pain. Obesity also results in a lower quality of life due
to conditions like obstructive sleep apnea and osteoarthritis, not to mention the many other affected aspects
of health and quality of life.
Obesity is the leading precursor to many of these chronic
diseases. If we want to prevent these diseases, shouldnt
we be treating the underlying cause? The answer is yes,
of course. If we wouldnt hold back giving someone
with type 2 diabetes a medicine, then why would we
not provide someone with obesity effective treatments?
We will get into effective treatment options later.
But fat just sits there as an energy storage depot! This
is where the pathophysiology of obesity gets really
interesting. We used to think of adipose tissue as an
inert substance, basically serving as a warehouse for
energy until when we needed it later. Researchers have

People
with central
obesity and
the metabolic
derangements
that result from
this condition
are said to have
adiposopathy,
or sick fat.

found that our fat is the largest endocrine organ in our


body! As readers of ERD are aware, there are hormones
called adipokines that our fat tissue releases. These
adipokines have various effects on our bodies, some
good, some bad. Where we store our fat has an effect on
the types of adipokines released as well. People with an
apple shape, with fat stored centrally (visceral) tend to
have the more deleterious types of adipokines, whereas
people with a pear shape (subcutaneous) tend to have
the more benign adipokine profile.
People with central obesity and the metabolic derangements that result from this condition are said to have
adiposopathy, or sick fat. This term was coined by obesity researcher and clinician Dr. Harold Bays. Not only
is the fat hormonally active, but due to its location (near
the liver and portal vein), a higher flux of free fatty
acids throughout the body is stored in the muscle, heart,

and other area of the body. The increase in free fatty


acids and adipokines are thought to be the cause of the
metabolic issues we see with obesity, like insulin resistance, dyslipidemia, hypertension, and other conditions.
The idea of inert fat is old and needs to be buried.
What about people with the pear shape and subcutaneously stored adipose? The metabolic issues described
above may not be as relevant, but these people still have
a condition called fat mass disease. This is the consequences of having too much body mass, as mentioned
above, and it includes osteoarthritis, obstructive sleep
apnea, and even symptoms like reflux.
Either way, obesity be considered a disease. If we think
issues caused by lifestyle shouldnt be called diseases,
then we should stop calling type 2 diabetes and hyper7

tension diseases too. Yes, there are non-lifestyle causes

As a physician, I often see patients who are taking

of the aforementioned diseases, but the same can be

multiple medicines that are thought to be helpful for

said for obesity.

certain symptoms or disease, but which cause weight


gain as a side effect. Kids are being put on powerful

The cause(s) of obesity


Much to Gary Taubes dismay, the fault of obesity
doesnt rest on the shoulders of a single macronutrient
like carbohydrates. While refined carbohydrates play a
role in the disease, there are many other strong factors
pushing us towards larger waistlines.
Obesity researcher and ERD reviewer, Dr. Stephan
Guyenet, often discusses food reward and hyper palatability of food. What seems as simple as avoiding
certain high caloric foods becomes a much tougher task

antipsychotics for an off-label use, without regard that


they will likely experience weight gain and metabolic derangement. Heck, many of my patients use over
the counter antihistamines, which could account for a
few pounds of weight gain if used chronically. For an
exhaustive list of medicines that cause weight gain, refer
to my book, The Fat Loss Prescription.
Of course, genetics also play a role in our body weight.
Researchers are constantly finding various single nucleotide polymorphisms (SNPs) related to our weight. We

[...] many of my patients use over


the counter antihistamines, which
could account for a few pounds of
weight gain if used chronically.
when scientists are trying to create foods that cause our
brain wiring to short circuit and crave more of them.
Our appetite regulation also doesnt rely only on the
volume of food we eat. The layers of complexities run
much deeper. The adipokines mentioned above and the
subsequent inflammation can disrupt our appetite and
food reward signaling. This partially explains why it
might be hard to lose weight once we have gained it.
The microbiome is also involved (another favorite of

cant do anything about our genetics. Even more annoying, we dont have control over what our parents and
grandparents did, which may have had a large effect on
our weight, too. Epigenetics, another fun ERD topic,
has been studied more recently in the context of obesity.
Turns out the effect our parents had on us in utero was
stronger than we once thought, and we may be more
likely to store fat than if our parents had chosen different lifestyles.

ERD readers). Its possible the bacteria in our guts con-

What can we do though?

trol part of our appetite and cravings. Even viruses have

Inevitably when I discuss this topic with someone who

been implicated in weight gain, like adenovirus-36.

is an eat less, more more pusher, they point out that


8

we still do need to eat less


and move more. They are
absolutely correct, but we
also need to find out how to
get the individual to be able
to actually do so.
There is a reason that weight
regain after initial weight
loss is so common. The environment, genetic, epigenetic,
biological, physiological, and
psychological drivers all collaborate to force us back the
wrong way. Think about all
of the people you know that
have obesity. Think of those
with obesity who have lost
weight. Have most kept it off
successfully? If most of the
people you know that have
had obesity in the past have
now lost the weight and kept
it off, then I want you to find
out their secret and patent it.
Research shows that unfortunately lifestyle counseling

Lets face it,


dieting is not
fun and often
our hunger and
cravings get the
best of us. The
forces that drive
us to regain are
strong and we
need strong
treatments to
combat them.

by itself is not very successful. This is due to the factors described above.

will help them with their


lifestyle.
Many fitness professionals
balk at the idea of a medicine that helps with weight
loss. The truth is that these
medicines work in the brain
to actually help you eat less
and move more. Instead
of feeling miserable on a
diet and feeling driven to
eat highly palatable foods,
these medicines work in the
parts of the brain that contain our appetite and food
reward centers to take the
edge off. As explained above,
our brains may not be functioning properly due to our
weight and other factors.
Why not use a deemed safe
medicine to push back the
other way, toward weight
loss?
There are currently four
medicines approved for

long-term weight loss in the U.S. Each work in different


ways in our brain to help with lifestyle adherence. Since

Lets face it, dieting is not fun and often our hunger

safety is a concern, there are long-term trials currently

and cravings get the best of us. The forces that drive us

going on to ensure the adverse effects of these medi-

to regain are strong and we need strong treatments to

cines are minimal and that our treatment of obesity is

combat them.

saving lives and/or improving quality of life.

As an obesity medicine specialist, my goal is to find the

While I am a medical bariatrician (nonsurgical weight

linchpin in a patients road map for long-term obesity

loss physician), I do understand that weight loss sur-

success. This includes creating a lifestyle they can follow

gery is actually the most powerful tool we have when

for life, making sure they are not on any medicines that

fighting obesity. Just like medicine, the surgery isnt a

cause weight gain or inhibit weight loss, and deciding

magical procedure that automatically makes someone

on whether they need a medicine and/or surgery that

lose weight and keep it off forever. Surgical weight loss


9

is another method that allows patients to stick to a life-

drivers of obesity (adipokines, gut hormones, micro

style over the long term and have a much higher chance

biome, etc). No matter the reason they work, they are the

of success than without (in many cases). In fact, weight

most efficacious treatment we have right now for obesity.

regain (bariatric surgery recidivism) is common when


So, do we still believe that obesity is just a matter of

the new lifestyle is not adhered to.

pushing ourselves away from the table? As heard


There are multiple bariatric surgeries available today,

from ERD reviewer and renowned obesity researcher

but the most common are the roux en y gastric bypass

Dr. Arya Sharma at an obesity conference, we wouldnt

and the vertical sleeve gastrectomy. It was thought these

tell someone with depression to just cheer up. Why

worked by shrinking the size of our stomach and there-

would we tell someone with obesity to just eat less and

fore our ability to eat large portions, but we are now

move more?

finding these procedures also affect the aforementioned

Dr. Spencer Nadolsky is a board certified Family Medicine Physician


and a Diplomate of the American Board of Obesity Medicine. He is
the medical editor for Examine.com. Dr. Nadolsky is the author of
The Fat Loss Prescription, now available on Amazon.com.
His love for lifestyle as medicine began in athletics, where he
worked using exercise and nutrition science to succeed in football and wrestling. After wrestling at UNC Chapel Hill as a Tar Heel
heavyweight and earning a degree in exercise science, he headed to Edward Via College of Osteopathic Medicine in Blacksburg.
During medical school, Dr. Nadolsky attended multiple obesity
medicine conferences and realized that he wanted to apply the same nutrition and exercise
information he learned during his athletics to the general population and health. After medical
school, he attended VCUs Riverside Family Medicine Residency in Newport News to hone his
skills. He is currently practicing in Olney, Maryland. He launched the book Skinny on Slim and
has a blog called Through Thick and Thin.

