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Abstract

Chronic inflammation negatively impacts all physiological functions, causing an array of degenerative conditions including diabetes; cancer; cardiovascular, osteo-articular, and neurodegenerative diseases; autoimmunity disorders; and aging. In particular, there is a growing knowledge of the role that gene transcription factors play in the inflammatory process. Obesity, metabolic syndrome, and diabetes represent multifactorial conditions resulting from improper balances of hormones and gene expression. In addition, these conditions have a strong inflammatory component that can potentially be impacted by the diet. It can reduce pro-inflammatory eicosanoids that can alter hormonal signaling cascades to the modulation of the innate immune system and gene transcription factors. Working knowledge of the impact of how nutrients, especially dietary fatty acids and polyphenols, can impact these various molecular targets makes it possible to develop a general outline of an anti-inflammatory diet that offers a unique, nonpharmacological approach in treating obesity, metabolic syndrome, and diabetes. Several important bioactive dietary components can exert their effect through selected inflammatory pathways that can affect metabolic and genetic changes. In fact, dietary components that can modulate glucose and insulin levels, as well as any other mediator that can activate nuclear factor-kB, can also trigger inflammation through common pathway master switches.
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Journal of the American College of Nutrition
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Diet and Inflammation: Possible Effects on
Immunity, Chronic Diseases, and Life Span
Camillo Ricordi MD, Marta Garcia-Contreras MSc, Sara Farnetti, MD, PhD &
Sara Farnetti
To cite this article: Camillo Ricordi MD, Marta Garcia-Contreras MSc, Sara Farnetti, MD,
PhD & Sara Farnetti (2015) Diet and Inflammation: Possible Effects on Immunity, Chronic
Diseases, and Life Span, Journal of the American College of Nutrition, 34:sup1, 10-13, DOI:
10.1080/07315724.2015.1080101
To link to this article: http://dx.doi.org/10.1080/07315724.2015.1080101
Published online: 23 Sep 2015.
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Diet and Inflammation: Possible Effects on Immunity,
Chronic Diseases, and Life Span
Camillo Ricordi, MD, Marta Garcia-Contreras, MSc, Sara Farnetti, MD, PhD
Diabetes Research Institute, University of Miami, Miami, Florida (C.R., M.G.-C., S.F.); RI Med Foundation, Palermo, ITALY (C.R.,
M.G.-C.); School of Medicine and Dentistry, Catholic University of Valencia, Valencia, SPAIN (M.G.-C.)
Key words: nutrition, diet, inflammation, AA/EPA ratio, telomere, longevity
Chronic inflammation negatively impacts all physiological functions, causing an array of degenerative
conditions including diabetes; cancer; cardiovascular, osteo-articular, and neurodegenerative diseases;
autoimmunity disorders; and aging.
In particular, there is a growing knowledge of the role that gene transcription factors play in the inflammatory
process. Obesity, metabolic syndrome, and diabetes represent multifactorial conditions resulting from improper
balances of hormones and gene expression. In addition, these conditions have a strong inflammatory component
that can potentially be impacted by the diet. It can reduce pro-inflammatory eicosanoids that can alter hormonal
signaling cascades to the modulation of the innate immune system and gene transcription factors. Working
knowledge of the impact of how nutrients, especially dietary fatty acids and polyphenols, can impact these
various molecular targets makes it possible to develop a general outline of an anti-inflammatory diet that offers
a unique, nonpharmacological approach in treating obesity, metabolic syndrome, and diabetes.
Several important bioactive dietary components can exert their effect through selected inflammatory
pathways that can affect metabolic and genetic changes. In fact, dietary components that can modulate glucose
and insulin levels, as well as any other mediator that can activate nuclear factor-kB, can also trigger
inflammation through common pathway master switches.
It is well known that nutrition can affect pro-inflammatory
molecular signatures both in the blood and in the intestinal
microbiome [1–3]. The persistance of an inflammatory envi-
ronment has been associated with the development of chronic
degenerative conditions, including obesity, diabetes, and auto-
immune and neurodegenerative conditions, to name a few.
