Diet in pregnancy—more than food

Abstract

Conclusion:
In this review, we will summarise the recommendations for diet composition in pregnancy, focusing on both diet quality and quantity. What is Known • High food quality, together with adequate macro- and micronutrient intake in pregnancy, is crucial for the health status of the mother and child. What is New • Recent findings suggest that the diet could be beneficial or harmful in the context of the well-being of the whole future population. Most conditions that occur in adulthood originate in foetal life. • Moreover, some epigenetic events, modified by diet impact more than one generation.

Full text

REVIEW
Diet in pregnancy—more than food
H. Danielewicz
1
&G. Myszczyszyn
2
&A. Dębińska
1
&A. Myszkal
2
&A. Boznański
1
&
L. Hirnle
2
Received: 8 July 2017 /Revised: 25 September 2017 /Accepted: 26 September 2017 /Published online: 3 November 2017
#The Author(s) 2017. This article is an open access publication
Abstract High food quality, together with adequate macro-
and micronutrient intake in pregnancy, is crucial for the health
status of the mother and child. Recent findings suggest that it
could also be beneficial or harmful in the context of the well-
being of the whole future population. According to the devel-
opmental origins of health and disease hypothesis, most con-
ditions that occur in adulthood originate in foetal life.
Moreover, some epigenetic events, modified inter alia by diet,
impact more than one generation. Still, the recommendations
in most countries are neither popularised nor very detailed.
While it seems to be important to direct diet trends towards
a healthier lifestyle, the methods of preventing specific disor-
ders like diabetes or asthma are not yet established and require
further investigation.
Conclusion: In this review, we will summarise the recom-
mendations for diet composition in pregnancy, focusing on
both diet quality and quantity.
舃What is Known
舃•High food quality, together with adequate macro- and micronutrient
intake in pregnancy, is crucial for the health status of the mother and
child.
舃What is New
舃•Recent findings suggest that the diet could be beneficial or harmful in
the context of the well-being of the whole future population. Most
conditions that occur in adulthood originate in foetal life.
舃•Moreover, some epigenetic events, modified by diet impact more than
one generation.
Keywords Pregnancy .Maternal diet .Developmental
programming
Abbreviations
AAD Allergic airway disease
ADHD Attention-deficit hyperactivity disorder
ALA Alpha linolenic acid
BMI Body mass index
BPA Bisphenol A
DC Dendritic cell
DHA Docosahexaenoic acid
EPA Eicosapentaenoic acid
GPR20 G protein-coupled receptor 20
GWG Gestational weight gain
HELP Haemolysis, elevated liver enzymes and low plate-
let count
IL-1βInterleukin-1beta
Communicated by Mario Bianchetti
*H. Danielewicz
hanna.danielewicz@umed.wroc.pl
G. Myszczyszyn
grzegorz.myszczyszyn@gmail.com
A. Dębińska
aanowak@gmail.com
A. Myszkal
ammyszkal@gmail.com
A. Boznański
andrzej.boznanski@gmail.com
L. Hirnle
lidia.hirnle@gmail.com
1
1st Department of Pediatrics, Allergy and Cardiology, Wroclaw
Medical University, Chalubinskiego 2a 50-368, Wroclaw, Poland
2
1st Department of Obstetrics and Gynecology, Wroclaw Medical
University, Chalubinskiego 3 50-368, Wroclaw, Poland
Eur J Pediatr (2017) 176:1573–1579
DOI 10.1007/s00431-017-3026-5
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

IL-6 Interleukin-6
IL-8 Interleukin-8
IOM Institute of Medicine
IUGR Intrauterine growth retardation
LBW Low birth weight
LPS Lipopolysaccharide
NF-κB Nucleic factor kappa B
NPPA Natriuretic peptide A
RDA Recommended dietary allowances
RvD Resolvin D
SCFA Short-chain fatty acid
SGA Small for gestational age
TLR Toll-like receptor
TNFαTumour necrosis factor alpha
Introduction
The substantial increase in the prevalence of common diseases
like asthma, atopy, obesity, hypertension and diabetes ob-
served over the past decades has directed attention to specific
changes in the environment as a possible cause of such an
unfavourable switch. Among environmental factors, the diet
is a crucial influencer of population health. According to the
developmental origins of health and disease hypothesis, most
conditions that occur in adulthood originate in foetal life.
Pregnancy is a specifically Bhot period^for the programming
of future condition. The relevance of the maternal diet to se-
rious pregnancy outcomes such as preeclampsia, hyperten-
sion, preterm birth and fertility hasalso been revealed [23,26].
