Prolactin

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Prolactin 

 

prolactin
Identifiers
Aliases	prolactin familylactotropinPRL
External IDs	GeneCards:
Orthologs
Species	Human	Mouse
Entrez	n/a	n/a
Ensembl	n/a	n/a
UniProt	n/a	n/a
RefSeq (mRNA)	n/a	n/a
RefSeq (protein)	n/a	n/a
Location (UCSC)	n/a	n/a
PubMed search	n/a	n/a

Prolactin (PRL), also known as lactotropin, is a protein best known for its role in enabling mammals (and birds), usually females, to produce milk. It is influential in over 300 separate processes in various vertebrates, including humans. Prolactin is secreted from the pituitary gland in response to eating, mating, estrogen treatment, ovulation and nursing. It is secreted heavily in pulses in between these events. Prolactin plays an essential role in metabolism, regulation of the immune system and pancreatic development.

Discovered in non-human animals around 1930 by Oscar Riddle and confirmed in humans in 1970 by Henry Friesen, prolactin is a peptide hormone, encoded by the PRL gene.

In mammals, prolactin is associated with milk production; in fish it is thought to be related to the control of water and salt balance. Prolactin also acts in a cytokine-like manner and as an important regulator of the immune system. It has important cell cycle-related functions as a growth  differentiating and anti-apoptotic factor. As a growth factor, binding to cytokine-like receptors, it influences hematopoiesis and angiogenesis, and is involved in the regulation of blood clotting through several pathways. The hormone acts in endocrine, autocrine and paracrine manner through the prolactin receptor and numerous cytokine receptors.

Pituitary prolactin secretion is regulated by endocrine neurons in the hypothalamus. The most important of these are the neurosecretory tuberoinfundibulum (TIDA) neurons of the arcuate nucleus that secrete dopamine (aka Prolactin Inhibitory Hormone) to act on the D₂ receptors of lactotrophs, causing inhibition of prolactin secretion. Thyrotropin-releasing factor (thyrotropin-releasing hormone) has a stimulatory effect on prolactin release, however prolactin is the only adenohypophyseal hormone whose principal control is inhibitory.

Several variants and forms are known per species. Many fish have variants prolactin A and prolactin B. Most vertebrates including humans also have the closely related somatolactin. In humans, three smaller (4, 16 and 22 kDa) and several larger (so called big and big-big) variants exist.

Functions

Prolactin has a wide variety of effects. It stimulates the mammary glands to produce milk (lactation): increased serum concentrations of prolactin during pregnancy cause enlargement of the mammary glands and prepare for milk production, which normally starts when levels of progesterone fall by the end of pregnancy and a suckling stimulus is present. Prolactin plays an important role in maternal behavior.

In general, dopamine inhibits prolactin but this process has feedback mechanisms.

Elevated levels of prolactin decrease the levels of sex hormones — estrogen in women and testosterone in men. The effects of mildly elevated levels of prolactin are much more variable, in women, substantially increasing or decreasing estrogen levels.

Prolactin is sometimes classified as a gonadotropin although in humans it has only a weak luteotropic effect while the effect of suppressing classical gonadotropic hormones is more important. Prolactin within the normal reference ranges can act as a weak gonadotropin, but at the same time suppresses GnRH secretion. The exact mechanism by which it inhibits GnRH is poorly understood. Although expression of prolactin receptors (PRL-R) have been demonstrated in rat hypothalamus, the same has not been observed in GnRH neurons. Physiologic levels of prolactin in males enhance luteinizing hormone-receptors in Leydig cells, resulting in testosterone secretion, which leads to spermatogenesis.

Prolactin also stimulates proliferation of oligodendrocyte precursor cells. These cells differentiate into oligodendrocytes, the cells responsible for the formation of myelin coatings on axons in the central nervous system.

