The association between trans fatty acids, infertility and fetal life: a review

Abstract

Trans fatty acids (TFAs) are thought to affect reproductive health by causing adverse effects on sperm morphology and ovum quality as a result of changing membrane lipid composition which, in turn, leads to impairment in metabolic pathways. This literature review examines the evidence for the effects of dietary TFAs on male and female infertility. Studies conducted between 2007 and 2017 on the effect of dietary TFAs on human reproductive health and fetal life have been included. They indicate that TFA intakes are inversely proportional to sperm concentration and total sperm count and exhibit a positive correlation with asthenospermia, as well as an adverse association on sperm concentration and semen quality. In the female TFAs intakes are associated with an increase in the risk of ovulatory infertility, adversely affect the length of gestation leading to fetal developmental defects and fetal loss. The findings suggest that high TFA intake (more than 1% of energy consumption) constitute a risk factor for infertility in both sexes.

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The association between trans fatty acids,
infertility and fetal life: a review
Hande Çekici & Yasemin Akdevelioğlu
To cite this article: Hande Çekici & Yasemin Akdevelioğlu (2018): The association
between trans fatty acids, infertility and fetal life: a review , Human Fertility, DOI:
10.1080/14647273.2018.1432078
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REVIEW ARTICLE
The association between trans fatty acids, infertility and fetal life: a review
Hande C¸ekici
a
and Yasemin Akdevelio
glu
b
a
College of Health, Department of Nutrition and Dietetics, Recep Tayyip Erdo
gan University, Rize, Turkey;
b
Faculty of Health Science,
Department of Nutrition and Dietetics, Gazi University, Ankara, Turkey
ABSTRACT
Trans fatty acids (TFAs) are thought to affect reproductive health by causing adverse effects on
sperm morphology and ovum quality as a result of changing membrane lipid composition
which, in turn, leads to impairment in metabolic pathways. This literature review examines the
evidence for the effects of dietary TFAs on male and female infertility. Studies conducted
between 2007 and 2017 on the effect of dietary TFAs on human reproductive health and fetal
life have been included. They indicate that TFA intakes are inversely proportional to sperm con-
centration and total sperm count and exhibit a positive correlation with asthenospermia, as well
as an adverse association on sperm concentration and semen quality. In the female TFAs intakes
are associated with an increase in the risk of ovulatory infertility, adversely affect the length of
gestation leading to fetal developmental defects and fetal loss. The findings suggest that high
TFA intake (more than 1% of energy consumption) constitute a risk factor for infertility in both
sexes.
ARTICLE HISTORY
Received 1 August 2017
Accepted 4 November 2017
KEYWORDS
Trans fatty acid; infertility;
asthenospermia; ovulatory
infertility; fetal loss; fetal
development
Introduction
Lipids are indispensable elements in the diet, both for
the provision of energy, and for the supply of essential
fatty acids, i.e. a-linolenic acid (a-LA), and linoleic acid
(LA). Fatty acids are responsible for tissue metabolism,
hormonal and other signals, regulation of membrane
structure and function, regulation of intracellular sig-
nalling pathways, transcription factor activity together
with gene expression, and regulation of the produc-
tion of bioactive lipid mediators (Z
arate, el Jaber-
Vazdekis, Tejera, P
erez, & Rodr

ıguez, 2017).
Lipid chains exist in two main forms: saturated
without the presence of double bonds, and unsatur-
ated, containing one or more double bonds, the latter
being of greater physiological importance because of
their medicinal properties. Unsaturated fatty acids con-
sist of the monounsaturated fatty acids (MUFAs) and
the polyunsaturated fatty acids (PUFAs). PUFAs can be
categorized as omega-3 (n–3) and omega-6 (n–6)
depending on the position of the first double bond
from the methyl end group of the fatty acid (Z
arate
et al., 2017). PUFAs can be directly obtained from
food, usually in limited amounts, but are largely pro-
duced from their essential fatty acid precursors, LA
and a-LA, through desaturation and elongation in the
liver. LA and a-LA, are considered to be essential,
because arachidonic acid (AA), eicosapentaenoic acid
(EPA), and docosahexaenoic acid (DHA), which serve
critical roles in human metabolism, can only be syn-
thesized from these precursors. A poor essential fatty
acid intake against the background of an inadequate
food intake has been considered a major factor
responsible for the reduced levels of AA and EPA
found in man (Burke, Ling, Forse, & Bistrian, 1999). EPA
can be produced when the starting substrate is a-LA.