In this narrative review, we will summarise the recommen-
dations for diet composition in pregnancy and existing devel-
opmental theories, focusing on both diet quality and quantity.
The aim of this review is to give the interpretative synthesis of
the current knowledge and highlight the developmental aspect
of maternal diet.
The literature search was provided via PubMed database with
the following search terms: Bdiet in pregnancy recommendation^,
Bspecific micro- or macronutrient and pregnancy^,Bspecific preg-
nancy outcome^,Bdiet in pregnancy and atopy/asthma^,
Bdevelopmental origin of disease^focusing on both more recent
reviews limited to specific aspects of diet and original papers.
Composition of the maternal diet—quality
Specific recommendations exist for different types of nutrients in
pregnancy. They differ in some points according to both the
eating tradition and nutrition status of the population. WHO an-
tenatal standards paper provides 39 recommendations related to 5
types of interventions. The healthy eating and physically active
styleoflifeispromotedtoprevent excessive gestational weight
gain (GWG). In the undernourished population, balanced energy
and protein intake are recommended to prevent LBW, SGA, and
stillbirths. Doses of iron and folate supplementation are given
with possible daily or intermittent routine. Supplementation of
vitamin A is suggested to be restricted only to areas where vita-
min A deficiency is a substantial public health problem.
Recommendation of calcium supplementation is limited to pop-
ulation with low-calcium intake. Vitamin B6, zinc, multi-nutrient
supplements and vitamin D supplementation are not advocated
as routine procedure. Avoiding of caffeine is suggested for wom-
en with high consumption [40]. Canadian consensus highlights
the need of the uptake of nutrient-dense and energy-appropriate
food with moderate increase of energy intake during pregnancy.
Particular concern is given to GWG, adequate folate, iron, cho-
line, omega-3 fatty acid and iodine input, as well as avoiding or
limiting specific food which contains bacteria or methyl mercury
and alcohol [25]. German National Consensus is quite detailed in
different aspects of diet in pregnancy. In the first paragraph, the
difference between slightly increase of energy needs in compar-
ison to a much greater increase of vitamin and minerals is
highlighted. According to these requirements, nutrient-dense
food eating, regular meals and regular exercises together with
moderate GWG are recommended. The specific concerns exist
for obese pregnant women for whom the standards of care and
weight lose still are not well established, vegetarian nutrition with
possible supplementation of iron and DHA and vegan where
specific medical counselling is required due to diet deficiency
of many nutrients [16]. Italian Consensus differs a little in the
points according to energy input and protein intake during preg-
nancy, where specific amounts are recommended in the particular
periods. The emphasis is put on the protein and fat composition,
iron supplementation, as well as iodine and calcium adequate
provision [17]. Standards of nutrition for Polish population,
reflecting WHO and EFSA recommendations, contain tables
for different groups according to age, sex and pregnancy status
for both micro- and macronutrients together with energy require-
ments and expenditure [7,14]. Similar tables are published by
Institute of Medicine [13,31]. Further in the text, the nutrient
requirements during pregnancy are described in details and
summarised in Table 1. Apart from the recommendations, there
is substantial body of reviews concerning specific aspects of
maternal nutrition. In the last 2 years, we identified important
papers in the subject relating to diet and fertility, interventions
for diabetic or obese pregnant women, metabolic consequences
of excessive GWG, the impact of the diet rich in polyphenols, the
use of probiotics and prebiotics, the maternal microbiome and the
development of neonatal immune system, the benefits of
Mediterranean diet and the epigenetic programming.
Macronutrients
Protein
Both the quantity and the composition of protein are important
in the context of diet quality. In a rat model, protein deficiency
1574 Eur J Pediatr (2017) 176:1573–1579
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

in pregnancy results in decreased birth weight, decreased heart
weight, increased heart rate and increased systolic blood pres-
sure [2]. In general, animal protein is of higher quality than
vegetable protein, suggesting that meat should be the main
source of protein in pregnancy, but mixing different types of
vegetables increases the quality of plant protein substantially.
Nevertheless, it should also be considered that specific
types of plant diets, such as vegetarian and vegan diets, are
associated with microelement and mineral deficiencies and
unfavourable pregnancy outcomes. In this context, a vegetar-
ian diet can result in vitamin B12 and iron deficiency, as well
as low birth weight, whereas a vegan diet can lead to inade-
quate intake of DHA, zinc and iron, as well as an increased
risk of preeclampsia and inadequate brain development.
However, still a well-balanced ovo-lacto vegetarian diet usu-
ally enables good nutrient status in pregnancy, when supple-
mented with vitamin D, folic acid, iodine, iron, vitamin B12
and zinc, and, in cases of a fish-free diet, with DHA [19].
