The Dietary Inflammatory Index: A New Tool for Assessing Diet Quality Based on Inflammatory Potential

Abstract

Background: Chronic inflammation is associated with a variety of chronic diseases and other conditions, and diet modulates inflammation. We developed a population-based literature-derived dietary inflammatory index (DII) to assess the inflammatory potential of an individual's overall diet, and compared DII scores across three different simulated diet plans. Methods: One day of intake was created for each of three diet plans (fast food, Mediterranean and macrobiotic) based on restaurant menus, literature and the Kushi Institute website. The DII score was calculated for each of the diet plans based on amounts of each of the 45 dietary components comprising the DII. A positive DII score represents a more pro-inflammatory diet, while a negative DII score represents a more anti-inflammatory diet. Results: The macrobiotic and Mediterranean diets produced strong anti-inflammatory DII scores (DII=-5.54 and-3.98, respectively) in comparison to the DII score for the fast food diet, which had strong pro-inflammatory potential (DII=+4.07). Conclusions: As expected, macrobiotic and Mediterranean meal plans exhibit anti-inflammatory potential, based on the derived DII scores, which may have the potential to exert beneficial effects on health. The DII represents a novel tool for assessing diet quality and has the potential to be used for evaluating and guiding individuals in setting dietary goals to help decrease levels of inflammation, thereby potentially reducing the risk of certain chronic health conditions.

Full text

TheDigest
Volume 49, Number 3 – Summer 2014
The Dietary Inammatory Index:
A New Tool for Assessing Diet Quality Based
on Inammatory Potential
Susan E. Steck, Ph.D., M.P.H., R.D. , Nitin Shivappa, M.B.B.S., M.P.H.,
Fred K. Tabung, M.S.P.H. , Brook E. Harmon, Ph.D., R.D.,
Michael D. Wirth, Ph.D., M.S.P.H., Thomas G. Hurley, M.S., James R. Hebert, Sc.D
Abstract
Background: Chronic inammation is associated with a variety of chronic diseases and
other conditions, and diet modulates inammation. We developed a population-based
literature-derived dietary inammatory index (DII) to assess the inammatory potential
of an individual’s overall diet, and compared DII scores across three dierent simulated
diet plans.
Methods: One day of intake was created for each of three diet plans (fast food,
Mediterranean and macrobiotic) based on restaurant menus, literature and the Kushi
Institute website. The DII score was calculated for each of the diet plans based on
amounts of each of the 45 dietary components comprising the DII. A positive DII score
represents a more pro-inammatory diet, while a negative DII score represents a more
anti-inammatory diet.
Results: The macrobiotic and Mediterranean diets produced strong anti-inammatory
DII scores (DII= -5.54 and -3.98, respectively) in comparison to the DII score for the fast
food diet, which had strong pro-inammatory potential (DII=+4.07).
Conclusions: As expected, macrobiotic and Mediterranean meal plans exhibit anti-
inammatory potential, based on the derived DII scores, which may have the potential
to exert benecial eects on health. The DII represents a novel tool for assessing
diet quality and has the potential to be used for evaluating and guiding individuals
in setting dietary goals to help decrease levels of inammation, thereby potentially
reducing the risk of certain chronic health conditions.
In this Issue:
The Dietary Inammatory Index: A
New Tool for Assessing Diet Quality
Based on Inammatory Potential
1-9
The Chair’s Message
10
Notes from the Secretary’s Desk…
11
Member Spotlight
Michelle Cardel, PhD, RD
12
Treasurer Report
13
Orthorexia Nervosa: How is this
Aecting the Male Population?
14-17
Upcoming Conferences
18
RDPG List of Ocial Volunteers
19

2 | Summer 14 | The Digest
Introduction
Inammation is a normal biologic
process involved in the immune
response. Normal inammatory
responses are typically self-limiting
and are necessary for wound healing
and combating infection. However,
chronic low-grade inammation can
occur as the result of a variety of
environmental insults and is particularly
common among obese individuals.1-4
This moderately elevated inammation
is associated with increased risk of
chronic diseases, such as cardiovascular
disease and some cancers.5-7
Dietary factors consistently have
been shown to aect inammation
through both pro-inammatory and
anti-inammatory mechanisms. The
Western-type diet, which is high in
sugar intake, fried foods, high-fat
dairy products, and rened grains,
is associated with higher levels of
inammatory biomarkers, such
as C-reactive protein (CRP) and
interleukin-6 (IL-6).8-10 On the other
hand, the Mediterranean diet, which
is high in whole grains, green leafy
vegetables, and sh, low in red meat
and butter, with moderate alcohol
and moderate to high olive oil intake,
is associated with lower levels of
inammation.11-15 The macrobiotic diet,
which represents a modication of the
traditional Japanese diet, tends to be
very high in whole grains, vegetables,
and beans, with low consumption
of sh, fruits, and sweeteners. A
macrobiotic diet may have benecial
eects on lipid proles and has
been suggested to reduce cancer
risk, though epidemiologic data are
sparse.16-18 Some dietary components
associated with lower inammation
levels include fruits and vegetables,19-21
omega-3 polyunsaturated fatty acids
(PUFAs),6,22-26 ber,8,27-30 moderate
alcohol intake,31-33 vitamin E,6,34-40
vitamin C,34,41-43 β-carotene,6,34,44-46
and magnesium.27,47-49 These dietary
components are generally known
to have a much wider safety margin
with habitual intake than do anti-
inammatory drugs.50,51
Given foods or nutrients are not
consumed alone but rather in
combination, we created a novel
dietary inammatory index (DII) to
assess the overall diet quality with
regard to inammation potential.52
Several dietary indices exist to assess
diet quality, but these mainly are
derived from one of three sources:
dietary recommendations, specic
foods unique to individual cultures, or
ndings from individual studies.53-56
Until the DII was developed, no other
index had focused on inammation as
the key theme in its development.
The purpose in creating the DII was
to provide a tool that could assess
an individual’s diet on a continuum
from maximally anti-inammatory
to maximally pro-inammatory. The
DII has been validated using CRP
measurements in the Seasonal Variation
in Blood Lipids Study (SEASONS), a
longitudinal study of approximately
500 individuals followed with intensive
dietary and physical activity monitoring
for a year.52,57,58 In SEASONS, the odds
ratio (OR) for having an elevated CRP
(>3.0 mg/L compared to ≤3.0mg/L) was
1.08 (95% condence interval [CI]: 1.01-
1.16) for a one-unit increase in the DII
(representing a more pro-inammatory
diet) based on multiple 24-hour dietary
recalls; and an OR of 1.10 (95% CI:
1.02-1.19) was obtained using a 7-day
dietary recall.58 The purpose of the
current study is to extend our previous
work by describing the DII, and
comparing three dierent simulated
dietary patterns to examine how DII
scores vary across a typical day’s usual
intake for fast food, Mediterranean, and
macrobiotic diets.
Methods
Study Design
In the current study, we modeled
a typical day’s intake on a 2,000
kcal/d diet for each of the three
dierent dietary patterns: fast food,
Mediterranean diet, and macrobiotic
diet (menus found in Table 1).
We then compared the DII scores
across the three diets. For the fast
food diet, foods were selected to
represent a typical selection from a
fast food restaurant menu. For the
Mediterranean diet, recipes and food
choices were selected from Greek
Revival Cooking for Life.59 For the
macrobiotic diet, foods were chosen
from recipes provided on the Kushi
Institute website60 and from expert
recommendations. All foods and
recipes were entered into the Nutrition
Data System for Research 2012 (NDSR)
for nutrient analysis.61 Flavonoid levels
(i.e., avonols, avones, avanones,
avan-3-ols, and anthocyanidins),
which are associated with reduced
levels of inammation,62-64 are not
provided by the NDSR system so were
calculated based on linkage with
the USDA’s Database for Flavonoid

