The authors have declared that no competeting intrests exists.
Conceived and designed the experiments: LF KMS IEG MKM HCB. Performed the experiments: MWM SS MKM HCB KMS IEG. Analyzed the data: JDR MWM. Wrote the paper: MWM IEG MKM LF JDR.
Essential fatty acid status as well as docosahexaenoic acid (DHA, 22:6n-3) declines during pregnancy and lactation. As a result, the DHA status may not be optimal for child development and may increase the risk for maternal postpartum depression. The objective of this study was to assess changes in the maternal fatty acid status from pregnancy to 12 months postpartum, and to study the impact of seafood consumption on the individual fatty acid status.
Blood samples and seafood consumption habits (gestation week 28, and three-, six- and 12 months postpartum) were collected in a longitudinal observational study of pregnant and postpartum women (n = 118). Multilevel linear modeling was used to assess both changes over time in the fatty acid status of red blood cells (RBC), and in the seafood consumption.
Six fatty acids varied the most (>80%) across the four time points analyzed, including the derivative of the essential α-linoleic acid (ALA, 18:3n-3), DHA; the essential linoleic acid (LA, 18:2 n-6); and the LA derivative, arachidonic acid (AA, 20:4n-6). Over all, a large variation in individuals’ DHA- and AA status was observed; however, over the 15-month study period only small inter-individual differences in the longitudinal trajectory of DHA- and AA abundance in the RBC were detected. The median intake of seafood was lower than recommended. Regardless, the total weekly frequency of seafood and eicosapentaenoic acid (EPA, 20:5n-3)/DHA-supplement intake predicted the maternal level of DHA (μg/g RBC).
The period of depletion of the maternal DHA status during pregnancy and lactation, seem to turn to repletion from about six months postpartum towards one year after childbirth, irrespective of RBC concentration of DHA during pregnancy. Seafood and EPA/DHA-supplement intake predicted the DHA levels over time.
Pregnancy and lactation are periods of increased nutritional vulnerability as nutrient needs are increased. To maintain the delicate balance between the needs of the mother and those of the fetus an adequate supply of nutrients is required. Some of the nutrients required protect maternal health while others affect birth outcome and infant health.
Inadequate nutrient supply may in the worst case cause a biological competition between the mother and the fetus [
The n-3 fatty acid docosahexaenoic acid (DHA, 22:6n-3), and the n-6 fatty acid, arachidonic acid (AA, 20:4n-6), derived from the essential fatty acids α-linoleic acid (ALA, 18:3n-3) and linoleic acid (LA, 18:2n-6) respectively, are fundamental structural components in the brain and the central nervous system and play an important role in the growth, development and structure of the brain [
During the last trimester of fetal life and the first two years of childhood, the brain undergoes a period of rapid growth termed the “brain growth spurt”. Lower fish consumption in pregnancy has been associated with suboptimum neurodevelopmental outcomes in children [
Seafood is a unique dietary source of important nutrients such as eicosapentaenoic acid (20:5n-3) EPA and DHA, vitamin D and B12, and the trace minerals iodine and selenium [
The aim of the present study was to conduct a longitudinal analysis to investigate changes in the total fatty acid status during pregnancy and the first year postpartum, within a population of Norwegian mothers. We also aim to elucidate the impact seafood consumption has on the fatty acid status of red blood cells (RBC) in the same study population.
The investigation originated from a community based study with a prospective cohort design performed in a municipality outside Bergen, Norway. The main objectives of the cohort were to study the associations between seafood consumption, mental health, and infant development. Enrolment was open for 20 months and the source population was all women, pregnant in their 24th week of gestation, between November 2009 and June 2011, in the municipality. Midwifes or medical doctors recruited the women at a routine visit in the 24th week of gestation. At the routine visit 2 and 6 weeks postpartum public health nurses recruited women who had already given birth when the enrolment started. Thus, participation after time point 1 is larger. The original cohort comprised four waves of follow-up: in the 28th gestational week (T1), and at three- (T2), six- (T3), and 12 (T4) months postpartum. Exclusion criteria were lack of Norwegian language skills or/and premature childbirth (over four weeks). Blood samples (non-fasting venous) were drawn from the participants at all time points. The study design has challenges due to recruitment at both T1 and T2. The reason for this was due to practical issues in the recruitments process in the municipality where the source population originated. The initial plan was that family doctors was going to recruit pregnant women to the study at the routine visit in gestational week 24. However, over 50% of the pregnant women had their routine visits with their midwives at the well-baby clinic in gestational week 24. To ensure that all women in the source population was asked to participate and minimize selection bias, public health care nurses started recruiting women that had already just given birth.