Other actions include contributing to pulmonary surfactant synthesis of the fetal lungs at the end of the pregnancy and immune tolerance of the fetus by the maternal organism during pregnancy. Prolactin promotes neurogenesis in maternal and fetal brains.

Functions in other vertebrate species

The primary function of prolactin in fish is osmoregulation, i.e., controlling the movement of water and salts between the tissues of the fish and the surrounding water. Like mammals, however, prolactin in fish also has reproductive functions, including promoting sexual maturation and inducing breeding cycles, as well as brooding and parental care. In the South American discus, prolactin may also regulate the production of a skin secretion that provides food for larval fry. An increase in brooding behaviour caused by prolactin has been reported in hens.

Prolactin and its receptor are expressed in the skin, specifically in the hair follicles, where they regulate hair growth and moulting in an autocrine fashion. Elevated levels of prolactin can inhibit hair growth, and knock-out mutations in the prolactin gene cause increased hair length in cattle and mice.

Conversely, mutations in the prolactin receptor can cause reduced hair growth, resulting in the "slick" phenotype in cattle. Additionally, prolactin delays hair regrowth in mice.

Analogous to its effects on hair growth and shedding in mammals, prolactin in birds controls the moulting of feathers, as well as the age at onset of feathering in both turkeys and chickens.

Regulation

In humans, prolactin is produced at least in the anterior pituitary, decidua, myometrium, breast, lymphocytes, leukocytes and prostate.

Pituitary PRL is controlled by the Pit-1 transcription factor that binds to the prolactin gene at several sites. Ultimately dopamine, extrapituitary PRL is controlled by a superdistal promoter and apparently unaffected by dopamine. The thyrotropin-releasing hormone and the vasoactive intestinal peptide stimulate the secretion of prolactin in experimental settings, however their physiological influence is unclear. The main stimulus for prolactin secretion is suckling, the effect of which is neuronally mediated. A key regulator of prolactin production is estrogens that enhance growth of prolactin-producing cells and stimulate prolactin production directly, as well as suppressing dopamine.

In decidual cells and in lymphocytes the distal promoter and thus prolactin expression is stimulated by cAMP. Responsivness to cAMP is mediated by an imperfect cAMP–responsive element and two CAAT/enhancer binding proteins (C/EBP). Progesterone upregulates prolactin synthesis in the endometrium and decreases it in myometrium and breast glandular tissue. Breast and other tissues may express the Pit-1 promoter in addition to the distal promoter.

Extrapituitary production of prolactin is thought to be special to humans and primates and may serve mostly tissue-specific paracrine and autocrine purposes. It has been hypothesized that in vertebrates such as mice a similar tissue-specific effect is achieved by a large family of prolactin-like proteins controlled by at least 26 paralogous PRL genes not present in primates.

Vasoactive intestinal peptide and peptide histidine isoleucine help to regulate prolactin secretion in humans, but the functions of these hormones in birds can be quite different.

Prolactin follows diurnal and ovulatory cycles. Prolactin levels peak during REM sleep and in the early morning. Many mammals experience a seasonal cycle.

During pregnancy, high circulating concentrations of estrogen and progesterone increase prolactin levels by 10- to 20-fold. Estrogen and progesterone inhibit the stimulatory effects of prolactin on milk production. The abrupt drop of estrogen and progesterone levels following delivery allow prolactin—which temporarily remains high—to induce lactation.

Sucking on the nipple offsets the fall in prolactin as the internal stimulus for them is removed. The sucking activates mechanoreceptors in and around the nipple. These signals are carried by nerve fibers through the spinal cord to the hypothalamus, where changes in the electrical activity of neurons that regulate the pituitary gland increase prolactin secretion. The suckling stimulus also triggers the release of oxytocin from the posterior pituitary gland, which triggers milk let-down: Prolactin controls milk production (lactogenesis) but not the milk-ejection reflex; the rise in prolactin fills the breast with milk in preparation for the next feed.