Inflammation can also negatively affect the efficacy and long-
term outcomes of organ transplantation, cellular therapies, and
regenerative medicine strategies, contributing, for example, to
immune rejection or recurrence of autoimmunity [4–6]. In fact,
nonspecific inflammation within the microenvironment of
organs, tissues, and cells at the time of transplantation can
result in an increased risk of rejection, recurrence of autoim-
munity, and ultimate failure of the transplanted cells, tissues,
or organs (e.g., prevention of rejection in intestinal and lungs
transplants is particularly challenging because of the inflamma-
tion often associated with this kind of procedure).
It will therefore be important to understand how modulation
of inflammation could affect the immune system, from
tolerance induction to alloimmunity and rejection transplanted
cells, tissues, and organs. It is, in fact, virtually impossible to
implement strategies for immune tolerance induction in the
presence of inflammation. The degree of inflammation in the
period that anticipates and follows transplantation (peritrans-
plant period) is critically important, and it has also been shown
for transplantation of isolated pancreatic islets, as in the case
of diabetes. Without an anti-inflammatory strategy at the
beginning of islet transplantation, for example, long-term
results indicated less than 15% success rate, compared to
approximately 50% in the case of implementation of a peri-
transplant anti-inflammatory strategy.
Another interesting aspect is the potential impact of inflam-
mation on metabolic syndrome and the development of type 2
diabetes, a disease condition typically associated with silent
inflammation in the bloodstream [1,2]. Several chronic degen-
erative disease conditions are indeed associated with an inflam-
matory condition, from obese subjects to prediabetes and
diabetes, but it could be argued that inflammation is not only
Address correspondence to: Camillo Ricordi, MD, Diabetes Research Institute at the University of Miami, 1450 NW 10 Avenue, Miami, FL 33136. E-mail:
ricordi@miami.edu
This article was presented at the Science in Nutrition 3rd International Congress in Milan, Italy, on March 14, 2014.
Color versions of one or more of the figures in the article can be found online at www.tandfonline.com/uacn.
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associated to the disease condition itself but could be involved
in its pathogenesis and progression.
Diet-induced epigenetic changes can occur over decades
and be responsible for the dramatic increase in chronic degen-
erative diseases documented in recent years. The mechanism
can be triggered by activation, via nutrition, of genetic tran-
scription factors involved in inflammation [2]. Therefore, it
can be said that inflammation is central to many physiologic
and pathologic conditions. Certainly we need the processes of
inflammation to survive—in fact, without an inflammatory
response to infection, injury, trauma, or poisoning, we would
die; in these cases we are dealing with acute inflammatory
responses. But there is another inflammatory condition, called
silent inflammation, that can be chronic, subliminal to the tres-
hold of pain, so it is not easily detected unless a blood test is
performed [1,2]. This kind of inflammation is typically trig-
gered and maintained by factors related to diet and the
environment.
It is interesting to note that the cellular mechanisms of tis-
sue repair and regeneration are linked to this type of inflamma-
tion, because it is necessary to repair and regenerate the
tissues. For example, endothelial progenitor cells are
“consumed” for repair of the microscopic lesions induced by
the inflammation associated with inappropriate diets.
It has been hypothesized that inactivation of the inflamma-
tory process and oxidative stress block wound healing. There
are simple tests on cell cultures in vitro where artificially pro-
ducing a wound (e.g., scratching the surface with a needle and
creating a linear defect or hole in the cell culture) can allow for
subsequent microscopic observation of the reparative process
of proliferation of endothelial progenitor cells and mesenchy-
mal tissue in order to close the artificially generated, in vitro
wound. If oxidative stress and inflammation are inactivated,
the wound does not heal. This indicates that if inflammation is
necessary for wound healing, then the resulting microscopic
tissue damage will require an increased activation/consumption
of repair mechanisms.
What are the consequences of these processes? The imme-
diate molecular response in the damaged tissue can activate a
natural defense mechanism in which the pericytes, cells located
on the capillaries, become mesenchymal cells. This was dis-
covered by Bruno P
eault, who showed that these cells are more
likely to become mesenchymal cells; however, not all pericytes
become mesenchymal cells, but all mesenchymal cells have
been pericytes [7,8].
Therefore, when there is inflammation or the tissue is dam-
aged, the pericytes are activated in mesenchymal cells and the
activated mesenchymal cells are anti-apoptotic, pro-angio-
genic, and regenerating but also immunomodulatory and anti-
inflammatory. So we have a system programmed to regenerate
damaged tissue within the native human capillary system and
in virtually all tissues.