1 Not all women from the source population were asked to participate in the study while still pregnant, partly for practical reasons and partly due to exclusion criteria (unable to understand Norwegian). 2 2 BS and 16 FFQ missing at random or passive dropout. 3 Women recruited 2–6 weeks postpartum to restrict selection bias as not the whole source population was asked to participate during pregnancy due to practical reasons. 4 Passive drop-out sometime between T1 and T2. 5 18 BS and 16 FFQ missing at random or passive drop-out. 6 21 BS and 21 FFQ missing at random or passive drop-out. 7 30 BS and 26 FFQ missing at random or passive drop-out. BS: blood sample; FFQ: food frequency questionnaire.
All volunteers provided written informed consent. Participants could withdraw from the study at any time, without reason. The procedures followed were in accordance with the Helsinki Declaration of 1975 (revised in 2008), and approved by the Regional Committee of Ethics in Medical Research West and the Norwegian Social Science Data Services. A research specific biobank was established and approved for storage of biological samples.
For preparation of red blood cells (RBC) venous blood from the elbow cavity was collected in ice water cooled 4 ml BD Vacutainer K2E 7.2 mg vials. Blood collected in K2E vials was centrifuged (10 min, 1000 g, RT) within 30 minutes. RBCs were adequately separated to ensure a clean blood fraction. Blood samples were stored at -20°C for 0–4 weeks prior to transportation on dry ice to a -80°C freezer where they were stored until analysis.
The fatty acid (FA) composition of total RBC was determined by ultrafast gas chromatography (UFGC) (Thermo Electron Corporation, Massachusetts, USA), a method developed by Araujo
A questionnaire designed for the study was sent by e-mail to all participants in the 28th gestational week (T1) and three moths postpartum (T2), and by postal mail six- (T3) and twelve months postpartum (T4). Questions regarding the seafood consumption were assessed using a semi-quantitative seafood food frequency questionnaire (FFQ). The FFQ was designed to capture the habitual intake of seafood and the use of dietary supplements [
Breastfeeding habits were assessed through a combination of a 24-hour dietary recall interview and an interviewer administered FFQ. The infant FFQ included questions on the frequency of breast milk feeding, followed by questions on exclusive breastfeeding. Breastfeeding was categorized in terms of yes/no based on daily breast feedings.
Descriptive statistics and analysis of differences between participants recruited at two different time points were calculated using the Statistical Package for the Social Sciences (IBM SPSS Statistics 21, IBM Corporation, Norway). Data was tested for normality using the Shapiro-Wilk test. Potential differences in fatty acid status, total seafood and fish oil supplementation, descriptive, socioeconomic- and behavioral characteristics were assessed using dependent t-tests if the assumption of normality was met; otherwise the Man-Whitney test was employed. Relative and absolute amounts of the FA as measured in RBC are presented as means (± 95% confidence intervals, CI). Independent sample t-tests were performed to assess if mean values of FA of participants whom we sampled blood from at all four time points were significantly different to those we did not sample blood from at all four timepointsat each time point.