10

High versus low fat diets


for insulin sensitivity

A high-fat, high-saturated fat diet decreases


insulin sensitivity without changing intraabdominal fat in weight-stable overweight
and obese adults

11

Introduction
Insulin is a hormone that regulates several physiological
functions, such as promoting glucose uptake from the
blood, inhibiting glucose release by the liver, and inhibiting fatty acid release from fat tissue. Insulins role is so
central to our survival that nearly every cell in the body
contains insulin receptors. When these cells become
less sensitive to insulins signal, more insulin must be
secreted by the body to compensate. This combination
of insulin resistance and compensatory hyperinsulinemia may be a fundamental driver of metabolic
syndrome and non-alcoholic fatty liver disease.
As depicted in Figure 1, typical insulin resistance is
thought to be caused in part by excessive inflammation
brought about by an abundance and dysfunction of fat
cells. The last few decades has seen an accumulation of
evidence showing that fat surrounding organs (visceral
or intra-abdominal) is particularly detrimental in this
regard. However, the traditional view that fat beneath
the skin (subcutaneous) is less detrimental or even

protective when compared to visceral fat has been challenged recently. In either case, the commonality is that
there is an excess amount of fat tissue.
Weight loss has been shown to reduce inflammation
and increase insulin sensitivity. Moreover, improvements in insulin sensitivity have been shown to
correlate most strongly with the magnitude of change
in visceral fat. Indeed, fat loss appears to be the primary determinant of improvements in insulin sensitivity
regardless of whether the individual is consuming a
low-fat or low-carbohydrate diet. However, not everyone who is over-fat and insulin resistant is actively
seeking to lose weight.
The study under review sought to examine the effects
of diets differing in their total and saturated fat content on measures of insulin sensitivity and glucose
tolerance during weight-stable conditions. Researchers
also investigated whether these changes were mediated
through changes in body fat distribution.

Figure 1: How inflammation may contribute to the development of diabetes

12

ticipants actually ate all their assigned foods and no


Insulin resistance is considered a hallmark of met-

non-study foods. Still, this design is quite rigorous and

abolic syndrome and fatty liver. It is commonly

far more accurate than just asking people what they ate

brought about by fat cell-mediated inflammation.

using a food frequency questionnaire or dietary recall.

Although fat loss has been shown to improve insulin


sensitivity and inflammation regardless of dietary

The participants consisted of a small group of mid-

composition, not everyone who is insulin resistant

dle-aged obese men (n=10) and women (n=3). Despite

and inflamed is seeking to lose weight. Thus, the

having an average BMI of 33.6, all the participants

current study sought to compare the effects of a high-

had normal glucose tolerance based on fasting and

fat diet to a low-fat diet on insulin sensitivity during

two-hour glucose levels after a standard oral glucose

weight-stable conditions.

tolerance test. However, NAFLD was present in 7 out of


13 participants.

Who and what was studied?


This was a randomized, controlled, crossover feeding
study with two four-week intervention periods. Each
intervention period was preceded by a 10-day control diet and separated by a six-week washout period.
During the control and intervention periods, all food
was provided to the participants in amounts designed
to maintain bodyweight. Each participant picked up
their food for off-site consumption and was weighed

The two intervention diets (broken down in Figure 2) were:


A high-fat diet (HFD) containing 55% of calories
from total fat, 25% from saturated fat, 27% from
carbohydrates, and 18% from protein, and ...
A low-fat diet (LFD) containing 20% calories from
total fat, 8% from saturated fat, 62% from carbohydrates, and 18% from protein.

twice weekly.

The control diet mimicked a standard American diet

Dietary compliance was monitored with a checklist,

47% from carbohydrates, and 18% from protein.

with 35% calories from total fat, 12% from saturated fat,

meaning that there was no guarantee that the par-

Figure 2: Kinds of fats in the different diets

13

The major sources of fat in all three diets were butter


and high-oleic (meaning high-monounsaturated fat)

This was a randomized, crossover, controlled feeding

safflower oil. Additionally, vegetable content between

study in which 13 middle-aged obese men and wom-

diets was matched, inulin fiber was added to the HFD

en with normal glucose tolerance consumed a low-fat

to match the LFD fiber content, and fructose was lim-

(20% fat, 8% saturated fat) or high-fat (55% fat, 25%

ited to less than 15 grams per 1000 kcal in all diets.

saturated fat) diet for four weeks each. Gold stan-

However, fructose content was not matched between

dard measurement methods were used to determine

diets, being roughly 4.5-fold greater in the LFD com-

body composition, abdominal and liver fat, insulin

pared to the HFD. Aside from knowing that the diets

sensitivity, and -cell function after each dietary

were based on typical American foods, we dont know

intervention period.

what specific foods were being eaten by the participants.


Study assessments were performed at the end of the
control diet and intervention diet phases. Body composition was assessed with DXA, abdominal fat was
assessed with MRI, and liver fat was assessed with
magnetic resonance spectroscopy (MRS). These measurement methods are all considered gold standards for

What were the findings?


Since this was a crossover study, the participants served as
their own controls for analysis. However, only seven participants completed both the LFD and HFD interventions,
whereas the other six completed only one. Therefore, a
lack of statistical power to detect differences between the

their respective uses in this study.

LFD and HFD is a potential limitation of this study.

Whole-body and liver-specific insulin sensitivity were

As intended by the study design, bodyweight remained

assessed with the hyperinsulinemic-euglycemic clamp.


This method was discussed previously in ERD #8, Blast
from the past: a paleo solution for type 2 diabetes, and is
widely accepted as the gold-standard for directly determining insulin sensitivity in humans. The clamp data
was complemented by an intravenous glucose tolerance
test (IVGGT), which provided information about insulin sensitivity, glucose tolerance, and -cell function.

stable during the LFD and HFD periods relative to the


respective control periods that preceded them. Despite
a stable bodyweight, the HFD showed a significant 6%
increase in subcutaneous fat, and the LFD showed a
significant 22% reduction in liver fat (absolute change
from 9.4 to 7.2%).
Figure 3 shows some of the main study results. The
hyperinsulinemic-euglycemic clamp data suggests that

Figure 3: How the high-fat diet compared to the low-fat diet

14

whole-body insulin sensitivity was reduced by 12-19%

associated with changes in VLDL concentrations of

on the HFD only, and this change was significantly

the omega-6 fatty acid docosapentaenoic acid (22:5

different from the non-significant increases observed in

n6). Additionally, only in the LFD was increased pal-

the LFD. Therefore, the HFD impaired the bodys ability

mitic acid predictive of increased insulin resistance in

to uptake glucose compared to the control diet and LFD.

the liver. No associations with insulin sensitivity were


observed for visceral fat, the subcutaneous to visceral

The reduction in whole-body insulin sensitivity appears

fat ratio, or liver fat.

to be primarily attributable to reduced insulin sensitivity in tissues other than the liver, since liver insulin
sensitivity wasnt different between the two intervention
diets (according to measures of endogenous glucose
production and hepatic insulin resistance).
The IVGTT data largely support the hyperinsulinemic-euglycemic clamp data. Glucose tolerance was

Four weeks on an HFD led to significant reductions


in the insulin sensitivity of tissues other than the liver, whereas the LFD led to significant improvements
in glucose tolerance and reductions in liver fat. These
changes were not related to changes in visceral or
liver fat.

significantly greater during the LFD compared to the


control diet and HFD. However, the HFD was not significantly different from the control diet and neither the
LFD or HFD affected beta-cell function.
The fatty acid composition of VLDL was also assessed
after each diet, with no significant changes observed for
the HFD. However, the LFD led to significant increases
in the relative proportions of stearic and palmitoleic
acid, a trend for an increase in palmitic acid, and a significant decrease in linoleic acid.
Finally, correlational analyses revealed that changes in
insulin sensitivity in both diets were positively associated with changes in subcutaneous fat and negatively

What does the study really


tell us?
This study suggests that a high-fat, high saturated fat
diet reduces whole-body insulin sensitivity within a relatively short timeframe of four weeks, but that a low-fat,
low saturated fat diet does not improve insulin sensitivity compared to a standard American diet.
One possible explanation for the detrimental effect of
the HFD but lack of positive effect in the LFD is that
the effects were mediated by the saturated fat content
rather than the total fat content of the diets. Insulin

No associations with insulin


sensitivity were observed for visceral
fat, the subcutaneous to visceral fat
ratio, or liver fat.
15

resistance is directly correlated to the amount of sat-

that of the current study (62% of calories). Additionally,

urated fat stored within the muscle (intramuscular

the proportion of stearic acid was increased, and there

triglycerides), as well as the proportion of saturated

is evidence in mice that this may be involved in insulin

fatty acids contained within the muscle cell membranes.

resistance of the liver.

Both of these have been shown to reflect the fat composition of the diet. As such, consuming a high saturated

It is tempting to add support to the DNL hypothesis by

fat diet would be expected to increase the amount of

noting the disproportionate intake of fructose among

saturated fat within the muscle tissue, which in turn

the LFD and HFD. However, this difference amount-

increases insulin resistance.

ed to 35 grams per day with a total fructose intake in


the LFD being around the

The above is in agreement


with the current study findings. It is possible that the
difference between the 12%
saturated fat content of the
control diet compared to the
to 8% of the LFD was not
pronounced enough to have
an effect on skeletal muscle
fat composition and insulin
sensitivity. By contrast, the
increase from the control diet
to the HFD was quite large
(12% to 25%). However, this
study was not designed to
investigate the specific effects
of saturated fat. The researchers changed two variables at
once, total and saturated fat,
and this precludes us from
determining which mediated

[...] the small


sample size
was a notable
limitation of
this study. Many
of the effects
were large but
not statistically
significant.

the observed outcomes.

average intake of Americans.


