A maternal erythrocyte DHA content of approximately 6 g% is the DHA status at which intrauterine DHA biomagnifications turns into bioattenuation and postnatal infant DHA equilibrium is reached.

PURPOSE: Higher long-chain polyunsaturated fatty acids (LCP) in infant compared with maternal lipids at delivery is named biomagnification. The decline of infant and maternal docosahexaenoic acid (DHA) status during lactation in Western countries suggests maternal depletion. We investigated whether biomagnification persists at lifelong high fish intakes and whether the latter prevents a postpartum decline of infant and/or maternal DHA status. METHODS: We studied 3 Tanzanian tribes with low (Maasai: 0/week), intermediate (Pare: 2-3/week), and high (Sengerema: 4-5/week) fish intakes. DHA and arachidonic acid (AA) were determined in maternal (m) and infant (i) erythrocytes (RBC) during pregnancy (1st trimester n = 14, 2nd = 103, 3rd = 88), and in mother-infant pairs at delivery (n = 63) and at 3 months postpartum (n = 104). RESULTS: At delivery, infants of all tribes had similar iRBC-AA which was higher than, and unrelated to, mRBC-AA. Transplacental DHA biomagnification occurred up to 5.6 g% mRBC-DHA; higher mRBC-DHA was associated with "bioattenuation" (i.e., iRBC-DHA < mRBC-DHA). Compared to delivery, mRBC-AA after 3 months was higher, while iRBC-AA was lower. mRBC-DHA after 3 months was lower, while iRBC-DHA was lower (low fish intake), equal (intermediate fish intake), and higher (high fish intake) compared to delivery. We estimated that postpartum iRBC-DHA equilibrium is reached at 5.9 g%, which corresponds to a mRBC-DHA of 6.1 g% throughout pregnancy. CONCLUSION: Uniform high iRBC-AA at delivery might indicate the importance of intrauterine infant AA status. Biomagnification reflects low maternal DHA status, and bioattenuation may prevent intrauterine competition of DHA with AA. A mRBC-DHA of about 6 g% during pregnancy predicts maternal-fetal equilibrium at delivery, postnatal iRBC-DHA equilibrium, but is unable to prevent a postnatal mRBC-DHA decline.

Postdelivery changes in maternal and infant erythrocyte fatty acids in 3 populations differing in fresh water fish intakes.

INTRODUCTION: Long-chain polyunsaturated (LCP) fatty acids (FA) are important during infant development. Mother-to-infant FA-transport occurs at the expense of the maternal status. Maternal and infant FA-status change rapidly after delivery. METHODS: Comparison of maternal (mRBC) and infant erythrocyte (iRBC)-FA-profiles at delivery and after 3 months exclusive breastfeeding in relation to freshwater-fish intakes. Approximation of de-novo-lipogenesis (DNL), stearoyl-CoA-desaturase (SCD), elongation-of-very-long-chain-FA-family-member-6 (Elovl-6), delta-5-desaturase (D5D) and delta-6-desaturase (D6D)-enzymatic activities from their product/essential-FA and product/substrate-ratios. RESULTS AND DISCUSSION: Increasing iRBC-14:0 derived from mammary-gland DNL. Decreasing mRBC-ω9, but increasing iRBC-ω9, suggest high ω9-FA-transfer via breastmilk. Decreasing (m+i)RBC-16:0, DNL- and SCD-activities, but increasing (m+i)RBC-18:0 and Elovl-6-activity suggest more pronounced postpartum decreases in DNL- and SCD-activities, compared to Elovl-6-activity. Increasing (m+i)RBC-18:3ω3, 20:5ω3, 22:5ω3, 18:2ω6, mRBC-20:4ω6 and (m+i)D5D-activity, but decreasing mRBC-22:6ω3 and (m+i)D6D-activity and dose-dependent changes in iRBC-22:6ω3 confirm that D6D-activity is rate-limiting and 22:6ω3 is important during lactation. Fish-intake related magnitudes of postpartum FA-changes suggest that LCPω3 influence DNL-, SCD- and desaturase-activities.

Postpartum changes in maternal and infant erythrocyte fatty acids are likely to be driven by restoring insulin sensitivity and DHA status.

