Propuesta de un modelo ecosistémico para la atención integral a la salud mental perinatal / An ecosystemic model for comprehensive perinatal mental health care

La atención a la salud mental tradicionalmente ha prestado poca atención a las madres. Son muy escasos en nuestro medio los programas de atención integral a la salud mental perinatal. Proponemos un modelo de encuadre que sirva para la atención integral a la perinatalidad, incluyendo los cuidados a los procesos psíquicos de la reproducción, embarazo, parto y posparto desde una visión ecosistémica inspirada en las propuestas de Urie Bronfenbrenner y John Bowlby, entre otros, integrando las aportaciones de la neurobiología, la epigenética, los modelos de transmisión intergeneracional del apego y el trauma, la sistémica, y añadiendo una perspectiva de género y ecológica que permita visibilizar las necesidades de la díada madre-bebé en el centro como punto de partida para la prevención y la atención en perinatalidad. Proponemos una mirada perinatal como modelo para continuar profundizando en la atención a madres y familias en el inicio de la vida, así como para cuidar también a las profesionales que los atienden. Apostamos por la escucha, el acompañamiento y la psicoterapia como herramientas básicas en la atención comunitaria e individual a madres, bebés y familias. (AU)

Mental health care has traditionally paid little attention to mothers. Comprehensive perinatal mental health care programs are very scarce in our environment. We propose a framing model that serves for comprehensive perinatal care, including care for the mental processes of reproduction, pregnancy, childbirth, and postpartum from an ecosystemic vision inspired by the proposals of Urie Bronfenbrenner and John Bowlby, among others. The model integrates data from neurobiology and epigenetics and theories from systemic and intergenerational transmission of attachment and trauma. It is embedded in a gender and ecological perspective that allows making visible the mother-baby dyad's needs in the center as a starting point for prevention and attention during the perinatal period. We propose a perinatal view as a model to continue deepening care for mothers and families at the beginning of life, as well as to care for the professionals who care for them. We bet on listening, support and psychotherapy as basic tools in community and individual care for mothers, babies, and families. (AU)

Placental fatty acid transfer: a key factor in fetal growth.

The functionality of the placenta may affect neonatal adiposity and fetal levels of key nutrients such as long-chain polyunsaturated fatty acids. Fetal macrosomia and its complications may occur even in adequately controlled gestational diabetic (GDM) mothers, suggesting that maternal glycemia is not the only determinant of fetal glycemic status and wellbeing. We studied in vivo the placental transfer of fatty acids (FA) labeled with stable isotopes administered to 11 control and 9 GDM pregnant women (6 treated with insulin). Subjects received orally ¹³C-palmitic, ¹³C-oleic, and ¹³C-linoleic acids and ¹³C-docosahexaenoic acid (¹³C-DHA) 12 h before an elective caesarean section. FA were quantified by gas chromatography and ¹³C enrichments by gas chromatography-isotope ratio mass spectrometry. The ¹³C-FA concentration was higher in total lipids of maternal plasma in GDM patients versus controls, except for ¹³C-DHA. Moreover, ¹³C-DHA showed a lower placenta/maternal plasma ratio in GDM patients versus controls and a significantly lower cord/maternal plasma ratio. Other FA ratios studied were not different between GDM and controls. A disturbed ¹³C-DHA placental uptake occurred in GDM patients treated with diet or insulin, while the latter also had lower ¹³C-DHA levels in the venous cord. The tracer study pointed towards an impaired placental DHA uptake as a critical step, while the transfer of other ¹³C-FA was less affected. Patients with GDM treated with insulin could also have a greater fetal fat storage, which may have contributed to the reduced ¹³C-DHA in the venous cord observed. The DHA transfer to the fetus was reduced in GDM pregnancies compared to controls. This might have an influence on fetal neurodevelopment and long-term consequences for the child.

Neuroendocrinology of childbirth and mother-child attachment: the basis of an etiopathogenic model of perinatal neurobiological disorders.

This review focuses on the neuroendocrine mechanisms in the mother and the newborn that are involved in the generation and consolidation of mother-child attachment. The role that different hormones and neurotransmitters play on the regulation of these mechanisms during parturition, the immediate postpartum period and lactation is discussed. Interferences in the initiation of mother-child attachment may have potential long-term effects for the behavior and affection of the newborn. Therefore, the possible consequences of alterations in the physiological neuroendocrine mechanisms of attachment, caused by elective Cesarean section, intrapartum hormonal manipulations, preterm delivery, mother-infant postpartum separation and bottle-feeding instead of breastfeeding are also discussed.

Materno-fetal transfer of docosahexaenoic acid is impaired by gestational diabetes mellitus.

