Postpartum depression

From Wikipedia, the free encyclopedia

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

 

Postpartum depression
Other names	Postnatal depression
Specialty	Psychiatry
Symptoms	Extreme sadness, low energy, anxiety, changes in sleeping or eating patterns, crying episodes, irritability
Usual onset	A week to a month after childbirth
Causes	Unclear
Risk factors	Prior postpartum depression, bipolar disorder, family history of depression, psychological stress, complications of childbirth, lack of support, drug use disorder
Diagnostic method	Based on symptoms
Differential diagnosis	Baby blues
Treatment	Counselling, medications
Frequency	~15% of births

Postpartum depression (PPD), also called postnatal depression, is a type of mood disorder associated with childbirth, which can affect both sexes. Symptoms may include extreme sadness, low energy, anxiety, crying episodes, irritability, and changes in sleeping or eating patterns. Onset is typically between one week and one month following childbirth. PPD can also negatively affect the newborn child.

While the exact cause of PPD is unclear, the cause is believed to be a combination of physical, emotional, genetic, and social factors. These may include factors such as hormonal changes and sleep deprivation. Risk factors include prior episodes of postpartum depression, bipolar disorder, a family history of depression, psychological stress, complications of childbirth, lack of support, or a drug use disorder. Diagnosis is based on a person's symptoms. While most women experience a brief period of worry or unhappiness after delivery, postpartum depression should be suspected when symptoms are severe and last over two weeks.

Among those at risk, providing psychosocial support may be protective in preventing PPD. This may include community support such as food, household chores, mother care, and companionship. Treatment for PPD may include counseling or medications. Types of counseling that have been found to be effective include interpersonal psychotherapy (IPT), cognitive behavioral therapy (CBT), and psychodynamic therapy. Tentative evidence supports the use of selective serotonin reuptake inhibitors (SSRIs).

Postpartum depression affects roughly 15% of women after childbirth. Moreover, this mood disorder is estimated to affect 1% to 26% of new fathers. Postpartum psychosis, a more severe form of postpartum mood disorder, occurs in about 1 to 2 per 1,000 women following childbirth. Postpartum psychosis is one of the leading causes of the murder of children less than one year of age, which occurs in about 8 per 100,000 births in the United States.

Signs and symptoms

Symptoms of PPD can occur any time in the first year postpartum. Typically, a diagnosis of postpartum depression is considered after signs and symptoms persist for at least two weeks.

Emotional

• Persistent sadness, anxiousness or "empty" mood
• Severe mood swings
• Frustration, irritability, restlessness, anger
• Feelings of hopelessness or helplessness
• Guilt, shame, worthlessness
• Low self-esteem
• Numbness, emptiness
• Exhaustion
• Inability to be comforted
• Trouble bonding with the baby
• Feeling inadequate in taking care of the baby
• Thoughts of self-harm or suicide

Behavioural

• Lack of interest or pleasure in usual activities
• Low libido
• Changes in appetite
• Fatigue, decreased energy and motivation
• Poor self-care
• Social withdrawal
• Insomnia or excessive sleep

Cognition

• Diminished ability to make decisions and think clearly
• Lack of concentration and poor memory
• Fear that you can not care for the baby or fear of the baby
• Worry about harming self, baby, or partner

Onset and duration

Postpartum depression onset usually begins between two weeks to a month after delivery. A study done at an inner-city mental health clinic has shown that 50% of postpartum depressive episodes there began prior to delivery. Therefore, in the DSM-5 postpartum depression is diagnosed under "depressive disorder with peripartum onset", in which "peripartum onset" is defined as anytime either during pregnancy or within the four weeks following delivery. PPD may last several months or even a year.

Postpartum depression can also occur in women who have suffered a miscarriage. For fathers, several studies show that men experience the highest levels of postpartum depression between 3–6 months postpartum.

Parent-infant relationship

Postpartum depression can interfere with normal maternal-infant bonding and adversely affect acute and longterm child development. Postpartum depression may lead mothers to be inconsistent with childcare. These childcare inconsistencies may include feeding routines, sleep routines, and health maintenance.

In rare cases, or about 1 to 2 per 1,000, the postpartum depression appears as postpartum psychosis. In these, or among women with a history of previous psychiatric hospital admissions, infanticide may occur. In the United States, postpartum depression is one of the leading causes of annual reported infanticide incidence rate of about 8 per 100,000 births.

