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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