Summer 14 | The Digest | 3
Content from Selected Foods (Release
3.1, December 2013).
The Dietary Inammatory Index
A description of the development of
the original DII and other supporting
materials can be found elsewhere.52,57,58
The goal in developing the DII was
to create a score for specic foods
and dietary constituents thought to
positively or negatively aect levels
of inammation. All research articles
through the year 2010 that were
identied as assessing the role of one
or more of 45 dierent foods and
dietary constituents (listed in Table 2)
on specic inammatory markers were
used to devise the scores. Because
of the large number of articles on
inammation, the literature search
was limited to six well-established
inammatory markers: CRP, IL-1β,
IL-4, IL-6, IL-10, and tumor necrosis
factor (TNF)-α out of which CRP, IL-1β,
IL-6 and TNF-α are considered pro-
inammatory biomarkers and IL-4 and
IL-10 are considered anti-inammatory
cytokines. A total of 1943 research
articles were reviewed and scored in
the creation of the DII.
One of three possible values was
assigned to each article based on
the eect of the food parameter on
inammation: “+1” was assigned if
the eects were pro-inammatory
(signicantly increased IL-1B, IL-6,
TNF-α, or CRP or decreased IL-4 or
IL-10); “-1” if the eects were anti-
inammatory (signicantly decreased
IL-1B, IL-6, TNF-α, or CRP or increased
IL-4 or IL-10) and “0” if the food
parameter did not produce any
signicant change in the inammatory
marker. Full details of the scoring
algorithm are available on request.
The research articles were rst
weighted by study characteristics, with
clinical trials in humans receiving the
greatest weight (i.e., 10 of possible 10)
to cell culture experimental studies
receiving the lowest weight (i.e., 3 of
possible 10). Using these weighted
values, the pro- and anti-inammatory
fractions for each food parameter were
calculated. The food parameter-specic
overall inammatory eect score was
then calculated by: 1) dividing the
weighted pro- and anti-inammatory
articles by total weighted number of
articles and 2) subtracting the anti-
inammatory fraction from the pro-
inammatory fraction. A cut point of
236, the median of the total weighted
number of articles across all the food
parameters, was chosen to indicate
an optimally robust pool of literature.
All food parameters with a weighted
number of articles ≥236 were assigned
the full value of the score. Foods and
constituents with a weighted number
of articles <236 were adjusted as follows:
1) number of weighted articles was
divided by 236; 2) the fraction was then
multiplied by the food parameter-specic
raw inammatory eect score, which
resulted in the food parameter-specic
overall inammatory eect score.
To avoid the arbitrariness resulting
from simply using raw intake
amounts (resulting in dierent units
of measurement for various nutrients
having large inuences on the overall
score) as had been done in the original
DII,57 the new version of the DII was
standardized to a representative
range of dietary intake based on
actual human consumption.52 This
was accomplished by constructing
a composite database representing
a wide range of diets across diverse
populations living in a variety of
countries in dierent regions of the
world. Authors of articles reporting
on data from nutrition surveys were
contacted to request access to
complete datasets. A total of 11 such
datasets were identied and used in
developing the composite database.
Calculation of the DII in a given study
is based on dietary intake data that are
then linked to the global mean intake
database derived from the 11 datasets.
An individual’s diet is then expressed
relative to the standard global mean
as a z-score. This is achieved by
subtracting the standard global mean
from the amount reported by the
individual and dividing this value by
its standard deviation. To minimize
the eect of “right skewing,” this value
is converted to a percentile score. To
achieve a symmetrical distribution
with values centered on 0 (null) and
bounded between -1 (maximally anti-
inammatory) and 1 (maximally pro-
inammatory) each percentile score
is doubled and then 1 is subtracted.
The centered-percentile value for each
food parameter is then multiplied by
its respective food parameter-specic
inammatory eect score to obtain
a food parameter-specic DII score.
Finally, all of the food parameter-
specic DII scores are summed to create
the overall DII score for an individual.

4 | Summer 14 | The Digest
More positive numbers represent a
more pro-inammatory diet whereas
more negative values represent a more
anti-inammatory diet.
Data Analyses
The overall DII scores and amount of
each of the 45 dietary constituents that
factor into the DII score were calculated
using the methods described above for
each of the three diets.
Results
The foods and portion sizes used to
model a typical day’s meal plan on
the three dierent diets (fast food,
Mediterranean diet, and macrobiotic
diet) are presented in Table 1. For
the purposes of comparing the DII
scores across the three diets, we
selected foods and portion sizes such
that energy intake would sum to an
isocaloric 2,000 kcal/d for each of
the three meal plans. In Table 2, the
overall DII scores are presented, along
with the amount of each of the 45
food parameters that are included in
the DII. The fast food diet had a high
pro-inammatory DII score (DII=+4.07),
while the macrobiotic diet (DII= -5.54)
and the Mediterranean diet (DII=
-3.96) scores indicated strong anti-
inammatory potential.
Discussion
A comparison of the DII scores across
three dierent simulated diets reveal
the macrobiotic and Mediterranean
diets exhibit strong anti-inammatory
potential. Indeed, these model diets
correspond to <10th percentile of
the DII score as shown in previous
simulated global intake estimates,52
representing high anti-inammatory
potential. By contrast, the fast food diet
exhibited a strong pro-inammatory
DII score corresponding to >90th
percentile of global intake.52 Given the
nutrient proles of the dierent diets
and the research on specic dietary
factors associated with inammation,
it is likely that the higher saturated
fat and trans fatty acids and lower
ber, vitamin, and avonoid values
of the fast food diet are the major
contributors to its pro-inammatory
score. In contrast, the incorporation
of more vegetables, fruits, and whole
grains into both the Mediterranean
and macrobiotic meal plans appears to
drive the anti-inammatory potential
of those diets. The macrobiotic diet
recommends very limited use of
saturated and polyunsaturated fatty
acids. Thus, in terms of macronutrient
intake, the macrobiotic diet would likely
be the most anti-inammatory of the
three diets and is consistent with our
results showing the lowest DII score
of the three diets. The relatively high
intake of spices and herbs that contain
biologically active anti-inammatory
compounds65 in the Mediterranean
diet may contribute to its very low DII
score. The anti-inammatory DII scores
associated with the macrobiotic and
Mediterranean diets are consistent
with the protective eect of controlling
chronic inammation as a mechanism
through which these diets exert their
benecial eects on health and chronic
disease prevention.16-18,66,67
The daily menus used were derived
from the literature, restaurant menus,
and expert recommendations. Using
these “modeled diets” (versus actual
intake data from human subjects) has
some inherent limitations. Our ndings
of dierences with inammatory
potential between the diets could be
due to our usage of a standardized
diet versus the range that would come
from actual intake data. For example,
fast food users may not typically
consume these foods at every meal
in a given day; thus, the DII score for
a full day of fast food may indicate a
higher inammatory potential than
actual diets that incorporate these
components less frequently. Selection
of items with more vegetables and
fruits from a fast food restaurant
menu could potentially decrease the
DII score for these diets, though it is
unlikely to be lowered to the extent
needed to meet the Mediterranean and
macrobiotic DII scores.
A 2,000 kcal/d diet was used across all
three diets so as to invoke isocaloric
comparisons and eliminate the
potential for dierences in DII scores
due to dierences in total energy
consumed. However, a typical
macrobiotic diet would likely consist
of fewer kcals/d, which would reduce
the portion sizes of the benecial
anti-inammatory dietary factors
(such as avonoids, onions, spices, and
ber), resulting in a slightly higher (i.e.,
less anti-inammatory) DII score. In
contrast, a fast food diet may consist of
more kcals/d than the 2,000 assumed,
resulting in either a higher or lower DII
score depending on the composition
of specic foods contributing to the
added energy. Thus, using typical intake
amounts, rather than conning to 2,000

Summer 14 | The Digest | 5
kcals/d for all diets, could have resulted
in either larger or smaller dierences in
the inammatory potential across the
three diets, depending on the foods
added to or subtracted from each of
the diets. We chose the Mediterranean
and macrobiotic diets for illustrative
purposes, but these are only two of
many possible diets representing
dietary patterns from around the
world that could be employed to
provide healthful alternatives to pro-
inammatory diets. It is very likely that
whole grain- and vegetable-based diets
consumed elsewhere in the world also
would result in low DII scores, indicative
of an anti-inammatory eect of diet.
There also are some potential
limitations of the DII. Because the
development of the DII scoring
algorithm was dependent on the
published literature, there is the
possibility of publication bias, such
that inclusion of signicant ndings
may be more likely than null ndings.
However, slightly under one-third
of all associations contributing to
the scoring of the DII were null. Also,
individual intakes are standardized to a
global population mean intake, which
may vary over time. However, a range
of intakes was used, and substantial
changes to the world mean intake
estimates are not anticipated in the
near future. The DII is based upon an
extensive literature search and takes
into account not only macronutrients,
vitamins, and minerals but also
incorporates commonly consumed
bioactive components including
avonoids and food items known to have
an eect on inammation like ginger,
turmeric and garlic. In addition, the
overall score takes into account the whole
diet, but this does preclude the ability to
assign DII scores to individual foods.
The DII represents a new tool for
assessing the inammatory potential
of the diet that can be applied to any
population in which dietary data have
been collected. In the modeled diets
presented here, the DII was calculated
based on the complete list of 45 food
and dietary constituents. In practice, a
complete list of all 45 food and dietary
constituents would be available only
from 24-hour recall- or food record-
derived data because traditional food
frequency questionnaires contain a
limited list of foods and beverages.
However, the DII can be used with
dietary data from any source, and we
are currently calculating it from food
frequency questionnaires that provide
a smaller list of dietary factors. These
data are being used in a variety of
datasets to examine the association
between the DII and chronic disease
risk. Results presented here, as well
as those obtained from our previous
work, highlight the potential of the DII
to be used in evaluating the eect of
dierent diets on a variety of health
outcomes. Continued application of
the DII in studies based in diverse
populations and using a variety of
health outcomes ultimately may help in
guiding individuals to set dietary goals
to decrease levels of inammation and
potentially reduce the risk of certain
chronic health conditions.

