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Keywords:

  • atopic diseases;
  • breast milk;
  • diet;
  • n-3 fatty acids;
  • n-6 fatty acids;
  • polyunsaturated fatty acids;
  • serum lipid

Abstract

  1. Top of page
  2. Abstract
  3. Material and methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References

Background: The increased consumption of n-6 polyunsaturated fatty acids (PUFA) has been shown to coincide with the increased prevalence of atopic diseases. We aimed to investigate whether maternal diet and atopic status influence the PUFA composition of breast milk and the serum lipid fatty acids of infants.

Methods: Maternal diet was assessed by a food questionnaire. The PUFA composition of breast milk obtained at 3 months from 20 allergic and 20 healthy mothers and of their infants' (10 atopic and 10 nonatopic/group of mothers) serum lipids was analyzed.

Results: Although no differences in maternal PUFA intake were observed, the breast milk of allergic mothers contained less γ-linolenic acid (18:3 n-6) than that of healthy mothers. Similarly, atopic infants had less γ-linolenic acid in phospholipids than healthy infants, although n-6 PUFA were elevated in other serum lipid fractions in atopic infants. The serum lipid fatty acids in atopic infants did not correlate with those in maternal breast milk.

Conclusions: Our results suggest that dietary n-6 PUFA are not as readily transferred into breast milk or incorporated into serum phospholipids, but may be utilized for other purposes, such as eicosanoid precursors, in allergic/atopic individuals. Subsequently, high dietary proportions of n-6 PUFA, or reduced proportions of regulatory PUFA, such as γ-linolenic acid and n-3 PUFA, may be a risk factor for the development of atopic disease.

The prevalence of atopic diseases has increased in industrialized countries over the last two decades (1). Breast-feeding has been demonstrated to protect against the development of atopic diseases (2), although infants may have atopic diseases even during exclusive breast-feeding (3). The reasons for this paradoxical phenomenon remain unexplained. One proposed explanation is the altered consumption of polyunsaturated fatty acids (PUFA) (4–6). The last two decades have seen a fall in the consumption of saturated fatty acids (SFA), whereas the consumption of PUFA has increased. This increase has mainly been attributed to increased use of margarine and vegetable oils rich in n-6 PUFA, whereas the consumption of n-3 PUFA has gradually decreased (4, 5).

Both linoleic acid (18:2 n-6) and α-linolenic acid (18:3 n-3) are essential PUFA and therefore must be provided by food. It has been suggested that man evolved on a diet with a 1:1 ratio of n-6 to n-3. However, in current Western diets, this ratio is approaching 10–25:1, indicating a deficiency in n-3 PUFA (5). Linoleic acid and α-linolenic acid both serve as precursors for longer chain PUFA, but are in continuous competition for the same desaturation and elongation enzymes. Due to altered dietary habits, the metabolism of n-6 fatty acids predominates, resulting in the production of longer chain derivatives of linoleic acid such as arachidonic acid (20:4 n-6). Prostaglandin E2 and leukotriene B4, eicosanoids derived from arachidonic acid, are important factors promoting atopic inflammation (7, 8). In contrast, n-3 fatty acids and eicosanoids derived from them have been demonstrated to possess anti-inflammatory properties (5, 9, 10).

As the mother's diet influences the fatty acid composition of breast milk (11), subsequent variations in the PUFA proportions of breast milk may explain why breast-feeding has a variable influence on the prevention of atopic diseases. However, studies investigating the role of maternal diet with regard to development of atopy in infants have been scarce. Moreover, an abnormal metabolism of PUFA has been proposed in atopic disease (6, 14, 15), although this hypothesis remains controversial (16). To take the maternal diet into account, we aimed to investigate

1) the influence of maternal diet on the fatty acid composition of breast milk

2) the effect of breast milk on the serum lipid fatty acids of infants

3) the association of these differences with the atopic status of mothers and the development of atopic disease in infants during the first 3 months of life.