In contrast, consumption of red meat, which was recently
revealed to be associated with cancer risk, raises some con-
cerns over pregnancy and protein requirements, but till now,
there are no any evidences that this diet can negatively impact
child’shealth[24].
Fat
Fat in the diet of pregnant woman is important mainly in
context of fatty acid composition, mainly that of DHA and
eicosapentaenoic acid (EPA). Omega-3 fatty acids are benefi-
cial for brain development and proper functioning of the ret-
ina. In many studies, maternal serum DHA concentration has
been associated with neuronal development and plasticity,
receptor-mediated signalling, membrane fluidity and the for-
mation of second messengers. This type of fatty acid also
impacts modulation of inflammation by affecting Toll-like
receptors (TLRs), related to adequate response to bacteria
and other microorganisms. DHA also plays a role as a precur-
sor of the anti-inflammatory lipid mediator RvD, which pre-
vents the formation of proinflammatory arachidonic acid
products, thus indicating the anti-inflammatory function of
these molecules [33].
Carbohydrates
Carbohydrates are an essential component of a healthy diet.
However, increased caloric intake associated with increased
fat and carbohydrate consumption with adequate protein has
been associated with neonatal adiposity, which is obviously
unfavourable [28]. Additionally, a preconception diet rich in
saturated fat, carbohydrates and take-away food has been as-
sociated with poor asthma control during pregnancy, thus af-
fecting child well-being [8]. Moreover, changing the maternal
eating pattern by decreasing carbohydrate load and increasing
physical activity could impact the inflammation status associ-
ated with obesity in pregnant women [32]. Similarly, modify-
ing the protein/carbohydrate ratio can decrease the expected
GWG [18].
Tab le 1 Micro- and macronutrients intake during pregnancy—
summary of the recommendations
Energy No additional input I trimester
340 kcal/day II trimester
452 kcal/day III trimester [31]
69 kcal/day I trimester
266–360 kcal/day II trimester
437–496 kcal/day III trimester [17]
10% increase in late pregnancy—260 kcal/day [16]
GWG •BMI < 18.5 kg/m
2
GWG 12.5–18 kg
•BMI 18.5–24.9 kg/m
2
GWG 11.5–16 kg
•BMI 25–29.9 kg/m
2
GWG 7–11.5 kg
•BMI > 30 kg/m
2
GWG 5–9kg[25,40]
Protein 10–35% of energy, 71 g/day [13]
Additional 1 g/day I trimester
8 g/day II trimester
26 g/day III trimester [17]
RDA 1.1 g/kg/day [25]
RDA 1.2 g/kg/day [14]
Carbohydrates 45–65% of energy, 175 g/day
Fat 20–35% of energy [13]
Additional 8–14 g/d II trimester
11–18 g/day III trimester [14]
n-6 13 g/day, 5–10% [13]
n-3 1.4 g/day, 0.6–1.2% [13]
EPA 250 mg/day
DHA 100–200 mg/day [14,16]
DHA 600–1000 mg in risk groups [7]
Fibre 28 g/day [13,31]
Iron Supplementation 30–60 mg/day [40]
RDA 27 mg/day [14,31]
Iodine RDA 220 mcg/day [14,31]
Supplementation 100–150 mcg/day [16]
Supplementation 200 mcg/day [7]
None additional supplementation [40]
Folate RDA 600 mcg/day [31]
Supplementation 0.4 mg/day [7,16,40]
Calcium RDA 1.0–1.3 g/day [31]
Supplementation 1.5–2 g/day in risk population (low
calcium intake) [40]
Vitamin D RDA 5 mcg (200 IU)/day [31]
RDA 15 mcg (600 IU)/day [17]
At least 600 IU/day RDA, 1500–2000 IU/day to
maintain the level above 30 ng/ml [11]
None additional supplementation in general [40]
Additional supplementation in risk groups 2000 IU/day
[7]
Eur J Pediatr (2017) 176:1573–1579 1575
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

Fibre
The main role of fibre is to modulate gut microbiome. A high-
fibre diet has been shown to prevent asthma by epigenetic
switch and by impacting the gut microbiota. In a mouse mod-
el, a diet differing only in fibre amount with the same fat,
protein, carbohydrates, energy and weight gain impacts the
development of allergic airway disease (AAD; a model of
human asthma). The mechanism is believed to be related to
the specific microbiota and level of short-chain fatty acids
(SCFAs) in faeces and serum. Specifically, SCFAs (acetate,
propionate and butyrate) regulate acetylation of Foxp3 and
Treg development and thus have an anti-inflammatory effect
but also affect epithelial integrity. The SCFA propionate also
impacts dendritic cell (DC) biology and the ability to promote
the T helper 2 (Th2) response and regulates NPPA gene ex-
pression in the lungs. All these phenomena happen only in
foetal life, possibly in the early stages of development, but
even later in pregnancy has some impact, where the high-
fibre diet has been shown to correlate with fewer GP visits
in the first year of life due to cough and wheezing [37].