In usual circumstances, in the absence of galactorrhea, lactation ceases within one or two weeks following the end of breastfeeding.

Levels can rise after exercise, high-protein meals, minor surgical procedures, following epileptic seizures or due to physical or emotional stress. In a study on female volunteers under hypnosis, prolactin surges resulted from the evocation, with rage, of humiliating experiences, but not from the fantasy of nursing.

Hypersecretion is more common than hyposecretion. Hyperprolactinemia is the most frequent abnormality of the anterior pituitary tumors, termed prolactinomas. Prolactinomas may disrupt the hypothalamic-pituitary-gonadal axis as prolactin tends to suppress the secretion of GnRH from the hypothalamus and in turn decreases the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary, therefore disrupting the ovulatory cycle. Such hormonal changes may manifest as amenorrhea and infertility in females as well as impotence in males. Inappropriate lactation (galactorrhoea) is another important clinical sign of prolactinomas.

Structure and isoforms

The structure of prolactin is similar to that of growth hormone and placental lactogen. The molecule is folded due to the activity of three disulfide bonds. Significant heterogeneity of the molecule has been described, thus bioassays and immunoassays can give different results due to differing glycosylation, phosphorylation and sulfation, as well as degradation. The non-glycosylated form of prolactin is the dominant form that is secreted by the pituitary gland.

The three different sizes of prolactin are:

• Little prolactin—the predominant form. It has a molecular weight of appxoximately 22-kDa. It is a single-chain polypeptide of 198 amino acids and is apparently the result of removal of some amino acids.
• Big prolactin—approximately 48 kDa. It may be the product of interaction of several prolactin molecules. It appears to have little, if any, biological activity.
• Big big prolactin—approximately 150 kDa. It appears to have a low biological activity.

The levels of larger ones are somewhat higher during the early postpartum period.

Prolactin receptor

Prolactin receptors are present in the mammillary glands, ovaries, pituitary glands, heart, lung, thymus, spleen, liver, pancreas, kidney, adrenal gland, uterus, skeletal muscle, skin and areas of the central nervous system. When prolactin binds to the receptor, it causes it to dimerize with another prolactin receptor. This results in the activation of Janus kinase 2, a tyrosine kinase that initiates the JAK-STAT pathway. Activation also results in the activation of mitogen-activated protein kinases and Src kinase.

Human prolactin receptors are insensitive to mouse prolactin.

Diagnostic use

Prolactin levels may be checked as part of a sex hormone workup, as elevated prolactin secretion can suppress the secretion of FSH and GnRH, leading to hypogonadism and sometimes causing erectile dysfunction.

Prolactin levels may be of some use in distinguishing epileptic seizures from psychogenic non-epileptic seizures. The serum prolactin level usually rises following an epileptic seizure.

Units and unit conversions

The serum concentration of prolactin can be given in mass concentration (µg/L or ng/mL), molar concentration (nmol/L or pmol/L) or in international units (typically mIU/L). The current IU is calibrated against the third International Standard for Prolactin, IS 84/500. Reference ampoules of IS 84/500 contain 2.5 µg of lyophilized human prolactin and have been assigned an activity of .053 International Units. Measurements that are calibrated against the current international standard can be converted into mass units using this ratio of grams to IUs; prolactin concentrations expressed in mIU/L can be converted to µg/L by dividing by 21.2. Previous standards use other ratios.

The first International Reference Preparation (or IRP) of human Prolactin for Immunoassay was established in 1978 (75/504 1st IRP for human Prolactin) at a time when purified human prolactin was in short supply. Previous standards relied on prolactin from animal sources. Purified human prolactin was scarce, heterogeneous, unstable and difficult to characterize. A preparation labelled 81/541 was distributed by the WHO Expert Committee on Biological Standardization without official status and given the assigned value of 50 mIU/ampoule based on an earlier collaborative study. It was determined that this preparation behaved anomalously in certain immunoassays and was not suitable as an IS.