Material and methods

  1. Top of page
  2. Abstract
  3. Material and methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References

Subjects and design

The study population comprised 40 women and their children; healthy mothers (n=20) of atopic (n=10) and healthy children (n=10), and mothers who had confirmed asthma, allergic rhinoconjunctivitis, or atopic eczema (n=20) and their children, who were either atopic (n=10) or healthy (n=10). Children with at least one positive skin prick test together with atopic eczema or food allergy were classified as atopic (17).

Breast-milk samples were collected when the children were 3 months old. Infants were allowed to suckle the nipple for a few minutes, and then a breast milk sample (10 ml) was taken and the feeding continued. The breast-milk samples were collected between 8 and 12 o'clock. The samples were immediately transferred to the freezer at −70°C until analysis. At the same time, completed food records were collected, and blood samples from infants were drawn by venous puncture. The blood samples were centrifuged and the serum was frozen and stored at −20°C.

Informed written consent was obtained from the mothers before the study. In accordance with the Helsinki Department, the Joint Ethical Committee of the University of Turku and Turku University Central Hospital approved the study.

Analysis of the fatty acid composition of breast milk

Lipids of breast-milk samples were extracted by the standardized method of the International Dairy Federation for determination of milk fat (18), except that the reagent volumes were adjusted to match the available sample volumes, and only one dose of petroleum ether/diethyl ether was used. The fatty acids of milk lipids (20 mg/sample) were then methylated with sodium methoxide plus methanol in hexane (19), but without solvent evaporation. In addition, the excess of methanol in the hexane layer was adsorbed on anhydrous CaCl2 before gas chromatography analysis.

Samples of fatty acid methyl esters in hexane were analyzed by a Hewlett-Packard 6890 gas chromatography device (Hewlett-Packard GmbH, Waldbronn, Germany) equipped with electronic gas control, automatic sampler and injector, split-splitless inlet, FocusLiner (SGE International Pty Ltd, Ringwood, Australia), a silica capillary column (length 100 m, inner diameter 0.25 mm) coated with 0.20 µm CP-Sil 88 cyano silicone phase (Chrompack International BV, Middelburg, The Netherlands), and a flame ionization detector. Instrument control and data processing were done with ChemStation A04.02 software on a Hewlett-Packard Vectra XM2 4/100i computer (Hewlett-Packard Co., Wilmington, DE, USA).

The injection volume was 1 µl, the inlet temperature 255°C, and the split ratio 50:1. The carrier gas was H2 produced by a Whatman 75-32-220 hydrogen generator (Whatman International Ltd, Maidstone, UK). The initial inlet pressure was 30 psi, but after 50 min of the run, it was programmed to rise 5 psi/min to 60 psi and held there to minimize run time. The initial oven temperature was 70°C, continuing for 4 min after injection. The temperature was then programmed to rise 8°C/min to 110°C and 5°C/min to 170°C, where there was a 10-min isothermal period, followed by a programmed 4°C/min rise to 240°C, which was held for 15 min. The detector temperature was 255°C.

One fatty acid analysis per milk sample was carried out. Peaks were identified by comparison of their retention times to the retention times of pure fatty acid methyl ester reference compounds or known fatty acid methyl ester mixtures, and by analyzing natural reference fats with literature data. Quantitative results were expressed as relative peak area percentage (its proportion of the sum of all fatty acid peak areas).

Fatty acid composition of serum lipids

Fatty acids were analyzed by the method described previously (20, 21). Lipids were extracted from serum samples of 100 µl with chloroform-methanol (2:1), and separated with an aminopropyl column into three fractions, i.e., cholesteryl esters (CE), triglycerides (TG), and phospholipids (PL). Fatty acids were then transmethylated with 14% borontrifluoride in methanol at 100°C for 1 h.

Fatty acid methyl esters were analyzed by a Hewlett-Packard 5890 series II gas chromatography device (Hewlett-Packard Company, Waldbronn, Germany) equipped with a FFAP-column (length 25 m, diameter 2 mm, and film thickness 0.3 µm) using helium as a carrier gas.