EPA is then extended to the 4-position unsaturated
docosapentaenoic acid (DPA) to produce DHA (Z
arate
et al., 2017).
Advances and diversification in food technologies
have caused an increase in the amount of dietary
trans fatty acids (TFAs). TFAs can occur naturally in
meat and dairy product and are produced industri-
ally. Such industrial hydrogenated fats, margarines,
and hydrogenated vegetable oils (shortenings) make
up 82–90% of all dietary lipid-based TFAs (Kahraman
&K
€
upl€
ul€
u, 2011). Hydrogenated vegetable oils, which
are found in many processed foods as well as in
fast food, are the main source of TFAs with their
high unsaturated fatty acid trans isomer content
(Kahraman & K€
upl€
ul€
u, 2011). The remaining 2–8% is
from animal source foods (Kiralan, Yorulmaz, &
Ercoskun, 2005).
CONTACT Hande C¸ekici handecekici@hotmail.com Recep Tayyip Erdo
gan University, College of Health, Department of Nutrition and Dietetics,
Rize, Turkey
ß2018 The British Fertility Society
HUMAN FERTILITY, 2018
https://doi.org/10.1080/14647273.2018.1432078

TFAs are important, because they cause health
problems as a result of various metabolic activities
(Kiralan et al., 2005). They are known to cause changes
in membrane enzyme functions and in certain cellular
reactions (Kahraman & K€
upl€
ul€
u, 2011) because they
block the oxidation of cis fatty acids, alter membrane
fluidity as a component of membrane phospholipids
and as a result of their high melting point. They have
been reported to block the synthesis of enzymes such
as oxygenase desaturase and prostaglandin synthetase
in the enzymatic pathway (Kahraman & K€
upl€
ul€
u, 2011).
Furthermore, TFAs have been shown to suppress the
desaturation and elongation reactions of essential fatty
acids, as well as decreasing AA levels and cyclooxyge-
nase activity. As a result, linoleic and gamma linoleic
acid are blocked from turning into longer chain unsat-
urated metabolites (Kahraman & K€
upl€
ul€
u, 2011; Tas¸an
& Daglıoglu, 2005).
Studying the health effects shows that TFAs induce
insulin resistance by changing the fatty acid compos-
ition in the membrane structure of adipocytes (Riserus,
2006). It is also suggested that excess TFA intake
(>2% of the energy from TFAs) may increase plas-
minogen activator inhibitor activity, which is a risk fac-
tor for fetal loss, by increasing the risk of type-2
diabetes and insulin resistance (Morrison, Glueck, &
Wang, 2008). Similarly, a 2% rise in total energy
derived from TFAs has been reported to be linked to a
23% rise in the risk of death from cardiovascular dis-
ease (CVD) and heart attack (Brouwer, Wanders, &
Katan, 2013; Mozaffarian, Aro, & Willett, 2009). They
have been reported to increase the risk of CVD
through high-density lipoprotein-cholesterol (HDL-c)
inhibition and low-density lipoprotein-cholesterol
(LDL-c) induction (Mozaffarian, Katan, Ascherio,
Stampfer, & Willet, 2006). Evidence suggests that in
addition to CVDs, TFA intake is also linked to diabetes,
Alzheimer’s, breast cancer, endometriosis, cholelithiasis,
fertility issues and infertility (Field, Willett, Lissner, &
Colditz, 2007; Smit, Willett, & Campos, 2010; Teegala,
Willett, & Mozaffarian, 2009). Table 1 summarizes the
adverse effects of TFA on health (Bhardwaj, Passi, &
Misra, 2011).
Figures 1 and 2summarize nutrition-related factors
in male and female infertility respectively.
The fact that certain dietary ingredients are deemed
responsible for male and female infertility makes it
crucial to study the effects of nutrition on infertility
and reproductive health. This is especially the case for
TFAs, which are reported to have adverse effects on
male and female reproductive health. Adverse effects
such as inhibiting the peroxisome proliferator-acti-
vated receptor-c(PPARc) (Chavarro, Rich-Edwards,
Rosner, & Willett, 2007; Esmaeili, Shahverdi,
Moghadasian, & Alizadeh, 2015) causing abnormalities
in the ovulation cycle by lowering the PPARcgene
mRNA expression (Chavarro et al., 2007); decreasing
the activity of D5 and D6-desaturases which affect
spermatogenesis (Chavarro et al., 2014); restricting the
integration of long-chain PUFAs, which play an active
role in spermatogenesis and epididymal sperm matur-
ation (Esmaeili et al., 2015); blocking the transfer of
n–3 (Cohen, Rifas-Shiman, Rimm, Oken, & Gillman,
2011); preventing the desaturation of a-LA to DHA and
LA to AA (Cohen et al., 2011) may cause infertility.