INTRODUCTION: Perinatal changes in maternal glucose and lipid fluxes and de novo lipogenesis (DNL) are driven by hormones and nutrients. Docosahexaenoic acid (DHA) reduces, whereas insulin augments, nuclear abundance of sterol-regulatory-element-binding-protein-1 (SREBP-1), which promotes DNL, stearoyl-CoA-desaturase (SCD, also Δ9-desaturase), fatty acid-(FA)-elongation (Elovl) and FA-desaturation (FADS). Decreasing maternal insulin sensitivity with advancing gestation and compensatory hyperinsulinemia cause augmented postprandial glucose levels, adipose tissue lipolysis and hepatic glucose- and VLDL-production. Hepatic VLDL is composed of dietary, body store and DNL derived FA. Decreasing insulin sensitivity increases the contribution of FA from hepatic-DNL in VLDL-triacylglycerols, and consequently saturated-FA and monounsaturated-FA (MUFA) in maternal serum lipids increase during pregnancy. Although other authors described changes in maternal serum and RBC essential-FA (EFA) after delivery, none went into detail about the changes in non-EFA and the mechanisms behind -and/or functions of- the observed changes. HYPOTHESIS: Postpartum FA-changes result from changing enzymatic activities that are influenced by the changing hormonal milieu after delivery and DHA-status. EMPIRICAL DATA: We studied FA-profiles and FA-ratios (as indices for enzymatic activities) of maternal and infant RBC at delivery and after 3 months exclusive breastfeeding in three populations with increasing freshwater-fish intakes. DNL-, SCD- and FADS2-activities decreased after delivery. Elongation-6 (Elovl-6)- and FADS1-activities increased. The most pronounced postpartum changes for mothers were increases in 18:0, linoleic (LA), arachidonic acid (AA) and decreases in 16:0, 18:1ω9 and DHA; and for infants increases in 18:1ω9, 22:5ω3, LA and decreases in 16:0 and AA. Changes were in line with the literature. DISCUSSION: Postpartum increases in 18:0, and decreases in 16:0 and 18:1ω9, might derive from reduced insulin-promoted DNL-activity, with more reduced SCD- than Elovl-activity that leaves more 16:0 to be converted to 18:0 (Elovl-activity) than to MUFA (SCD-activity). Postpartum changes in ΣDNL, saturated-FA and MUFA related negatively to RBC-DHA. This concurs with suppression of both SCD- and Elovl-6 activities by DHA, through its influence on SREBP. Infant MUFA and LA increased at expense of their mothers. Sustained transport might be important for myelination (MUFA) and skin barrier development (LA). Maternal postpartum decreases in FADS2-, and apparent increases in FADS1-activity, together with increases in LA, AA, and 22:5ω3, but decrease in DHA, confirm that FADS2 is rate limiting in EFA-desaturation. Maternal LA and AA increases might be the result of rerouting from transplacental transfer to the incorporation into milk lipids and discontinued placental AA-utilization. IMPLICATIONS: Perinatal changes in maternal and infant FA status may be strongly driven by changing insulin sensitivity and DHA status.

Maternal DHA equilibrium during pregnancy and lactation is reached at an erythrocyte DHA content of 8 g/100 g fatty acids.

Low long-chain PUFA (LC-PUFA, or LCP) consumption relates to suboptimal neurodevelopment, coronary artery disease, and [postpartum (PP)] depression. Maternal-to-infant LCP transport during pregnancy and lactation is at the expense of maternal status, a process known as biomagnification. Despite biomagnification, maternal and infant LCP status generally declines during lactation. To assess the 1) turning point of biomagnification [level from which maternal (m)LCP status exceeds infant (i)LCP status]; 2) LCP equilibrium (steady-state-level from which mRBC-LCP stop declining during lactation); 3) corresponding iLCP-status; and 4) the relationship between RBC-DHA and RBC-arachidonic acid (AA), we measured RBC-fatty acids in 193 Tanzanian mother-infant pairs with no, intermediate (2-3 times/wk), and high (4-5 times/wk) freshwater fish consumption at delivery and after 3 mo of exclusive breast-feeding. At 3 mo, mRBC-DHA was lower than the corresponding iRBC-DHA up to a mRBC-DHA of 7.9 g%. mRBC-DHA equilibrium, with equivalent mRBC-DHA at both delivery and at 3 mo PP, occurred at 8.1 g%. This mRBC-DHA equilibrium of 8.1 g% corresponded with an iRBC-DHA of 7.1-7.2 g% at delivery that increased to 8.0 g% at 3 mo. We found between-group differences in mRBC-AA; however, no differences in iRBC-AA were observed at delivery or 3 mo. Relations between RBC-DHA and RBC-AA were bell-shaped. We conclude that, at steady-state LCP intakes during lactation: 1) biomagnification occurs up to 8 g% mRBC-DHA; 2) mRBC-DHA equilibrium is reached at 8 g%; 3) mRBC-DHA equilibrium corresponds with an iRBC-DHA of 7 g% at delivery and 8 g% after 3 mo; 4) unlike RBC-DHA, mRBC-AA and iRBC-AA are independently regulated in these populations; and 5) bell-shaped RBC-DHA vs. RBC-AA-relations might support uniform iRBC-AA. A (maternal) RBC-DHA of 8 g% might be optimal for infant neurodevelopment and adult cardiovascular disease incidence.