Marc Penn et al. conducted a study in which mesenchymal
cells were labeled with dye, in order to identify them, and
injected into a guinea pig in the absence of injuries or surgery.
In these mice the injected mesenchymal cells disappear within a
few days. If a myocardial infarction is induced, mesenchymal
cells are concentrated in the cardiac area to heal. In contrast, in
the control group in which the same incision was performed
without inducing an ischemic lesion of the heart, the labeled
mesenchymal cells selectively migrated to the incisional wound
but not to the heart, indicating that this very clever tissue repair
system can sense inflammation and tissue injury and selectively
home to the site that requires repair/regeneration [9].
How do the mechanisms of tissue repair and regeneration
correlate with nutrition and diet-induced silent inflammation?
Diet-induced silent inflammation [1,2] can progressively con-
sume the cell types that are chronically utilized to repair
inflammation associated with tissue injury. Over time, this
chronic process can progressively deplete the native regenera-
tive potential; for example, in the continuous effort to repair
atherosclerotic plaque deposition. Once the repair potential is
exhausted, progression of coronary disease accelerates. Expos-
ing the body to chronic inflammation by nutrition and/or life-
style can lead to more rapid consumption of stem and
progenitor cells that are naturally present to heal damaged tis-
sue. This is important especially if this chronic condition con-
tinues for decades, during which these cells are activated every
day; it is intuitive that there is a possibility that their regenera-
tive power could be exhausted faster compared to subjects
exposed to noninflammatory lifestyles and diets.
There are several markers of silent inflammation; for exam-
ple, oxidative stress markers and high levels of glucose in the
blood, which are often related to inflammation. It is due to the
discoveries of Dr. Jenkins and others such as Jennie Brand-
Miller (Sydney, Australia) [12] that we have learned of the
importance of the glycemic index of food and its effect on
blood glucose levels. Now, when we go shopping at the super-
market we must pay attention to the types of food to buy and
avoid foods with a high glycemic index that aggravate the
inflammation. For example, you can choose carbohydrates
with a glycemic index equal to, if not less than, some low-car-
bohydrate foods. Barry Sears outlined very well the way our
diet has evolved over the past 30 years [1,2], with an increase
in refined vegetable oils (rich in linoleic acid) and refined car-
bohydrates (high glycemic index) and a decrease in omega-3
fatty acids and polyphenols.
This led to 2 negative and synergistic effects:
1. The promotion of inflammation by the combination of
foods with a high linoleic acid content and high glycemic
index, because insulin catalyzes (through desaturase
enzymes) the conversion pathway of linoleic acid to the
pro-inflammatory arachidonic acid.
Diet and Inflammation
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2. A decrease in anti-inflammatory protective factors associ-
ated with the decreased consumption of polyphenols and
omega-3s [1,2].
This nutritional change has become evident even in Italy. In
fact, in recent years the Italian population has adopted several
of Americans’ poor eating habits (e.g., fast food and sugar-
added beverages) and the obesity epidemic has now reached
Italy as well, where children and young adults have some of
the highest rates of overweight in Europe. This trend was asso-
ciated with the highest degree of silent inflammation measured
by blood markers, such as the arachidonic acid : eicosapentae-
noic acid (AA:EPA) ratio that was comparable to the ratios
observed in inflammatory disease conditions such as diabetes.
Normally this ratio should be less than 2. In fact, the population
of Japan, which benefits from one of the longest healthy life
spans on Earth, has an AA:EPA ratio of approximately 1.5,
whereas a value of 16–18 is found in subjects with inflamma-
tory conditions such as diabetes; when these children grow and
become adults, this could have significant consequences for
their health, in particular for the increased risk of developing
chronic degenerative disease conditions. It is worrisome that
this generation of children could be the first one with a life
span inferior to their parents.
It is difficult to study longevity or its impact on health or
life span, because studies with projections of many decades
should be conducted. However, a study published on Plos One
showed that simple changes in lifestyle can prolong the life
span by 14 years [10]. The study indicated that adherence to 4
factors was associated with a longer life span, individually but
with an incremental combinatory effect. The 4 factors were
absence of smoking, vitamin C levels greater than or equal to
50 nmol/L in the blood, alcohol consumption up to 14 servings
per week, and moderate physical activity. These 4 simple fac-
tors combined could result in a positive effect on longevity
with an increased life expectancy of about 14 years [10].