Articles studying the effects of TFAs on male and
female reproductive system mechanisms have been
examined as part of this review.
Table 1. Adverse effects of TFA on health (Bhardwaj et al., 2011).
Effect Scientific results
CVD TFAs increase VLDL-c and LDL-c levels, while decreasing HDL-c levels. They
also trigger CVD by causing reduced TG intake and free fatty acid
production.
Diminished cognitive state and neurological diseases Prospective epidemiological studies have reported that excess TFA and low
PUFA consumption starting at middle age may lead to a quick decline in
cognitive state. It can also be linked to neurodegenerative diseases.
Fetal development A significant correlation between C18:1 (trans-9) concentration in maternal
plasma phospholipids and low birth weight has been established. TFAs
have been reported to adversely affect growth and development by
inhibiting normal essential fatty acid metabolism. TFAs have also been
proven to directly affect fetal membrane composition. They indirectly
decrease the cis essential amino acid intake of the mother and the fetus.
Ovulatory infertility Shown to increase ovulatory infertility in women.
Insulin resistance and metabolic syndrome Cardiometabolic effect is linked to insulin resistance and metabolic syn-
drome. Shown to induce insulin resistance.
Atherosclerosis TFAs contribute to developing atherosclerosis by increasing biological
markers in the circulatory system thus causing endothelial dysfunction.
Systemic inflammation Contributes to systemic inflammation by increasing CRP levels.
CRP: C-reactive protein; TG: triglycerides; TFA: trans fatty acid; VLDL-c: very-low-density lipoprotein cholesterol; LDL-c: low-density lipopro-
tein cholesterol; CVD: cardiovascular diseases; PUFA: polyunsaturated fatty acid.
2H. C¸EKICI AND Y. AKDEVELIO

GLU

Methods
In order to research the effects of TFAs on reproductive
health, Gazi University and Recep Tayyip Erdo
gan
University access networks were used between
September and January 2016 to search PubMed,
Nature, Science Direct, Clinical Keys and Google aca-
demic databases for the last 10 years for the keywords
‘trans fatty acids and infertility’,‘trans fatty acids and
reproductive system’,‘trans fatty acids and
asthenospermia’,‘trans fatty acids and sperm’,‘trans
fatty acids and ovulatory infertility’,‘female
reproductive health’,‘male reproductive health’in both
Turkish and English. The word ‘and’was used to ascer-
tain the correlation between TFAs and reproductive
health. Clinical studies and compilation articles in both
English and Turkish were included in this study, if they
were accessible in their entirety. Thesis papers and oral
and poster presentations from conferences on the sub-
ject were not included in the study.
Findings
Fifteen studies in total were included based on the cri-
teria; four on the association between TFAs and fetal
loss and fetal development, eight between TFAs and
semen quality and semen parameters, and three
between TFAs and ovulatory infertility. Table 2 summa-
rizes these studies and their results.
Results
Effects of trans fatty acids on sperm quality and
sperm parameters
Sperm membrane lipid composition has a distinct
effect on the functional properties of sperm. High TFA
levels in sperm were reported to be associated with
low sperm concentration (Esmaeili et al., 2015). DHA
density in the sperm tail affects the fluidity and flexi-
bility of the sperm (Esmaeili et al., 2015). The DHA pro-
portion is notably higher in sperm membrane
phospholipids than in other cells. Consequently, PUFA
High alcohol and caffeine consumption
(>5 cups of coffee/day or >500mg)
High sweets, sweetened food and drink
and sugar consumption
High fat, saturated fat and TFA
consumption (calorie intake as fat
>35%, calorie intake as TFA > 1%)
Excess consumption of soy and soy
products ( 0.30 serving/day) and
potatoes
High cheese, full fat milk and dairy
consumption
Low intake of fruits and vegetables
(<5 serving/day)
Fruit and vegetable consumption
Whole-grain based dietary fibre intake
Fish, seafood,crustacean and chicken
consumption
Low fat milk and dairy consumption
Sufficient antioxidant intake
(Vitamins E, D and C, β-Carotene,
selenium, zinc, cryptoxanthin, lycopene,
and folate)
Nutritional factors that increase risk of
infertility
Nutritional factors that decrease risk of
infertility
Male Infertility
(Abnormal sperm parameters and hormone levels)
Figure 1. Nutrition-related factors in male infertility (Chavarro, Rich-Edwards, Rosner, & Willett, 2008; Kazemi, Ramezanzadeh, &
Nasr-Esfahani, 2014; Mendiola et al., 2009; Ricci et al., 2017; Rossi, Abusief, & Missmer, 2014; Salas-Huetos, Bull
o, & Salas-Salvad
o,
2017).