Causes

The cause of PPD is unknown. Hormonal and physical changes, personal and family history of depression, and the stress of caring for a new baby all may contribute to the development of postpartum depression.

Evidence suggests that hormonal changes may play a role. Hormones which have been studied include estrogen, progesterone, thyroid hormone, testosterone, corticotropin releasing hormone, endorphins, and cortisol. Estrogen and progesterone levels drop back to pre-pregnancy levels within 24 hours of giving birth, and that sudden change may cause it. The use of synthetic oxytocin, a birth-inducing drug, has been linked to increased rates of postpartum depression and anxiety.

Fathers, who are not undergoing profound hormonal changes, can also have postpartum depression. The cause may be distinct in males.

Profound lifestyle changes that are brought about by caring for the infant are also frequently hypothesized to cause PPD. However, little evidence supports this hypothesis. Mothers who have had several previous children without suffering PPD can nonetheless suffer it with their latest child. Despite the biological and psychosocial changes that may accompany pregnancy and the postpartum period, most women are not diagnosed with PPD. Many mothers are unable to get the rest they need to fully recover from giving birth. Sleep deprivation can lead to physical discomfort and exhaustion, which can contribute to the symptoms of postpartum depression.

Risk factors

While the causes of PPD are not understood, a number of factors have been suggested to increase the risk:

• Prenatal depression or anxiety
• A personal or family history of depression
• Moderate to severe premenstrual symptoms
• Stressful life events experienced during pregnancy
• Postpartum blues
• Birth-related psychological trauma
• Birth-related physical trauma
• History of sexual abuse
• Childhood trauma
• Previous stillbirth or miscarriage
• Formula-feeding rather than breast-feeding
• Cigarette smoking
• Low self-esteem
• Childcare or life stress
• Low social support
• Poor marital relationship or single marital status
• Low socioeconomic status
• A lack of strong emotional support from spouse, partner, family, or friends
• Infant temperament problems/colic
• Unplanned/unwanted pregnancy
• Low vitamin D levels
• Breastfeeding difficulties
• Administration of labor-inducing medication synthetic oxytocin

Of these risk factors a history of depression, and cigarette smoking have been shown to have additive effects. Some studies have found a link with low levels of DHA in the mother.

These above factors are known to correlate with PPD. This correlation does not mean these factors are causal. Rather, they might both be caused by some third factor. Contrastingly, some factors almost certainly attribute to the cause of postpartum depression, such as lack of social support. The relationship between breastfeeding and PPD is not clear.

Women with fewer resources indicate a higher level of postpartum depression and stress than those women with more resources, such as financial. Rates of PPD have been shown to decrease as income increases. Women with fewer resources may be more likely to have an unintended or unwanted pregnancy, increasing risk of PPD. Women with fewer resources may also include single mothers of low income. Single mothers of low income may have more limited access to resources while transitioning into motherhood.

Studies have also shown a correlation between a mother's race and postpartum depression. African American mothers have been shown to have the highest risk of PPD at 25%, while Asian mothers had the lowest at 11.5%, after controlling for social factors such as age, income, education, marital status, and baby's health. The PPD rates for First Nations, Caucasian and Hispanic women fell in between.

Migration away from a cultural community of support can be a factor in PPD. Traditional cultures around the world prioritize organized support during postpartum care to ensure the mother's mental and physical health, wellbeing, and recovery.

One of the strongest predictors of paternal PPD is having a partner who has PPD, with fathers developing PPD 50% of the time when their female partner has PPD.

Sexual orientation has also been studied as a risk factor for PPD. In a 2007 study conducted by Ross and colleagues, lesbian and bisexual mothers were tested for PPD and then compared with a heterosexual sample group. It was found that lesbian and bisexual biological mothers had significantly higher Edinburgh Postnatal Depression Scale scores than did the heterosexual women in the sample. These higher rates of PPD in lesbian/bisexual mothers may reflect less social support, particularly from their families of origin and additional stress due to homophobic discrimination in society.

A correlation between postpartum thyroiditis and postpartum depression has been proposed but remains controversial. There may also be a link between postpartum depression and anti-thyroid antibodies.