6 | Summer 14 | The Digest
Table 1. Modeled Meal Plans for Fast Food, Mediterranean and Macrobiotic Diets
Breakfast Lunch Dinner
Fast Food Diet1 1 bacon, egg and cheese biscuit 1 double cheeseburger 1 crispy chicken sandwich
1 coee, small 1 French fries, small 1 French fries, small
1 diet citrus soda, 1 citrus soda, caeine-free,
caeine-free, medium medium
Mediterranean Diet2 1.5 cup yogurt 10.6 oz Greek salad (with 1 cup couscous, cooked
1 cup green seedless grapes spinach, lettuce, feta cheese, 4 oz tilapia, cooked
0.5 cup shelled walnuts tomatoes, cucumber, olives) 2 tbsp olive oil
3 tsp honey 1 tbsp olive oil 1 garlic clove
1 cup herbal tea 1 tbsp vinegar 0.5 cup fennel
1 whole wheat pita 0.5 red pepper
0.25 cup hummus 0.5 onion
1 small coee 0.5 tomato
2 tbsp milk 0.25 cup mint leaves
0.5 cup blueberries
4 oz red wine
Macrobiotic Diet3 0.75 serving of tofu cilantro 2 cups short grain brown rice, 2 cups short grain brown rice,
and veggie dish: cooked cooked
3.33 oz tofu, steamed, extra rm 1cup miso soup 1 cup miso soup
0.26 oz fresh cilantro 1 serving of stir fried vegetables: 2 serving of azuki, squash dish:
0.75 quarter head of Napa cabbage 0.25 medium carrot 0.5 cup azuki beans
0.75 medium carrot 0.125 cup cooked lotus root 0.5 cup cubed butternut squash
0.75 medium spring onion 0.25 medium onion 0.25 sheet dehydrated seaweed
0.75 tablespoon brown rice vinegar 0.25 broccoli ower 0.5 tbsp parsley
1 cup cooked oatmeal 0.75 leaves Chinese cabbage 0.5 serving of cucumber and
0.5 cup blackberries 0.5 shiitake mushrooms wakame salad:
1 cup green tea 0.5 tbsp sesame oil 0.5 cup cucumber salad with vinegar
0.5 tbsp soy sauce 0.25 cup wakame
0.5 tbsp vinegar 0.5 tbsp soy sauce
0.5 tbsp arrowroot our 0.5 tsp brown rice vinegar
0.25 tsp ground ginger 1 serving of squash pudding:
0.5 small spring onions 0.25 cup cubed butternut squash
0.5 cup apple juice 0.13 oz kelp
1 cup green tea 0.5 tbsp cooked barleY
0.25 tbsp tahini
0.25 tbsp arrowroot our
1 cup green tea
1 Items selected from fast food restaurant menu
2 Recipes from Greek Revival: Cooking for Life59
3 Recipes from Kushi Institute website60

Summer 14 | The Digest | 7
Table 2. Dietary Inammatory Index Scores, Nutrients, and Dietary Factors for Modeled 2,000kcal/d Diet Plans
Fast Food Diet Mediterranean Diet Macrobiotic Diet
DII Score* +4.07 -3.96 -5.54
Food parameters (units):
Energy intake (kcals/day) 2003 2001 2001
Total fat (g/d) 102.25 109.24 35.81
Total carbohydrate (g/d) 188.30 193.57 355.56
Total protein (g/d) 85.34 61.25 78.58
Alcohol (g/d) 0.00 12.02 0.00
Cholesterol (mg/d) 364.25 105.85 0.00
Saturated fat (g/d) 32.74 20.84 5.71
Monounsaturated fat (g/d) 36.64 45.74 14.61
Polyunsaturated fat (g/d) 24.74 36.75 12.88
Trans fatty acid (g/d) 3.69 0.53 0.04
Omega 3 fatty acids (g/d) 2.70 6.42 0.88
Omega 6 fatty acids (g/d) 24.27 30.29 11.31
Total dietary ber (g/d) 12.98 26.81 63.97
Vitamin A (RE/d) 245.92 1097.68 1509.94
Beta Carotene (mcg/d) 147.22 5780.23 13587.89
Vitamin D (mcg/d) 2.67 5.45 0.09
Vitamin E (AT EQ/d) 10.41 14.92 5.32
Vitamin C (mg/d) 34.78 181.64 120.36
Thiamin (mg/d) 1.24 1.18 2.04
Riboavin (mg/d) 1.45 1.54 1.49
Niacin (mg/d) 23.12 21.39 25.57
Vitamin B6 (mg/d) 1.94 1.74 3.17
Total folate (mcg/d) 213.93 423.66 902.95
Vitamin B12 (mcg/d) 3.81 2.75 0.01
Magnesium (mg/d) 194.39 371.62 858.92
Iron (mg/d) 9.28 12.40 28.36
Zinc (mg/d) 10.04 8.67 16.83
Selenium (mcg/d) 104.07 75.56 131.32
Caeine (mg/d) 0.10 0.09 0.14
Flavonols (g/d) 3.54 48.75 47.30
Flavones (g/d) 0.03 6.37 6.26
Isoavones (g/d) 0.18 0.25 70.07
Anthocyanidins (g/d) 0.00 204.36 87.96
Flavonones (g/d) 0.27 9.02 0.00
Flavan-3-ol (g/d) 0.19 736.66 977.30
Garlic (g/d) 0.00 3.75 0.00
Ginger (g/d) 0.00 0.00 2.60
Onion (g/d) 0.00 55.00 161.67
Pepper (g/d) 0.00 0.00 0.00
Rosemary (mg/d) 0.00 0.00 0.00
Saron (g/d) 0.00 0.00 0.00
Thyme/Oregano (mg/d) 0.00 0.00 0.00
Turmeric (g/d) 0.00 0.00 0.00
Eugenol (g/d) 0.00 0.00 0.00
Green/Black Tea (g/d) 0.00 0.00 4.47
*A negative number reects a more anti-inammatory score, while a positive number reects a more pro-inammatory score