Nutritional factors that increase risk of
infertility
Fem
(Fertilization and miscarriage rate)
m
ale Infertili
tty (Fecundati
Tea consumption exceeding daily safe limits
(regardless of caffeine content)
Caffeine consumption (consuming at least 2 or
more caffeinated soft drinks per day or
>300mg/d day total caffeine intake)
High fat consumption (consumption of a diet in
which 60% of calories come from fat)
Red and processed meat consumption (total
protein energy ≥23%, animal protein energy
≥6%)
ion)
Figure 2. Nutrition-related factors in female infertility (Cao,
Ren, Feng, Yang, & Liu, 2016; Chavarro et al., 2008; Chavarro,
Rich-Edwards, Rosner, & Willett, 2009; Salas-Huetos et al.,
2017; Skaznik-Wikiel, Swindle, Allshouse, Polotsky, &
McManaman, 2016).
HUMAN FERTILITY 3

Table 2. Literature related to trans fatty acids and infertility.
Study Sample Findings Conclusion
Chavarro et al., 2007 18,555 women with no infertility his-
tory, who tried to get pregnant or
got pregnant between 1991 and
1999
438 cases of infertility. Each 2% rise
in energy from TFAs has been
linked to 73% higher risk of ovula-
tory infertility. Two percent of
energy from TFAs doubles the risk
of infertility.
Consuming TFAs instead of unhydro-
genated oil, carbohydrates or
unsaturated fats may increase the
risk of infertility.
Morrison et al., 2008 104 women with insulin data, who
reported one more pregnancies
A significant, curvilinear, independent
relationship between a rise in per-
centage of energy from TFAs and
fetal loss has been discovered. As
percentage of energy from TFAs
rises a sharp increase in one or
more fetal loss rate was observed.
A sharp increase in fetal loss was
observed when percentage of
energy from TFAs is more than
4.7%.
Dirix et al., 2009a 782 mother–baby pairings No significant correlation was found
between TFA isomer 18:1t in
maternal plasma phospholipids
and birth weight.
No significant correlation was found
between TFA and birth weight.
Dirix et al., 2009b 782 mother–baby pairings An inverse proportion was found
between 18:1t concentrations in
umbilical cord phospholipids and
birth weight.
TFAs decrease birth weight.
Cohen et al., 2011 1369 pregnant women As a result of blocking omega-3
transfer, TFA intake can cause fetal
development abnormalities espe-
cially in the second trimester.
TFAs were reported to possibly cause
fetal development abnormalities.
Chavarro, Furtado et al., 2011 33 men undergoing infertility evalu-
ation at an medical centre
High TFAs in western-type diet have
shown a negative correlation with
sperm concentration.
TFAs have an adverse effect on sperm
concentration.
Chavarro, Attaman, et al., 2011 99 men from an infertility clinic No significant correlation was
detected between TFAs and sperm
motility, sperm morphology; how-
ever, a negative correlation was
determined between TFAs and
sperm concentration.
TFAs were reported as having an
adverse effect on semen concen-
tration by inhibiting the generation
of DHA and EPA.
Attaman et al., 2012 99 fertile men A negative correlation was deter-
mined between TFA intake and
sperm concentration and total
sperm count.
TFAs decrease total sperm count and
sperm concentration.
Jensen et al., 2013 701 young men A negative correlation was deter-
mined between TFAs and sperm
concentration and total sperm
count.
TFAs decrease total sperm count and
sperm concentration.
Chavarro et al., 2014 209 healthy young university students
18–23 years of age
When TFA intake increases from
0.37% of total energy intake to
1.03%, sperm concentration regis-
ters a significant decrease from
135 10
6
–94.9 10
6
.