One fatty acid analysis per serum sample was performed. Peaks were identified by comparison of their retention times to the retention times of pure fatty acid methyl ester reference compounds, with heptadecanoate acid as an internal standard to quantify the fatty acids. Quantitative results are presented as molar percentages of total fatty acids.

Food records

Altogether, 28 (18 atopic and 10 healthy) out of the 40 mothers completed food records adequately with household measures on 4 consecutive days, as described previously (3). These days were chosen freely by the mothers, and they were regarded to reflect the period of exclusive breast-feeding.

Calculations of energy and fat intake were made with the Micro-Nutrica computer program (version 2.0, Research Centre of the Social Insurance Institution, Turku, Finland), which uses the food and nutrient database of the Social Insurance Institution (22) and is continuously updated. The total intake of SFA, monounsaturated fatty acids (MUFA), and PUFA was calculated. Of the PUFA, only the intake of linoleic and α-linolenic acid was calculated, since the Micro-Nutrica database did not include other individual PUFA.

Statistical analysis

Statistical analyses were performed by the SPSS for Windows program (Version 8.0, SPSS, Inc., Chicago, IL, USA). Normal distribution of variables was confirmed with the Kolmorov-Smirnov test. The general approach we took was first to perform an analysis of variance (here multivariate ANOVA) to detect differences, and then use a multiple-comparison procedures (unpaired t-test or Bonferroni t-test) to isolate the parameters producing the different results. For diet (mother allergic vs healthy and child atopic vs healthy), breast milk (mother allergic vs. healthy and child atopic vs healthy), and serum lipid fatty acids (child atopic vs healthy), comparisons between the two groups were performed with an unpaired t-test, while for comparisons of breast milk in subgroups (allergic vs healthy mothers in relation to atopic status of their children), a t-test with Bonferroni correction was used. The level of significance was set to P<0.05. The correlations between fatty acid intake and fatty acid composition of breast milk and composition of breast milk and serum lipid fatty acids were analyzed by linear regression and the Spearman rank correlation test. The significance level for correlations was set to P<0.01. The interpretation of data was focused on the general results, i.e., n-6 to n-3 ratio, total n-6, and total n-3 PUFA, in which the power with the present sample size was satisfactory. The results for continuous variables are expressed as means (SD).

Results

  1. Top of page
  2. Abstract
  3. Material and methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References

Maternal diet and breast-milk fatty acids

The mean (SD) energy intake of mothers was 8.3 (1.8) MJ. Protein intake comprised 15.7% (2.3), fat 36.4% (5.8), and carbohydrate 47.3% (5.4) of the total energy intake. The proportions of SFA, MUFA, and PUFA of the total fat intake were 43.1% (3.6), 34.3% (3.2), and 15.1% (2.3), respectively. The intake of linoleic acid and α-linolenic acid varied from 8.2% to 17.8%, with a mean of 12.1% (2.3), and from 1.2% to 5.7%, mean 2.0% (0.8), of the total fat intake, respectively, giving an overall n-6 to n-3 ratio of 6.5 (1.8).

There were no differences in the intake of energy or PUFA among allergic and healthy mothers. When food records were analyzed according to children's atopic status, mothers having a healthy child consumed less fat in their diet than mothers whose child suffered from atopic dermatitis, 74.3 g/day (22.2) vs 92.7 g/day (18.1), P=0.04, and more linoleic acid (relative percentage: 12.8% (2.2) vs 10.6% (1.8), P=0.05. The intake of n-3 PUFA from marine sources was generally very low, as only 8/28 mothers (five allergic and three healthy mothers) consumed oily fish during the recording days. Of their children, two (children of allergic mothers) developed atopy by the age of 3 months.