Three different human pituitary extracts containing prolactin were subsequently obtained as candidates for an IS. These were distributed into ampoules coded 83/562, 83/573 and 84/500. Collaborative studies involving 20 different laboratories found little difference between these three preparations. 83/562 appeared to be the most stable. This preparation was largely free of dimers and polymers of prolactin. On the basis of these investigations 83/562 was established as the Second IS for human Prolactin. Once stocks of these ampoules were depleted, 84/500 was established as the Third IS for human Prolactin.

Reference ranges

General guidelines for diagnosing prolactin excess (hyperprolactinemia) define the upper threshold of normal prolactin at 25 µg/L for women and 20 µg/L for men. Similarly, guidelines for diagnosing prolactin deficiency (hypoprolactinemia) are defined as prolactin levels below 3 µg/L in women and 5 µg/L in men. However, different assays and methods for measuring prolactin are employed by different laboratories and as such the serum reference range for prolactin is often determined by the laboratory performing the measurement. Furthermore, prolactin levels vary according to factors as age, sex, menstrual cycle stage, and pregnancy. The circumstances surrounding a given prolactin measurement (assay, patient condition, etc.) must therefore be considered before the measurement can be accurately interpreted.

The following chart illustrates the variations seen in normal prolactin measurements across different populations. Prolactin values were obtained from specific control groups of varying sizes using the IMMULITE assay.

Typical prolactin values

Proband	Prolactin, µg/L
women, follicular phase (n = 803)	12.1
women, luteal phase (n = 699)	13.9
women, mid-cycle (n = 53)	17
women, whole cycle (n = 1555)	13.0
women, pregnant, 1st trimester (n = 39)	16
women, pregnant, 2nd trimester (n = 52)	49
women, pregnant, 3rd trimester (n = 54)	113
Men, 21–30 (n = 50)	9.2
Men, 31–40 (n = 50)	7.1
Men, 41–50 (n = 50)	7.0
Men, 51–60 (n = 50)	6.2
Men, 61–70 (n = 50)	6.9

Inter-method variability

The following table illustrates variability in reference ranges of serum prolactin between some commonly used assay methods (as of 2008), using a control group of healthy health care professionals (53 males, age 20–64 years, median 28 years; 97 females, age 19–59 years, median 29 years) in Essex, England:

Assay method	Mean Prolactin		Lower limit 2.5th percentile		Upper limit 97.5th percentile
	µg/L	mIU/L	µg/L	mIU/L	µg/L	mIU/L
Females
Centaur	7.92	168	3.35	71	16.4	348
Immulite	9.25	196	3.54	75	18.7	396
Access	9.06	192	3.63	77	19.3	408
AIA	9.52	257	3.89	105	20.3	548
Elecsys	10.5	222	4.15	88	23.2	492
Architect	10.6	225	4.62	98	21.1	447
Males
Access	6.89	146	2.74	58	13.1	277
Centaur	7.88	167	2.97	63	12.4	262
Immulite	7.45	158	3.30	70	13.3	281
AIA	7.81	211	3.30	89	13.5[60]	365
Elecsys	8.49	180	3.40	72	15.6	331
Architect	8.87	188	4.01	85	14.6	310

An example of the use of the above table is, if using the Centaur assay to estimate prolactin values in µg/L for females, the mean is 7.92 µg/L and the reference range is 3.35–16.4 µg/L.

Conditions

Elevated levels

Hyperprolactinaemia, or excess serum prolactin, is associated with hypoestrogenism, anovulatory infertility, oligomenorrhoea, amenorrhoea, unexpected lactation and loss of libido in women and erectile dysfunction and loss of libido in men.