As discussed in ERD #9,
Fructose: the sweet truth,
fructose use in experimental trials averaged more
than double this amount,
often in isolation. Moreover,
fructose does not appear to
have a detrimental impact
on liver fat accumulation
when exchanged for other
carbohydrates with total
caloric intake held constant.
It therefore seems unlikely
that the difference between
the groups in fructose intake
played any substantial role in
the observed outcomes.
As already mentioned, the
small sample size was a
notable limitation of this

study. Many of the effects were large but not statistically


Alternatively, it is possible that the lack of benefit from

significant. This is why future work with a larger sample

the LFD was owed to an increase in deleterious met-

size is needed to corroborate this study.

abolic pathways that counterbalanced any beneficial


effects. The observed increase in the proportion of pal-

Another limitation is that the saturated to unsaturat-

mitic acid within the VLDL particles during the LFD

ed fatty acid ratios of the diets were not matched. It

may reflect an increase in de novo lipogenesis (DNL, or

has been argued that the quality of dietary fat is more

the synthesis of new lipids in the body), which is also

important than the quantity of fat with regard to insulin

known to occur with high carbohydrate intakes such as

resistance and the development of metabolic syndrome.


16

There is also evidence to suggest that a threshold for fat

high-fat (50-55%) and low-fat (20-25%) diets for two to

intake exists, below which mono- and polyunsaturated

three weeks with no observed changes in insulin sensi-

fatty acids have a more favorable impact than saturated

tivity. Unfortunately, these studies do not indicate how

fatty acids, but above which all fatty acids are similarly

much of the fat was saturated. However, an 11-day study

detrimental to insulin sensitivity. This threshold was

in healthy men failed to show a difference in peripher-

suggested to be 34% of calories. Thus, the different ratios

al insulin sensitivity they ate diets with zero, 41%, and

could have had a different impact on the LFD with its

83% of calories from total fat when the ratio of saturat-

20% total fat, compared to the 55% total fat of the HFD.

ed to unsaturated fatty acids remained constant.

Despite these limitations, the control diet preceding

The primary difference between these studies and the

each intervention diet was an important strength of

current one is the population. The study under review

this study as it allowed for a standardization of dietary

was in obese (BMI of 33.6) individuals, while the above

parameters before making changes and eliminat-

studies were not. It is possible that the reduction in insu-

ed the possibility that the participants habitual diet

lin sensitivity is owed to an inability to readily switch

confounded the results. Additionally, the methods of

fuel sources, often referred to as metabolic flexibility.

measurement were all considered to be at or near gold


standards, thus lending strong support that the observed

The current study also showed no improvement in

outcomes were not a result of measurement error.

insulin sensitivity with a low-fat, low saturated fat diet.


This is in contrast to a study analyzing 548 participants

Several questions that remain include the effects of a

across five different dietary interventions that showed

very-low carbohydrate or ketogenic diet (with fat less

that insulin sensitivity increases when consuming a diet

than 10% of daily calories), the effects of consuming

containing 28% total fat and 10% saturated fat. This

more protein, the effects of physical activity, the effects

may be owed in part to the type of carbohydrate being

of carbohydrate type and quality, the effects of different

consumed. The current study modeled the standard

types of fatty acids, and the effects over the long-term.

American diet in food choice, while this other study


utilized low-glycemic carbohydrates. Notably, one

This study suggests that a high-fat, high saturated


fat diet reduces whole-body insulin sensitivity when
compared to a low-fat, low saturated fat diet and
standard American diet (control). However, the study
design precludes conclusions about the cause.

of the other five dietary interventions was the same


low-fat prescription with high-glycemic index carbohydrates, and this dietary group actually worsened their
insulin sensitivity.
In both this and the abovementioned study, the participants were obese. It does also appear that DNL is more

The big picture

pronounced in overweight-obese men compared to lean

The current study supports the notion that a high-fat,

hydrates override any potential benefit of a low-fat diet.

high saturated fat diet impairs insulin-mediated glucose


uptake into tissues other than the liver. However, not

men, and this may explain why higher glycemic carboHowever, we cannot make any definitive conclusions.

all experimental evidence does. Two other studies that


utilized the hyperinsulinemic-euglycemic clamp had
overweight and primarily normal-weight men consume

17

blood and tissue, and adverse health outcomes such as


It appears that the effects of high- and low-fat diets

metabolic syndrome in adults and adolescents, hyper-

on insulin sensitivity are dependent on the carbohy-

triglyceridemia, type-2 diabetes, coronary heart disease,

drate quality of the diet and the metabolic flexibility

and prostate cancer. However, since none of these stud-

of the individual. High-fat diets may be more detri-

ies establish causality, it is possible that these conditions

mental in overweight-obese individuals because of

lead to higher proportions of palmitoleic acid.

an inability to readily switch between using glucose


and fat for energy. Low-fat diets may only confer
benefits when the increased carbohydrates come
from low-glycemic sources.

What should I know?


Consuming a high-fat, high-saturated fat diet may
be detrimental to insulin sensitivity if you are
overweight-obese, and consuming a low-fat, low-sat-

Frequently asked questions

What is DNL and why is it seen as detrimental?

A consequence of overconsumption of carbohydrates


is increased de novo lipogenesis (DNL), which is a
process that involves the synthesis of fatty acids from
non-lipid sources. The major end-product of DNL is
the saturated fat palmitic acid, which can be desaturated within the body to form the monounsaturated fat
palmitoleic acid.

urated fat diet may be beneficial if you are consuming


low-glycemic carbohydrates. However, there are many
potential confounding variables that prevent drawing
firm conclusions, and this small study does not address
many of these.

The most annoying answer to any research question is


it depends. Yet that is the answer to many questions,
including the one of fat impact on glucose regulation.
Talk it over at the ERD Facebook forum.

There are numerous studies showing associations


between higher proportions of palmitoleic acid in

18

Root rage: The impact


of ashwagandha on
muscle
Examining the effect of Withania
somnifera supplementation on muscle
strength and recovery: a randomized
controlled trial.

19

Introduction

ashwagandha in humans may decrease the stress hor-

Being stressed sucks. However, stress has its benefits.


Its been long-known that a moderate amount of psychological stress can improve physical performance.
And, as many of our readers probably know, exercise is
a stressor on the body that actually strengthens it in the
long run.

mone cortisol, increase testosterone, and even improve


cardiovascular performance. Yet many of these studies
were published in lower-impact journals, which may
somewhat call into question the validity of the results.
With that many effects to its name, it is plausible that
ashwagandha may also be beneficial for strength train-

Recently there has been increased interest in a class


of herbal supplements known as adaptogens (some

ing. This is the question the authors of the study under


review intended to answer.

common ones are shown in Figure 1). Adaptogens are


purported to help the body cope with both physical and

Ashwagandha is classified under the loose umbrella

mental stressors. Well-known examples of adaptogens

of adaptogen, meaning an herbal supplement that

include ginseng and rhodiola.

helps the body cope with stressors. The purpose of


this study was to determine if ashwagandha sup-

Another adaptogen that may help in this context is the

plementation could improve strength gains during

root of Withania somnifera, also known as ashwagand-

resistance training.

ha, Indian Ginseng, or Winter Cherry. Ashwagandha


is a perennial shrub that grows primarily in parts
of Asia, and is a member of the nightshade family.
Ashwagandha root is classified in traditional Indian
Ayurvedic medicine as a rasayana, or a rejuvenator.
Initial research on ashwagandha has indicated that it
may live up to this classification. Supplementation of

Who and what was studied?


Healthy men aged 18-50 were recruited for this study.
People were excluded if they took performance-enhancing medications, smoked or drank excessively,

Figure 1: Some common adaptogens

20

had an injury in the past six months. Researchers also

Secondary endpoints were also measured. These

excluded participants if they had medical conditions

included muscle size as measured on the mid-upper

deemed problematic for the study. Participants were

arm, chest, and upper thigh, body fat as measured by

also excluded if they engaged in resistance training in

bioelectrical impedance, serum testosterone, and serum

the past 18 months. Fifty-seven men who met these

creatine kinase (a measure of muscle damage caused

criteria were recruited for the study. They were asked

by exertion) 24 and 48 hours after working out at the

not to take anti-inflammatory medications for the eight

beginning and end of the study. Participants were also

weeks duration of the study.

asked to report any side effects.

The participants were then randomized to receive either


twice-daily placebo (28 people) or 300 milligrams of
KSM-66 twice-daily (29 people). KSM-66 is a commercial high-concentration ashwagandha water extract
standardized to 5% withanolides, one of the primary
active ingredients found in ashwagandha.
Both groups then began the same resistance training

Healthy men were randomized to take either placebo or 300 milligrams of ashwagandha twice a day
during eight weeks of resistance training. Strength
gains before and after were measured as the primary
outcome, along with a host of secondary outcomes,
including muscle size, body fat, testosterone levels,
and serum creatinine kinase.

program. The program consisted of two weeks of an


acclimation phase consisting of multiple free weight
and machine exercises done until failure, with a goal of
15 reps. This phase was followed by six weeks of a periodization scheme, where the target reps per set rotated
between 5-13 on different days, with the weight also
being adjusted accordingly.
The main outcome measured for this study was strength
gains as measured by the one repetition maximum
(1RM) for leg extension and a machine bench press.
Similar exercises were part of the training protocol.
These were measured on the first day of the acclimation
phase and two days after the eight-week training protocol was complete.