Qlucore Omics Explorer version 2.3 (Qlucore AB, Lund, Sweden) was used to perform unsupervised principal component analysis (PCA). For PCA analysis, each variable was standardized by subtraction of its mean value and division by its standard deviation across all samples. Variance filtering was applied to limit the number of FA in the standardized data set to the ones explaining >80% of the variation in the data. Heat maps were generated to visualize the abundance values of the FA, detected > limit of quantification for FA determination by UFGC, over time. The time course of the FA was analyzed further using multilevel linear models in the statistical package R (version 3.0.2) emulating the modelling approaches described in [
Descriptive characteristics of the study population at all four time points are presented as cross section data in
Characteristics | T1 Count (%) |
T2 Count (%) |
T3 Count (%) |
T4 Count (%) |
Difference between recruitment time point |
---|---|---|---|---|---|
Age (mean ± SD) | 30±4.8 | 31±5.3 | 31±5.5 | 32±5.5 | p < 0.05 |
BMI (mean ± SD) | 24±3.9 |
25±4.8 | 25±4.4 | 24±4.2 | |
Education | |||||
Junior high school | 0 (0) | 4 (4.3) | 5 (6.1) | 6 (7.7) | |
High school | 16 (29.1) | 29 (31.5) | 27 (32.9) | 25 (32.1) | |
< 4 years of university education |
24 (43.6) | 34 (37.0) | 35 (42.7) | 35 (44.9) | |
≥ 4 years of university education |
15 (27.3) | 25 (27.2) | 15 (18.3) | 12 (15.4) | |
Employment | |||||
Full-time (80–100%) | 48 (87.3) | 78 (84.8) | |||
Part-time (50–79%) | 2 (3.6) | 6 (6.5) | NA |
NA |
|
Part-time (<50%) | 1 (1.8) | 0 (0) | |||
Homemaker | 1 (1.8) | 2 (2.2) | |||
Other | 3 (5.5) | 6 (6.5) | |||
Marital status | |||||
Married | 23 (43.4) |
43 (46.7) | NA |
NA |
|
Cohabiting | 28 (52.8) | 46 (50.0) | |||
Single | 2 (3.8) | 3 (3.3) | |||
Own income in NOK |
|||||
No income | 0 (0) | 2 (2.2) | |||
< 150.000 | 2 (3.6) | 6 (6.5) | |||
150.000–199.999 | 1 (1.8) | 3 (3.3) | NA |
NA |
|
200.000–299.999 | 12 (21.8) | 11 (12.0) | |||
300.000–399.999 | 27 (49.1) | 47 (51.1) | |||
400.000–499.999 | 10 (18.2) | 14 (15.2) | |||
> 500.000 NOK | 3 (5.5) | 9 (9.8) | |||
Breastfeeding | |||||
Yes | NA | 79 (81.4) | 66 (70.2) | 27 (32.5) | |
No | 18 (18.6) | 28 (29.8) | 56 (67.5) |
* An independent sample t-test was applied to normal data (age) and Man-Whitney for non-normal data (BMI, education, employment, marital status, own income and breastfeeding)
1 Age and BMI are presented as mean ± SD
2 BMI pre-pregnancy
3 University or University College
4 Data not requested at time point 3 and 4 (no new recruitment)
5 100 000 NOK ≈ 14 000 EUR
Means and 95% CI of all quantified FA at all four time points are presented in