8 | Summer 14 | The Digest
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tumor promoter in cancer induction. Semin Cancer Biol
2004;14:433-9.
8. King DE, Egan BM, Geesey ME. Relation of dietary fat
and ber to elevation of C-reactive protein.[erratum
appears in Am J Cardiol. 2004 Mar 15;93(6):812].
Am J Cardiol 2003;92:1335-9.
9. Esmaillzadeh A, Kimiagar M, Mehrabi Y, et al. Dietary
patterns and markers of systemic inammation among
Iranian women. J Nutr 2007;137:992-8.
10. Aeberli I, Gerber PA, Hochuli M, et al. Low to moderate
sugar-sweetened beverage consumption impairs
glucose and lipid metabolism and promotes
inammation in healthy young men: A randomized
controlled trial. Am J Clin Nutr 2011;94:479-85.
11. Dalziel K, Segal L, de Lorgeril M. A Mediterranean
diet is cost-eective in patients with previous
myocardial infarction. J Nutr 2006;136:1879-85.
12. Chrysohoou C, Panagiotakos DB, Pitsavos C, Das UN,
Stefanadis C. Adherence to the Mediterranean diet
attenuates inammation and coagulation process in
healthy adults: The ATTICA Study. J Am Coll Cardiol
2004;44:152-8.
13. Esposito K, Marfella R, Ciotola M, et al. Eect of a
Mediterranean-style diet on endothelial dysfunction
and markers of vascular inammation in the metabolic
syndrome: A randomized trial. Jama 2004;292:1440-6.
14. Estruch R, Martinez-Gonzalez MA, Corella D, et al. Eects
of a Mediterranean-style diet on cardiovascular risk
factors: A randomized trial. Ann Intern Med 2006;145:1-11.
15. Serrano-Mar tinez M, Palacios M, Martinez-Losa E, et al.
A Mediterranean dietary style inuences TNF-alpha and
VCAM-1 coronary blood levels in unstable angina
patients. Eur J Nutr 2005;44:348-54.
16. Porrata-Maury C, Hernandez-Triana M, Rodriguez- ....
Sotero E, et al. Medium- and short-term interventions
with ma-pi 2 macrobiotic diet in type 2 diabetic adults
of Bauta, Havana. J Nutr Metab 2012;2012:856342.
17. Kushi LH, Cunningham J, Hebert JR, et al. The
macrobiotic diet in cancer. J Nutr 2001;131:3056S-64S.
18. Weitzman S. Complementary and alternative (CAM)
dietary therapies for cancer. [Review]. Pediatric Blood
Cancer 2008;50:494-7.
19. Gao X, Bermudez OI, Tucker KL. Plasma C-reactive
protein and homocysteine concentrations are related to
frequent fruit and vegetable intake in Hispanic and
non-Hispanic white elders. J Nutr 2004;134:913-8.
20. Watzl B, Kulling SE, Moseneder J, Barth SW, Bub A.
A 4-wk intervention with high intake of carotenoid-rich
vegetables and fruit reduces plasma C-reactive protein
in healthy, nonsmoking men. Am J Clin Nutr
2005;82:1052-8.
21. Esmaillzadeh A, Kimiagar M, Mehrabi Y, et al. Fruit
and vegetable intakes, C-reactive protein, and the
metabolic syndrome. Am J Clin Nutr 2006;84:1489-97.
22. Ferrucci L, Cherubini A, Bandinelli S, et al. Relationship
of plasma polyunsaturated fatty acids to circulating
inammatory markers. J Clin Endocrinol Metab ...........
2006;91:439-46.
23. Lopez-Garcia E, Schulze MB, Manson JE, et al.
Consumption of (n-3) fatty acids is related to plasma
biomarkers of inammation and endothelial activation
in women. J Nutr 2004;134:1806-11.
24. Niu K, Hozawa A, Kuriyama S, et al. Dietary long-chain
n-3 fatty acids of marine origin and serum C-reactive
protein concentrations are associated in a population
with a diet rich in marine products. Am J Clin Nutr
2006;84:223-9.
25. Zampelas A, Panagiotakos DB, Pitsavos C, et al. Fish
consumption among healthy adults is associated
with decreased levels of inammatory markers related
to cardiovascular disease: The ATTICA Study. J Am Coll
Cardiol 2005;46:120-4.
26. Zhao Y, Joshi-Barve S, Barve S, Chen LH.
Eicosapentaenoic acid prevents LPS-induced TNF-alpha
expression by preventing NF-kappab activation. Am Coll
Nutr 2004;23:71-8.
27. Bo S, Durazzo M, Guidi S, et al. Dietary magnesium and
ber intakes and inammatory and metabolic
indicators in middle-aged subjects from a population-
based cohort. Am J Clin Nutr 2006;84:1062-9.
28. Ajani UA, Ford ES, Mokdad AH. Dietary ber and
C-reactive protein: Findings from National Health and
Nutrition Examination Survey data. J Nutr
2004;134:1181-5.
29. King DE, Egan BM, Woolson RF, et al. Eect of a high-
ber diet vs a ber-supplemented diet on C-reactive
protein level. Arch Intern Med 2007;167:502-6.
30. Ma Y, Grith JA, Chasan-Taber L, et al. Association
between dietary ber and serum C-reactive protein.
Am J Clin Nutr 2006;83:760-6.
31. Avellone G, Di Garbo V, Campisi D, et al. Eects of
moderate Sicilian red wine consumption on
inammatory biomarkers of atherosclerosis. Eur J Clin
Nutr 2006;60:41-7.
32. Sierksma A, van der Gaag MS, Kluft C, Hendriks HF.
Moderate alcohol consumption reduces plasma
C-reactive protein and brinogen levels; a randomized,
diet-controlled intervention study. Eur J Clin Nutr
2002;56:1130-6.
33. Imhof A, Froehlich M, Brenner H, et al. Eect of alcohol
consumption on systemic markers of inammation.
Lancet 2001;357:763-7.
34. van Herpen-Broekmans WMR, Klopping-Ketelaars IAA,
Bots ML, et al. Serum carotenoids and vitamins
in relation to markers of endothelial function and
inammation. Eur J Epidemiol 2004;19:915-21.
35. Ber tran N, Camps J, Fernandez-Ballart J, et al. Diet
and lifestyle are associated with serum C-reactive
protein concentrations in a population-based study.
J Lab Clin Med 2005;145:41-6.