High TFAs in western-style diet dis-
play a negative correlation with
sperm concentration.
Ghaffarzad et al., 2014 35 infertile women with PCOS and 29
healthy women
Among the red blood cell TFAs, only
trans-linoleate (18:2t) is signifi-
cantly higher compared to the
control group. Tendency of the
PCOS group to consume foods rich
in TFAs is higher compared to the
control group.
A correlation was discovered only
between 18:2t and risk of ovula-
tory infertility in PCOS. TFAs are
regarded as a precursor for
increased risk of ovulatory infertil-
ity in women with PCOS.
Eslamian et al., 2015 Total of 107 asthenospermic men and
235 age appropriate healthy men
TFA’s, palmitic acid and stearic acid
were found to have a positive cor-
relation with asthenospermia.
Conversely, higher omega-3, PUFA
and DHA intake was discovered to
have a significant correlation with
low asthenospermia rate.
Excess TFA intake was found to have
positive correlation with
asthenospermia.
Jamioł-Milc et al., 2015 53 pregnant women between the
ages of 18 and 39 and newborns
Elaidic and vaccenic acid levels were
found in maternal and umbilical
plasma.
TFA levels were found to have no
effect on neonatal birth weight
and body height.
Arvizu et al., 2015 141 couples undergoing ART in a fer-
tility clinic
Fertilization rates were found to be
lowest in couples with highest TFA
intake (energy from TFA 1.20%) of
the male partner.
Higher TFA intake in men was found
to be linked to fertilization rates in
couples undergoing ART.
Eslamian et al., 2016 107 men with asthenospermia
between the ages of 20 and 40
and control group (n¼235)
Western-type diet (rich in fast food,
saturated fats, TFAs and animal
based food) was found to have a
positive correlation with
asthenospermia.
Western-type diet is a potential risk
factor for asthenospermia.
TFA: trans fatty acid; DHA: docosahexaenoic acid; EPA: eicosapentaenoic acid; PCOS: polycystic ovary syndrome; PUFA: plyunsaturated fatty acid; ART:
assisted reproductive technologies.
4H. C¸EKICI AND Y. AKDEVELIO

GLU

metabolism in the testes is more active during sperm-
atogenesis and epididymal sperm maturation com-
pared to PUFA metabolism in other human tissues. It
has recently been suggested that lipid concentrations
can affect semen parameters and that this effect is
more distinct in sperm head morphology (Esmaeili
et al., 2015). Dietary n–3 fatty acids may improve
sperm function by manipulating sperm head and tail
fatty acid profiles. In contrast, dietary TFAs have an
adverse effect on semen quality and may cause infer-
tility by inhibiting PUFA metabolism essential for the
sperm (Esmaeili et al., 2015).
The negative correlation between excess TFA intake
and sperm markers has made a more rigorous study
of fatty acid profiles in the reproductive system neces-
sary. TFAs have an adverse effect on semen function
(motility, fluidity and density, etc.) by changing the
membrane lipid composition of the sperm. Adversely
affected semen quality constitutes a primary contribu-
ting factor for infertility (Esmaeili et al., 2015).
Furthermore, dietary TFAs in the male are reported to
decrease the chance of fertilization (Arvizu, Tanrikut,
Hauser, Keller, & Chavarro, 2015). A study conducted
on 141 couples undergoing ART, reported that sperm
from men with the highest TFA intake (1.20% of total
energy intake) gave the lowest rate of fertilization.
Furthermore, TFA intake correlates positively with low
total testosterone and calculated free testosterone
concentration, but has a negative correlation with tes-
ticular volume (Arvizu et al., 2015). These findings sug-
gest that TFAs may affect testicular function. Men in
the top 25% of TFA intake have been reported as hav-
ing 37% lower total sperm count, 15% lower testoster-
one levels and 4% less testicular volume than men
with lowest TFA consumption (M

ınguez-Alarc
on et al.,
2017). Sperm TFA levels are reported to be inversely
proportional to sperm concentration (M

ınguez-Alarc
on
et al., 2017). Similarly, TFA exposure in male mice
causes TFA accumulation in the testes leading to lower
serum testosterone concentrations and sperm count.
Inhibition of spermatogenesis and testicular degener-
ation are severe reproductive disorders associated with
TFAs (Hanis, Zidek, Sachova, Klir, & Deyl, 1989; Veaute
et al., 2007).