Different letter indicate statistically different values.
Fatty acids in red blood cells | T1 (n = 69) expressed as: | T2 (n = 90) expressed as: | T3 (n = 88) expressed as: | T4 (n = 78) expressed as: | ||||
---|---|---|---|---|---|---|---|---|
% of total FA | μg / g RBC | % of total FA | μg / g RBC | % of total FA | μg / g RBC | % of total FA | μg / g RBC | |
Mean ± 95% CI | ||||||||
14:0 | 0.6 ± 0.0 | 19 ± 2a | 0.4 ± 0.0 | 9 ± 1b | 0.4 ± 0.0 | 8 ± 1 b | 0.4 ± 0.0 | 9 ± 1 b |
16:0 PA | 23.0 ± 0.4 | 662 ± 26 a | 21.0 ± 0.3 | 515 ± 12 b | 21.0 ± 0.4 | 471 ± 13 c | 20.0 ± 0.6 | 469 ± 16 c |
17:0 | 0.4 ± 0.0 | 10 ± 1 a | 0.3 ± 0.0 | 7 ± 0 b, |
0.3 ± 0.0 | 7 ± 0 b, |
0.3 ± 0.0 | 7 ± 0 b, |
18:0 SA | 14.0 ± 0.4 | 390 ± 7 a | 16.0 ± 0.3 | 384 ± 10 a | 16.0 ± 0.4 | 350 ± 5 b | 15.0 ± 0.5 | 342 ± 11 b |
20:0 | 0.3 ± 0.0 | 9 ± 0 a | 0.4 ± 0.0 | 9 ± 1 a, b | 0.4 ± 0.0 | 8 ± 0 b | 0.4 ± 0.0 | 9 ± 0 a |
22:0 | 0.7 ± 0.0 | 19 ± 1 | 1.0 ± 0.1 | 25 ± 2 | 1.0 ± 0.0 | 24 ± 2 | 1.1 ± 0.0 | 25 ± 1 |
24:0 | 0.1 ± 0.1 | 2 ± 3 3 | 0.3 ± 0.2 | 7 ± 4 2 | 0.4 ± 0.1 | 7 ± 2 |
0.0±0.0 | 0±0 3 |
16:1 |
0.9 ± 0.1 | 28 ± 4 a | 0.6 ± 0.0 | 14 ± 1 b | 0.5 ± 0.0 | 12 ± 2 b | 0.6 ± 0.0 | 15 ± 1 b |
18:1 |
16.0 ± 0.4 | 452 ± 25 a | 14.0 ± 0.3 | 344 ± 10 b | 14.0 ± 0.4 | 320 ± 10 c | 13.0 ± 0.4 | 311 ± 12 c |
24:1n-9 | 1.7 ± 0.1 | 47 ± 2 a | 2.7 ± 0.1 | 65 ± 3 b | 1.9 ± 0.2 | 45 ± 5 a | 2.7 ± 0.1 | 62 ± 3 b |
18:2n-6 LA | 13.0 ± 0.7 | 390 ± 33 a | 13.0 ± 0.4 | 303 ± 11 b | 12.0 ± 0.4 | 267 ± 10 c | 11.0 ± 0.5 | 254 ± 12 c |
16:3n-3 | 0 ± 0 | 0 ± 0 3 | 0.4 ± 0.1 | 9 ± 1 |
0.6 ± 0.1 | 15 ± 2 | 0.7 ± 0.1 | 16 ± 2 |
20:2n-6 | 0.3 ± 0.0 | 8 ± 1 a, |
0.2 ± 0 | 5 ± 1 b, |
0.2 ± 0.0 | 4 ± 1 b, |
0.2 ± 0.0 | 4 ± 1 b, |
20:3n-6 | 1.7 ± 0.1 | 48 ± 3 a | 0 ± 0 | 36 ± 2 b | 1.4 ± 0.1 | 31 ± 2 c | 0.2 ± 0.0 | 33 ± 2 c |
20:4n-6 AA | 11.0 ± 0.4 | 320 ± 12 a | 13.0 ± 0.4 | 324 ± 11 a | 12.7 ± 0.4 | 286 ± 6 b | 12.0 ± 0.5 | 290 ± 12 b |
22:4n-6 | 1.9 ± 0.1 | 55 ± 3 a | 2.0 ± 0.1 | 50 ± 3 a, b | 2.0± 0.1 | 45 ± 3 b | 2.5 ± 0.3 | 57 ± 7 a |
21:5n-3 | 1.0 ± 0.2 | 38 ± 6 a | 1.0 ± 0.2 | 14 ± 5 b | 0.0 ± 0.0 | 0 ± 0 c, |
0.1 ± 0.1 | 1 ± 1 c, |
22:5n-6 | 0.3 ± 0.0 | 10 ± 1 a | 0.2 ± 0.0 | 6 ± 1 b, |
1.0 ± 0.2 | 22 ± 5 c | 0.5 ± 0.1 | 11 ± 3 a |
18:3n-3 ALA | 0.3 ± 0.0 | 9 ± 1 a, 2 | 0 ± 0 | 1 ± 0 b, |
0.1 ± 0.0 | 9 ± 11 a, b, c, |
0.2 ± 0.0 | 4 ± 1 c, |
20:5n-3 EPA | 0.8 ± 0.1 | 22 ± 3 a, b | 1.0 ± 0.1 | 25 ± 3 a | 0.9 ± 0.1 | 20 ± 3 a, b | 0.8 ± 0.1 | 18 ± 2 a, b |
22:5n-3 DPA | 1.8 ± 0.1 | 50 ± 3 a, b | 2.3 ± 0.1 | 55 ± 2 a | 2.0 ± 0.1 | 46 ± 2 b | 2.0 ± 0.1 | 46 ± 2 b |
22:6n-3 DHA | 6.0 ± 0.3 | 164 ± 9 a | 6.0 ± 0.3 | 132 ± 7 b | 5.9 ± 0.3 | 137 ± 10 b | 7.2 ± 0.2 | 165 ± 7 a |