What were the findings?


Three people in the placebo group and four people in
the treatment group stopped the resistance training
program before completing the study, leaving 25 people
in each group who completed the study. There were no
major side effects or adverse events in either group.
The study findings are summarized in Figure 2. At the
end of the eight weeks, both groups gained strength.
However, the ashwagandha group seemed to outperform the placebo group. The ashwagandha group
improved their bench press 1RM by a whopping 20
kilograms (or 44 pounds) more than the placebo group

With that many effects to its name,


it is plausible that ashwagandha may
also be beneficial for strength training.
21

Figure 2: Gains over placebo from ashwagandha


supplementation combined with resistance training

(46 kilogram or 101 pound gain vs. 26 kilogram or a 57

Serum testosterone rose in the ashwagandha group by

pound gain). The 1RM gains for the leg extension exer-

about 15%, while it remained unchanged in the place-

cise of the treatment group was about 4.5 kilograms

bo group.

(10 pounds) more than the placebo groups gains (14.5


kilograms vs. 9.8 kilograms or 32 vs 22 pounds). Each

Finally, muscle recovery, as measured by serum creatine

of the differences between groups were statistically sig-

kinase levels found in the blood 24 and 48 hours after

nificant, and will be discussed further later.

working out, improved in both groups over the eight


weeks. The ashwagandha group improved more, to a

Both groups also gained muscle size over the eight-week

statistically significant degree. However, the difference

trial. The ashwagandha group gained more size in the

between the two groups after the eight weeks was much

upper arm. They also had an increased chest girth of

smaller than the improvement over the eight-week

about two centimeters more than the placebo group, on

trial in both groups: the serum creatine kinase levels

average. Thigh size was not different between the groups.

after working out in both groups dropped around 100fold over the eight weeks. But the difference between

Both groups also reduced their body fat percentage.

the two groups at the end of the study was only about

Both groups started at around 22% body fat. The pla-

five-fold. In other words, training over time accounted

cebo group dropped by 1.5%, while the ashwagandha

for most of the improved muscle recovery seen in this

group lost about 3.5%, which was also a statistically

study, and not supplementation.

significant difference.
22

How does resistance training


affect testosterone levels?
In general, serum testosterone rises immediately following resistance training in men, but
returns to baseline, or even below baseline, after about 30 minutes. Several factors may
affect the specific testosterone response to working out, however. For instance, high intensity or high volume alone isnt enough to induce a testosterone response. A response is
induced by meeting a minimum threshold for both.
In women, some studies have also found short-term increases in serum testosterone, but
others havent, so the results are more equivocal.
The measurements of serum testosterone taken in this study were done prior to any activity, so the fact that the placebo groups levels remained unchanged between the initial and
final measurements isnt out of the ordinary, since they were both taken in the morning,
before resistance training sessions started.

Firstly, although the gains seen in the bench press and


The ashwagandha group gained a lot more strength

leg extension 1RM seemed quite large, they also had

in the bench press and moderately more strength

a pretty large error associated with them. For instance,

in the leg extension compared to the placebo group.

the 95% confidence interval (essentially the range of

They also lost more body fat, bulked up a little more,

values you can be 95% confident the real value lies

had a higher testosterone level, and recovered faster.

within) for the 1RM gain for the ashwagandha group in

No side effects were reported.

the bench press was 36.56-55.54 kg and for the placebo


group 19.52-33.32 kg. Note that the lower estimate of

What does the study really


tell us?
The results of this study seem to be pretty impressive at
first glance, perhaps even unbelievable. Especially the
gains seen in the bench press, which were almost double that of the placebo group. In short, this study found
that ashwagandha supplementation, when combined
with a sensible resistance training program, improves
strength and size in previously untrained men, and
with no reports of side effects to boot.
However impressive these results seem, though, there
are some important limitations.

36.56 for the ashwagandha group is close to the higher


estimate of 33.32 for the placebo group. So, there may
be a difference between groups, but the data from this
study are consistent with the difference being small. For
the leg extension, the 95% confidence intervals between
ashwagandha and placebo actually overlap, so there
could in theory be no difference in that measurement.
In short: the large gains in strength seen in this study
could be in large part just due to chance.
In addition, this was only an eight-week study. Thus,
the safety and efficacy over more extended periods
has not been well-tested. In fact, other studies exploring ashwagandhas safety have been of an even shorter
duration (and one showed an adverse reaction involv-

23

If, by random chance, participants in


the ashwaganda group adhered better
to the training protocol than those in
the placebo group, it could account for
the differences seen between groups.
ing hallucinogenic effects with vertigo at the lowest

There were also a couple of weird things going on in the

dose). So, theres definitely more work to be done to

way the study was reported. The paper had an import-

make sure that ashwagandha supplementation is safe in

ant omission concerning compliance to the resistance

the long term.

training protocol. While the authors mention treatment


compliance in terms of pill count, no mention of how

Also, muscle recovery was not measured directly

well the participants adhered to the strength training

by asking participants about soreness or by testing

protocol itself was mentioned. If, by random chance,

strength reductions after exercise. Instead, serum cre-

participants in the ashwaganda group adhered better to

atine kinase measures were taken to be a marker of

the training protocol than those in the placebo group, it

muscle recover. While theres some evidence that higher

could account for the differences seen between groups.

levels of this correlates well with soreness and reduc-

Since these data werent reported, this possibility couldnt

tions in strength, other studies have found that creatine

be ruled out on the basis of the original paper. However,

kinase correlates poorly with functional measures of

we contacted the authors, and they indeed tracked the

recovery. So, we cant necessarily say that the reductions

resistance training protocol between groups and found

in creatine kinase seen in this study would necessarily

no difference. This increases the plausibility that it was

translate into better performance.

indeed the ashwagandha that lead to the gains.

Another limitation of this study was that it only recruit-

One other item of note was the exclusion criteria in the

ed men with little experience in resistance training,

study. One of these criteria was that the authors exclud-

according to the authors. Whether or not women or

ed people with any other conditions which [were]

more experienced lifters would experience similar ben-

judged problematic for participation in the study. This

efits is an open question since the results from this study,

is a pretty broad category, and may have skewed the

which only recruited men, may not generalize to women.

outcome as well as introduced researcher bias into the


sample used in this study. Thus, theres a chance the

The fat loss measurements should also be taken with

population studied here may not be representative of

a grain of salt, since the method used (bioelectrical

the general population.

impedance) is somewhat unreliable.

24

one exception. One small study reported no side effects


The results of this study are only over the short-term

in healthy young people performing cardio exercise

and only in relatively untrained men. The results also

over eight weeks. Another small study in healthy vol-

have pretty large errors associated with them, so the

unteers reported one adverse event, where a participant

actual effect of ashwagandha may be smaller than

experienced increased appetite, libido, and halluci-

seen in this study. Whether ashwagandha is safe and

nogenic effects with vertigo at the lowest dose, and

effective in experienced strength trainers, women, or

was withdrawn from the study. No other participants

over the long-term is still unknown.

reported any adverse effects. A third study with participants under chronic stress reported that adverse events

The big picture


This is the first study to the authors (and our) knowledge that took a look at ashwagandhas effects on
resistance training in particular. However, ashwagandha has been studied in other contexts, many of which

were mild and no different from placebo.


Ashwagandhas effect on increasing testosterone has
also been seen in two studies looking at men with
stress-related infertility or low sperm count.

also show positive results.

Ashwagandha has also been studied in other athlet-

The safety of ashwagandha has been tentatively estab-

3. The study on healthy volunteers mentioned above

lished in the short-term in a few different studies, with

ic-related contexts and shown benefit, as seen in Figure


showed mild improvements in back and quad strength

Figure 3: Ashwagandhas effects on physical performance in other studies

25

over 30 days, even though the participants were not


told to train and did not participate in any exercise
program in the month before enrolling in the study.
Another study in healthy, untrained young people
showed improvements in cardiovascular fitness and
jumping power after taking 500 milligrams of ashwagandha extract for eight weeks. A third study in trained,
elite cyclists found improvements in cardiovascular
function after eight weeks of 500 milligram supplementation as well.
While this study fits well with the literature on ashwagandha, the literature currently consists of only a few
short-term studies of small sample sizes. And in these
respects, the current study is no different. While longer-term and larger studies are needed to confirm its
effects, the early research on ashwagandha seems
quite promising.