Violence

A meta-analysis reviewing research on the association of violence and postpartum depression showed that violence against women increases the incidence of postpartum depression. About one-third of women throughout the world will experience physical or sexual violence at some point in their lives. Violence against women occurs in conflict, post-conflict, and non-conflict areas. It is important to note that the research reviewed only looked at violence experienced by women from male perpetrators, but did not consider violence inflicted on men or women by women. Further, violence against women was defined as "any act of gender-based violence that results in, or is likely to result in, physical, sexual, or psychological harm or suffering to women". Psychological and cultural factors associated with increased incidence of postpartum depression include family history of depression, stressful life events during early puberty or pregnancy, anxiety or depression during pregnancy, and low social support. Violence against women is a chronic stressor, so depression may occur when someone is no longer able to respond to the violence.

Diagnosis

Criteria

Postpartum depression in the DSM-5 is known as "depressive disorder with peripartum onset". Peripartum onset is defined as starting anytime during pregnancy or within the four weeks following delivery. There is no longer a distinction made between depressive episodes that occur during pregnancy or those that occur after delivery. Nevertheless, the majority of experts continue to diagnose postpartum depression as depression with onset anytime within the first year after delivery.

The criteria required for the diagnosis of postpartum depression are the same as those required to make a diagnosis of non-childbirth related major depression or minor depression. The criteria include at least five of the following nine symptoms, within a two-week period:

• Feelings of sadness, emptiness, or hopelessness, nearly every day, for most of the day or the observation of a depressed mood made by others
• Loss of interest or pleasure in activities
• Weight loss or decreased appetite
• Changes in sleep patterns
• Feelings of restlessness
• Loss of energy
• Feelings of worthlessness or guilt
• Loss of concentration or increased indecisiveness
• Recurrent thoughts of death, with or without plans of suicide

Differential diagnosis

Postpartum blues

Postpartum blues, commonly known as "baby blues," is a transient postpartum mood disorder characterized by milder depressive symptoms than postpartum depression. This type of depression can occur in up to 80% of all mothers following delivery. Symptoms typically resolve within two weeks. Symptoms lasting longer than two weeks are a sign of a more serious type of depression. Women who experience "baby blues" may have a higher risk of experiencing a more serious episode of depression later on.

Psychosis

Postpartum psychosis is not a formal diagnosis, but is widely used to describe a psychiatric emergency that appears to occur in about 1 in a 1000 pregnancies, in which symptoms of high mood and racing thoughts (mania), depression, severe confusion, loss of inhibition, paranoia, hallucinations and delusions begin suddenly in the first two weeks after delivery; the symptoms vary and can change quickly. It is different from postpartum depression and from maternity blues. It may be a form of bipolar disorder. It is important not to confuse psychosis with other symptoms that may occur after delivery, such as delirium. Delirium typically includes a loss of awareness or inability to pay attention.

About half of women who experience postpartum psychosis have no risk factors; but a prior history of mental illness, especially bipolar disorder, a history of prior episodes of postpartum psychosis, or a family history put some at a higher risk.

Postpartum psychosis often requires hospitalization, where treatment is antipsychotic medications, mood stabilizers, and in cases of strong risk for suicide, electroconvulsive therapy.

The most severe symptoms last from 2 to 12 weeks, and recovery takes 6 months to a year. Women who have been hospitalized for a psychiatric condition immediately after delivery are at a much higher risk of suicide during the first year after delivery.

Screening

In the US, the American College of Obstetricians and Gynecologists suggests healthcare providers consider depression screening for perinatal women. Additionally, the American Academy of Pediatrics recommends pediatricians screen mothers for PPD at 1-month, 2-month and 4-month visits. However, many providers do not consistently provide screening and appropriate follow-up. For example, in Canada, Alberta is the only province with universal PPD screening. This screening is carried out by Public Health nurses with the baby's immunization schedule.

The Edinburgh Postnatal Depression Scale, a standardized self-reported questionnaire, may be used to identify women who have postpartum depression. If the new mother scores 13 or more, she likely has PPD and further assessment should follow.

Healthcare providers may take a blood sample to test if another disorder is contributing to depression during the screening.