Physiological Coitus Exercise Lactation Pregnancy Sleep Stress Depression

Pharmacological Anesthetics Anticonvulsant Antihistamines (H2) Antihypertensives Cholinergic agonist Drug-induced hypersecretion Catecholamine depletor Dopamine receptor blockers Dopamine synthesis inhibitor Estrogens Oral contraceptives Oral contraceptive withdrawal Neuroleptics Antipsychotics Neuropeptides Opiates and opiate antagonists

Pathological Hypothalamic-pituitary stalk damage Granulomas Infiltrations Radiation Rathke's cyst Trauma Pituitary stalk resection Suprasellar surgery Tumors Craniopharyngioma Germinoma Hypothalamic metastases Meningioma Suprasellar pituitary mass extension Surgery

Pituitary Acromegaly Idiopathic Lymphocytic hypophysitis or parasellar mass Macroadenoma (compressive) Macroprolactinemia Plurihumoral adenoma Prolactinoma Systemic disorders Chest-neurologic chest wall trauma Herpes Zoster Chronic renal failure Cirrhosis Cranial radiation Epileptic seizures Polycystic ovarian disease Pseudocyesis Chronic low levels of thyroid hormone

Decreased levels

Hypoprolactinemia, or serum prolactin deficiency, is associated with ovarian dysfunction in women, and arteriogenic erectile dysfunction, premature ejaculation, oligozoospermia, asthenospermia, hypofunction of seminal vesicles and hypoandrogenism in men. In one study, normal sperm characteristics were restored when prolactin levels were raised to normal values in hypoprolactinemic men.

Hypoprolactinemia can result from hypopituitarism, excessive dopaminergic action in the tuberoinfundibular pathway and ingestion of D₂ receptor agonists such as bromocriptine.

While there is evidence that women who smoke tend to breast feed for shorter periods, there is a wide variation of breast-feeding rates in women who do smoke. This suggest that psychosocial factors rather than physiological mechanisms (e.g., nicotine suppressing prolactin levels) are responsible for the lower rates of breast feeding in women who do smoke.

In medicine

Prolactin is available commercially for use in other animals, but not in humans. It is used to stimulate lactation in animals. The biological half-life of prolactin in humans is around 15–20 minutes. The D₂ receptor is involved in the regulation of prolactin secretion, and agonists of the receptor such as bromocriptine and cabergoline decrease prolactin levels while antagonists of the receptor such as domperidone, metoclopramide, haloperidol, risperidone, and sulpiride increase prolactin levels. D₂ receptor antagonists like domperidone, metoclopramide, and sulpiride are used as galactogogues to increase prolactin secretion in pituitary gland and induce lactation in humans.

Breastfeeding and mental health

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Breastfeeding_and_mental_health 

 

The relationship between breastfeeding and mental health of mothers and their children is under investigation.

Breastfeeding and mental health is the relationship between postpartum breastfeeding and the mother’s and child’s mental health. Research indicates breastfeeding has positive effects on the mother’s and child’s mental health. These benefits include improved mood and stress levels in the mother, lower risk of postpartum depression, enhanced social emotional development in the child, stronger mother-child bonding and more. Given the benefits of breastfeeding, the World Health Organization (WHO), the European Commission for Public Health (ECPH) and the American Academy of Pediatrics (AAP) suggest exclusive breastfeeding for the first six months of life. Despite these suggestions, estimates indicate 70% of mothers breastfeed their child after birth and 13.5% of infants in the United States are exclusively breastfed. Breastfeeding promotion and support for mothers who are experiencing difficulties or early cessation in breastfeeding is considered a health priority.

The exact nature of the relationship between breastfeeding and some aspects of mental health is still unclear to scientists. The causal links are uncertain due to the variability of how breastfeeding and its effects are measured across studies. There are complex interactions between numerous psychological, sociocultural and biochemical factors which are not yet fully understood.

