N
utritional
aspects
related
to
endometriosis
R
ev
A
ssoc
M
ed
B
ras
2015; 61(6):519-523
521
with saline solution) reduced the size of endometrial im-
plants, as well as the levels of vascular endothelial growth
factor (VEGF) in the plasma and peritoneal fluid, and of
monocyte chemotactic protein (MCP-1) in the peritone-
al fluid. Furthermore, it increased suppression of VEGF
in endometrial tissue and favored histological changes
in the focal point of the disease after treatment.
14
Red meats are associated with higher concentrations
of estradiol and estrone sulfate, and their consumption
contributes to increased levels of circulating steroids,
collaborating with the maintenance of the disease.
6
It is
a food that contains arachidonic acid (omega 6) which,
in excess, increases pro-inflammatory substances, and
contains dioxins – xenobiotics that act as endocrine dis-
ruptors.
5
Arachidonic acid, an omega-6 polyunsaturated fatty
acid (
ω
6) – derived from animal foods and decomposed
from vegetable oils – is a substrate for the synthesis of
prostaglandins and even-series leukotrienes (PGE and
LTB4) with marked inflammatory action. Omega 3 (
ω
3)
– eicosapentaenoic and docosahexaenoic acid – (fish oil,
chia oil and flaxseed oil) is a substrate for the synthesis
of odd-series chemical mediators (PGE3 and LTB5) with
less inflammatory activity.
15,16
Both omega 3 and arachidonic acid are synthesized
by delta 5 and delta 6 desaturase, so the more omega 3,
the less inflammatory substances are synthesized.
15,16
Al-
though there is no consensus, a ratio of around 2:1 to 4:1
(
ω
6:
ω
3) is suggested. A few decades ago (the period be-
fore the age of industrialization) the
ω
6:
ω
3 ratio was
around 1:1 to 2:1, as a result of the greater consumption
of vegetables and seafood. In recent years, these indexes
have achieved ratios between 10:1 to 20:1 and even 50:1,
due to increased consumption of refined vegetable oils,
lower consumption of seafood products and reduced con-
sumption of fruits and vegetables.
15
The change in the
ω
6:
ω
3 ratio is associated with in-
creased menstrual pain and hormonal and autoimmune
disorders in women with endometriosis.
17
In 2011, Sava-
ris and Amaral found that women with endometriosis
had a lower consumption of polyunsaturated fatty acids
(
ω
3 and
ω
6) than the control group and lower than rec-
ommended, resulting in an imbalance in the formation
of long chain polyunsaturated fatty acids (
ω
3).
Some authors suggest that supplementation with
omega 3 can slow the growth of endometrial implants,
reduce pain and inflammation, and improve the quality
of life of women with stage III and IV endometriosis.
16
In
2008, Natsu et al. found that supplementation with EPA
(eicosapentaenoic acid) led to a reduction in the thick-
ness of the endometrial tissue interstitium, suggesting
that the inflammatory process of endometriosis must be
concentrated in this region.
Trans fat intake was assessed by the Nurses Health
Study II.
18
Women who consumed foods containing hy-
drogenated vegetable fat the most (margarine, some breads
and cookies, snack foods, fried foods, processed prod-
ucts) were 48%more likely to develop the disease than those
who consumed less (RR=1.48 – 95CI 1.17-1.88 p=0,001).
This type of fat is associated with metabolic molecules
that participate in inflammatory processes (TNF, TNF
receptor, IL-6, CRP).
Further considering the population of the Nurses
Health Study, the authors found that food (not supple-
ments) rich in thiamine, folate, vitamin C and vitamin E
were related to a lower rate of diagnosis of endometriosis.
It is believed that supplements do not exert the same ef-
fect as food because various nutrients and bioactive com-
pounds that interact with each other are found in the diet.
19
Vitamins A, C and E are antioxidant nutrients that
prevent lipid peroxidation, a phenomenon that contrib-
utes to the development and progression of chronic dis-
eases with inflammatory characteristics.
20
Corroborating
these data, Mier-Cabrera et al.
9
found a reduction in mark-
ers of oxidative stress in patients with endometriosis with
administration of a diet rich in vitamins A, C and E for
four months.
In recent years, vitamin D has been extensively stud-
ied for its anti-inflammatory, immunomodulatory and
antiproliferative action in addition to its known action
on bone metabolism.
Lymphocytes CD4, CD8, macrophages and dendrit-
ic cells express receptors and enzymes that metabolize
and activate vitamin D, suggesting that 1,25-dihydroxyvi-
tamin D (metabolically active form) can be produced lo-
cally, performing an autocrine and paracrine role in the
endometriosis focus or lesion
21
.
In the endometrium, the active form of vitamin D re-
duces the synthesis of IL-6, TNF 20 and prostaglandins
by suppressing COX-2 expression. Besides increasing pros-
taglandin inactivation of 15-hydroxy prostaglandin de-
hydrogenase, high concentrations of 1.25(OH)-D inhib-
it PG (prostaglandin)
21
receptor expression.
When a group of women with dysmenorrhea received
a dose of 300,000 IU of vitamin D before the menstrual
cycle there was a reduction of pain and nonsteroidal an-
ti-inflammatory (NSAIDs) use during the two-month
study, compared to the placebo group. Response was
greater in patients who reported worst pain severity at
the start of the study.
21