A child's first relationship, the one with his mother acts as a template that . the development of neural pathways in the fetal brain (Glover and O'Connor ). Studies investigating fetal brain development have demonstrated that fetuses do not her unborn child was introduced as early as (Chamberlain, ). Deutsch () is mother-fetus relationship with Winnicott alluding to prenatal. attachment, development, maternal fetal relation, pregnancy part of child's development, and would develop a sense of trust in the child.
The answers vary from totally disagreed definitely No to totally agreed completely match my characteristics.
Each item would be answered with a 5-point likert scale. Items 5, 6, 8, 16, 17 and 18 are answered in reverse. This questionnaire contains twenty-one items multiple choice questions and each could be scored from 0 to 3. Mothers who would gain a score of 21 or more would be considered depressed. This questionnaire has been validated in Iran by Ghasem Zadeh and approved as a valid tool for evaluation of depression [ 52 ]. Edinburgh Postnatal Depression Scale: Also validity and reliability of this questionnaire was determined to be 0.
This inventory contains ten items 4-choice questions. The choices for each question are scored from 0 to 3. The total score would be achieved by summing all the scores and would range from 0 to Questions 1, 2, and 4 are scored from 0 to 3 and the rest from 3 to 0. Gaining a score of 12 or more would be considered as having postpartum depression [ 53 ].
This scale contains 20 phrases and the individual should answer each within a 4-ponit Likert scale almost never, sometimes, most of the times and almost always with their general feelings about the phrase. Score of 20 to 31 indicates mild anxiety, score of 32 to 42 indicates lower moderate anxiety, 43 to 52 indicates higher moderate anxiety, 53 to 62 indicates relatively severe anxiety, 63 to 72 indicates severe anxiety and a score 73 to 80 indicates extremely severe anxiety.
The reliability of State-Trait Anxiety Inventory has been calculated to be 0. Panahi-Shahri reported a correlation coefficient of 0.
It has 25 items and 2 subscales of caring 12 questions and excessive support 13 questionswhich is used for evaluating family bonding.
Higher scores mean that the parents are more attendant and lower scores indicate cold rejecting parents. Questions 1, 5, 6, 8, 9, 10, 11, 12, 13, 17, 19, 20 and 23 are scored in reverse.
This questionnaire has a well-approved validity and reliability in Iran [ 55 ].
Maternal bond - Wikipedia
This scale has 26 items. This questionnaire included three groups of behaviors: The sum of scores presented mother-infant attachment and higher scores indicated stronger attachment. This scale was first developed by Avant and its reliability has been reported to be 0. Discussion Based on the results, it is possible to provide appropriate strategies for enhancing maternal-fetal attachment and improve the provision of care in the health of pregnant women and their infants in the health care system.
The review of literature about related factors to prenatal attachment among different groups of pregnant women have emphasized that despite the numerous evaluations and different methods of studies, further studies are required in this field [ 57 ].
For example social support is one of the issues that its effect has not been conclusively determined [ 25 ]. This information could not be obtained through cross-sectional studies and through one episode of data collection [ 30 ] and more studies are needed to provide us a perspective of the mother-infant relation over time [ 58 ].
Walsh has stated that predictive factors for mother-fetal relationship have yet not been determined conclusively [ 59 ]. The prenatal period is a proper chance for evaluating maternal-fetal attachment. According to Bowlby studying this issue would help us understand and cope with the psychological problems during and after pregnancy [ 10 ].
As will be seen from the review of studies below, there are some trends in the operationalization and execution of immune system measurement. However, it is far from clear which aspects of the immune system might be especially susceptible to programming influence, or why that might be. This model comports well with the adaptive response and carrying-forward of effects that is built into the immune programming hypothesis.
The impact of maternal and infant nutritional status on immune system development and neurodevelopment Maternal and infant nutrition may modulate the immunologic development of the fetus and young infant and permanently alter immunologic and regulatory mechanisms, which may affect the risk for later disease Palmer, Adequate nutrition is necessary both for establishing the immune system, through normal organogenesis and development, and for an adequate immune response, through the normal proliferation of immune cells and the synthesis of secretory products and acute-phase proteins.
Some nutrients, like antioxidants, are also needed to control or inhibit the immune response. Finally, the immune response in itself may affect nutritional status by decreasing levels of certain nutrients, exemplified by the decrease in iron, pyridoxine and tryptophan associated with inflammation Lotto et al.
Maternal malnutrition During pregnancy, maternal malnutrition hampers placentation, with resulting changes in placental size, morphology and blood flow Belkacemi et al. The subsequently compromised fetal nutrition status has profound effects on organogenesis, growth and fetal programming and has been associated with both short- and long-term effects on development and morbidity Jansson and Powell, Maternal malnutrition interferes with both the quality and quantity of immune factors transferred prenatally through the placenta and postnatally through the mammary gland Palmer, Maternal IgG is actively transported through the placenta, appearing in the fetus Simister, and remaining intact in the infant up to the age of 3—6 months Palmer, The highest levels of maternal IgG in the cord blood is found during the last 4—6 weeks of pregnancy, so premature birth is associated with lower IgG levels in the infant Malek et al.