This is the the first study to examine ashwagandhas effects on strength training. However, previous
studies have noted safety in most people over short
time periods, as well as increased testosterone plus
improved cardiovascular and muscle performance in
untrained or cardiovascularly trained populations.
Longer-term and larger studies are needed to con-

While this
study fits
well with the
literature on
ashwagandha,
the literature
currently
consists of only
a few shortterm studies of
small sample
sizes.

firm these effects.


anti-inflammatory and analgesic properties as well. The

Frequently asked questions

By what mechanisms might ashwagandha improve


strength?

Nobody is really sure, but the authors of this study offer


one suggestion: ashwagandha improves muscle recovery while also helping muscle development.
This study saw improved serum creatine kinase levels
with ashwagandha supplementation, which is suggestive (but not definitivesee above) of improved
muscle recovery after training. Ashwagandha has some

authors suggest that improved muscle healing alongside


less pain allowed the ashwagandha group to train harder, thereby increasing their gains.
In terms of muscle development, evidence suggests
that supplementation could increase testosterone levels,
which may be one contributing factor. But ashwagandha may also increase the bodys use and/or production
of creatine. A previous study found increased levels
of the breakdown product of creatine in the blood of
healthy people taking ashwagandha, accompanied by
mild increases in strength. Thus, the authors of the cur26

rent study suggest that ashwagandha may also stimulate

Finally, recall that the safety of ashwagandha supple-

creatine utilization through an unknown mechanism.

mentation has only been evaluated on the time scale of


a month or two at best. Creatine supplementation, on

But, again, these mechanisms are mostly speculation at

the other hand, has had much longer term safety stud-

this point.

ies in various populations and has fared quite well.

Speaking of creatine, how do the gains found in this study

So, it may not be wise to drop creatine in favor of ash-

compare to those found with creatine supplementation?

wagandha just yet.

If the results of this study are to be taken at face value, ashwagandha has a stronger effect. Thats a big if

What other effects is ashwagandha purported to have?

though. A meta-analysis of creatine supplementation

Preliminary evidence suggests that ashwagandha may

found a difference in 1-3RM performance on the bench

improve semen quality and anxiety, and may improve

press of about seven kilograms (15 pounds) versus pla-

glycemic control and cholesterol in diabetics as well.

cebo. In this study, an improvement of 20 kilograms (44

You can check out the details at Examine.coms ashwa-

pounds) over placebo on the bench press was seen.

gandha entry.

Before you drop your creatine and run for the ashwa-

What should I know?

gandha, there are some caveats to keep in mind.


First, keep in mind there was some error associated
with the measurements in strength gain, and that the
results of this study are also consistent with smaller
gains. This was discussed above.
Second, the meta-analysis mentions that almost all of the
studies included in the calculation to get the seven kilogram number were done on experienced lifters. Recall
that the study under review recruited untrained people.
So, a large part of the difference between creatine and
ashwagandha may be the result of beginner gains.

This is the first study to examine the effects of ashwagandha on participants undergoing resistance training.
The researchers found that ashwagandha supplementation combined with training over eight weeks improved
strength quite significantly, as well as muscle size, in
untrained healthy men with no reported side effects.
While these results are promising, they would be
unprecedented if replicable. The sheer magnitude of the
effects (which are more similar to steroid-influenced
gains than that of a normal supplement) definitely
warrants further research. Longer-term, larger studies
are needed to confirm both the safety and the beneficial
effects of ashwagandha.

Also, creatine is a very well-studied supplement at


this point, and its effects and safety are quite estab-

Pumped up to discuss ashwagandha? Head on over to

lished (you can check out the nitty-gritty details on

the private ERD Facebook forum!

the Examine.com creatine page). While ashwagandha


seems promising, its evidence base is much smaller. The
great results you see here may diminish or disappear
when further research is done, or unpublished research
is uncovered. This is actually a common phenomenon
in science, known as the decline effect.

27

Not-so-safe
supplements

Emergency Department Visits


for Adverse Events Related to
Dietary Supplements

28

Introduction
Dietary supplements are sometimes erroneously perceived as inherently healthy. And because of the way
many supplements are advertised, its easy to overlook that
improper administration can lead to adverse outcomes.
The classification of a supplement is defined in
the United States Dietary Supplement Health and
Education Act of 1994 (DSHEA) as a vitamin, mineral, herb or botanical, amino acid, and any concentrate,
metabolite, constituent, or extract of these substances.
In the U.S., the Food and Drug Administration (FDA)
is the governing body that oversees the regulation of
dietary supplements. If a supplement has been reported to be causing serious adverse events or reactions,
the FDA has the authority to pull it from the market.
However, no safety testing or FDA approval is required
before a company can market their supplement. The

ments. An independent survey has echoed these results,


finding that 67.2% of respondents felt extremely or
somewhat confident in supplement efficacy and 70.8%
felt extremely or somewhat confident about their safety.
While the majority of Americans trust in their supplements, more than one-third have not told their
physician about using them. There are numerous documented drug-supplement interactions ranging from the
mild to the severe. The herb St. Johns Wort is thought
to be able to reduce symptoms in people with mild to
moderate depression. But this natural supplement also
has 200 documented major drug interactions, including
some with common depression medication. However,
no good data currently exists to document how common adverse events related to dietary supplements may
be. The authors of the present study have used surveillance data to try and fill this knowledge gap.

lack of oversight authority given to the FDA has even


drawn the attention of late night talk shows hosts like

Due to DSHEA, supplements remain largely unreg-

John Oliver, who humorously covered the issue in this

ulated by the FDA. But dietary supplements are

YouTube video.

becoming ever more popular, as about half of U.S.


adults report using one or more in the past 30 days.

Many adults are using one or more supplements to

Trust in the safety and efficacy of these supplements

address illnesses or symptoms, and to maintain or

also remains high. The authors of this study aimed

improve health. Half of all U.S. adults have report-

to investigate how many annual adverse events are

ed using at least one supplement in the past 30 days.

caused by improper supplement usage.

Twelve percent of college students have reported taking


five or more supplements a week. Now, more than ever,
there are seemingly endless options to choose from.
The number of supplement products currently available on the market is thought to be in excess of 55,000.
Compare that to the mere 4,000 available in 1994, when
DSHEA was passed.
Furthermore, confidence in the safety and efficacy of
these supplements is very high despite the lack of rigorous oversight by the FDA. A survey conducted by the
trade association, Council for Responsible Nutrition,
found that 85% of American adults are confident in
the safety, quality and effectiveness of dietary supple-

Who and what was studied?


The researchers looked at 10 years of data (2004-2013) to
estimate the adverse events associated with dietary supplements in the United States from 63 different hospitals.
The selection of these hospitals was meant to be nationally representative and included locations that had
24-hour emergency departments. Trained patient record
abstractors reviewed the reports from each hospital to
identify cases where supplements had been implicated
as the likely source of the adverse event. These abstractors have been trained to analyze and compile medical
information contained in patient records.
29

Cases were scanned for emergency room visits where

ing intentional self-harm, drug abuse, therapeutic

the treating clinician had explicitly ascribed dietary

failures, nonadherence, and withdrawal.

supplements as the root cause of the medical issue. This


included herbal or complementary nutritional products
such as botanicals, microbial additives, and amino acids,
in addition to micronutrients like vitamins and minerals.
Products that may typically be classified as food were
excluded, like energy drinks and herbal tea beverages.
Topical herbal items and homeopathic products were
included in the analysis even though they do not fall
under the regulatory definition of dietary supplements.
Adverse events were classified as anything causing
adverse or allergic reactions, excess doses, unsupervised ingestion by children, or other events like
choking. Due to the non-standard death registration
practices among different hospitals, cases involving a
mortality were not included, as were any cases involv-

Researchers examined patient records from 2004 to


2013 from 63 different hospitals. Cases where the
treating clinician had identified a supplement as
the cause of the medical emergency were extracted
from the dataset. However, deaths associated with or
caused by supplements were not included, as hospitals differ in their practice of registering mortalities.

What were the findings?


Some of the major findings are summarized in Figure
1. Over 3,600 cases were identified within the predetermined 10-year period. The researchers extrapolated
from these data that the U.S. experienced an average

Figure 1: Supplement safety by the numbers

30

of 23,000 supplement-related emergency department

of ER visits (65.9%) were due to herbal or complemen-

visits per year, with estimates ranging from 18,600 to

tary nutritional products. The top five products in this

27,400. Of these 23,000 emergency room visits, it was

category included the following: weight loss (25.5%),

calculated that about 2,150 (9.4%) of these result in

energy (10.0%), sexual enhancement (3.4%), cardiovas-

hospitalization. About 88% of these ER visits were

cular health (3.1%), and sleep, sedation, or anxiolysis

attributed to a single supplement, as opposed to inter-

(i.e. anti-anxiety) (2.9%). Multivitamins or unspecified

actions or mixtures of multiple supplements. The

vitamin products were the biggest contributors to ER

average age of patients treated for supplement-related

visits under the micronutrient product category.

adverse events was 32 years, and the majority of these


cases were female.

ER visits also varied according to gender and age.