Studying why TFAs affect semen quality has
invoked the influence of PPARc. The PPARs, which
have some similarity with steroid and thyroid hormone
receptors, are ligand-activated nuclear transcription
factors. Both PPARaand PPARcresponsive genes are
involved in lipid homeostasis, especially glucose and
lipid homeostasis. Both oviducts includes oviduct-
derived soluble factors and embryos derived-autocrine
factors are sources of PPAR ligands (Huang, 2008).
PPAR forms which are activated by binding of PUFAs
are expressed in different parts of the reproductive
system (hypothalamus, pituitary, ovaries, uterus and
testis). TFAs inhibit PPARc’s main role on sperm
metabolism by down-regulating PPARcmRNA expres-
sion. Such adverse effects of TFAs have been claimed
to be responsible for infertility (Esmaeili et al., 2015).
A cross-sectional study has revealed that while TFAs
have no correlation with sperm motility and sperm
morphology, they have a negative correlation with
sperm concentration (Chavarro, Attaman, et al., 2011).
While TFA intake was found to have a positive correl-
ation with sperm and seminal plasma TFA levels, it has
a negative correlation with DHA sperm levels and EPA
seminal plasma levels. TFAs were reported to have an
adverse effect on semen concentration by their effect
on inhibition of DHA and EPA generation (Chavarro,
Attaman, et al., 2011).
It is still unclear how an increase in TFA concentra-
tions in semen of subfertile and infertile men regard-
less of the source of TFAs (diet or synthesis) affects
infertility. Recent studies have shown a negative cor-
relation between western-type diets high in TFAs and
sperm concentration (Chavarro et al., 2014; Chavarro,
Furtado, et al., 2011). For example, Chavarro et al.
(2014) reported that when TFA intake increased from
0.37% of total energy intake to 1.03% in healthy men
between the ages of 18 and 23 years, sperm concen-
tration registered a significant drop, from 135 10
6
to
94.9 10
6
. However, analysis of the components of
the diet, data on a possible correlation between TFA
intake and semen quality remains inconclusive.
However, seminal plasma TFAs were found to have a
negative correlation with sperm concentration and
total sperm count in fertile patients (Attaman et al.,
2012; Jensen et al., 2013). Similarly, evidence in rodent
models suggests that TFA intake may lead to defects
in spermatogenesis and testicular damage (Hanis et al.,
1989).
A possible effect of TFAs on diminished sperm
count may be in terms of a decrease in the activity of
D5 and D6-desaturases which affect spermatogenesis,
potentially restricting the integration of long-chain
PUFAs into sperm membranes (Chavarro et al., 2014).
The association between asthenospermia, which is
defined as decreased sperm motility, and nutrition is
still unknown. The correlation between TFAs and
asthenospermia is especially striking. Thus, in a current
case control study on men with asthenospermia;
evaluation of dietary intake, semen quality and endo-
crinological parameters has shown that TFAs, palmitic
acid and stearic acid have a positive relationship with
asthenospermia (Eslamian et al., 2015). Conversely,
HUMAN FERTILITY 5

high levels of n–3 fatty acid and DHA intake has been
linked to lower rates of asthenospermia. Consequently,
findings from various studies suggest that TFA intake
increases the risk of asthenospermia (Eslamian,
Amirjannati, Rashidkhani, & Sadeghi, 2012; Eslamian
et al., 2015). Similarly, a controlled study on 107 male
patients with asthenospermia aged between 20 and
40 years has revealed that a western-style diet not
only had a positive correlation with asthenospermia,
but that constituted an undesirable risk factor.
Effects of trans fatty acids on ovulatory infertility
Anovulation is an important gynaecological problem
and commonly present with irregular menstruation
oramenorrhea. In case of anovulation, women have
adequate oestrogens but no ovulation (Chandeying &
Pantasri, 2015). Menstrual irregularity is almost always
the result of anovulatory cycles but the reverse is not
true; monthly menstrual regularity does not necessarily
indicate underlying regular ovulatory cyclicity
(Rosenfield, 2013). Chronic anovulation is defined as a
prolonged interval between menstrual cycles for more
than 35 days, or amenorrhea for at least 6 months.
Many diseases and conditions, such as polycystic ovary
syndrome (PCOS), Cushing’s syndrome, hyperthyroid-
ism or hypothyroidism, hypothalamic disorders, late-
onset congenital adrenal hyperplasia, adrenal and
ovarian tumors are associated with chronic anovula-
tion (Chandeying & Pantasri, 2015).