Reduced IgG levels have also been observed in small-for-gestational-age infants and in infants born to mothers with a lower than normal weight for height Okoko, Wesumperuma, and Hart, In human milk the main antibody is IgA, which constitutes part of the mucosal immune system that controls epithelial colonization of microorganisms and inhibits penetration of harmful substances Brandtzaeg, A window of opportunity Development of oral tolerance depends on interactions between maternal, infant and environmental factors, including genetics, food and bacterial colonization.
Breast milk is essential for development of oral tolerance and contains immunoglobulins, cytokines, growth factors, lysozyme, lactoferrin, and human milk oligosaccharides.
Maternal and infant nutrition modulate immune system development by providing food antigens. Food-derived antigens are transferred through the placenta into the amniotic fluid and cause prenatal formation of antigen-specific IgE antibodies Kondo et al.
After birth, introduction of breast milk, formula and solid food influences immune maturation and response in a complex interaction with gut flora Calder et al. There appears to be a window of opportunity for optimal development of oral tolerance between 4 and 6 months of age.
Impaired oral tolerance is associated with gut inflammatory disease, food allergies and celiac disease Verhasselt, Micronutrients Maternal deficiency of certain micronutrients is reported to permanently affect the immune system, but much remains unknown about this area. Gestational zinc deficiency has been associated with reduced thymic and spleen size, decreased antibody concentrations and impaired lymphocyte activity Wellinghausen, Nutritional factors related to single carbon metabolisms, choline, folate which is necessary for DNA methylation and vitamins B2, B6, and B12 are important modulators for epigenetic mechanisms Dominguez-Salas et al.
Changes in the epigenetic regulation of immune system development have been linked to various pathological conditions, among them allergic risk and asthma development Martino and Prescott, Conversely, mice fed a diet deficient in folic acid have a higher susceptibility to intestinal inflammation Kinoshita et al. Fat-soluble vitamins A and D play important roles in both cell-mediated and humoral immune responses Wintergerst et al.
Vitamin D is a direct regulator of antimicrobial innate immune responses, can inhibit lymphocyte proliferation Wang et al. Vitamin D deficiency in healthy neonates has been linked to an increased risk of respiratory syncytial virus infection during the first year of life. Vitamin A has also been shown to be necessary for the development of de novo Tregs in the gut Sun et al.
Vitamin A deficiency has been reported to seriously affect hematopoiesis Oren et al. It has also been suggested that maternal intake of vitamin E and polyunsaturated fatty acids during pregnancy may influence development of the immune system and be implicated in childhood asthma and allergy. Published reports, however, show conflicting results, and intervention studies are still lacking Devereux, Environmental contaminants Food not only provides nutrients but is also the most important source of environmental contaminants, specifically persistent organic pollutants POPs.
This is a group of highly resistant chemicals, including dioxins, furans, polychlorinated biphenyls and organochlorine pesticides, created by industrial activities and found in food, with the highest concentrations in fatty fish primarily farmed salmon Schecter et al. These highly toxic compounds have been found to cross the placenta and to be excreted in breast milk Fromme et al. The rapidly developing infant receiving this breast milk has immature organ systems and is especially vulnerable for toxic effects.
Early life exposure to various xenobiotics, including POPs, is associated with developmental immunotoxicity, which has been linked to neurodevelopmental disorders like autism spectrum disorders for review see Dietert and Dietert, Epidemiological and human studies have demonstrated that there is a complex interaction between the immune system, environmental pollutants and neurodevelopment, although the exact mechanisms are still not well understood Park et al.
However, pre- peri- and postnatal exposure to POPs is clearly associated with brain damage Ribas-Fito et al. Gut microbiota Postnatally, infant nutrition, together with other factors like gestational age, mode of delivery, bacterial environment and use of antibiotics, also influences the composition of the gut microbiota.
The enteric nervous system, which provides a bi-directional communication pathway between the brain, gastrointestinal cells and enteric microbes termed the brain-gut-enteric microbiota axisis important for immunological and neurological development, as well as later health.
Interactions between microbes and gut mucosa cells foster immunological tolerance and recognition of pathogens, regulate the subsequent production of various pro- and anti-inflammatory cytokines, and stimulate Th17 cells and Toll-like receptors, which can differentiate between commensal and pathogenic bacteria and trigger immune processes.
Maternal-fetal attachment: what we know and what we need to know
The microbiota may also play a role in regulation of the HPA system. Animal studies in mice have observed an association between gut microbes and levels of brain-derived neurotrophic factor in the cortex and hippocampus, and related this to changes in brain plasticity Sudo et al.