Weight loss and micronutrient supplements dispro-

Figure 2 shows age and supplement category related

portionately landed females in the ER, while sexual

results. About a quarter of ER visits involved people

enhancement and bodybuilding products largely affect-

between the ages of 20 to 34, but people older than 65

ed males. Among patients younger than four years old

years old were more likely to have a visit that resulted

and adults over 65, micronutrients were the number

in hospitalization. Of patients above 65 admitted to the

one cause of emergency department visits. This is in

ER, 16% had to be hospitalized. Surprisingly, one-fifth

contrast to the other age groups, where herbal and

of supplement-related ER visits were due to accidental

complementary nutritional products were the biggest

ingestion by children. When the data covering unsuper-

contributor. In people ages five to 34, weight loss prod-

vised ingestion of dietary supplements by children was

ucts or energy products were implicated in more than

not included, the researchers found that the majority

50% of ER visits. Weight loss products mostly affected

Figure 2: Summary of which types of supplements lead to ER visits by age

Source: Geller AI et al. N Engl J Med. 2015 Oct.

31

patients from 20 to 34 years of age, while the micro-

ed dietary supplements as fundamentally healthy. That is,

nutrients iron, calcium, and potassium mostly affected

the general public overwhelmingly perceives these prod-

those older than 65.

ucts to be safe and effective, but the present data does not
support this notion (ERD readers excluded. We think

About 23,000 people go to the ER for supplement-related visits every year. The biggest contributors to
this are herbal or complementary nutritional products like weight loss and energy supplements, which
largely affect people between the ages of five to 34.
Females are more likely than males to end up in the
ER due to adverse supplement reactions. Those over
the age of 65 are most at risk for an ER visit due to
micronutrient supplements such as iron, calcium,
and potassium.

you are all ahead of the curve on this one).


However, it should also be noted that overall incidences
of supplement-related ER visits have remained constant over time. No significant changes were detected
between 2004 and 2013 when accounting for population increases. The only increase that occurred was
ER visits associated with micronutrient supplements,
which jumped 42.5%, from 3,212 to 4,578 cases in this
same time frame.
Unlike their highly regulated pharmaceutical coun-

What does the study really


tell us?
While 23,000 annual supplement-related emergency visits may sound high, this is less than 5% of pharmaceutical
product-related ER visits. However, these ER admittance
rates do not line up with the marketing that has promot-

terparts, there are no legal requirements for dietary


supplements to identify any potential adverse effects or
major drug interactions on their packaging. The lack of
adequate warning labels may be a contributing factor
to why histories of dietary supplement usage are rarely
obtained by clinicians. This can be due to a combination of clinicians not asking proper patient screening
questions and to a lack of disclosure by the patient.

Proprietary Blends
The FDA has established labeling standards dictating what must appear on a supplements
packaging. Manufacturers must list out each ingredient, and are required to display the amount
or percentage of daily value of those ingredients.
A proprietary blend falls under a slightly different set of regulations. Blends are a unique mixture of ingredients that are typically developed by the manufacturer. The FDA requires that all
ingredients of a proprietary blend be listed on the label in descending order according to predominance of weight. While the amount of the blend as a whole must be listed, the amount of
each ingredient included in the blend does not.
Blends are used to help prevent the competition from knowing what the specific formulation is.
But it can also hide the fact that very little of an active ingredient may be in the bottle. So while
a proven performance enhancing ingredient like creatine may be listed in a proprietary blend, it
could be well below what is considered to be an effective dose.
32

Given that there is a tendency to underreport sup-

In light of this lack of regulatory oversight, if you are

plement usage, the researchers have noted that their

currently taking or thinking about adding a supplement

calculations of emergency department visits attributed

to your diet, be sure to notify your doctor. Supplements

to supplement-related adverse events are probably an

can interact with prescription medication or could

underestimation. A further limitation was the relative-

exacerbate certain medical conditions. Warfarin

ly small sample of hospitals used. But this method of

(Coumadin) is a good example. It is a blood-thinning

data collection is likely to yield more accurate results

medication that can be prescribed to people at risk of

over voluntary reporting despite the fact that volun-

forming blood clots. To ensure that the medication

tary reporting would have likely allowed for a larger

works properly, these patients are usually placed on a

sample population.

low vitamin K diet, as vitamin K plays an essential role


in forming blood clots. If these patients do not disclose

While 23,000 annual supplement-related emergency visits may not be a large contributor to ER
visits in the larger scheme of things, it does provide
a counter-narrative to the marketing that often

that they are taking a multivitamin with vitamin K,


multivitamins being one of the most commonly used
supplements, they could be putting themselves at risk
for developing unwanted clots.

portrays supplements as always health promoting. Supplements are not required to come with

Currently, the supplement industry is partially

labels warning of adverse events or potential drug

policed by itself. Companies that market and sell

interactions, which can be a contributing factor to

supplement products do not have to show the FDA

supplement-related ER visits.

data of safety or efficacy in the same fashion that


pharmaceutical companies do. The FDA can step in

The big picture


The supplement industry is the wild west of nutrition.
By and large, DSHEA has hampered the ability of the
FDA to adequately regulate supplements. If you have
ever taken a supplement that makes a health claim,

when a supplement has been shown to cause harm


and pull it from the market. It is important to discuss all supplements you may be taking with your
doctor to avoid unpleasant or dangerous interactions.
Be sure to tell them even if they do not ask during
your screening.

you may have encountered this statement on the label:


These statements have not been evaluated by the Food
and Drug Administration. This product is not intended

Frequently asked questions

to diagnose, treat, cure, or prevent any disease. While

Is there any way to ensure that Im purchasing a quality

all ingredients must be declared on the label, there is lit-

supplement??

tle oversight to ensure that these ingredients are present

There are companies out there that do supply third-par-

in the supplement, at the doses that are advertised on

ty certifications to supplement manufacturers. These

the packaging. Under DSHEA, there is no requirement

companies will verify that the supplements listed on

for companies to provide any data to the FDA showing

the ingredient list are present in the concentrations

that their supplement is safe and effective, unless they

claimed. There are four major companies that provide

are introducing a new or novel ingredient. It falls on

these certifications, which are shown in Figure 3: NSF

the FDA to show that a supplement is unsafe before any

International, Informed Choice, Consumer Lab, and

action can be taken.

U.S. Pharmacopeia. With the exception of Consumer

33

Lab, all of these third-party certifiers print their seal on

related deaths were not included in the ER visit pro-

the products they have screened.

jection, which could lead to an underestimation, it is


also possible that emergency department physicians

The testing process often involves looking at the puri-

may have incorrectly ascribed certain signs and symp-

ty, strength, and bioavailability of the product. Good

toms to supplements, which could consequently lead to

manufacturing practices, which help to provide systems

overestimation. Essentially, the 23,000 annual ER visits

that track proper design, monitoring, and control of the

should be viewed as a very rough estimation.

manufacturing process and facilities, are also frequently


taken into account. Many employ continuous random

If you are currently taking or planning to introduce

testing in order for a given supplement to remain cer-

a supplement to your diet, be sure that you are con-

tified. It is very important to note that these companies

suming the recommended dose for that product and

do not test for efficacy. That is to say, these certifications

consult your doctor before hand. Supplements are not

do not ensure that any health claims made about the

automatically beneficial for health, no matter what the

supplement are truthful.

marketing says. Treat dietary supplements the way you


would treat medication, with caution and respect for

What should I know?

their ability to both help and harm your health.

While 23,000 dietary-supplement related ER visits may


not seem like a lot when compared to something like

An incredibly effective supplement may also be incred-

the 610,000 deaths caused by heart disease every year

ibly harmful given the right (well wrong) context.

in the U.S., it is something that can be easily prevented

Talk about the under-discussed issue of supplement

with education and awareness. Although supplement

safety at the ERD Facebook forum.

Figure 3: Third-party supplement certifications

34

Throwdown: plant vs
animal protein for
metabolic syndrome

Type and amount of dietary protein in


the treatment of metabolic syndrome: a
randomized controlled trial

35

Introduction
Metabolic syndrome is a cluster of risk factors that
greatly increases the risk of dying from any cause (1.5fold) and especially cardiovascular disease (CVD)
specific causes (2.4-fold). This condition is diagnosed
as either having or being on medications to treat at least
three of the five following criteria:
Abdominal obesity (waist circumference greater
than 40 inches (men) or 35 inches (women)),
Elevated fasting blood glucose (more than 110 mg/
dL),
Elevated fasting triglycerides (more than 150 mg/
dL),
Low HDL-c (less than 40 (men) or 50 (women)
mg/dL), and

In the OmniHeart (Optimal Macronutrient Intake Trial


for Heart Health) trial, two variations of the DASH
dietary pattern were compared with DASH. One
variation replaced 10% of total daily energy from carbohydrate with protein, and the other replaced the same
amount of carbohydrate with unsaturated fat. Both
variations led to greater reductions of estimated CVD
risk than the standard DASH diet. Notably, all three
tested diets had a roughly even split between animaland plant-based protein.
This study sought to expand upon the findings of the
OmniHeart trial by comparing the effects of three variations of the DASH diet, which differed in protein type
(plant vs. animal) and amount (18% vs. 27%), on metabolic syndrome criteria.