1 The fatty acids 6:0, 8:0, 10:0, 12:0, 16:2n-4, 20:3n-3, 16:4n3, 18:4n3 and 20:3n9 were quantified as 0
2 Mean < the limit of quantification for the method (LOQ 10 μg / g RBC).
3 Mean < the limit of detection for the method (LOD 3 μg / g RBC).
4 The method does not specify monounsaturated fatty acids.
Fatty acids | n | Mean ± 95% CI | Fatty acids | n | Mean ± 95% CI | ||||||
---|---|---|---|---|---|---|---|---|---|---|---|
18:2n-6 LA % | A | 35 | 13±8 | 18:2n-6 LA % | A | 35 | 12±7 | ||||
B | 34 | 13±11 | B | 55 | 13±5 | ||||||
18:2n-6 LA μg / g | A | 35 | 396±42 | 18:2n-6 LA μg / g | A | 35 | 301±18 | ||||
B | 34 | 383±52 | B | 55 | 305±15 | ||||||
20:4n-6 AA % | A | 35 | 11±6 | 20:4n-6 AA % | A | 35 | 14±6 | ||||
B | 34 | 11±5 | B | 55 | 13±5 | ||||||
20:4n-6 AA μg / g | A | 35 | 323±17 | 20:4n-6 AA μg / g | A | 35 | 336±18 | ||||
B | 34 | 317±18 | B | 55 | 316±13 | ||||||
22:6n-3 DHA % | A | 35 | 6±4 | 22:6n-3 DHA % | A | 35 | 5±4 | ||||
B | 34 | 6±5 | B | 55 | 5±4 | ||||||
22:6n-3 DHA μg / g | A | 35 | 168±13 | 22:6n-3 DHA μg / g | A | 35 | 133±10 | ||||
B | 34 | 161±13 | B | 55 | 132±9 | ||||||
18:2n-6 LA % | A | 35 | 12±6 | 18:2n-6 LA % | A | 35 | 11±5 | ||||
B | 52 | 12±6 | B | 43 | 11±4 | ||||||
18:2n-6 LA μg / g | A | 35 | 273±20 | 18:2n-6 LA μg / g | A | 35 | 256±16 | ||||
B | 52 | 264±11 | B | 43 | 259±13 | ||||||
20:4n-6 AA % | A | 35 | 13±6 | 20:4n-6 AA % | A | 35 | 13±4 | ||||
B | 52 | 13±5 | B | 43 | 13±5 | ||||||
20:4n-6 AA μg / g | A | 35 | 290±12 | 20:4n-6 AA μg / g | A | 35 | 298±14 | ||||
B | 52 | 283±8 | B | 43 | 290±15 | ||||||
22:6n-3 DHA % | A | 35 | 6±6 | 22:6n-3 DHA % | A | 35 | 7±3 | ||||
B | 52 | 6±5 | B | 43 | 7±3 | ||||||
22:6n-3 DHA μg / g | A | 35 | 140±16 | 22:6n-3 DHA μg / g | A | 35 | 168±8 | ||||
B | 52 | 135±14 | B | 43 | 167±9 |
1 Independent sample t-test, significant level 0.05.
Six months after birth 33% of the participants were below the 2.5 percentile (113 μg/g RBC) for DHA (μg/g RBC), using T4 as reference. The corresponding fractions were 27% 3 months after birth and 7% in pregnancy.
The FA whose abundance profiles over time explained over 80% of the variation in the data were: palmitic acid (PA, 16:0), stearic acid (SA, 18:0), the sum of the monounsaturated 18:1 fatty acids, LA, AA and DHA (
Panel A shows a heat map visualizing the abundance values of the FA across the repeated measurement. Red represents higher values and green represent lower values. A dendrogram on the left hand side of the heat map indicates similarity in the change over time in abundance profiles. Panel B, C and D represent raw data (yellow) of individually growth trajectories for
In this study, multilevel linear models or polynomials (linear, quadratic, cubic) were used to study the rate of change of fatty acid status in red blood cells over time, from pregnancy until 12 months postpartum. In addition, it was assessed if a statistical model can be found that best describes the change over time.
There were significant between-subject variations in average DHA status (μg/g RBC) over the time (data not shown). The effect of time,
Likewise, there were significant between-subject variations in the average LA status (μg/g RBC) over time points (data not shown). The effect of time,
There were significant between-subject variations in the average AA status (μg/g RBC) over time points (data not shown). The effect of time,
Multilevel linear models were also used to study any change in the seafood consumption over the 15-month time period, from pregnancy until 12 months postpartum. The median weekly frequency of seafood as dinner was 1.5 (0.2–3.0) in pregnancy, and 1.5 (0–3.0), 1.5 (0.2–3.0) and 1.5 (0.2–3.0) 3-, 6- and 12 months postpartum.