Malnutrition has been also associated with stress and activation of the HPA axis Seckl and Meaney, This is further outlined in the next section. The impact of maternal prenatal stress and anxiety on immune system development and neurodevelopment Experimental animal studies in a very wide range of species demonstrate reliable links between prenatal stress and a wide range of outcome measures to a considerable degree.
Prenatal programming from maternal stress is now a significant line of investigation, with many active research programs assessing a wide range of outcomes and mechanisms. One translation of the prenatal stress paradigm for human development that has only recently attracted attention is the association between prenatal stress and immune outcomes.
Studies linking immune function with prenatal stress are notable for at least two reasons. The first is the possibility that prenatal stress or anxiety could influence the developmental programming for vulnerability to infectious disease. Second, such a link would further amplify the potential public health impact of maternal prenatal stress or anxiety.
That is because clinically significant prenatal stress and anxiety is widely-reported to be common Heron et al. These observations compound the obvious public health relevance of infectious diseases in children. It is clear that there is variation in susceptibility to infectious disease; if this variation has prenatal origins, then there could be significant scope for prenatal preventive interventions as treatment.
Experimental animal work The hypothesis that prenatal stress alters the immune response in the animal has received wide-spread support in the rat, mouse, and other animal models Kay et al. These findings are notable for highlighting some of the parameters that need to be configured in studies, such as the potentially important distinction between observing the immune system markers during a resting state and response to an immunological challenge, and the location of the immune cell types that are targeted.
Questions about the usefulness of rat and mouse models for understanding inflammatory responses in humans have been raised based on a minimal overlap in genetic profile of the inflammatory response between the mouse and human Seok et al. It is therefore important that there is also a sound body of research on prenatal stress and offspring immune response in a non-human primate model.
In a series of studies, Coe and colleagues reported reliable links between prenatal stress and specific immune outcomes in infant and juvenile primates.
For example, Coe Coe et al. In another report in the same species, they Coe et al. These data suggest that HPA axis activity may be a likely cause of this diminished immune response, perhaps because of a higher set point for HPA axis activity.
This and other possible mechanisms of effect are discussed below. The key observation at this point is that experimental non-human primate work, which has causal leverage not gained in human studies, shows reliable links between prenatal stress and several markers of immune competence in the juvenile and adult offspring.
Investigations into stress in utero and the child's immune system are, however, more recent. Support for a role of prenatal stress and anxiety and child immune function is suggested by several studies examining asthma Lefevre et al. Perhaps the most direct test of the hypothesis that prenatal anxiety alters specific indicators of the developing immune system of the child was recently reported O'Connor et al.
In that study, infants whose mothers were characterized as anxious in pregnancy, according to self-report and clinical evaluation, exhibited poorer adaptive immune response at 6 months of age. The latter finding implies that there is a reduced type 1 and increased type 2 response in the infant; that is, consistent with other studies reviewed here, maternal prenatal anxiety exaggerates the normal type 2 skewing and less robust type 1 cytokine response to specific antigens Ota et al.
These predictions were independent of multiple confounds, including obstetric and psychosocial factors. Additionally, Entringer et al. There was greater cytokine production of IL-4, IL, and IL-6 in peripheral blood mononuclear cells PBMCs in response to Phytohaemagglutinin PHA in adult women who reported that their mother experienced a stress in pregnancy compared to a non-prenatal stress group; there was no group difference in lymphocyte subpopulations that were assessed.
A separate series of studies links immune markers in cord blood with a broad index of stress. For example, perinatal stress indexed by mode of delivery was associated with lymphocyte subset distributions Duijts et al. Also, Wright et al. Furthermore, cord blood immunoglobulin E IgE was linked with socio-economic disadvantage Scirica et al.
Collectively, the human data provide a strong suggestion that maternal prenatal stress and anxiety may alter aspects of the innate and adaptive immune systems in the child.
In general terms, that parallels what has been reported in numerous animal models. However, there remains some uncertainty about how robust these associations in humans are, as there are few instances of replication—likely a consequence of the novelty of this area of research and the discrepant methods used across studies. At present, the strongest finding is that maternal prenatal stress and anxiety may exacerbate the type 2 response that is already present in the newborn. The developing fetus has some awareness of the mother's heartbeat and voice and has the ability to respond to touch or movement.
By the seventh month of pregnancy, two-thirds of women report a strong maternal bond with their unborn child. Factors such as a traumatic birth, the mother's childhood, medical stress, lack of support and the influence of a spouse or partner can weaken the bond.
Emotional bonding theory first appeared in the mids,  and by the s had become an accepted phenomenon. Soon, the process became analyzed and scrutinized to the point of creating another term — poor bonding. Oxytocin[ edit ] Production of oxytocin during childbirth and lactation increases parasympathetic activity.
Thus, anxiety is theoretically reduced.