Hypertension (systolic blood pressure higher than


130 mmHg and/or diastolic blood pressure higher

Metabolic syndrome is a cluster of risk factors that

than 85 mmHg).

greatly increases the risk of cardiovascular diseases,


the treatment of which includes diet and exercise to

Reducing these risk factors for CVD is the primary

facilitate weight loss. The DASH diet is considered

goal of managing metabolic syndrome, which is often

a prudent dietary pattern to address these risk fac-

done through lifestyle modification. Notably, changes

tors, but other research has shown variations of the

to diet and exercise that facilitate a 5-10% weight loss

diet to be more efficient. The study under review was

can address and significantly improve each risk fac-

designed to determine how protein type (plant vs.

tor. While a variety of dietary approaches can result in

animal) and amount (18% vs. 27%) affected metabol-

weight loss in overweight and obese adults, as explored

ic syndrome criteria.

in ERD Issue #6 (April, 2015), some dietary approaches may benefit people with metabolic syndrome more
than other approaches.
One currently accepted dietary pattern to reduce
CVD risk factors is the Dietary Approaches to Stop
Hypertension (DASH) diet, which is high in vegetables,
fruit, low-fat dairy products, whole grains, poultry, fish,
and nuts. The diet is low in sweets, sugar-sweetened
beverages, and red meats. The DASH diet is designed
to be low in saturated fat, total fat, and cholesterol, and
rich in fiber, potassium, magnesium, and calcium.

Who and what was studied?


This six-month, randomized, parallel-arm, controlled-feeding study recruited 62 sedentary overweight
and obese adults with metabolic syndrome. The participants were free of established cardiovascular diseases,
diabetes, or liver, kidney, and autoimmune diseases.
Two participants on glucose-lowering drugs and seven
participants on lipid-lowering medications were asked
to discontinue their use for the duration of the study,
but the eight participants taking medication for high
blood pressure were allowed to continue.

36

The entire study consisted of four phases:

WM, and WL phases, but only one meal per day was
consumed under the supervision of research personnel.

1. A two-week healthy American diet (HAD) run-

The remainder of the food was packed for taking home.

in period to establish a baseline for comparison

This means that even though all experimental diets were

during the subsequent phases and establish

tightly controlled, there was no guarantee that the par-

weight-maintenance caloric intake for each

ticipants would eat all of the food provided to them, and

participant.

only the food provided (i.e. no outside food or drink).

2. A five-week weight maintenance (WM) phase following one of three experimental diets.
3. A six-week weight loss (WL) phase consuming

The experimental diets were a modified-DASH


(M-DASH) diet rich in plant protein (18% of the calo-

the same experimental diet as in WM but with a

ries from protein, two-thirds from plants), an M-DASH

minimum 500 kcal per day deficit through dietary

diet rich in animal protein (BOLD, which stands

restriction and increased physical activity; and

for Beef in an Optimal Lean Diet; 18% protein, two-

4. A 12-week free living (FL) phase where participants were asked to continue their assigned

thirds from animals), and a higher-protein BOLD diet


(BOLD+; 27% protein, two-thirds from animals).

hypocaloric diets and physical activity, but without the provision of food and drinks. To prepare

These diets were matched for total fat (as seen in Figure

for this phase, each participant met with a dieti-

1), saturated fat, monounsaturated fat, polyunsaturat-

tian three times during the WL phase. They were

ed fat, cholesterol, sodium, potassium, calcium, and

educated on the unique features of their assigned

magnesium so as to help isolate the effects of differ-

diet and given practical advice, including suggest-

ent amounts and sources of protein. However, the

ed menus and recipes.

M-DASH diet was significantly higher in fiber (55 vs.


38 grams) than the other two diets because of the reli-

All food and drink were prepared by a metabolic kitch-

ance on plant-based protein sources. Examples of each

en and provided to the participants during the HAD,

study diets are shown in Table 1.

Figure 1: Macronutrient breakdown of the four diets

37

differences in any outcome between the three dietary


Overweight and obese adults with metabolic syndrome

groups. Most of the significant health improvements

were randomized to follow a modified DASH diet rich

occurred only after the WL phase. Accordingly, there

in either plant protein (M-DASH) or animal protein

was no change in the prevalence of metabolic syndrome

(BOLD), or a higher protein BOLD diet (BOLD+) for

among the participants from baseline through WM, but

a five-week weight maintenance phase and a six-week

prevalence dropped substantially to 50-60% after the

weight loss phase, with all food and drink prepared

WL phase and was maintained through the FL phase. In

and provided by the research staff. Afterward, the par-

other words, roughly half of the participants were no

ticipants were asked to continue their respective diets

longer classified as suffering from metabolic syndrome

for 12 weeks under free-living conditions.

after the WL phase. A summary of the study findings is


shown in Figure 2.

What were the findings?

The resolution of metabolic syndrome was the result of

Over the entire six-month intervention, there were no

significant improvements in every criterion except for


blood glucose levels. On average, after the WL phase

Table 1: Examples of the four study diets: Menus for the test diets

Breakfast

Lunch

Dinner

Snack

HAD
Pancakes with butter
and light syrup
Peaches, canned
in juice
Cottage cheese (1%)
Apple Juice

M-DASH
Pancakes with butter
and light syrup
Blueberries
Skim Milk
Orange Juice

Spinach/baby greens
salad with cherry
Turkey, provolone
tomatoes, mandarin,
cheese, and lettuce
oranges, grilled chicken
sandwich on white
breast, and dressing
bread with mayonnaise
Edamame beans
Granola bar
Whole-wheat dinner
roll with butter
Pistachios
Szechuan stir-fry entr Ratatouille (eggplant/
with pork and white rice
peppers) with pasta
White dinner roll
Spinach salad
with butter
with carrots, cherry
Romaine lettuce
tomatoes, red bell
salad with carrots
pepper, chickpeas,
and italian dressing
and dressing

Plain bagel with


cream cheese

Light yogurt
High-fiber cereal
Almonds

BOLD
Bran flakes with
raisins and skim milk
Whole-wheat minibagel and margarine
Orange Juice
Banana
Barbeque beef
sandwich on wholewheat bun
Spinach salad with
cherry tomatoes
and dressing
Thin pretzels
Pear

BOLD+
Bran Flakes with
raisins and skim milk
Cottage cheese (1%)
Orange Juice

Beef chili with


shredded cheddar
cheese (low fat) and
while-wheat crackers
Peaches, canned
in juice

Pot roast with mashed


Spinach and beef
potatoes and gracy
skillet with ribeye steak
White dinner roll
Brown rice
with margarine
Mixed baby greens
Broccoli and
salad with carrots,
edamame beans
cherry tomatoes,
Romaine salad with
and dressing
cherry tomatoes
and dressing
Hummus with
Light yogurt
whole wheat pita
Orange
and baby carrots
Almonds
Trail mix
38

and compared to the WM phase, there was a three


to four centimeter (about 3%) reduction in waist circumference, a 13-30% reduction in triglycerides, a one
to four mmHg reduction in systolic blood pressure,

Figure 2: Effects of all the diets on


metabolic syndrome factors

a one to three mmHg reduction in diastolic blood


pressure, and a 4-9% increase in HDL-c. Additionally,
total and LDL-cholesterol were reduced from baseline
during both the WM and WL phases, possibly due to
the reduced saturated fat intake among all diets, but
returned to baseline values during the FL phase. The
WL phase also led to significant improvements in CRP
(a marker for inflammation), endothelial function, and
vascular stiffness.
The only difference between the WM and WL phases
was a 500 kcal reduction in the food provided to the
participants and a significant increase in the number of
daily pedometer-measured steps taken, from 6,300 to
10,500. Together, this resulted in a significant 5% weight
loss across all groups, with roughly 80% coming from
fat mass. Since metabolic syndrome resolved only after
the WL phase, these findings suggest that weight loss
was the primary driver of health improvement.
Compliance during the WM and WL phases was
determined through daily questionnaires. Participants
were classified as noncompliant on any day that they
consumed a non-study food or beverage or did not
consume a study food or beverage. Accordingly, dietary
compliance ranged from 70-90% throughout the WM
and WL phases, but appeared to be higher in the
M-DASH (82-90%) group than the BOLD (70-75%) or
BOLD+ (77-80%) groups.

Regardless of diet, weight loss appeared to be the


primary driver of improved health among the participants. In all diet groups, the number of individuals
with metabolic syndrome was reduced by 40-50%
after they lost about 5% of their bodyweight during

Note: ranges are based on average changes across all the diets.
None of the diets effects were statistically different from one another.

the weight-loss phase.

39

What does the study really


tell us?

teins. This finding is consistent with numerous other

The researchers conducting this study sought to explore

ence between lean red and white meats and suggests

how protein type and amount affects the health of

that red meat can be safely included in an otherwise

people with metabolic syndrome through three dif-

healthy diet.

compared to a diet supplying mainly plant-based prointervention trials (1, 2, 3, 4, 5, 6) showing no differ-

ferent phases of energy balance: weight maintenance,


weight loss, and free living. The results indicate that nei-

The current study had a strong design, with ample time

ther protein type or amount have a significant impact

in each phase to allow for changes in CVD risk markers

on health at any stage, and that clinically significant

to occur. However, the trial was designed to be statisti-

weight loss (5% in this study) is the primary driver for

cally powered only to detect changes over time in each

reductions in abdominal obesity, triglycerides, blood

diet group, meaning that any between-group differenc-

pressure, and inflammation (CRP).

es may not have manifested due to a lack of statistical


power. This may be most apparent when acknowledg-

Current DASH diet recommendations include limit-

ing the lack of difference between the normal protein

ing the consumption of red meat. Many other dietary

and higher protein diet in terms of changes in body

patterns that are considered healthy, such as the

composition.