The PUFA profiles of breast milk are shown in Table 1. When the breast-milk composition was analyzed according to atopic status of the children, the n-6 to n-3 ratio in breast milk from mothers of healthy children was lower (3.92 [0.52]) than the ratio seen in breast milk from mothers of atopic children (4.47 [1.14]), P<0.05. On the other hand, breast milk from healthy mothers contained more γ-linolenic acid (18:3 n-6) and less docosahexaenoic acid (22:6 n-3) than the breast milk of allergic mothers (P=0.04 and 0.03, respectively). The ratio of n-6 to n-3 PUFA was therefore higher in healthy mothers (4.49 [1.08]) than in allergic mothers (3.90 [0.62]), P=0.04. Healthy mothers with atopic children had a higher n-6 to n-3 ratio in their breast milk than allergic mothers with atopic children; 5.08 (1.22) in the former compared to 3.85 (0.66) in the latter (P=0.01).

Table 1.  PUFA composition in breast milk (mean [SD]) of allergic and healthy mothers in relation to atopic status of their children at age of 3 months
Allergic/atopic statusnBreast-milk fatty acids
MotherChild18:2 n-618:3 n-620:4 n-618:3 n-320:5 n-322:6 n-3n-6:n-3Σ n-6Σ n-3
  1. * Statistically significant difference (P<0.05) between atopic and healthy children, and between allergic and healthy mothers (unpaired t-test). ** Statistically significant difference between healthy mothers with atopic children and allergic mothers with atopic children (MANOVA, P<0.05), Bonferroni t-test, P=0.01.

 Atopic209.56 (2.82)0.08 (0.03)0.33 (0.10)1.67 (0.71)0.09 (0.06)0.27 (0.19)4.47 (1.14)*10.55 (2.95)2.46 (0.77)
 Healthy209.00 (1.42)0.07 (0.03)0.30 (0.06)1.74 (0.51)0.09 (0.04)0.30 (0.10)3.92 (0.52)9.92 (1.52)2.58 (0.56)
Allergic 208.92 (1.84)0.06 (0.03)*0.30 (0.08)1.63 (0.60)0.10 (0.06)0.33 (0.19)*3.90 (0.62)*9.81 (1.96)2.59 (0.67)
Healthy 209.64 (2.54)0.08 (0.03)0.32 (0.09)1.78 (0.63)0.08 (0.03)0.23 (0.09)4.49 (1.08)10.66 (2.65)2.46 (0.68)
HealthyAtopic1010.22 (3.21)0.08 (0.04)0.36 (0.11)1.68 (0.68)0.07 (0.03)0.19 (0.04)5.08 (1.22)**11.33 (3.31)2.31 (0.73)
HealthyHealthy109.06 (1.62)0.08 (0.02)0.29 (0.04)1.88 (0.59)0.10 (0.03)0.28 (0.10)3.89 (0.43)9.99 (1.69)2.61 (0.62)
AllergicAtopic108.90 (2.36)0.07 (0.03)0.30 (0.09)1.66 (0.77)0.12 (0.08)0.34 (0.25)3.85 (0.66)9.77 (2.48)2.61 (0.82)
AllergicHealthy108.93 (1.26)0.06 (0.03)0.31 (0.08)1.60 (0.39)0.08 (0.04)0.31 (0.10)3.93 (0.62)9.84 (1.41)2.56 (0.52)

A significant correlation was observed between the SFA consumed and the sum of SFA in the breast milk of allergic mothers (r=0.61, P<0.01). No correlation between PUFA intake and proportions of individual PUFA in breast milk was observed in either group.