Micronutrients
Iron
Iron is one of the most important micronutrients. The usual
absorption from plants is low and could be further decreased
by phytates and polyphenols, which are present in some plant-
based products. The absorption of haem iron from meat is
much higher.
Inadequate iron intake during pregnancy is associated with
cardiovascular risk to the offspring in adulthood. In animal
models, maternal iron deficiency has been associated with
obesity, hypertension and adverse cardiovascular outcomes
[1,29].
Iodine
Iodine is another very important micronutrient. Iodine defi-
ciency has been revealed to be associated with postpartum
hyperthyroidism, perinatal mortality and neonatal hypothy-
roidism. Inadequate iodine intake during pregnancy causes
an increased risk of spontaneous abortion, higher mortality,
birth defects, neurological disorders and brain damage [10].
Fish and shellfish, fruits, vegetables, milk, eggs and meat are
the main source of iodine from the usual diet.
Calcium and vitamin D
The main source of calcium is milk and milk products (50%),
cereals (11%) and vegetables (11%). It is crucial for bone
metabolism but also related to birth weight, risk of preterm
labour and appropriate blood pressure [12].
Early studies concerning vitamin D in pregnancy
showed an association with preeclampsia and caesarean
section but also glucose tolerance, abnormal foetal
grown pattern, preterm birth and reproductive failure.
In the first weeks of pregnancy, the level of the vitamin
D metabolite 1,25(OH)D3 increases 2–3-fold, regardless
of the level of intake, but the significance of this phe-
nomenon is unknown. This mechanism could possibly
maintain the required level during pregnancy if precon-
ception stores were normal. Below adequate levels of
25(OH)D3 (< 20 ng/ml) are related to adverse outcomes
later in life, such as asthma, multiple sclerosis, neuro-
logical disorders and autoimmune conditions.
The main dietary sources of vitamin D are cod liver oil and
fish. Smaller amounts are present in eggs, butter and cheese;
however, the most important contributor to the general level is
skin production upon exposure to UV radiation and additional
supplementation [21].
Folates
Folates are extremely important for the prevention of neural
tube defects. The RDA increases by up to 50% in pregnancy,
and the recommended supplementation dose is 400–800 μg
from 2 months prior to conception onward, which is essential
in the first trimester and could be continued after the 12th
week of pregnancy [39].
BPA
Environmental exposure to harmful substances in pregnancy,
especially those present in the diet, raises concerns. BPA is
used for different types of food packaging and as food addi-
tives and has now become the focus of interest. Exposure to
this substance has been associated with adiposity, energy bal-
ance [38] and neurogenesis [22] and thus can be related to
obesity and neurological disorders such as ADHD, anxiety,
depression and sexual dimorphic behaviours.
Composition of the maternal diet—quantity
Gestational weight gain
According to US epidemiological data, 69% of the popu-
lation is overweight and 35% is obese. This change in
prevalence is related to changes in lifestyle, but some
prenatal events are also important. Gestational weight
gain GWG has been shown to be a predictor of pregnancy
complications and future health problems in the child [15,
30]. GWG is strongly associated with birth weight and
values exceeding 4000 g are associated with a 2-fold
1576 Eur J Pediatr (2017) 176:1573–1579
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

greater risk of obesity later in life. Excess intake of calo-
ries during pregnancy has been associated with miscar-
riage, diabetes and preeclampsia in mothers and obesity
and type 2 diabetes in children. This diabetic effect seems
to be transgenerational. The mechanism is possibly related
to placental gene-expression changes [35].
Surprisingly, opposite effect was described by Barker and
colleagues who observed that nutritional insufficiency in the
foetal period reflected by LBW or SGA is also related to
glucose intolerance, diabetes, hypertension and coronary dis-
ease later in life [3]. These observations are the basis of the so-
called thirsty phenotype hypothesis, which reflects the chang-
es in the metabolism as it increases efficiency. The values for
appropriate GWG are given in Table 1.
Metabolic programming, cardiovascular risk and cortisol
metabolism
A substantial number of studies have proven the causa-
tive relationship between birth weight, weight catch-up
and cardio-metabolic risk reflected by alternation in liver
and pancreatic functions [36]. BFatty liver^in normal-
weight offspring could be both a result of a high-fat
maternal diet or protein restriction. Later in life, both
poor weight gain and accelerated weight gain in the first
months of infancy increase the risk of non-alcoholic fatty
liver disease (NAFLD) [27]. What is more, maternal pro-
tein restriction in animal models modifies the offspring’s
islet cell ontogeny and the number of beta cells [5,34].