Mediterranean diet, tend to have relatively less animal


protein, with relatively more protein from whole grains

After all, it is recognized that higher protein diets, such

and legumes. The current study used unprocessed

as those used in this study (27%), lead to greater fat

lean beef (select grade top round, ribeye, chuck shoul-

loss and retention of muscle mass than normal protein

der, and 95% ground beef) and found that consuming

diets. Additionally, higher protein diets facilitate weight

nearly seven ounces (200 grams) per day had no det-

loss through increased satiety. Unfortunately, the

rimental (or beneficial) impact on CVD risk factors

controlled-feeding design of this study required partic-

The current study used


unprocessed lean beef and found that
consuming nearly seven ounces (200
grams) per day had no detrimental (or
beneficial) impact on CVD risk factors
compared to a diet supplying mainly
plant-based proteins.
40

ipants to eat all food provided to them, eliminating the

address an increasing rate of hypertension among

satiety advantage. While not statistically significant, it

the general public. One of the unique features of the

is noteworthy that only the BOLD+ diet continued to

DASH diet is that it focuses on dietary patterns rath-

demonstrate weight and fat loss alongside increases in

er than single nutrients, based on past observational

lean body mass during the free-living phase, when the

evidence combined with knowledge of select vitamins

benefits of a higher protein diet could be realized.

and minerals. Accordingly, the DASH diet was built


on a foundation of natural foods such including fruit,

Alternatively, the high and low protein diet groups were

vegetables, whole grains, nuts, legumes, and seeds that

consuming 2.5 and 1.7 grams of protein per kilogram

are good sources of potassium, magnesium, and dietary

of lean-body mass, respectively, and it has been sug-

fiber. Additionally, it incorporates low-fat dairy prod-

gested that optimal intake for resistance-trained obese

ucts, fish, chicken, and lean meats to reduce total and

adults is around 1.9 grams per kilogram. The current

saturated fat consumption and increase protein and

study did not utilize resistance training, so an optimal

calcium intake.

amount of protein would likely be lower and possibly


around that of the lower protein diets. Accordingly, the

Because nutrition is not static, this successful dietary

lower protein diet may have been sufficient in protein

pattern has undergone small changes in the last two

to account for the insignificant difference in weight loss

decades, such as limited red meat in favor of fish and

or lean mass kept from a higher protein intake.

poultry. This change was based on observational evidence suggesting a link between red meat and CVD.

Lastly, the recruitment goals of the study were not met,

As follow-up research has shown, this recommenda-

which may have limited the statistical power to detect

tion may have been premature. Associations are not

significant changes over time within each dietary group.

cause-and-effect relationships and there are countless

However, there were no trends that presumably may

potential explanations for why an association exists.

have reached significance with additional participants.

Against that background, it is all the more important to


highlight that the study under review just like sever-

Clinically meaningful weight loss (about 5%)


appears to benefit health regardless of protein type
or amount. Although this study showed no benefit to
higher protein intake, a potential lack of statistical
power to detect between-group changes, as has been
observed in previous studies evaluating the effect
of protein on body composition, suggests the finding should be accepted with caution. In agreement
with other intervention trials, unprocessed lean red
meat may be safely included as part of an otherwise
healthy diet.

al previous studies found no evidence that lean red


meat poses a CVD risk, at least not one that is detectable by the measurement of common CVD risk markers.
This is certainly not the first time policy makers have
based recommendations on associations, only to be
unsupported by subsequent intervention trials. In
ERD Issue #7 (May, 2015), we discussed the DIABEGG
study that sought to clarify whether eggs could be
safely included in the diet of people with type 2 diabetes. This research was needed because observational
evidence showed that people with type 2 diabetes who
ate eggs more than once per day were 69% more likely

The big picture

to develop CVD comorbidity than those who ate eggs

The DASH diet was developed in the mid-1990s to

for each four-per-week increase in egg intake, the risk

less than once per week. Other research showed that

41

of CVD increased by 40%. Not only did the DIABEGG

What is the difference between red meat and white

study show that eggs had no impact on blood lipids

meat, other than color?

or glycemic control, it showed that eggs increased

Red meat is a general term referring to meat from

post-breakfast satiety and resulted in a more enjoyable

land mammals, including cattle, lamb, goat, and sheep,

dietary experience by the participants.

whereas white meat is a general term referring to meat


from poultry, lean game like rabbit, and non-fatty

Observational evidence is important for noticing potential links between diet and health, but it
serves only as a starting point that requires further
and more rigorous testing. It is not uncommon for
dietary recommendations to incorporate observational evidence that is later shown to be incorrect

fish, such as cod and pollock. The primary difference


between these types of meat is their primary muscle
fiber type: red meat is slow-twitch and white meat is
fast-twitch. It should be noted that both types of fibers
exist in the meat, and these terms refer to the dominant
fiber type.

by experimental trials. The study at hand is a great


example, showing that the observational link
between red meat and CVD may be a bit misleading,
based previous trial evidence plus this study showing
a lack of difference in CVD risk markers between the
plant- and animal-based protein groups.

Frequently asked questions

Are there other dietary patterns with evidence for


improving metabolic syndrome?

Ultimately, any diet that results in fat loss will help with
metabolic syndrome. However, some dietary patterns
may better facilitate the necessary caloric deficit. For
instance, a paleolithic diet excluding cereal grains, dairy,
and legumes in favor of lean meats, fruit, fibrous and
starchy vegetables, and nuts has been shown to result
in more favorable health outcomes than a healthy reference diet, as discussed in ERD Issue #6 (April, 2015).
The paleo diet referenced above is unique in that it promotes the consumption of lean unprocessed meats. This
is in contrast to observational evidence that suggests
protective dietary patterns are low in red and processed
meats, providing yet more evidence that the exclusion
of lean red meat is not what makes these other dietary
patterns beneficial.

Ultimately,
any diet that
results in fat
loss will help
with metabolic
syndrome.
However,
some dietary
patterns may
better facilitate
the necessary
caloric deficit.
42

Slow-twitch fibers are designed to contract continu-

considered a prudent dietary pattern to address these

ously for long periods of time and thus rely heavily on

risk factors, but some components of it are based largely

oxygen for energy production via the aerobic path-

on observational evidence, such as the suggestion to

way. The protein myoglobin stores oxygen in muscle

limit red meat.

cells and is richly pigmented, so the more myoglobin


there is in the cells, the redder, or darker, the meat. By

The current study tested the validity of this recommen-

contrast, fast-twitch muscles are designed to contract

dation and showed that consuming up to seven ounces

forcefully and rapidly for very short periods of time and

(200 grams) of unprocessed lean red meat per day as

rely more on glucose than oxygen to function properly.

a primary protein source has no differential impact on

Therefore, they dont store a lot of myoglobin, instead

CVD risk factors and metabolic syndrome than a diet

favoring glycogen, and thus appear more glossy white.

where the majority of protein is obtained from plants.


Overall, the results suggest that clinically meaningful

From a nutritional perspective, the two types of meat

weight loss (about 5%) will benefit health regardless

are very similar. White meat is much leaner on average,

of protein type or amount. However, protein-specific

but there are also many types of lean red meat such as

benefits on other health outcomes like body composi-

bison and beef steak cut from the round of the cow. Red

tion require further research, as the current study may

meat also tends to be higher in vitamin B12, zinc, and

not have been adequately powered to detect significant

iron, while white meat contains more niacin and panto-

differences.

thenic acid.

What should I know?

The DASH diet has been studied in countless trials, but


this is the first to show that its low-red-meat stipula-

Metabolic syndrome is a cluster of cardiovascular dis-

tion may be misguided. Head over the ERD Facebook

ease risk factors, the treatment of which includes diet

forum to talk more about this study.

and exercise to facilitate weight loss. The DASH diet is

Overall, the results suggest that


clinically meaningful weight loss (about
5%) will benefit health regardless of
protein type or amount.

43

In closing...
Thanks again for reading ERD. We enjoy helping people stay up to date on research,
whether youre dietitians, trainers, physicians, or simply people interested in improving your health.
Click here to learn more about how Examine.com evolved over the past five years.

The Examine.com Research Digest is my


go-to resource for nutrition information.
It helps keep up up to date on the latest
studies that are relevant to my clients and
I, and its presentation and readability
make it beneficial for both the seasoned
researcher and the layman.
- Greg Nuckols

Kamal Patel, Editor-in-Chief

44

Credits
Copy Editor: Dmitri Barvinok
Infographics: Antonius Khengdro, Hieu Nguyen, Jessie Alley & Calla Lee
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45