Summer 14 | The Digest | 9
36. Upritchard JE, Sutherland WH, Mann JI. Eect of
supplementation with tomato juice, vitamin E, and
vitamin C on LDL oxidation and products of
inammatory activity in type 2 diabetes. Diabetes Care
2000;23:733-8.
37. Devaraj S, Li D, Jialal I. The eects of alpha tocopherol
supplementation on monocyte function. Decreased
lipid oxidation, interleukin 1 beta secretion, and
monocyte adhesion to endothelium. J Clin Invest
1996;98:756-63.
38. van Tits LJ, Demacker PN, de Graaf J, Hak-Lemmers HL,
Stalenhoef AF. Alpha-tocopherol supplementation
decreases production of superoxide and cytokines
by leukocytes ex vivo in both normolipidemic
and hypertriglyceridemic individuals. Am J Clin Nutr
2000;71:458-64.
39. Devaraj S, Jialal I. Alpha tocopherol supplementation
decreases serum C-reactive protein and monocyte
interleukin-6 levels in normal volunteers and type 2
diabetic patients. Free Radic Biol Med 2000;29:790-2.
40. Murphy RT, Foley JB, Tome MT, et al. Vitamin E
modulation of C-reactive protein in smokers with acute
coronary syndromes. Free Radic Biol Med 2004;36:959-65.
41. Chien CT, Chang WT, Chen HW, et al. Ascorbate
supplement reduces oxidative stress in dyslipidemic
patients undergoing apheresis. Arterioscler Thromb Vasc
Biol 2004;24:1111-7.
42. Korantzopoulos P, Kolettis TM, Kountouris E, et al. Oral
vitamin c administration reduces early recurrence rates
after electrical cardioversion of persistent atrial
brillation and attenuates associated inammation.
Int J Cardiol 2005;102:321-6.
43. Wannamethee SG, Lowe GDO, Rumley A, Bruckdorfer
KR, Whincup PH. Associations of vitamin C status,
fruit and vegetable intakes, and markers of
inammation and hemostasis. Am J Clin Nutr
2006;83:567-74.
44. Folsom AR, Desvarieux M, Nieto FJ, et al. B vitamin
status and inammatory markers. Atherosclerosis
2003;169:169-74.
45. Erlinger TP, Guallar E, Miller ER, 3rd, Stolzenberg-
Solomon R, Appel LJ. Relationship between systemic
markers of inammation and serum beta-carotene
levels. Arch Intern Med 2001;161:1903-8.
46. Kritchevsky SB, Bush AJ, Pahor M, Gross MD. Serum
carotenoids and markers of inammation in
nonsmokers. Am J Epidemiol 2000;152:1065-71.
47. King DE, Mainous AG, 3rd, Geesey ME, Woolson RF.
Dietary magnesium and C-reactive protein levels.
Am Coll Nutr 2005;24:166-71.
48. Song Y, Li TY, van Dam RM, Manson JE, Hu FB.
Magnesium intake and plasma concentrations of
markers of systemic inammation and endothelial
dysfunction in women. Am J Clin Nutr 2007;85:1068-74.
49. Song Y, Ridker PM, Manson JE, et al. Magnesium
intake, C-reactive protein, and the prevalence of
metabolic syndrome in middle-aged and older U.S.
Women. Diabetes Care 2005;28:1438-44.
50. Dannhardt G, Kiefer W. Cyclooxygenase inhibitors-
-current status and future prospects. Eur J Med Chem
2001;36:109-26.
51. Rao CV, Rivenson A, Simi B, Reddy BS. Chemoprevention
of colon carcinogenesis by dietary curcumin, a naturally
occurring plant phenolic compound. Cancer Res
1995;55:259-66.
52. Shivappa N, Steck SE, Hurley TG, Hussey JR, Hebert JR.
Designing and developing a literature-derived,
population-based dietary inammatory index. Public
Health Nutr 2013:1-8.
53. Haines P, Siega-Riz AM, Popkin BM. The Diet Quality
Index revised: A measurement instrument for
populations. J Am Diet Assoc 1999;99:697-704.
54. Martinez-Gonzalez MA, Fernandez-Jarne E, Serrano-
Martinez M, et al. Mediterranean diet and reduction in
the risk of a rst acute myocardial infarction: An
operational healthy dietary score. Eur J Nutr
2002;41:153-60.
55. Guenther PM, Reedy, J., Krebs-Smith, S.M., Reeve,
B.B., & Basiotis, P.P. Development and evaluation of
the Healthy Eating Index-2005: Technical report. Center
for Nutrition Policy and Promotion, US Department
of Agriculture Available at http://www.cnpp.usda.gov/
HealthyEatingIndex.htm 2007.
56. Kwan ML, Weltzien E, Kushi LH, et al. Dietary patterns
and breast cancer recurrence and survival among
women with early-stage breast cancer. J Clin Oncol
2009;27:919-26.
57. Cavicchia PP, Steck SE, Hurley TG, et al. A new dietary
inammatory index predicts interval changes in serum
high-sensitivity C-reactive protein. J Nutr
2009;139:2365-72.
58. Shivappa N, Steck SE, Hurley TG, et al. A population-
based dietary inammatory index predicts levels of
C-reactive protein in the Seasonal Variation of Blood
Cholesterol Study (SEASONS). Public Health Nutr 2013:1-9.
59. Moore-Pastides P. Greek revival : Cooking for life.
Columbia, S.C.: University of South Carolina Press; 2010.
60. Kushi institute recipes. (Accessed February 23, 2014, at
http://www.kushiinstitute.org/library-resources/
recipes/.)
61. The Nutrition Data System for Research (NDS-R version
4.03_31). Minneapolis, MN: Developed by the
Nutrition Coordinating Center (NCC), University of
Minnesota; 2001.
62. Macready AL, George TW, Chong MF, et al. Flavonoid-
rich fruit and vegetables improve microvascular
reactivity and inammatory status in men at risk of
cardiovascular disease--FLAVURS: A randomized
controlled trial. Am J Clin Nutr 2014;99:479-89.
63. Jennings A, Welch AA, Spector T, Macgregor A, Cassidy
A. Intakes of anthocyanins and avones are associated
with biomarkers of insulin resistance and inammation
in women. J Nutr 2014;144:202-8.
64. Mahmoud MF, Hassan NA, El Bassossy HM, Fahmy A.
Quercetin protects against diabetes-induced
exaggerated vasoconstriction in rats: Eect on low
grade inammation. PLoS One 2013;8:e63784.
65. Rubio L, Motilva MJ, Romero MP. Recent advances in
biologically active compounds in herbs and spices:
A review of the most eective antioxidant and anti-
inammatory active principles. Crit Rev Food Sci Nutr
2013;53:943-53.
66. Estruch R, Ros E, Salas-Salvado J, et al. Primary
prevention of cardiovascular disease with a
Mediterranean diet. N Engl J Med 2013;368:1279-90.
67. Rees K, Har tley L, Flowers N, et al. 'Mediterranean'
dietary pattern for the primary prevention of
cardiovascular disease. Cochrane Database Syst Rev
2013;8:CD009825.

10 | Summer 14 | The Digest
It is a New Year for the Research DPG!
As we begin the 2014-15 year, I extend
a warm welcome to new and returning
Research DPG members! Our Executive
Committee team includes Chair Elect
Karin Pennington, Past Chair Nancy
Emenaker, Secretary Lauri Byerley,
Treasurer Elizabeth Reverri, Nominating
Committee Chair Sabrina Trudo, and me
as Chair. New committee chairs have
been appointed, and some positions
are soon to be lled. Our Executive
Committee is committed to continuing
activities and collaborations that
enhance the relevance and visibility
of the Research DPG and, more
importantly, benet the members.
This year will be focused on a number
of initiatives including updating our
website with a modern look and
expanding content, enhancing our
research expertise through a new series
of webinars, and expanding outreach to
students.
I hope to meet many Research DPG
members at the Food & Nutrition
Conference & ExpoTM (FNCE®) 2014
being held in Atlanta, GA on October
18-21. You will be learning more about
the Research DPG activities planned for
FNCE in upcoming eblasts, but mark
your calendar for the following events:
• Saturday, October 18,
11 am – 3 pm: Research DPG Pre-
conference Workshop entitled
“National Dietary Data: Building
Blocks to Expand Your Research
Portfolio”
Learn about dietary intakedata
collection, survey databases,
and research products that
augment analysis from What We
Eat in America (WWEIA), NHANES
in a hands-on workshop that
will provide attendees with a
variety of resources (bring your
laptop). Attendance is free to
Research DPG members and
$25.00 for non-members.
(This fee will include a one-year
membership to the Research DPG.)
• Monday, October 20, 7 – 8:30 am:
Research DPG Member Breakfast,
Omni at CNN Center, Dogwood Room
Enjoy breakfast, learn about new
activities of the DPG, catch up with
acquaintances, and connect with
new colleagues. Plans are
underway for enhancing student
involvement at the breakfast
sponsored by Solae.
• Monday, October 20,
9:30 am – 12:30 pm:
Research DPG Showcase,
Level 3 Foyer, Booth 10, Georgia
World Congress Center
Stop by to meet Research DPG
Executive Committee Members
and learn about ways to become
involved in the Research DPG.
As I work with the many members of
the Research DPG, whether elected
ocers or appointed committee
members, I am very thankful for these
volunteers who generously give their
time and talents. I especially want
to thank the outgoing Chair, Nancy
Emenaker, and the other outgoing
Executive Committee members for their
many contributions. The Executive
Committee is continually working
to enhance benets to members. I
welcome suggestions of potential ways
we can serve you better. I look forward
to serving you for the next year.
The Chair’s Message
Alanna Moshfegh, MS, RD
Chair, Research DPG

Summer 14 | The Digest | 11
Wow! We have rolled over into a new
year…2014-2015. I will continue to
serve the RDPG as secretary for the
next year. We have several new faces
including a new chair at the helm,
Alanna Moshfegh. Nancy Emenaker
will continue on as past chair helping
to steer us in the right direction. I want
to thank Nancy for her many hours of
service to the practice group.
Volunteers needed! Positions are
posted in a variety of places – the
EML (electronic mailing list), LinkedIn,
monthly email blast and the website.
If you don’t belong to the EML, there
are directions below. If you have
questions about volunteering or want
more information, send me an email at
lbyerley@msn.com.
LinkedIn: You are invited to join the
Research Dietetics Practice Group on
LinkedIn! We are a private member
community. Just send Nancy Emenaker
(emenaken@mail.nih.gov) a request to
join. See you there!
Electronic Mailing List: If you want to
subscribe to the EML, then send an
email message to ResearchDieteticPG@
googlegroups.com. Please include
your name in the body of the email.
When I receive your email, I will send
you back an email from the EML.
When you receive this email, you must
respond in order to become a member.
Within the EML, you are allowed to set
options. For example, you might not
want to receive an email every time
something is posted on the EML. You
can modify your EML settings to receive
notications less frequently.
If you already participate in the
EML, you should be receiving emails
occasionally from the EML, Research
DPG with the subject line showing
ResearchDieteticPG. If you are not
getting these, please contact Inés
Anchondo at Ines.Anchondo@ttuhsc.
edu.
If you have diculty accessing the
EML or posting on the EML, send Inés
Anchondo an email at Ines.Anchondo@
ttuhsc.edu The email address used to
contact the EML must match the email
address in the EML database. If it does
not, your message will bounce back to
you.
Enjoy the summer!
Notes from the Secretary’s Desk…
Lauri O. Byerley, PhD, RDN, LDN