Prevention

A 2013 Cochrane review found evidence that psychosocial or psychological intervention after childbirth helped reduce the risk of postnatal depression. These interventions included home visits, telephone-based peer support, and interpersonal psychotherapy. Support is an important aspect of prevention, as depressed mothers commonly state that their feelings of depression were brought on by "lack of support" and "feeling isolated."

Across different cultures, traditional rituals for postpartum care may be preventative for PPD, but are more effective when the support is welcomed by the mother.

In couples, emotional closeness and global support by the partner protect against both perinatal depression and anxiety. Further factors such as communication between the couple and relationship satisfaction have a protective effect against anxiety alone.

In those who are at risk counselling is recommended. In 2018, 24% of areas in the UK have no access to perinatal mental health specialist services.

Preventative treatment with antidepressants may be considered for those who have had PPD previously. However, as of 2017, the evidence supporting such use is weak.

Treatments

Treatment for mild to moderate PPD includes psychological interventions or antidepressants. Women with moderate to severe PPD would likely experience a greater benefit with a combination of psychological and medical interventions. Light aerobic exercise has been found to be useful for mild and moderate cases.

Therapy

Both individual social and psychological interventions appear equally effective in the treatment of PPD. Social interventions include individual counseling and peer support, while psychological interventions include cognitive behavioral therapy (CBT) and interpersonal therapy (IPT). Other forms of therapy, such as group therapy, home visits, counseling, and ensuring greater sleep for the mother may also have a benefit.

Internet-based cognitive behavioral therapy (iCBT) has shown promising results with lower negative parenting behavior scores and lower rates of anxiety, stress, and depression. iCBT may be beneficial for mothers who have limitations in accessing in person CBT. However, the long term benefits have not been determined.

Medication

A 2010 review found few studies of medications for treating PPD noting small sample sizes and generally weak evidence. Some evidence suggests that mothers with PPD will respond similarly to people with major depressive disorder. There is evidence which suggests that selective serotonin reuptake inhibitors (SSRIs) are effective treatment for PPD. The first-line anti-depressant medication of choice is sertraline, an SSRI, as very little of the it passes into the breast milk and, as a result, to the child. However, a recent study has found that adding sertraline to psychotherapy does not appear to confer any additional benefit. Therefore, it is not completely clear which antidepressants, if any, are most effective for treatment of PPD, and for whom antidepressants would be a better option than non-pharmacotherapy.

Some studies show that hormone therapy may be effective in women with PPD, supported by the idea that the drop in estrogen and progesterone levels post-delivery contribute to depressive symptoms.

However, there is some controversy with this form of treatment because estrogen should not be given to people who are at higher risk of blood clots, which include women up to 12 weeks after delivery.

Additionally, none of the existing studies included women who were breastfeeding. However, there is some evidence that the use of estradiol patches might help with PPD symptoms.

In 2019, the FDA approved brexanolone, a synthetic analog of the neurosteroid allopregnanolone, for use intravenously in postpartum depression. Allopregnanolone levels drop after giving birth, which may lead to women becoming depressed and anxious. Some trials have demonstrated an effect on PPD within 48 hours from the start of infusion. Other new allopregnanolone analogs under evaluation for use in the treatment of PPD include SAGE-2017 and ganaxolone.

Brexanolone has risks that can occur during administration, including excessive sedation and sudden loss of consciousness, and therefore has been approved under the Risk Evaluation and Mitigation Strategy (REMS) program. The mother is to enrolled prior to receiving the medication. It is only available to those at certified health care facilities with a health care provider who can continually monitor the patient. The infusion itself is a 60-hour, or 2.5 day, process. People's oxygen levels are to be monitored with a pulse oximeter. Side effects of the medication include dry mouth, sleepiness, somnolence, flushing and loss of consciousness. It is also important to monitor for early signs of suicidal thoughts or behaviors.

Breastfeeding

Antidepressant medications are generally considered safe to use during breastfeeding. Most antidepressants are excreted in breast milk. However, there are limited studies showing the effects and safety of these antidepressants on breastfed babies. Regarding allopregnanolone, very limited data did not indicate a risk for the infant.

Other

Electroconvulsive therapy (ECT) has shown efficacy in women with severe PPD that have either failed multiple trials of medication-based treatment or cannot tolerate the available antidepressants. Tentative evidence supports the use of repetitive transcranial magnetic stimulation (rTMS).