Breastfeeding and mother's mental health

Benefits on mood and stress levels

Breastfeeding positively influences the mother’s mental and emotional wellbeing as it improves mood and stress levels, and it is referred to as a ‘stress buffer’ for mothers during the postpartum period. The activity facilitates a calmer psychological state and decreases feelings of anxiousness, negative emotions and stress. This is reflected in their physiological response to breastfeeding, where the mother’s cardiac vagal tone modulation enhances, and blood pressure and heart rate decreases. The stress-buffering effect of breastfeeding results from the hormones oxytocin and prolactin. Mothers who breastfeed experience enhanced sleep duration and quality, while instances of sleep disturbances are decreased. The activity positively influences how mothers respond to social situations, which facilitates improved relationships and interactions. Mothers who engage in breastfeeding respond less to negative facial expressions (e.g. anger) and increase their response to positive facial expressions (e.g. happiness). Breastfeeding also help mothers feel confident and empowered given the knowledge that breastfeeding is beneficial to their child.

Postpartum depression

Effects of postpartum depression on breastfeeding

Studies indicate mothers with postpartum depression breastfeed their infant with lower frequency. Breastfeeding is an intimate activity with requires sustained mother-child physical contact and new mothers with symptoms of depression, including increased anxiety and tendency to avoid their child, are less likely to breastfeed their child. Postpartum depressive anxiety can decrease the mother’s milk production which reduces the mother’s ability to breastfeed her child. Mothers who take certain antidepressants to treat their depression are not recommended to breastfeed their child. The ingredients in the medication may be transferred to the child through breast milk and this may have detrimental consequences on their development. A woman should consult with her doctor to understand if her specific medication might be problematic in this regard.  Mothers with symptoms of postpartum depression commonly report more difficulties with breastfeeding and lower levels of breastfeeding self-efficiacy. Mothers with postpartum depression are more likely to have a negative perception of breastfeeding. They also initiate breastfeeding later, breastfeed less, and are more likely to cease breastfeeding early on during the postpartum period.

Effects of breastfeeding on postpartum depression

Breastfeeding may provide protection against postpartum depression or reduce some of its symptoms, and it is suggested that the benefits of breastfeeding may outweigh the benefits of antidepressants. The abstinence of breastfeeding, or decreased breastfeeding can increase the mother’s likelihood developing of this mental disorder. Oxytocin and prolactin, which is released during breastfeeding, may improve the mother’s mood and reduce her risk of depression. Breastfeeding women have lower rates of postpartum depression in comparison to formula-feeding women. Stress is one of the strongest risk factors in the development of depression, and as breastfeeding reduces stress it may decrease the risk of postpartum depression in mothers. Improved sleep patterns, improvements in mother-child bonding and an increased sense of self-efficacy due to breastfeeding also reduces the risk of developing depression. Breastfed infants generally have improved temperaments and less health issues. This may also have positive influences on the mother’s mental health.

Breastfeeding difficulties and postpartum depression

Breastfeeding difficulties and interruption lead to poorer maternal mood and increase the risk of developing postpartum depression. A 2011 study conducted by Nielson and colleagues found women who were unable to breastfeed were 2.4 times more likely to develop symptoms of depression 16 weeks after birth. Reasons for being unable to breastfeed include nipple pain, child temperamental issues, lack of milk production, breast surgery and mastitis. The lack of self-confidence or difficult experiences during breastfeeding is a common concern for mothers with postpartum depression. It is suggested that mothers who experience problems during breastfeeding require immediate additional support or should be screened for any signs of depression. Encouragement and guidance from professionals promotes self-efficacy and help mothers feel capable and empowered. As a child’s temperament may affect the breastfeeding process, mothers are also encouraged to gain a deeper understanding of how infants feed during breastfeeding so potential problems can be anticipated and addressed.

Nature of relationship between breastfeeding and postpartum depression

There is a clear link between breastfeeding and postpartum depression; however, the exact nature of the relationship between breastfeeding and postpartum depression is unclear to scientists. This is due to several reasons including:

• Complex interactions between multiple physiological, sociocultural and psychological factors that are not yet fully understood.
• Different methods adopted by scientists to study this relationship may have led to different results.
• Conflicting scientific studies have indicated either that there is no link between breastfeeding and postpartum depression or that breastfeeding leads to increased risk of developing depression.