12 | Summer 14 | The Digest
Our spotlight member for this edition
is Michelle Cardel, PhD, RD. Dr. Cardel
is a post-doctoral fellow and registered
dietitian at the University of Colorado
Anschutz Medical Campus. In her
current position, she spends about
90% of her time conducting research
in pediatric obesity and 10% of her
time seeing patients for weight
management. As a post-doctoral
fellow, Dr. Cardel is crossing the bridge
between her professional training and
becoming an independent scientist.
Read below to learn how her personal
desire to help others led her to choose
a career in pediatric obesity research.
Dr. Cardel, please tell us about your
background. How did you get to
where you are now?
Growing up, a teacher shared with me
Winston Churchill’s famous quote, “We
make a living by what we get, we make
a life by what we give.” Not until I was
an adult did I begin to understand
what this adage truly meant and have
since strived to live by those words
both personally and professionally. The
world of childhood obesity and health
disparities research allows me to make a
living doing work I am passionate about,
while also providing me the opportunity
to help others. Each morning I show
up to work and know that today is not
about padding my resume or getting a
pat on the back. The reason I do what I
do is simple: I want to improve the health
and quality of life of others in this world,
and I believe I can make a dierence. The
training that I have completed to be able
to do this work is a bachelor’s of science
in Biology with a minor in Chemistry,
a master’s of science degree in Clinical
Nutrition, a doctorate in Nutritional
Sciences, and I became a registered
dietitian. I am grateful to be part of such a
dynamic and impactful eld.
Could you please summarize your
current research for us?
In my post-doctoral fellowship, I
have utilized my research and clinical
background in order to participate in
collaborative and multidisciplinary
translational clinical research. My training
has focused on the development,
implementation, and evaluation of
community-based, family-centered
obesity prevention and treatment in
diverse children and their families.
Additionally, I am the principal
investigator on a pilot study investigating
the eect of social status condition
on acute energy intakes and eating
behavior in Hispanic adolescents. The
culmination of the above research
program may have public health
implications for creating cost eective
programs that use evidence-based
practices to target psychosocial variables
to produce sustainable, long term weight
loss in children and families of diverse
populations. My combined research
eorts has contributed to my long
term goal of developing meaningful
and sustainable community based
interventions to improve obesity-related
outcomes in underserved populations.
How did you become involved/
interested in your current line of
research?
As a registered dietitian and longtime
hospice volunteer, I have seen many
of my patients, particularly those from
underserved communities, suer from
weight-related medical conditions such
as hypertension, diabetes, cardiovascular
disease, and stroke. To me, it became
abundantly clear that we needed to
start preventing the development of
obesity early in life to decrease the risk of
developing these adverse body weight-
related diseases. That is why I have focused
my research career on understanding the
etiology of pediatric obesity.
Dr. Cardel,
what advice
would you give
to a young
researcher for
developing
a successful line
of research?
Review the literature. Find a eld of
interest that you are really passionate
about. You are going to need that passion
to sustain you when you are in the middle
of writing your 7th grant that year.
What are your career goals?
My professional goal is to become a
successful independent researcher
focused on the development of
sustainable and eective weight
management interventions in pediatric
minority and low income populations. I
also hope to serve as a liaison between
the scientic community and the
public, providing evidence based
education and recommendations to the
greater community.
How has your aliation with the
Academy impacted your career
progression?
As someone who did not decide to
become a registered dietitian until I was
in the middle of my doctoral program, I
believe I have a unique perspective on
the Academy. The Academy has impacted
my career by providing me with clinical
expertise and support that has only
helped my research career. I think that my
research background has helped to make
me a better clinician, while my clinical
work has greatly informed my research
career…wins all around!
If someone were to ask you to explain
why research is important to the eld
of dietetics, what would you say?
I would say that without the research,
you wouldn’t have a eld of dietetics. It is
the very foundation of the dietetics eld.
Member Spotlight
Michelle Cardel, PhD, RD
Michelle Cardel, PhD, RD

Summer 14 | The Digest | 13
My name is Beth Reverri, and I am a
Postdoctoral Scholar at the Jean Mayer
USDA Human Nutrition Research Center
on Aging at Tufts University. I am excited
to be the incoming RDPG Treasurer
and look forward to becoming more
involved with the RDPG. If you have
additional ideas for the RDPG members,
please email me, Elizabeth.Reverri@
tufts.edu, or one of the other Executive
Committee members.
The new scal year started on June 1 and
the nal annual budget will be released
by the end of the summer. Below are the
preliminary numbers to reect how we
have done overall. The most recent past
expenses include the RDPG’s presence at
the Public Policy Workshop via Mary-Jon
Ludy, an Academy Foundation donation,
and payment for the spring issue of The
Digest production. We submitted bids
and decided on a dierent company
to take advantage of high quality
publishing while also reducing costs.
Membership continues to drive our
income for the RDPG. The reserve of
137% currently puts the RDPG in good
nancial standing as we move forward
with WebEx trainings and website
redesign. Based on our current nances
and projected expenses/income for
the next year, we will end the 2014-15
scal year at 95% reserve. We are in the
process of securing funding for grant
awards which will aect this estimated
reserve.
Treasurer Report
Summer Greetings
Research DPG Members!
Elizabeth J. Reverri, PhD, RD and Karin Pennington, MS, RD, LD, FAND
Incoming RDPG Treasurer Outgoing RDPG Treasurer and Incoming RDPG Chair-Elect
Elizabeth J. Reverri, PhD, RD
Treasurer Repo rt
Summer Greeti ngs Research DPG Members !
My name is Beth Reverri, and I am a Postdoctora l Scholar at the Jean Mayer USD A Human Nutrition
Research Center on Aging at Tufts University. I a m excited to be the incoming R DPG Treasurer and look forward
to becoming mo re involved with the RDPG. If yo u have additional ideas for the R DPG members, please email me ,
Elizabeth.Reverri@tufts.edu, or on e of the other Executive Commi ttee members.
The new fiscal ye ar started on June 1 and the fin al annual budget will be release d by the end of the
summer. Below are the preliminary numbers to reflect how we have done overa ll. The most recent past
expenses includ e the RDPG’s presence at the Pu blic Policy Workshop via Mary-J on Ludy, an Academy
Foundation don ation, and payment for the sprin g issue of The Digest productio n. We submitted bids and
decided on a dif ferent company to take advanta ge of high quality publishing w hile also reducing costs.
Membership con tinues to drive our income for t he RDPG. The reserve of 137% c urrently puts the RDPG
in good financia l standing as we move forward w ith WebEx trainings and websi te redesign. Based on our curren t
finances and pro jected expenses/income for the next year, we will end the 2014 -15 fiscal year at 95% reserve.
We are in the pro cess of securing funding for gra nt awards which will affect this e stimated reserve.
Elizabeth J. Rev erri, PhD, RD and Karin Penn ington, MS, RD, LD, FAND
Incoming RDPG Treasurer Outgoing R DPG Treasurer and Incoming RD PG Chair-Elect
Research DPG 2 013-14 Budget
Annual Budg et ($) As of Apr 2014 ($)
Revenue Membership 18,580 16,453
Grants/Contract s
Interest Income
8,000
---
3,000
3,826
26,580 19,453
Expenses Lodging/Subsistence 1,393 1,259
Transportation 5,310 1,996
Professional/Con sulting 1,500 2,580
Postage/Mailing Services
Teleconferences
Advertising/Prom otion
Member Dues/F ees
Outside Services
150
90
0
973
5,200
31
94
774
1,831
200
Awards
Audio Visual
4,600
3,000
4,000
1,223
Food Service 5,250 2,330
Printing/Copyin g 10 0 19
AND Foundation 50 50
28,116 16,387
NET -1,536 3,066
Reserve Apr 2014 Rese rve 28,116 38,544
Reserve Percentage --- 137%
Ginger 6/18/14 7:56 AM
Comment: Placepictureof“E lizabethJordan
Reverri”withthisdocument
Research DPG 2014-15 Budget
Annual Budget ($)
Revenue Membership 18,250
Grants/Contracts
Interest Income
- - -
- - -
18,250
Expenses Lodging/Subsistence 924
Transportation 6,000
Professional/Consulting 3,000
Postage/Mailing Services
Teleconferences
Webex Seminars
Advertising/Promotion
Member Dues/Fees
Outside Services
50
135
588
250
1062
4,400
Awards
Audio Visual
Expo / Meeting Services
3,100
2,000
400
Food Service 6,000
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14 | Summer 14 | The Digest
Introduction to Orthorexia Nervosa
Health. Wellness. Longevity. The
justication for such terms can be met
with aspects such as, the “rising cost
of health care”, the “obesity epidemic”,
and the “green movement” (1)
manifesting themselves heavily on the
minds of health-conscious individuals.
Orthorexia Nervosa (ON) occurs
when an individual adopts unhealthy
obsessions with healthy eating (2),
subsequently resulting in extensive
dietary restrictions, a distortion
of priorities, obsessive tendencies
associated with food, and severe social
isolation (3,4,5). Stemming from the
Greek words “orthós” (straight, right,
proper) and “orexsis” (appetite), ON was
coined by Steven Bratman, MD, who
rst wrote about this condition in an
October 1997 issue of Yoga Journal. But
how is it possible for eating healthy to
actually cause harm to one’s health?
An individual struggling with ON will
follow a strict diet, of which major
food groups are often not suciently
consumed, resulting in a shortage
of essential nutrients, modication
of social and personal relationships,
and change in the individual’s general
psychosocial condition (6). Essentially,
the desire to eat healthy foods is not
itself a cause for concern, yet the
obsessions for these foods, coinciding
with the loss of moderation, balance,
and withdrawal from life, can result in
the fostering of this condition (3). What
can start as diet tied to philosophy
or theory, quickly adopts “pure” and
“spiritual” connotations in the ON
individuals mind (3,5). Additionally,
feelings of superiority can arise when
compared to the eating lifestyle and
dietary habits of others (3). Often,
specic foods, whole food groups,
and food preparation methods
deemed perilous to his/her health will
be avoided by a person with ON, as
ingesting what he/she considers to be
quality food becomes of paramount
importance. (3,4).
Obsessive expressions towards food
are qualitative in an individual with ON,
unlike cases of anorexia nervosa (AN)
or bulimia nervosa (BN), in which food
quantity becomes a motivating factor
to regulate weight status (3). The more
qualitatively restrictive and complicated
the diet, the more an individual with
ON will be attracted to it (7). It has even
been reported that in extreme cases, a
number of ON individuals would rather
starve than consume foods regarded
as “impure” or “unnatural” (3). Currently,
the Diagnostic and Statistical Manual
of Mental Disorders (DSM-V) does not
recognize this recent eating behavior
as a disease, but research has begun
to highlight the stark prevalence of
ON. Donini (3) reported that 28 of
404 Italian subjects (6.9%) displayed
orthorexic behavior. Ramacciotti
(8) also indicated a 57.6% (N=102)
prominence of ON among a general
Italian population sample. A “highly
sensitive eating behavior disorder” or
ON, was assessed in a sample of 318
resident medical doctors in Ankura,
Turkey, utilizing the ORTO-15 test.
Results from this test indicated that
45.5% of the study group scored below
40, dening them as orthorexic (6).
Fidan (9) demonstrated that 43.6% of
the 878 medical students of Ataturk
University Medical School in Erzurum,
Turkey, expressed ON tendencies using
ORTO-11, the ORTO-15 test translated
into Turkish. ON has even been
reported to occur among dietitians (10),
athletes (11), and performance artists
including opera singers, ballet dancers,
and orchestra artists (12).
A Dual Manifestation of Orthorexia
Nervosa within the Male Population
Albeit limited, much of the recent
research indicates a prevalence of
ON among males, highlighting the
idea that ON aects males equally,
and potentially more frequently than
females. Donini (3), Fidan (9), Garcia
(11), and Aksoydan (12), have all
determined that males experienced
higher rates of ON occurrence when
compared to females, with factors such
as age, and weight further categorizing
incidence of ON within the gender.
ON tendencies among males have
been reported to maintain a direct
relationship with increasing age (3) and
weight (12). One possible explanation
for this could be the need to adopt
a higher sensitivity toward nutrition,
fueling a desire to prevent or treat
illness and improve general health
(5,12). Older males have an increased
susceptibility to experience chronic
illness, with eorts to avoid disease
prompting the assessment of diet
as an area of concern, justifying the
modication and adoption of particular
health conscious dietary behaviors. The
media can be a primary contributor to
the idea that eating well is important
for keeping wellness (9), as knowledge
Orthorexia Nervosa: How is this Aecting
the Male Population?
Dylan A. Bailey
© 2014, BHN Newsletter; Behavioral Health Nutrition a dietetic practice group of the Academy of Nutrition and Dietetics. Used with permission.