Chronic degenerative diseases are influenced by our mod-
ern lifestyle: nutrition, stress, and drugs can interfere with the
body’s ability to heal. There is an interesting emerging
research branch, resoleomics, that studies native mechanisms
of self-healing that occur when the human body repairs itself
and resolves inflammation; but this natural process can be pre-
vented by some of the anti-inflammatory or pain medication
administered. For example, some classes of analgesic used to
treat pain associated with inflammatory conditions could in
fact suppress self-healing mechanisms and their chronic sys-
temic use may not be indicated. Now there are much more inte-
grated approaches under consideration. For example, for
arthritis there are groups recommending more combinatorial,
integrated approaches to therapy, including diet, medication,
and changes in lifestyle.
To simplify the impact of diet on long-term reparative
systems and their possible impact on longevity, we could
assess telomere length. Each cell has a final DNA part
called a telomere; every time the cell divides it undergoes a
reduction in size (telomere shortening). The overall residual
length of telomers could be oversimplified as an indicator of
residual longevity potential. Themorecellsthatarerequired
to divide and replenish temselves to fight the effects of
chronic silent inflammation, the faster telomeres will
shorten. If we assume, for example, that the life potential
could be 140 years, this could be reduced to 70 years or
less when we are exposed to pro-inflammatory nutrition
and/or environment. Therefore, an inflammatory diet could
be associated with faster “consumption” of repair potential
and subsequent accelerated aging, compared to an anti-
inflammatory diet. For example, if the regenerative potential
of a subject exposed to an inflammatory diet is evaluated
after the first 40 years of age, it could suggest that a loss of
two thirds of their reparative potential has already occurred.
In contrast, a subject adopting an anti-inflammatory diet
would show a loss of only one third of such potential by
age 40. Physical appearance in this case could be misleading
because a football player, for example, following 20–
25 years of an inflammatory diet, could appear stronger and
healthier at age 40 compared to a subject who does moder-
ate exercise and spends most of his time working at a com-
puter but who consumes a vegetarian or noninflammatory
diet. However, by the age of 70, the inflammatory diet could
have consumed the regenerative potential of this subject,
who may now begin to experience strokes, heart attacks,
neurodegenerative diseases, and other chronic degenerative
conditions. The subject adhering to an anti-inflammatory
diet can instead still enjoy over one third of his life potential
(Fig. 1). This diet-induced consumption of the native regen-
erative potential (Fig. 1) is supported by recent evidence
indicating that adherence to a Mediterranean diet is associ-
ated with larger telomeres [11].
At the base of an anti-inflammatory diet, there are 6
basic rules described in the book The End of Pain by Peter
Wehling, in which innovative approaches are proposed for
the treatment of arthritis [13]. Wehling based his book on
nutrition rules to follow for the treatment of arthritis, with
several requirements considered in addition to avoidance of
foods that are direct triggers of inflammation. These
requirements/guidelines include avoidance of allergies and
other inflammatory reactions to foods, avoidance of foods
rich in starch and sugar that affect the level of glucose in
the blood and therefore insulin requirements, and eating
foods that reduce inflammation. Additional recommenda-
tions include taking supplements that reduce inflammation
and keeping one’s weight down, because obesity increases
inflammation. This book also pointed out that while focus-
ing on the rules one by one, we must remember that it is
necessary to implement a global approach where each ele-
ment enhances the other synergistically. It is impossible to
Diet and Inflammation
12 VOL. 34, NO. S1
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get full results using only individual components or ele-
ments that appear easier to adhere to.
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Diet and Inflammation
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... Many studies have found that chronic inflammation is related to a wide variety of human diseases, including diabetes, cardiovascular diseases (CVDs), autoimmune diseases, and cancer [1,2]. It has been proposed that dietary strategies can modulate inflammatory activity [3,4]. Several important bioactive dietary components can interfere with selective inflammatory pathways to affect metabolic and genetic changes [3]. ...
... It has been proposed that dietary strategies can modulate inflammatory activity [3,4]. Several important bioactive dietary components can interfere with selective inflammatory pathways to affect metabolic and genetic changes [3]. The whole-diet approach seems particularly promising for reducing the levels of inflammation compared with individual foods or food constituents [5,6]. ...
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