In humans, LBW is associated with pancreatic beta cell
hyperplasia, and SGA causes a reduction of beta cell
number. Consequently, SGA or LBW results in insulin
resistance or diabetes in adulthood. Rapid weight catch-
up during early infancy in children with LBW increases
the risk of unfavourable metabolic events [4].
On the other hand, altering the foetal neuroendocrine
environment specifically by impacting on the ACTH/
cortisol level affects brain development. The foetus could
be protected against increased levels of maternal cortisol
by the placental enzyme 11β-HSD. This barrier, howev-
er, is disrupted by obstetric complications like pre-
eclampsia and preterm birth as well as IUGR (intrauter-
ine growth retardation), medication and diet. In an ani-
mal model, a maternal high-fat diet could increase anxi-
ety in offspring by the interplay with serotonin, dopa-
mine and HPA (hypothalamic-pituitary-adrenal) axis. In
this model, also maternal anxiety, reflected by increased
levels of cortisol, has been shown to cause impaired
cognition, deficits in learning and memory, sex-atypical
behaviours, heightened emotionality and general anxiety.
It also impacts reactivity to stress and sensitivity to nic-
otine and other addictive substances. Rats prenatally
stressed react with a faster, stronger and prolonged
cortisol response later in life. In humans, a relationship
between maternal stress in the third trimester and lower
scores in attention and reactivity in newborns has been
shown in some of them, as has a relation to Bayley
Scales of Infant Development (BSID) and mental/motor
development at 8 months. Data from epidemiological
studies suggest links between maternal obesity and met-
abolic complications with neurological disorders like
ADHD, ASD, schizophrenia, anxiety and depression [6,
20].
Atopy and asthma programming
Perhaps not surprisingly, because food allergy is usually the
first manifestation of atopy in life, atopy and asthma are con-
ditions associated strongly with the maternal diet. Different
diets have been studied in relation to this conditions risk. A
diet focused on avoiding the main allergens was shown not to
be related to atopic outcome in offspring. A holistic diet rich in
a variety of foods is believed to be beneficial. Specifically, a
diet rich in fish oil and PUFAs, probiotics, antioxidants and
vitamins has been shown to be protective. Folate, a known
methyl donor impacting methylation status, at specific doses
has the reverse effect, due to the epigenetic mechanism.
Specifically, high doses of folic acid (≥5 mg/day) in late
pregnancy are an established risk factor for allergy. In contrast,
nicotinamide, another methyl donor, decreases the risk of ec-
zema at 12 months. Its main sources are vitamin B3 and tryp-
tophan [9].
Conclusion
Here, we tried to answer questions concerning pregnan-
cy: What to eat? How much eat? Why is it important?
Recommendations proposed by different authorities are
based on the solid knowledge. However, there are some
differences—population specific, they depend on the eat-
ing customs and tradition, and interventions which have
been already introduced for the whole population. Some
concerns exist for adequate folate supplementation, ap-
propriate dose of DHA and iodine. Still, it seems to be
difficult for ordinary pregnant woman to design proper
diet. Novel electronic applications could be helpful; how-
ever, the algorithm should be approved by local health
authorities. Hopefully healthy eating becomes trendy
nowadays, which is the promise of good health for future
population.
Authors’contributions H. Danielewicz: preparing the manuscript, re-
view of the literature, final approval. Grzegorz Myszczyszyn: review of
the literature, final approval, Anna Dębińska: review of the literature,
final approval, Anna Myszkal: review of the literature, final approval,
Eur J Pediatr (2017) 176:1573–1579 1577
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

Andrzej Boznański: review of the lietrature, consulting, final approval,
Lidia Hirnle: review of the literature, consulting, final approval.
Funding This study was funded by National Science Center, Poland,
DEC-2015/19/B/NZ5/00041.
Compliance with ethical standards
Conflict of interest Author Hanna Danielewicz has received a speaker
honorarium from GPharma—administrator of Allergy and Pulmonology
2016 Conference—activity outside submitted work. Grzegorz
Myszczyszyn declares that he has no conflict of interest. Anna
Dębińska declares that she has no conflict of interest. Anna Myszkal
declares that she has no conflict of interest. Lidia Hirnle declares that
she has no conflict of interest. Andrzej Boznański declares that he has
no conflict of interest.
Ethical approval This article does not contain any studies with human
participants performed by any of the authors.