The influence of breast milk on serum lipid fatty acid profiles in infants

Table 2 compares the fatty acid composition of serum CE, PL, and TG in 20 children with atopic dermatitis to that in 20 healthy controls. γ-Linoleic acid in the PL fraction was higher in healthy infants than in the atopic group (P<0.05), while linoleic acid was lower in the TG fraction (P=0.03). The ratio of n-6 to n-3 and the sum of n-6 in the TG fraction differed between the groups. Atopic infants had a higher sum of n-6 fatty acids and subsequently a higher n-6 to n-3 ratio (P=0.02 for both). In the CE fraction, healthy infants had a higher proportion of docosahexaenoic acid (22:6 n-3), P=0.03. The sum of n-3 fatty acids was also higher in the serum lipid CE of healthy infants (P=0.05). This resulted in a lowered n-6 to n-3 ratio (P=0.02) in the CE fraction of healthy infants.

Table 2.  Serum lipid PUFA composition (mean [SD]) in atopic and healthy children aged 3 months
PUFATGCEPL
Atopic child (n=20)Healthy child (n=20)Atopic child (n=20)Healthy child (n=20)Atopic child (n=20)Healthy child (n=20)
  1. * Statistically significant difference between atopic and nonatopic children, P<0.05 (unpaired t-test).

18:2 n-614.22 (2.89)*12.57 (1.99)46.21 (4.38)45.20 (4.85)21.28 (2.89)21.28 (2.95)
18:3 n-60.21 (0.06)0.18 (0.05)0.47 (0.22)0.40 (0.12)0.12 (0.06)*0.16 (0.03)
20:3 n-60.21 (0.06)0.23 (0.07)0.50 (0.13)0.50 (0.12)2.80 (0.60)2.80 (0.59)
20:4 n-60.98 (0.34)0.81 (0.44)5.62 (1.78)5.31 (1.41)8.22 (1.73)7.74 (1.68)
22:4 n-6    0.20 (0.05)0.19 (0.04)
18:3 n-31.19 (0.61)1.46 (0.34)0.51 (0.17)0.57 (0.11)0.22 (0.07)0.22 (0.04)
20:5 n-30.23 (0.12)0.22 (0.13)0.44 (0.22)0.51 (0.19)0.58 (0.24)0.53 (0.19)
22:5 n-30.21 (0.10)0.17 (0.07)  0.58 (0.15)0.62 (0.15)
22:6 n-30.46 (0.30)0.51 (0.35)0.41 (0.19)*0.54 (0.22)3.43 (0.92)3.74 (0.98)
n-6:n-37.32 (4.91)*5.83 (2.01)38.47 (9.56)*31.73 (9.49)6.82 (2.99)6.30 (2.60)
Σ n-615.52 (2.86)*13.77 (2.01)52.70 (4.30)51.41 (4.17)32.61 (1.87)32.17 (1.57)
Σ n-32.13 (0.79)2.57 (0.59)1.37 (0.47)*1.62 (0.40)4.78 (1.24)5.12 (1.20)

Several PUFA in breast milk correlated with subse-quent serum lipid fatty acid proportions in healthy infants. The proportion of arachidonic acid (r=0.736, P<0.01) in the PL fraction positively correlated with corresponding proportions in breast milk. Similarly, there was a significant positive correlation between serum CE and breast milk γ-linolenic acid (r=0.790, P<0.001) and arachidonic acid (r=0.731, P<0.01). In the TG fraction, γ-linolenic acid (r=0.723, P<0.01), α-linolenic acid (r=0.668, P<0.01), and docosahexaenoic acid (r=0.766, P<0.001) correlated with breast-milk proportions.

In atopic infants, no correlations were observed in the PL fraction. However, the sum of n-3 PUFA (r=0.990, P<0.001) in serum TG and the sum of n-6 PUFA (r=0.679, P<0.01) in serum CE positively correlated with corresponding proportions of breast-milk PUFA.

Discussion

  1. Top of page
  2. Abstract
  3. Material and methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References

The Western lifestyle has been held to be responsible for the increasing susceptibility to atopic sensitization. One explanation for such a development is the so-called hygiene hypothesis (23), and another the dietary hypothesis, according to which the increased prevalence of atopic diseases has been linked to an increase in PUFA consumption (4, 5).