Summer 14 | The Digest | 15
concerning the relationship between
diet, health, and illness, can transition
into obsession, and the development
of ON. Being overweight or obese
can additionally result in possible
ON occurrence, as society has begun
placing an increasing amount of
importance on health and body image.
Further, an obesogenic environment
has given rise to the stigmatization
of fatness, as male-centric ideals
(muscularity, strength, power,
athleticism) have gained heightened
societal focus.
Moreover, ON is occurring within
younger males maintaining lower
weight status, and a previously existing
risk for eating disorders (EDs) (9,11). In
correlation with the strict physical and
aesthetic stereotypes associated with
males, in which “six pack” abdominal
muscles dominate billboards, adopting
the “health-fanatic” lifestyle can be seen
as an acceptable action, legitimizing
an individual’s maniacal obsession with
healthy eating. Even though weight
loss is not a motivational factor for the
dietary extremes expressed within ON,
eating healthfully is seen as positive,
and males are beginning to adopt this
knowledge. Yet males, being new to a
world lled with aesthetic and health
lled expectations, can experience
anxiousness and susceptibility
toward bombarding social messages
concerning food, pathologically
exacerbating ON occurrence (3).
ON prevalence has illustrated a
relationship to the tness industry
and athletic roots, as evidenced by
ON manifestation in Italian male
athletes (11), performance artists (12),
and recreational tness participants
(13). Athletes are often well aware
that nutrition plays a crucial role for
enhancing performance and recovery,
reaching an ideal weight, shaping
the body (male specic pursuit of
muscularity) and preventing physical
detriments, which can lead to food
control as a necessary factor to
maintain intensive exercise practice
and to achieve optimal performance
(11). Knowledge concerning the
signicant role nutrition upholds in
athletics, coupled with the prevalent
availability of dietary information
from unqualied sources, and the
self-motivation character trait seen
in athletes (14), can promote swift
implementations of inadequate dietary
practices. This can be detrimental for
athletes displaying ON tendencies,
as the potential avoidance of whole
foods or food groups can result in
nutrient deciencies, and low energy
availability within a population for
whom adequate nutrition and energy
intakes are essential for advantageous
sport performance. Additionally,
sports nutritionists or other health
professionals dealing with male athletes
need to understand that reluctance
to discuss eating problems may occur,
as diculties can arise due to the
shame and embarrassment associated
with displaying stereotypically female
dilemmas (14).
Implications for Dietetic
Professionals and ON Treatment
Although ON subjects are not obsessed
with food quantity intake as observed
in AN and BN, some aspects of ON
and clinically recognized EDs can be
observed as similar including a genetic
predisposition to perfectionism,
anxiety, rigidity, a need for control of
life transferred to eating, and character
traits of detailed, careful, and tidy
personas with an exaggerated need
for self-care and protection (4). Zamora
(15) explains that ON patients display
obsessive-compulsive mechanisms with
personality traits, phobic mechanisms,
and hypochondriac mechanisms similar
to those of restrictive anorexia. Might
someone who is heavily obsessed
with achieving the perfect diet,
constantly thinking about food, and
dedicating signicant time to planning,
purchasing, preparing, and consuming
it, be categorized as having obsessive-
compulsive disorder (OCD)?
Individuals with greater orthorexic
tendencies were reported to have
higher obsessive-compulsive
symptoms (4). Garcia (11) conrmed
that ON showed a strong relationship
with Yale Brown Cornell Eating Disorder
Scale (YBC-EDS) positivity, food and
eating preoccupations, and eating and
exercise rituals, making the association
between ON and obsessive-compulsive
symptoms clear. Ultimately, the specic
clinical implication of ON is still under
debate. ONs signicance within the ED
or OCD spectrum is certainly unknown,
as future research can clarify its exact
diagnostic placement.
Nonetheless, treatment solutions
should utilize cognitive behavioral
therapy (CBT) to challenge the patient’s
distorted belief system, by tapping