Open Access This article is distributed under the terms of the Creative
Commons Attribution 4.0 International License (http://
creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
distribution, and reproduction in any medium, provided you give appro-
priate credit to the original author(s) and the source, provide a link to the
Creative Commons license, and indicate if changes were made.
References
1. Alwan N, Hamamy H (2015) Maternal ironstatus in pregnancy and
long-term health outcomes in the offspring. J Pediatr Genet 4:111–
123. https://doi.org/10.1055/s-0035-1556742
2. Amer MG, Mohamed NM, Shaalan AAM (2017) Gestational pro-
tein restriction: study of the probable effects on cardiac muscle
structure and function in adult rats. Histol Histopathol 11883.
https://doi.org/10.14670/HH-11-883
3. Barker DJ (1992) Fetal growth and adult disease. Br J Obstet
Gynaecol 99:275–276
4. Barker D, Eriksson J, Forsén T, Osmond C (2002) Fetal origins of
adult disease: strength of effects and biological basis. Int J
Epidemiol 31:1235–1239. https://doi.org/10.1093/ije/31.6.1235
5. Calzada L, Morales A, Sosa-Larios TC et al (2016) Maternal pro-
tein restriction during gestation impairs female offspring pancreas
development in the rat. Nutr Res 36:855–862. https://doi.org/10.
1016/j.nutres.2016.03.007
6. Egliston K-A, McMahon C, Austin M-P (2007) Stress in pregnancy
and infant HPA axis function: Conceptual and methodological is-
sues relating to the use of salivary cortisol as an outcome measure.
Psychoneuroendocrinology 32:1–13. https://doi.org/10.1016/j.
psyneuen.2006.10.003
7. Karowicz-BilińskaA,Nowak-MarkwitzE,OpalaTetal(2014)
Rekomendacje Polskiego Towarzystwa Ginekologicznego w
zakresie stosowania witamin i mikroelementów u kobiet
planujących ciążę,ciężarnych i karmiących. Ginekologia Polska
85:395–399
8. Grieger JA, Grzeskowiak LE, Wood LG, Clifton VL (2016)
Asthma control in pregnancy is associated with pre-conception di-
etary patterns. Public Health Nutr 19:332–338. https://doi.org/10.
1017/S1368980015001226
9. Grieger JA, Clifton VL, Tuck AR et al (2016) In utero program-
ming of allergic susceptibility. Int Arch Allergy Immunol 169:80–
92. https://doi.org/10.1159/000443961
10. Harding KB, Peña-Rosas JP, Webster AC et al (2017) Iodine sup-
plementation for women during the preconception, pregnancy and
postpartum period. In: Peña-Rosas JP (ed) Cochrane Database Syst.
Rev. John Wiley & Sons, Chichester, p CD011761
11. Holick MF, Binkley NC, Bischoff-Ferrari HA et al (2011)
Evaluation, treatment, and prevention of vitamin D deficiency: an
endocrine society clinical practice guideline. J Clin Endocrinol
Metab 96:1911–1930. https://doi.org/10.1210/jc.2011-0385
12. Hyde NK, Brennan-Olsen SL, Bennett K et al (2016) Maternal
nutrition during pregnancy: intake of nutrients important for bone
health. Matern Child Health J:1–7. https://doi.org/10.1007/s10995-
016-2178-7
13. Institute of Medicine of the National Academies (2015) Dietary
Reference Intakes: Macronutrients Nutrient 2002/2005 http://
www.iom.edu/~/media/Files/Activity%20Files/
14. Jarosz M, Traczyk I, StośK et al (2012) Normy Żywienia dla
Populacji Polskiej. Instytut Żywności i Żywienia
15. King V, Hibbert N, Seckl JR et al (2013) The effects of an
obesogenic diet during pregnancy on fetal growth and placental
gene expression are gestation dependent. Placenta 34:1087–1090.
https://doi.org/10.1016/j.placenta.2013.09.006
16. Koletzko B, Bauer CP, Bung P et al (2013) German national con-
sensus recommendations on nutrition and lifestyle in pregnancy by
the BHealthy Start - Young Family Network^. Ann Nutr Metab 63:
311–322. https://doi.org/10.1159/000358398
17. Marangoni F, Cetin I, Verduci E et al (2016) Maternal diet and
nutrient requirements in pregnancy and breastfeeding. An Italian
consensus document. Nutrients. https://doi.org/10.3390/
nu8100629
18. Maslova E, Halldorsson TI, Astrup A, Olsen SF (2015) Dietary
protein-to-carbohydrate ratio and added sugar as determinants of
excessive gestational weight gain: a prospective cohort study.