As in a recent study by Hoppu et al. (24), we observed that the energy intake of the mothers was low and a notably high proportion of the energy was derived from fat. Moreover, a maternal diet rich in SFA was associated with the atopic status of the children. We also demonstrated a significant correlation between maternal diet and breast-milk content of SFA, although the intake and breast-milk proportions of linoleic and α-linolenic acids did not correlate in either group of mothers. Francois et al. (25) concluded that the long-chain PUFA content of breast milk is not closely related to maternal intake of their parent fatty acids. Other factors influencing PUFA levels in human milk, such as liberation from maternal stores and endogenous synthesis from precursors, have been suggested (26). Overall, it appears that maternal diet during breast-feeding does influence the fatty acid composition of breast milk. Emphasis must be placed on the maternal diet during pregnancy, as these fatty acid stores may influence the transfer of lipids into breast milk even during lactation.

The PUFA content of the breast milk of atopic mothers has been demonstrated to differ from that of healthy mothers. Breast milk obtained from healthy mothers of infants with newly developed atopic dermatitis had more linoleic acid and decreased proportions of longer chain n-6 PUFA than the breast milk of healthy mothers of nonatopic infants (12, 13), whereas the breast milk of healthy mothers of healthy infants contained more γ-linolenic acid and α-linolenic acid than the breast milk of their atopic controls (6). Accordingly, we observed that γ-linolenic acid and the n-6 to n-3 ratio were lower in the breast milk of allergic mothers than in that of healthy mothers. This kind of difference has been attributed to disturbances in PUFA metabolism in the breast milk of atopic mothers (13). Yet, we did not detect any difference in linoleic acid proportions between allergic and healthy mothers; thus, our results do not entirely support the proposed impaired PUFA metabolism in atopic subjects. Another possible explanation could be that n-6 PUFA in allergic mothers are not as readily transferred from body stores to breast milk because they are used for eicosanoid synthesis, as also evinced by the elevated PGE2 and LTB4 levels observed in atopic subjects (7, 27).

Dietary supplementation of γ-linolenic acid has been shown to reduce the severity of skin symptoms in children with atopic dermatitis (28). The beneficial effects are expected to be directly attributable to deficits of the γ-linolenic acid required for normal skin functions. If applied before immunologic sensitization, as in the breast milk of healthy mothers here, γ-linolenic acid may protect against atopic sensitization (29). Moreover, the proportions of n-3 fatty acids have been demonstrated to possess anti-inflammatory properties and to compete with n-6 PUFA for the same desaturation and elongation enzymes (5, 27). Here, we found that the breast milk of mothers with healthy children tended to contain more n-3 fatty acids. Whether the shortage of regulatory PUFA, such as γ-linolenic acid and n-3 PUFA, in the breast milk could promote intestinal inflammation, subsequently increasing the permeability of the gut barrier, remains unknown. Yet, these adverse reactions would confirm the atopic sensitization of children.

The serum lipid fatty acids observed in atopic and healthy infants in the current study were in accordance with earlier reports (14, 16). There is epidemiologic evidence linking the increase in n-6 PUFA consumption to atopic sensitization, seen both at the dietary and serum fatty acid levels (4, 14, 30). Like the PUFA content of breast milk, linoleic acid in serum PL has been shown to be elevated and its long-chain derivatives lowered in atopic subjects (14, 15). These abnormalities have been explained by dysfunction of Δ-6 desaturase in atopic subjects (14, 15, 31), although this hypothesis remains controversial (16). In the present study, atopic infants had more n-6 fatty acids and less n-3 fatty acids in serum TG and CE fractions, indicating that atopic infants (exclusively breast-fed) consumed relatively more n-6 fatty acids. Still, except for γ-linolenic acid proportions that were slightly lower in atopic infants, n-6 PUFA compositions in serum PL were comparable in both groups. These results suggest that either the incorporation of n-6 fatty acids into serum PL may be hindered or these fatty acids may be utilized for other purposes in atopic infants.