Recent reports indicate that a reciprocal or bidirectional relationship exists between breastfeeding and postpartum depression. That is, postpartum depression results in reduced breastfeeding activity and early cessation, and abstinence from breastfeeding or irregularity in practicing it increases risk of developing postpartum depression.

Mechanisms of action

The relationship between breastfeeding and the mother’s mental health may be due to direct causes such as the following:

• Guilt, shame and/or disappointment: Mothers who are experiencing difficulties during breastfeeding or are unable to breastfeed may feel guilt, shame and disappointment as they believe they’re unable to provide the child with what they require. This may lead to symptoms of postpartum depression.
• Negative perceptions of breastfeeding: The mother’s perception of breastfeeding may affect her mood. Mothers with symptoms of postpartum depression are more likely to believe breastfeeding is restrictive and private. Depressed mothers tend to feel unsatisfied with breastfeeding and experience a decreased sense of self-efficacy when it comes to breastfeeding. Mothers who worry about breastfeeding are also more likely to be diagnosed with postpartum depression.
• Improved mother-infant bonding: Breastfeeding may also enhance the bond between the mother and child. This facilitates improved mental health.

Physiological mechanisms

The underlying physiological explanation of the benefits of breastfeeding on the mother’s mental health is attributed to neuroendocrine processes. Breast milk contains lactogenic hormones, oxytocin and prolactin, which contain antidepressant effects and reduces anxiety. Prolactin is the primary hormone responsible for milk production and its levels are proportional to breastfeeding frequency and the child’s milk requirements. Prolactin facilitates maternal behaviour, acts as an analgesic and decreases stress responsiveness. This hormone level is higher in women who breastfeed compared to women who do not breastfeed. Oxytocin decreases stress and promotes relaxation and nurturing behaviour. Prior to breastfeeding, oxytocin is released into the blood stream to aid in milk release. Oxytocin and prolactin are also released during nipple stimulation when the child suckles. The nerve fibres linked to the hypothalamus controls this release and the hormones are released in pulsating patterns. The increased levels of these hormones during breastfeeding have a beneficial effect on the mother’s mental health. When exposed to physical or psychological stress, breastfeeding mothers also have a reduced cortisol response due to decreased production of stress hormones and improvements in their sleep. Physical contact during this activity attenuates the cortisol response. Postpartum depression and breastfeeding failure are also attributed to neuroendocrine mechanisms.

Postpartum depression is also closely associated with inflammation caused by postpartum pain or sleep deprivation, which are common experiences of motherhood. Breastfeeding decreases this inflammation response which is beneficial to the mother’s mental health.

Breastfeeding and child's mental health

Social and emotional health and development

Breastfeeding is associated with improved social and emotional health and development of the child.

 The breastfeeding activity induces calming and analgesic effects in the infant. During this activity, their heart and metabolic rates decrease and their sensitivity to pain is reduced.

Research indicate infants who are breastfed for more than 3 or 4 months develop fewer behavioural and conduct disorders. Breastfeeding may also facilitate decreased aggression and antisocial tendencies in infants; and it is suggested this effect carries on into adulthood. In a longitudinal study conducted by Merjonen and colleagues (2011), it was found adults who were not breastfed during infancy demonstrated higher levels of hostility and aggression. Infants who are breastfed also demonstrate more ‘vigour’ and intense reactions compared to bottle-fed infants. To signal to their parents and have their needs attended to, infants who are breastfed may display greater distress and frustration.