BMJ Open 5:e005839–e005839. https://doi.org/10.1136/bmjopen-
2014-005839
19. Melina RDVM, Craig MPHWR, Levin RDCSSDSM (2016)
Position of the academy of nutrition and dietetics: vegetarian diets.
J Acad Nutr Diet 116:1970–1980. https://doi.org/10.1016/j.jand.
2016.09.025
20. Moody L, Chen H, Pan Y-X (2017) Early-life nutritional program-
ming of cognition—the fundamental role of epigenetic mechanisms
in mediating the relation between early-life environment and learn-
ing and memory process. Adv Nutr An Int Rev J 8:337–350. https://
doi.org/10.3945/an.116.014209
21. Moon RJ, Harvey NC, Cooper C et al (2016) Determinants of the
maternal 25-hydroxyvitamin D response to vitamin D supplemen-
tation during pregnancy. J Clin Endocrinol Metab 101:5012–5020.
https://doi.org/10.1210/jc.2016-2869
22. Mustieles V, Pérez-Lobato R, Olea N, Fernández MF (2015)
Bisphenol A: human exposure and neurobehavior.
Neurotoxicology 49:174–184. https://doi.org/10.1016/j.neuro.
2015.06.002
23. Nash DM, Gilliland JA, Evers SE et al (2013) Determinants of diet
quality in pregnancy: sociodemographic, pregnancy-specific, and
food environment influences. J Nutr Educ Behav 45:627–634.
https://doi.org/10.1016/j.jneb.2013.04.268
24. O’Callaghan-Gordo C, Kogevinas M, Pedersen M et al (2016)
Maternal diet during pregnancy and micronuclei frequency in pe-
ripheral blood T lymphocytes in mothers and newborns (Rhea co-
hort, Crete). Eur J Nutr:1–10. https://doi.org/10.1007/s00394-016-
1310-1
25. O’Connor DL, Blake J, Bell R et al (2016) Canadian consensus on
female nutrition: adolescence, reproduction, menopause, and be-
yond. J Obstet Gynaecol Can 38:508–554.e18. https://doi.org/10.
1016/j.jogc.2016.01.001
26. Oken E, Ning Y, Rifas-Shiman SL et al (2007) Diet during preg-
nancy and risk of preeclampsia or gestational hypertension. Ann
1578 Eur J Pediatr (2017) 176:1573–1579
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

Epidemiol 17:663–668. https://doi.org/10.1016/j.annepidem.2007.
03.003
27. Oliveira LS, Souza LL, Souza AFP et al (2016) Perinatal maternal
high-fat diet promotes alterations in hepatic lipid metabolism and
resistance to the hypolipidemic effect of fish oil in adolescent rat
offspring. Mol Nutr Food Res 60:2493–2504. https://doi.org/10.
1002/mnfr.201600171
28. Pereira-da-Silva L, Cabo C, Moreira A et al (2013) The adjusted
effect of maternal body mass index, energy and macronutrient in-
takes during pregnancy, and gestational weight gain on body com-
position of full-term neonates. Am J Perinatol 31:875–882. https://
doi.org/10.1055/s-0033-1363502
29. Petry N, Olofin I, Boy E et al (2016) The effect of lowdose iron and
zinc intake on child micronutrient status and development during
the first 1000 days of life: a systematic review and meta-analysis.
Nutrients. https://doi.org/10.3390/nu8120773
30. Poston L (2012) Maternal obesity, gestational weight gain and diet
as determinants of offspring long term health. Best Pract Res Clin
Endocrinol Metab 26:627–639. https://doi.org/10.1016/j.beem.