The present study demonstrated the carryover effect of dietary fatty acids from the maternal diet via breast milk into infants' serum lipid fatty acids. Low maternal consumption of foods rich in n-3 PUFA was noted and evinced as a high n-6 to n-3 PUFA ratio in the breast milk of both groups. Allergic mothers had less γ-linolenic acid in their breast milk than healthy mothers. Similarly, the γ-linolenic acid was lower, but proportions of other n-6 PUFA were comparable in the serum PL of infants, although atopic infants had more n-6 PUFA in serum TG and CE than healthy infants. Breast-feeding directly influenced the serum lipid fatty acid profiles of healthy infants, but, in atopic infants, correlation was found only between breast milk and serum TG and CE fractions. Although other reports have concluded that abnormalities in breast milk and serum PUFA in atopic individuals may be due to impaired capacity to metabolize PUFA, our results cannot unconditionally confirm this conclusion. As an alternative explanation, we suggest that instead of transferring n-6 PUFA into breast milk in mothers or incorporating them into PL in infants, they may be utilized for other purposes such as eicosanoid precursors in allergic/atopic individuals. In accordance with the observation of Hodge et al. (27), we suggest that the excess dietary supply of n-6 PUFA or reduced proportions of regulatory PUFA, such as γ-linolenic acid and n-3 PUFA, may be a risk factor for the development of atopic disease.

Acknowledgments

  1. Top of page
  2. Abstract
  3. Material and methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References

This work was financially supported by the Technology Development Agency of Finland (TEKES), the Academy of Finland, and the Wäinö Edvard Miettinen Foundation. We gratefully acknowledge the cooperation of the participants in the study. We thank E. Sarkkinen, PhD, for advice on interpretation of serum lipid fatty acid data; U. Hoppu, MSc, and L. Seppo, MSc, for food record calculations; and R. Crittenden, PhD, for his valuable comments on and revision of the English text.