16 | Summer 14 | The Digest
into current faulty beliefs and altering
them (7). Individuals with ON need
to understand that food quality is
not the only determinant of health.
Furthermore, nutrition education
should emphasize eating techniques
which will inhibit a relapse of obsessive
tendencies. Medications, specically
selective serotonin reuptake inhibitors
(SSRIs), have also been reported to be
useful during ON treatment (7), but
patients obsessed with dietary purity
may be hesitant to adopt a prescribed
drug regimen. Conversely, unlike
patients with other ED’s, subjects
with ON may be more responsive to
treatment due to their overall concern
with health and self-care (7).
Now, even though the treatment of
ON requires a multifaceted team of
physicians, psychotherapists, and
nurses, registered dietitians (RDs)
can be the rst in line to intercept an
individual displaying ON tendencies.
A person with ON may seek an RD
for more information in regards to
maintaining an optimal way of eating,
with input to dietary concerns aligning
with the disordered behavior (7).
Registered dietitians need to be aware
that the male population is currently
displaying a growing incidence of
problematic obsessions or xations
regarding healthy eating behaviors
referred to as ON. By understanding
the symptomology associated with
ON, RDs have an opportunity to play
a pivotal role in treatment via the
referral of patients to other appropriate
professionals or primary care facilities.
Behavioral & Psychological Aspects
of the Orthorexic Patient (3,16,17)
Distortion of Priorities
• Longing to spend less time xating
on food, and more time with others
• Thinking with critical concern
about what will be eaten on that
day or the following day
• Belief that creating and following
the perfect diet is uncompromisable
• Constant worry regarding food
quality
Social Isolation
• Beyond ability to eat a meal
prepared by someone else
• Positioning on a nutritional
pedestal, consistent scrutiny of
others and their diet
• Discussions on food are
always based around having the
perfect diet
• Hopes to spend less time on food
and more time with friends, living
and loving
Obsessive habits and repercussions of
the lifestyle
• Needs to take their own food
wherever they go
• Sense of control upon following a
“correct” diet
• Straying from “correct” diet
is met with feelings of
guilt or self-loathing
• Lack of self-assessment capabilities
regarding dietary behaviors,
reduced capacity to criticize
About the Author
Dylan A. Bailey is a current senior
dietetics undergraduate student
enrolled at Montclair State University,
Montclair, New Jersey.
Phone: 862-686-2359
Email: baileyd7@montclair.edu
References
1. Mellowspring, A. Orthorexia nervosa: A primer. IDEA
Fitness Journal. 2010; 7(10), 67-70.
2. Bratman, S. About “orthorexia”. Available at
http://www.orthorexia.com/about/.
Accessed Jan. 10, 2014.
3. Donini, L., Marsili, D., Graziani, M., et al. Orthorexia
nervosa: A preliminary study with a proposal for
diagnosis and an attempt to measure the dimensions
of the phenomenon. Eating Weight disorders. 2004;
9(2), 151-157.
4. Brytek-Matera, A. Orthorexia nervosa – an eating
disorder, obsessive- -compulsive disorder or disturbed
eating habit?. Archives of Psychiatry and Psychotherapy.
2012; 1: 55-60.
5. Bratman, S. (1997). The health food eating disorder.
Available at http://www.orthorexia.com/original-
orthorexia-essay/. Accessed Jan. 3, 2014.
6. Bosi, T., Çamur, D., & Güler , C. Prevalence of orthorexia
nervosa in resident medical doctors in the faculty of
medicine (ankara, turkey). Appetite. 2007; 49(3), 661-
666. doi:10.1016/j.appet.2007.04.007
7. Mathieu, J. What is orthorexia?. Journal of the American
Dietetic Association. 2005; 105(10), 1510-1512. doi:
10.1016/j.jada.2005.08.021
8. Ramacciotti, C., Perrone, P., Coli, E., et al. Orthorexia
nervosa in the general population: A preliminary
screening using a self-administered questionnaire
(ORTO-15). Eating and Weight Disorders. 2011; 16(2),
2011.
9. Fidan, T., Ertekin, V., Işikay, S., et al. Prevalence
of orthorexia among medical students in erzurum,
turkey. Comprehensive Psychiatry. 2010; 51(1), 49-54.
doi:10.1016/j.comppsych.2009.03.001
10. Kinzl, J., Hauer, K., & Traweger, C. Orthorexia nervosa
in dietitians. Psychotherapy and Psychosomatics. 2006;
75, 395-396. doi:10.1159/000095447
11. Segura-García, C., Papaianni, M., Caglioti, F., et al.
Orthorexia nervosa: A frequent eating disordered
behavior in athletes. Eating and Weight Disorders. 2012;
17(4), 226-233. doi: 10.3275/8272

Summer 14 | The Digest | 17
12. Aksoydan, E., & Camci, N. Prevalence of orthorexia
nervosa among turkish performance artists. Eating and
Weight Disorders. 2009; 14(1), 33-37.
13. Eriksson, L., Baigi, A., Marklund, B., et al. Social
physique anxiety and sociocultural attitudes toward
appearance impact on orthorexia test in tness
participants. Scandinavian Journal of Medicine &
Science in Sports. 2007; 18, 389-394. doi:
10.1111/j.1600-0838.2007.00723.x
14. Bonci, C., Bonci, L., Granger, L., et al. National athletic
trainers’ association position statement: Preventing,
detecting, and managing disordered eating in athletes.
Journal of Athletic Training. 2008; 43(1), 80-108.
15. Zamora, M., Bonaechea, B., Sanchez, F., et al. Orthorexia
nervosa: A new eating behavior disorder?. Actas Esp
Psiquiatr. 2005; 33(1), 66-68.
16. Torres-McGehee, T. O rthorexia: The direct impact
of energy availability among female and male athletes.
Available at http://vimeopro.com/nata1950/2013-
special-topics/video/71055930. Accessed Jan. 10, 2014.
17. Kratina, K. Orthorexia nervosa: National eating
disorders association. Available at http://www.
nationaleatingdisorders.org/orthorexia-nervosa.
Accessed Jan. 25, 2014.

18 | Summer 14 | The Digest
August 6-9, 2014
American Association of Diabetes
Educators Annual Meeting
(Orlando, FL)
Call for abstracts: Closed
Website: http://aade-365.ascendevent-
media.com/
October 11-14, 2014
American Academy of Pediatrics
National Conference & Exhibition
(San Diego, CA)
Call for abstracts: Closed
Website: http://www.aapexperience.org/
October 18-21, 2014
Food & Nutrition Conference
& ExpoTM
(Atlanta, GA)
Call for abstracts: Closed
Website: http://www.eatright.org/fnce/
abstractsubmission/
November 2-7, 2014
Obesity Society Annual Scientic
Meeting
(Boston, MA)
Call for abstracts: Closed
Website: http://www.obesityweek.com
March 18-21, 2015
Society of Adolescent Medicine and
Health Annual Meeting
(Los Angeles, CA)
Call for abstracts: TBD
Website: http://www.adolescenthealth.
org/Meetings/Future-Meetings.aspx
March 18-20, 2015
International Conference on Eating
Disorders
(London, UK)
Call for abstracts: Open until September
2014
Website: http://www.mahealthca-
reevents.co.uk/cgi-bin/go.pl/conferences/
detail.html?conference_uid=408
April 16-19, 2015
Women’s Health 2015: The 22nd
Annual Congress
(Washington, DC)
Call for abstracts: TBD
Website: http://academyofwomen-
shealth.org/
March 28-April 1, 2015
Experimental Biology
Call for abstracts: TBD
Website: http://experimentalbiology.
org/2014/About-EB/Future-Meeting-
Dates.aspx
Upcoming Conferences

Summer 14 | The Digest | 19
Executive Committee Chair
Alanna Moshfegh, MS, RD
Beltsville Human Nutrition Research Center
United States Department of Agriculture
Beltsville, MD
Alanna.Moshfegh@ars.usda.gov
Chair-elect
Karin Pennington, MS, RD, LD
St. Louis, MO
karin.pennington@gmail.com
Secretary
Lauri O. Byerley, PhD, RD, LDN
Department of Physiology
Louisiana State University Health
New Orleans, LA
704-340-4482
lbyerley@msn.com
Treasurer
Elizabeth J. Reverri, PhD, RD
Tufts University
Jean Mayer USDA Human Research
Center on Aging in the Cardiovascular
Nutrition Lab
Boston, MA
Elizabeth.Reverri@tufts.edu
Past-chair (2013-14)
Nancy Emenaker, PhD, RD
Division of Cancer Prevention
National Cancer Institute
Bethesda, MD
301-496-0116
emenaken@mail.nih.gov
Nominating Committee Chair
Sabrina Peterson Trudo, PhD, RD
trudo@umn.edu
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Joan.E.Milton@providence.org
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LD, CSP
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