Better knowledge on the disturbed mechanisms implicated in materno-fetal long-chain polyunsaturated fatty acid (LC-PUFA) transfer in pregnancies with gestational diabetes mellitus (GDM) may have potentially high implications for later on in effective LC-PUFA supplementation. We studied in vivo placental transfer of fatty acids (FA) using stable isotope tracers administrated to 11 control and 9 GDM pregnant women (6 treated with insulin). Subjects received orally [(13)C]palmitic, [(13)C]oleic and [(13)C]linoleic acids, and [(13)C]docosahexaenoic acid ((13)C-DHA) 12 h before elective caesarean section. Maternal blood samples were collected at -12, -3, -2, and -1 h, delivery, and +1 h. Placental tissue and venous cord blood were also collected. FA were quantified by gas chromatography (GC) and (13)C enrichments by GC-isotope ratio mass spectrometry. [(13)C]FA concentration was higher in total lipids of maternal plasma in GDM vs. controls, except for [(13)C]DHA. Moreover, [(13)C]DHA showed lower placenta/maternal plasma ratio in GDM vs. controls and significantly lower cord/maternal plasma ratio. For the other studied FA, ratios were not different between GDM and controls. Disturbed [(13)C]DHA placental uptake occurs in both GDM treated with diet or insulin, whereas the last ones also have lower [(13)C]DHA in venous cord. The tracer study pointed toward impaired placental DHA uptake as critical step, whereas the transfer of the rest of [(13)C]FA was less affected. GDM under insulin treatment could also have higher fetal fat storage, contributing to reduce [(13)C]DHA in venous cord. DHA transfer to the fetus was reduced in GDM pregnancies compared with controls, which might affect the programming of neurodevelopment in their neonates.

Omega 3 fatty acids, gestation and pregnancy outcomes.

Pregnancy is associated with a reduction in maternal serum docosahexaenoic acid (DHA, 22:6 n-3) percentage and its possible depletion in the maternal store. Since the synthesis of long chain polyunsaturated fatty acids (LCPUFA) in the fetus and placenta is low, both the maternal LCPUFA status and placental function are critical for their supply to the fetus. Maternal supplementation with DHA up to 1 g/d or 2·7 g n-3 LCPUFA did not have any harmful effect. DHA supplementation in large studies slightly the enhanced length of gestation (by about 2 days), which may increase the birth weight by about 50 g at delivery. However no advice can be given on their general using to avoid preterm deliveries in low or high risk pregnancies. Several studies, but not all, reported improvements of the offspring in some neurodevelopmental tests as a result of DHA supplementation during gestation, or, at least, positive relationships between maternal or cord serum DHA percentages and cognitive skills in young children. The effect seems more evident in children with low DHA proportions, which raises the question of how to identify those mothers who might have a poor DHA status and who could benefit from such supplementation. Most studies on the effects of n-3 LCPUFA supplementation during pregnancy on maternal depression were judged to be of low-to-moderate quality, mainly due to small sample sizes and failure to adhere to Consolidated Standards of Reporting Trials guidelines. In contrast, the effects of n-3 LCPUFA supplementation on reducing allergic diseases in offspring are promising.

Current understanding of placental fatty acid transport.

PURPOSE OF REVIEW: The amount and activity of placental enzymes, receptors, and transport proteins will determine the extent of lipid transfer to the fetus that strongly contributes to fetal fat accretion. RECENT FINDINGS: Several studies have shown an association between the percentage of maternal plasma docosahexaenoic acid during gestation and the development of cognitive functions in the neonate. The functionality of the placenta could affect neonatal adiposity and fetal levels of long-chain polyunsaturated fatty acids in the offspring. SUMMARY: Both in-vitro and human in-vivo studies using labeled fatty acids (FAs) reported a preferential placental-fetal transfer of long-chain polyunsaturated fatty acids, although the mechanisms are still uncertain. The placenta uptakes the maternal circulating nonesterified fatty acids (NEFAs) and FAs released by maternal lipoprotein lipase and endothelial lipase. These NEFAs enter the cell through passive diffusion or by membrane carrier proteins. NEFAs bind to cytosolic fatty-acid-binding proteins to interact with subcellular organelles, including the endoplasmic reticulum, mitochondria, lipid droplets and peroxisomes. Knowledge about FA metabolism and adaptations in response to obesity or diabetes in human placenta is more limited, and contradictory results are available in their influence on placental lipases and carriers.

Placental transfer of fatty acids and fetal implications.