References

  1. Top of page
  2. Abstract
  3. Material and methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References
  • 1
    International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee. Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAAC. Lancet 1998;351:12251232.DOI: 10.1016/s0140-6736(97)07302-9
  • 2
    Oddy WH, Holt PD, Sly PD, et al. Association between breast feeding and asthma in 6 year old children: findings of prospective birth cohort study. BMJ 1999;319:815819.
  • 3
    Isolauri E, Tahvanainen A, Peltola T, Arvola T. Breast-feeding of allergic infants. J Pediatr 1999;134:2732.
  • 4
    Black PN & Sharpe S. Dietary fat and asthma: is there a connection? Eur Respir J 1997;10:612.
  • 5
    Simopoulos AP. Omega-3 fatty acids in health and disease and in growth and development. Am J Clin Nutr 1991;55:438463.
  • 6
    Duchen K, Yu G, Björkstén B. Atopic sensitization during the first year of life in relation to long chain poly-unsaturated fatty acid levels in human milk. Pediatr Res 1998;44:478484.
  • 7
    Chan SC, Kim J-W, Henderson Wr Jr, Hanifin JM. Altered prostaglandin E2 regulation of cytokine production in atopic dermatitis. J Immunol 1993;151:33453352.
  • 8
    Ohtsuka Y, Yamashiro Y, Shimizu T, et al. Reducing cell membrane n-6 fatty acids attenuates mucosal damage in food-sensitive enteropathy in mice. Pediatr Res 1997;42:835839.
  • 9
    Alexander JW. Immunonutrition: the role of ω-3 fatty acids. J Nutr 1998;14:627633.
  • 10
    Calder PC. Fat chance of immuno-modulation. Immunol Today 1998;19:244247.DOI: 10.1016/s0167-5699(98)01264-x
  • 11
    Mellies MJ, Ishikawa TT, Gartside PS, et al. Effects of varying maternal dietary fatty acids in lactating women and their infants. Am J Clin Nutr 1979;32:299303.
  • 12
    Businco L, Loppi M, Morse NL, Nisini R, Wright S. Breast milk from mothers of children with newly developed atopic eczema has low levels of long chain polyunsaturated fatty acids. J Allergy Clin Immunol 1993;91:11341139.
  • 13
    Yu G, Duchen K, Björkstén B. Fatty acid composition in colostrum and mature milk from non-atopic and atopic mothers during the first months of lactation. Acta Pediatr 1998;87:729736.
  • 14
    Yu G & Björkstén B. Serum levels of phospholipid fatty acids in mothers and their babies in relation to allergic disease. Eur J Pediatr 1998;157:298303.DOI: 10.1007/s004310050815
  • 15
    Manku MS, Horrobin DF, Morse NL, Wright S, Burton JL. Essential fatty acids in the plasma phospholipids of patients with atopic eczema. Br J Dermatol 1984;110:643648.
  • 16
    Leichsenring M, Kochsiek U, Paul K. (n-6)-Fatty acids in plasma lipids of children with atopic bronchial asthma. Pediatr Allergy Immunol 1995;6:209212.
  • 17
    Hanifin JM. Epidemiology of atopic dermatitis. Monogr Allergy 1987;21:116131.
  • 18
    Fédération Internatinale de Laiterie – International Dairy Federation. Determination of fat. . 1987;1C:18.
  • 19
    Christie WW. A simple procedure for rapid transmethylation of glycerolipids and cholesteryl esters. J Lipid Res 1982;23:10721075.
  • 20
    Erkkilä AT, Sarkkinen ES, Koukkunen H, et al. Concordance of diet with the recommended cholesterol lowering diet in patients with coronary heart disease. Eur J Clin Nutr 1998;52:279285.
  • 21
    Ågren JJ, Julkunen A, Penttilä I. Rapid separation of serum lipids for fatty acid analysis by a single amino-propyl column. J Lipid Res 1992;33:18711876.
  • 22
    Rastas M, Seppänen R, Knuts LR, Karvetti RL, Varo P. Nutrient composition of foods. Helsinki: Publication of the Social Insurance Institution, 1993.
  • 23
    Wahn U. What drives the allergic march? Allergy 2000;55:591599.DOI: 10.1034/j.1398-9995.2000.00111.x
  • 24
    Hoppu U, Kalliomäki M, Isolauri E. Maternal diet rich in saturated fat during breastfeeding is associated with atopic sensitization of the infant. Eur J Clin Nutr 2000;55:702705.
  • 25
    Francois CA, Connor SL, Wander RC, Connor WE. Acute effects of dietary fatty acids on the fatty acids of human milk. Am J Clin Nutr 1998;67:301308.
  • 26
    Sauerwald TU, Demmelmair H, Fidler N, Koletzko B. Polyunsaturated fatty acid supply with human milk. Physio-logical aspects and in vivo studies of metabolism. Adv Exp Med Biol 2000;478:261270.
  • 27
    Hodge L, Salome CM, Peat JK, Haby MM, Xuan W, Woolcock AJ. Con-sumption of oily fish and childhood asthma risk. Med J Austr 1996;164:137140.
  • 28
    Shimasaki H. PUFA content and effect of dietary intake of γ-linolenic acid-rich oil on profiles of n-6, n-3 metabolites in plasma of children with atopic eczema. J Clin Biochem Nutr 1995;19:183192.
  • 29
    Horrobin DF. Essential fatty acid metabolism and its modification in atopic eczema. Am J Clin Nutr 2000;71 Suppl 1:367S372S.
  • 30
    Nagakomi T, Itaya H, Tominaga T, Yamaki M, Hisamatsu S, Nagakomi O. Is atopy increasing? Lancet 1994;343:121122.
  • 31
    Manku MS, Horrobin DF, Morse NL, et al. Reduced levels of prostaglandin precursors in the blood of atopic patients: defective delta-6-desaturase function as a biochemical basis of atopy. Prostaglandins Leukot Med 1982;9:615628.