2012.03.010
31. Institute of Medicine (US) and National Research Council (US)
Committee to Reexamine IOM Pregnancy Weight Guidelines;
Rasmussen KM, Yaktine AL (eds) (2009) Weight gain during preg-
nancy: reexamining the guidelines. National Academies Press (US),
Washington (DC)
32. Renault KM, Carlsen EM, Hædersdal S et al (2017) Impact of
lifestyle intervention for obese women during pregnancy on mater-
nal metabolic and inflammatory markers. Int J Obes. https://doi.org/
10.1038/ijo.2017.9
33. Rogers LK, Valentine CJ, Keim SA (2013) DHA supplementation:
current implications in pregnancy and childhood. Pharmacol Res
70:13–19. https://doi.org/10.1016/j.phrs.2012.12.003
34. Saad MI, Abdelkhalek TM, Haiba MM et al (2016) Maternal obe-
sity and malnourishment exacerbate perinatal oxidative stress
resulting in diabetogenic programming in F1 offspring. J
Endocrinol Investig 39:643–655. https://doi.org/10.1007/s40618-
015-0413-5
35. Sandler V, Reisetter AC, Bain JR et al (2017) Associations of ma-
ternal BMI and insulin resistance with the maternal metabolome
and newborn outcomes. Diabetologia 60:518–530. https://doi.org/
10.1007/s00125-016-4182-2
36. Smith CJ, Ryckman KK, Barnabei VM et al (2016) The impact of
birth weight on cardiovascular disease risk in the Women’sHealth
Initiative. Nutr Metab Cardiovasc Dis 26:239–245. https://doi.org/
10.1016/j.numecd.2015.10.015
37. Thorburn AN, McKenzie CI, Shen S et al (2015) Evidence that
asthma is a developmental origin disease influenced by maternal
diet and bacterial metabolites. Nat Commun 6:7320. https://doi.org/
10.1038/ncomms8320
38. Vafeiadi M, Roumeliotaki T, Myridakis A et al (2016) Association
of early life exposure to bisphenol Awith obesity and cardiometa-
bolic traits in childhood. Environ Res 146:379–387. https://doi.org/
10.1016/j.envres.2016.01.017
39. WHO (2015) Guideline: optimal serum and red blood cell folate
concentrations in women of reproductive age for prevention of
neural tube defects. World Health Organization, Geneva
40. WHO (2016) WHO recommendations on antenatal care for a pos-
itive pregnancy experience. World Health Organization, Geneva
Eur J Pediatr (2017) 176:1573–1579 1579
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

1.
2.
3.
4.
5.
6.
Terms and Conditions
Springer Nature journal content, brought to you courtesy of Springer Nature Customer Service Center GmbH (“Springer Nature”).
Springer Nature supports a reasonable amount of sharing of research papers by authors, subscribers and authorised users (“Users”), for small-
scale personal, non-commercial use provided that all copyright, trade and service marks and other proprietary notices are maintained. By
accessing, sharing, receiving or otherwise using the Springer Nature journal content you agree to these terms of use (“Terms”). For these
purposes, Springer Nature considers academic use (by researchers and students) to be non-commercial.
These Terms are supplementary and will apply in addition to any applicable website terms and conditions, a relevant site licence or a personal
subscription. These Terms will prevail over any conflict or ambiguity with regards to the relevant terms, a site licence or a personal subscription
(to the extent of the conflict or ambiguity only). For Creative Commons-licensed articles, the terms of the Creative Commons license used will
apply.
We collect and use personal data to provide access to the Springer Nature journal content. We may also use these personal data internally within
ResearchGate and Springer Nature and as agreed share it, in an anonymised way, for purposes of tracking, analysis and reporting. We will not
otherwise disclose your personal data outside the ResearchGate or the Springer Nature group of companies unless we have your permission as
detailed in the Privacy Policy.
While Users may use the Springer Nature journal content for small scale, personal non-commercial use, it is important to note that Users may
not:
use such content for the purpose of providing other users with access on a regular or large scale basis or as a means to circumvent access
control;
use such content where to do so would be considered a criminal or statutory offence in any jurisdiction, or gives rise to civil liability, or is
otherwise unlawful;
falsely or misleadingly imply or suggest endorsement, approval , sponsorship, or association unless explicitly agreed to by Springer Nature in
writing;
use bots or other automated methods to access the content or redirect messages
override any security feature or exclusionary protocol; or
share the content in order to create substitute for Springer Nature products or services or a systematic database of Springer Nature journal
content.
In line with the restriction against commercial use, Springer Nature does not permit the creation of a product or service that creates revenue,
royalties, rent or income from our content or its inclusion as part of a paid for service or for other commercial gain. Springer Nature journal
content cannot be used for inter-library loans and librarians may not upload Springer Nature journal content on a large scale into their, or any
other, institutional repository.
These terms of use are reviewed regularly and may be amended at any time. Springer Nature is not obligated to publish any information or
content on this website and may remove it or features or functionality at our sole discretion, at any time with or without notice. Springer Nature
may revoke this licence to you at any time and remove access to any copies of the Springer Nature journal content which have been saved.
To the fullest extent permitted by law, Springer Nature makes no warranties, representations or guarantees to Users, either express or implied
with respect to the Springer nature journal content and all parties disclaim and waive any implied warranties or warranties imposed by law,
including merchantability or fitness for any particular purpose.
Please note that these rights do not automatically extend to content, data or other material published by Springer Nature that may be licensed
from third parties.
If you would like to use or distribute our Springer Nature journal content to a wider audience or on a regular basis or in any other manner not
expressly permitted by these Terms, please contact Springer Nature at
onlineservice@springernature.com