A prominent finding in female reproductive health
regarding the correlation between TFAs and infertility
is ovulatory infertility. TFAs constitute a major albeit
modifiable risk factor for ovulatory infertility disorder.
The mechanism of ovulation plainly demonstrates the
adverse effect of TFAs. Low levels of plasma EPA and
erythrocyte DHA are seen in infertile women and TFAs
have been proposed as responsible for low levels of
EPA and DHA. Each 2% rise in TFA intake increases the
relative risk of ovulatory infertility from 1.73 to 2.31
(Chavarro et al., 2007). Seli, Babayev, Collins, Nemeth,
and Horvath, (2014) have reported that a diet high in
TFAs adversely affects fertility through lipotoxicity and
increases the risk of ovulatory infertility.
Similarly, in a study conducted on 18,555 women
with no history of infertility, who have previously tried
to be pregnant or become pregnant; 438 cases of ovu-
latory infertility were observed while total fat intake,
cholesterol and fatty acid intake did not appear to
have a significant correlation with ovulatory infertility.
The amount of TFAs in the diet as a proportion of
total energy intake is considered to have a stronger
effect on infertility compared to that of other
nutrients. In terms of the contribution made to total
energy intake, each 2% rise in energy from TFAs, as
opposed to carbohydrates and n–3 fatty acids, is
linked to 73% higher risk of ovulatory infertility. In
addition, a 2% contribution of energy from TFAs to
the total energy intake instead of from n–6 polyunsat-
urated fats doubles the risk of ovulatory infertility. It
follows that when consumed instead of carbohydrates
(Chavarro et al., 2007), TFAs can increase the risk of
infertility. In a controlled study on 35 infertile women
with PCOS, only trans-linoleate (18:2t) was significantly
higher in women with PCOS compared to the control
group. Women with PCOS also displayed a higher ten-
dency to consume foods rich in TFAs compared to the
control (Ghaffarzad et al., 2014). A closer look at the
type of TFAs revealed that risk of ovulatory infertility
in PCOS only related positively with 18:2t. These find-
ings suggest that TFAs may constitute a precursor for
increased risk of ovulatory infertility in women with
PCOS and other women (Ghaffarzad et al., 2014).
Effects of trans fatty acids on fetal development
and fetal loss
In addition to their known adverse effects on male
and female reproductive system, TFAs are also seen as
a risk factor for fetal loss and are deemed responsible
for fetal developmental disorders. TFA exposure at the
fetal level is known to increase the risk of developing
lifelong metabolic disorders (Mennitti et al., 2015).
Known adverse effects of TFAs on fetal development
include triggering insulin resistance and diabetes, asso-
ciated abnormalities in liver and adipose tissue func-
tions and negatively impact on the metabolism of
PUFAs which are essential for fetal development. In
light of this information, maternal nutritional status
and fatty acid composition of the mother’s nutrition
are closely linked to normal fetal and postnatal devel-
opment, as well affecting individual risks in fetal devel-
opment (Mennitti et al., 2015).
The potential adverse effects of dietary TFA intake
during pregnancy on growth and development are
striking (Amusquivar, S
anchez-Blanco, Clayton,
Cammarata, & Herrera, 2014). It is suggested that TFAs
interfere with the regulation of the hormones,
enzymes and genes involved in down-regulating
PPARcgene expression, which is involved in maintain-
ing placental maturation and function, as well as hor-
mone secretion (Esmaeili et al., 2015; Mozaffarian
et al., 2006). Moreover, Morrison, Glueck, and Wang,
(2008) have reported that TFAs may increase plasmino-
gen activator inhibitor activity, which is a risk factor
for fetal loss. Thus, high TFA intake is viewed as an
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indirect risk factor for fetal loss. In a study on 104
women who had reported one or more pregnancies;
the proportion of dietary energy from TFAs showed a
significant correlation with fetal loss. A significant rise
in the number of fetuses lost was also a function of
the proportion of energy from TFAs (Morrison et al.,
2008). When the percentage of energy from TFAs
reached over 4.7% of total energy, a severe increase in
fetal loss was observed (Morrison et al., 2008).