Mechanisms of action

The calming, analgesic effect and reduced sensitivity to pain is due to several factors:

• Suckling the nipple stimulates the child’s oropharynx. This focuses the child's attention on the area and reduces attention to other influences.
• The act of suckling and intestinal adsorption of fat increases the hormone cholecystokinin, which enhances relaxation and pain relief.
• Breast milk is sweet and this stimulates the release of opioids which decreases the infant’s sensitivity to pain.
• Physical contact stabilises blood glucose levels, body temperature and respiration rates, aids neurobehavioural self-regulation, reduces stress hormone release and blood pressure.
• Social interaction and physical contact promotes release of oxytocin.

The reduction of antisocial behaviour and aggression is be attributed to increased levels of oxytocin in the infant during breastfeeding. Human breastmilk contains oxytocin and this hormone is also released in the child due to physical contact and warmth during breastfeeding. Increased levels of oxytocin promotes social and emotional development, and this facilitates lower levels of aggression and other antisocial behaviours.

The act of breastfeeding may also be an indicator of the mother’s maternal behaviour. The abstinence or unnecessary prolonging of breastfeeding may suggest the mother is not mentally well and this contributes to increasingly antisocial behaviour in the child.

Autism spectrum disorder (ASD)

Research suggests breastfeeding may protect children from developing autism spectrum disorder (ASD), a mental disorder characterised by impaired social and communicative skills. Infants who are not breastfed, are breastfed later or breastfed for a short duration have a higher risk of being diagnosed with ASD. The exact physiological mechanism of this link is unclear but this association may be due to the lack of colostrum intake from breast milk which contains essential antibodies, protein and immune cells that are necessary for typical socio-emotional development and health.

However, scientists have emphasised the need to avoid assigning a causal role to breastfeeding in the development of ASD in infants. There is a possibility that children who are later diagnosed with ASD already possess behavioural traits which prevent regular breastfeeding activities. Children with ASD have reduced joint control, decreased social interaction or lack of cooperativeness; and this can lead to irregular breastfeeding patterns. The existence of research which do not show a relationship between breastfeeding and the development of ASD is also noted. For example, Husk and Keim (2015) conducted a large-scale survey with parents of 2 to 5 year old infants and found no significant correlation between ASD development and presence/absence of breastfeeding or length of breastfeeding duration. More studies are required to improve the understanding of breastfeeding and its link with ASD, and the underlying physiological mechanisms.

Breastfeeding and mother-child bonding

The mother and child's bond enhances during breastfeeding.

Breastfeeding enhances the emotional and social bond between the mother and child, and this attachment is important for the their mental health. This bond increases the mother's and child's abilities to control their emotions, reduce the stress response and encourages healthy social development in the child. Physical contact during breastfeeding increases levels of oxytocin in the mother and child, which improves the mother-child bond. Breastfed infants become more dependent on their mothers and develop a deep social and emotional connection. Likewise, breastfeeding facilitates mothers’ emotional connection with their child and thus mothers generally display more warmth and sensitivity.

Compared to non-breastfeeding mother-child pairs, in breastfeeding mother-child pairs:

• Mothers are more responsive and sensitive to their infant’s needs.
• Mothers spend more time and attention on their infant.
• Mothers generally touch and speak to their infant more.
• Infants demonstrate a greater sense of ‘attachment security’ and lower ‘attachment disorganisation.
• Infants suckle their mother’s breast longer than with bottles.
• Mothers and infants spend more time gazing at each other.
• Mothers are more positive and smile at their child more.

Brain imaging research indicates breastfeeding mothers who listen to their infant crying demonstrate greater activity in limbic regions of the brain. This suggests the mother’s enhanced emotional, empathetic and sensitive response to their child, which supports mother-infant bonding.

Studies which do not demonstrate a significant relationship between breastfeeding and mother-infant bonding exist. For example, Britton and colleagues (2006) did not find a significant association between breastfeeding and mother-infant bonding but found that mothers displaying more sensitivity were more likely to breastfeed than bottlefeed. This suggests that the mother’s sensitivity may have a more direct effect on mother-child bonding as more sensitive mothers are more likely to breastfeed and display greater emotional sensitivity.