Considerable amounts of long-chain polyunsaturated fatty acids (LC-PUFAs), particularly arachidonic acid and docosahexaenoic acid (DHA, 22:6n-3), are deposited in fetal tissues during pregnancy; and this process is facilitated by placental delivery. Nevertheless, the mechanisms involved in LC-PUFA placental transfer remain unclear. Stable isotope techniques have been used to study human placental fatty acid transfer in vivo. These studies have shown a significantly higher ratio of (13)C-DHA in cord to maternal plasma compared with other fatty acids, which reflects a higher placental DHA transfer. In addition, a selective DHA accumulation in placental tissue, relative to other fatty acids, has been reported. The materno-fetal transfer of fatty acids is a slow process that requires ≥12 h. A high incorporation of dietary (13)C-DHA into maternal plasma phospholipids appears to be important for placental uptake and transfer. DHA in cord blood lipids correlates with placental messenger RNA expression of fatty acid transport protein (FATP)-4, compatible with a role of FATP-4 in DHA transfer. Impaired materno-fetal LC-PUFA transport has been proposed in pregnancies complicated by abnormal placental function (eg, due to gestational diabetes mellitus or intrauterine growth restriction), which should be addressed in future studies. Given that placental DHA transfer is important for child outcomes, elucidation of its potential modulation by transport mechanisms, maternal diet, and disease appears to be important.

Mechanisms involved in the selective transfer of long chain polyunsaturated Fatty acids to the fetus.

The concentration of long chain polyunsaturated fatty acid (LCPUFA) in the fetal brain increases dramatically from the third trimester until 18 months of life. Several studies have shown an association between the percentage of maternal plasma docosahexaenoic acid (DHA) during gestation and development of cognitive functions in the neonate. Since only very low levels of LCPUFA are synthesized in the fetus and placenta, their primary source for the fetus is the maternal circulation. Both in vitro and human in vivo studies using labeled fatty acids have shown preferential transfer of LCPUFA from the placenta to the fetus compared with other fatty acids, although the mechanisms involved are still uncertain. The placenta takes up circulating maternal non-esterified fatty acids (NEFA) and fatty acids released mainly by maternal lipoprotein lipase and endothelial lipase. These NEFA may enter the cell by passive diffusion or by means of membrane carrier proteins. Once in the cytosol, NEFA bind to cytosolic fatty acid-binding proteins for transfer to the fetal circulation or can be oxidized within the trophoblasts, and even re-esterified and stored in lipid droplets. Although trophoblast cells are not specialized for lipid storage, LCPUFA may up-regulate peroxisome proliferator activated receptor-γ (PPARγ) and hence the gene expression of fatty acid transport carriers, fatty acid acyl-CoA-synthetases and adipophilin or other enzymes involved in lipolysis, modifying the rate of placental transfer, and metabolism. The placental transfer of LCPUFA during pregnancy seems to be a key factor in the neurological development of the fetus. Increased knowledge of the factors that modify placental transfer of fatty acids would contribute to our understanding of this complex process.

Maternal-fetal in vivo transfer of [13C]docosahexaenoic and other fatty acids across the human placenta 12 h after maternal oral intake.

BACKGROUND: Fetal growth and development require n-3 (omega-3) long-chain polyunsaturated fatty acids, but mechanisms for their placental transfer are not well understood. OBJECTIVE: We assessed distribution and human placental transfer of (13)C-labeled fatty acids (FAs) 12 h after oral application. DESIGN: Eleven pregnant women received 0.5 mg [(13)C]palmitic acid ((13)C-PA; 16:0), 0.5 mg [(13)C]oleic acid ((13)C-OA; 18:1n-9), 0.5 mg [(13)C]linoleic acid ((13)C-LA; 18:2n-6), and 0.1 mg [(13)C]docosahexaenoic acid ((13)C-DHA; 22:6n-3) per kilogram of body weight orally 12 h before elective cesarean section. Maternal blood samples were collected before tracer intake (-12 h) and at -3, -2, -1, 0, and +1 h relative to the time of cesarean section. At birth, venous cord blood and placental tissue were collected, and FA concentrations in individual lipid fractions and their tracer content (atom percent excess values) were determined. RESULTS: Relatively stable tracer enrichment was achieved in maternal lipid fractions 12 h after tracer administration. In maternal plasma, most (13)C-PA and (13)C-OA were found in triglycerides, whereas (13)C-LA and (13)C-DHA were found mainly in plasma phospholipids and triglycerides. In placental tissue, (13)C-FAs were mainly found in phospholipids, which comprise 80% of placental tissue lipids. Placenta-maternal plasma ratios and fetal-maternal plasma ratios for (13)C-DHA were significantly higher than those for any other FA. CONCLUSIONS: Twelve hours after oral application of (13)C-labeled FAs, relatively stable tracer enrichment was achieved. We found a significantly higher ratio of (13)C-DHA concentrations in cord plasma than in maternal plasma, which was higher than that for the other studied FAs. (13)C-DHA is predominantly esterified into phospholipids and triglycerides in maternal plasma, which may facilitate its placental uptake and transfer.