Lipid levels in cord blood of term babies and mater-
nal plasma are similar, emphasizing the importance of
TFA flow between the mother and the fetus. A direct
correlation was determined between elaidic acid levels
in maternal plasma and fetal tissue (Amusquivar et al.,
2014) and it has been reported that TFAs are passed
to the fetus through the placenta. In umbilical cord
plasma lipids in newborns, a negative correlation has
been reported between TFAs and DHA and AA both of
which are crucial for fetal development. It is possible
that TFAs may block the transfer of PUFAs to the fetus
or interfere with their metabolism (Innis, 2007). The
main mechanism of action is that they cause changes
to the desaturation form of fatty acids which may pre-
vent the desaturation of a-LA to DHA and LA to AA,
adversely affecting fetal growth (Cohen et al., 2011).
Some studies have examined possible effects of
TFAs on fetal growth (Dirix, Kester, & Hornstra, 2009a,
2009b; Elias & Innis, 2001). A study conducted on 84
pregnant Canadian women reported that naturally
occurring or industrially manufactured TFA intake is
inversely related to length of gestation (Elias & Innis,
2001). A study conducted on 782 mother–baby pair-
ings based on gestational age found no link between
the TFA isomer 18:1t in maternal plasma phospholipids
and birth weight (Dirix et al., 2009a). However, 18:1t
concentrations in erythrocyte phospholipids from the
umbilical cord showed a negative correlation with
birth weight (Dirix, Kester, & Hornstra, 2009b).
Cohen et al. (2011) have reported that TFAs can
block the transfer of n–3 fatty acids from the placenta
to the fetus or interfere and that TFAs can lead to fetal
developmental disorders by blocking n–3 transfer,
especially by interfering with fetal growth in the
second trimester, with no effect in the first trimester
(Cohen et al., 2011). In terms of the effects of TFAs on
the neurological health of the fetus and the baby;
Decsi and Boehm (2013) found that TFAs obtained
from umbilical lipids were related to the neurological
condition of 18 month old healthy children. Children
with minimal neurological dysfunction had significantly
higher cord vein wall trans octadecadienoic acid val-
ues compared to normal children. Total TFA values in
umbilical vein wall lipids, as well as total 18-carbon
TFA values were negatively correlated with neuro-
logical optimality score. In light of these findings, TFAs
may constitute a confounder in the relation between
fetal fatty acid composition and intrauterine growth
(Decsi & Boehm, 2013). It has been revealed that TFA
intake during pregnancy and lactation causes hypo-
thalamic inflammation in the baby through the TLR4/
NFjBp65 signalling pathway and that harmful meta-
bolic results persist even after TFA intake is terminated
(Pimentel et al., 2012). However, a study on the effects
of TFAs on fetal development has determined that
TFA levels have no effect on neonatal birth weight
and body height (Jamioł-Milc, Stachowska, Janus,
Barcz, & Chlubek, 2015). Similarly, Amusquivar et al.
(2014) have reported no differences in fetal and new-
born rats fed TFAs and olive oil in relation to
anthropometric variables. The effects of TFAs on fetal
development and human health may vary depending
on TFA sources (ruminant or industrial) (Enke et al.,
2011).
Conclusion and suggestions
The articles considered in this review have indicated
an association between a dietary TFA intake of greater
than 1% of total energy and low sperm concentration
and semen quality. When energy from dietary TFA
intake is more than 2% of total energy this is a link to
ovulatory infertility in women. In addition to infertility,
TFAs are related to fetal developmental disorders and
fetal loss through an adverse effect on DHA and AA
which are crucial for fetal development—blocking the
transfer of PUFAs to the fetus or interfering with the
metabolism of these fatty acids.
In light of these results, limiting the amount of
energy from dietary TFAs to lower than 1% of total
energy, and replacing TFAs in the diet with PUFAs will
likely have a positive impact on minimizing infertility
and negative results on fetal life. To achieve this a
Mediterranean diet rich in n–3 fatty acids, vitamins
and minerals, is recommended. In order to minimize
the risk of infertility, sufficient zinc, folic acid, vitamins
C and E intake should be included. While biological
indicators on the impact of TFAs in male infertility sup-
port these conclusions, it is crucial that further
research where multiple variables are taken into
account is conducted before a definitive conclusion is
reached. Since each 2% rise in energy from TFAs is
linked to a greater than 73% higher risk of ovulatory
infertility in women, TFA intake should be avoided and
nutritional choices made accordingly.
HUMAN FERTILITY 7

Disclosure statement
No potential conflict of interest was reported by the authors.
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