There was no significant between-subject variation in the
“The DHA status (μg/g RBC) did not differ between women that were breastfeeding (T2: 133 (65, 215) μg/g RBC, T3: 145 (52, 263) μg/g RBC, T4: 163 (56, 208) μg/g RBC) and women that were not breastfeeding (T2: 124 (54, 180) μg/g RBC, T3: 136 (43, 187) μg/g RBC, T4: 170 (116, 220) μg/g RBC),
The
The AA status was not predicted by the
The results from the present study provides novel data regarding maternal DHA stores which decrease after birth and are determined by the DHA status in pregnancy. The maternal seafood consumption and intake of EPA/DHA-supplements positively predicted the DHA status in pregnancy and postpartum. To our knowledge, this is the first study that presents the time course of the maternal FA status during pregnancy and the first year postpartum associated to seafood consumption. An important feature of this study was that all detected FA were submitted to analyses and DHA, AA and LA were among the FA whose abundance profiles varied the most over the 15-month period. For all three the amount in RBC decreased from pregnancy towards six months postpartum, however, different factors predicted the observed changes in FA statuses, respectively.
The maternal DHA status decreased from pregnancy towards three months- and reached a minimum six months after birth. As suggested by Houwelingen
Nevertheless, although women have physiological mechanisms to adapt to the high demands of DHA [
In order to determine whether an individual has a low DHA status, absolute amounts of RBC DHA (μg/g) in non pregnant, non lactating premenopausal women could be used as a reference. We used the two and a half percentile DHA status twelve months after delivery as a proxy, detecting the percentage of women with low DHA status in pregnancy, and three and six months after birth. The lowest values were measured three and six months after birth when about one third of the participants had RBC DHA status below the two and a half percentile, which corresponds to an n-3 index of just below 4% in pregnancy [
In the present study, the LA status, which decreased from pregnancy to postpartum, was negatively associated with education. Conversely, AA, which did not decrease before after 3 months postpartum, was not affected by any of the predictors. LA is predominantly found in processed foods with a high content of vegetable oils, soybean oil in particular. Excessive dietary intakes of LA may promote obesity [
Despite large variation in the DHA status the decrease in RBC DHA between pregnancy and three months post-partum was found to be significant. The observed decrease is likely due to normal biological changes causing an altered DHA metabolism in pregnancy and breastmilk production/lactation. Without clinical reference values we do not know which potential consequences a lower DHA status can lead to. Using the DHA status one year after birth as a reference, it was found that approximately one third of the women displayed DHA levels below the 2.5 percentile three and six months after birth, respectively. Observational studies and clinical trials have evaluated the possible role of omega-3 fatty acids consumption in the etiology of postpartum depression and suggest an association between low levels of marine omega-3 fatty acids and the occurrence of depression in the postpartum period [
The present study faced challenges due to recruitment issues at both T1 and T2 (28th gestational week) and T2 (three months postpartum) resulting in an untraditional longitudinal study design. The rationale for further recruiting after T1, the cohorts first and most important time point, was to represent a wide spectrum of women form the source population to minimize selection bias and maintain statistical power of the analysis, respectively. However, while inevitable, the additional recruiting may weaken the conclusions to be drawn from the longitudinal analysis performed in the present study. By chance the DHA status of participants entering the study at T2 could have had been very different to the DHA status of those participants who entered at T1. If this were the case, the significant decrease in DHA status from T1 to T2 would therefore be in parts due to new participants’ entering the study. To address this limitation, we compared participants whom we sampled blood from at all four time points and those we did not at each time point. There were no significant differences in the relative or absolute amount of LA-, AA-, or DHA in the RBC between the two “groups”. Thus, there is reason to believe that participants recruited at T2 do not differ to those recruited at T1 in their pregnancy DHA status. Thus, while not ideal, we believe that the additional recruiting did not invalidate the study design or the conclusions to be drawn.
Our results suggest that the maternal DHA status in pregnancy is pivotal for the DHA status the first year postpartum. The continuous decrease of maternal DHA status from pregnancy until six months postpartum may suggest that the maternal capacity to meet the high fetal requirements for DHA is inadequate. The functional implications of pregnancy-associated reduction in the maternal LA, AA and DHA status for fetal and neonatal development need further studies. In addition, the results indicate that increasing maternal seafood consumption or EPA/DHA-supplement intake during pregnancy may be beneficial to the mother and child ensuring sufficiently high DHA levels. These findings further indicate that promoting adequate maternal dietary intake of DHA before, during and after pregnancy is important to maintain sufficiently high levels of DHA that meet the requirements of fetal and infant development as well as requirements of the mother.
We are grateful to the participating women who, together with their infants gave their valuable time to take part in this study. In addition, we thank to the health care workers who were involved in recruiting and blood sampling of the participants in this study. The technical staff at NIFES is highly acknowledged for their analytical skills and for carrying out the fatty acid analyses.