As of 2013 it is unclear if acupuncture, massage, bright lights, or taking omega-3 fatty acids are useful.

Epidemiology

Postpartum depression is found across the globe, with rates varying from 11% to 42%. Around 3% to 6% of women will experience depression during pregnancy or shortly after giving birth. About 1 in 750 mothers will have postpartum depression with psychosis and their risk is higher if they have had postpartum episodes in the past.

History

Prior to the 19th century

Western medical science's understanding and construction of postpartum depression has evolved over the centuries. Ideas surrounding women’s moods and states have been around for a long time, typically recorded by men. In 460 B.C., Hippocrates wrote about puerperal fever, agitation, delirium, and mania experienced by women after child birth. Hippocrates' ideas still linger in how postpartum depression is seen today.

A woman who lived in the 14th century, Margery Kempe, was a Christian mystic. She was a pilgrim known as "Madwoman" after having a tough labor and delivery. There was a long physical recovery period during which she started descending into "madness" and became suicidal. Based on her descriptions of visions of demons and conversations she wrote about that she had with religious figures like God and the Virgin Mary, historians have identified what Margery Kempe was suffering from as "postnatal psychosis" and not postpartum depression. This distinction became important to emphasize the difference between postpartum depression and postpartum psychosis. A 16th century physician, Castello Branco, documented a case of postpartum depression without the formal title as a relatively healthy woman who suffered from melancholy after childbirth, remained insane for a month, and recovered with treatment. Although this treatment was not described, experimental treatments began to be implemented for postpartum depression for the centuries that followed. Connections between female reproductive function and mental illness would continue to center around reproductive organs from this time all the way through to modern age, with a slowly evolving discussion around "female madness".

19th century and after

With the 19th century came a new attitude about the relationship between female mental illness and pregnancy, childbirth, or menstruation. The famous short story, "The Yellow Wallpaper", was published by Charlotte Perkins Gilman in this period. In the story, an unnamed woman journals her life when she is treated by her physician husband, John, for hysterical and depressive tendencies after the birth of their baby. Gilman wrote the story to protest societal oppression of women as the result of her own experience as a patient.

Also during the 19th century, gynecologists embraced the idea that female reproductive organs, and the natural processes they were involved in, were at fault for "female insanity." Approximately 10% of asylum admissions during this time period are connected to “puerperal insanity,” the named intersection between pregnancy or childbirth and female mental illness. It wasn't until the onset of the twentieth century that the attitude of the scientific community shifted once again: the consensus amongst gynecologists and other medical experts was to turn away from the idea of diseased reproductive organs and instead towards more "scientific theories" that encompassed a broadening medical perspective on mental illness.

Society and culture

Malay culture holds a belief in Hantu Meroyan; a spirit that resides in the placenta and amniotic fluid. When this spirit is unsatisfied and venting resentment, it causes the mother to experience frequent crying, loss of appetite, and trouble sleeping, known collectively as "sakit meroyan". The mother can be cured with the help of a shaman, who performs a séance to force the spirits to leave.

Some cultures believe that the symptoms of postpartum depression or similar illnesses can be avoided through protective rituals in the period after birth. These may include offering structures of organized support, hygiene care, diet, rest, infant care, and breastfeeding instruction. The rituals appear to be most effective when the support is welcomed by the mother. Globalization and migration can disconnect women from their traditional communities of maternal support, which can be positive or negative depending on the traditions and on the mother's wishes.

Some Chinese women participate in a ritual that is known as "doing the month" (confinement) in which they spend the first 30 days after giving birth resting in bed, while the mother or mother-in-law takes care of domestic duties and childcare. In addition, the new mother is not allowed to bathe or shower, wash her hair, clean her teeth, leave the house, or be blown by the wind.

In the US, the Patient Protection and Affordable Care Act included a section focusing on research into postpartum conditions including postpartum depression. Some argue that more resources in the form of policies, programs, and health objectives need to be directed to the care of those with PPD.

The stigma of mental health - with or without support from family members and health professionals - often deters women from seeking help for their PPD. When medical help is achieved, some women find the diagnosis helpful and encourage a higher profile for PPD amongst the health professional community.

Media

Certain cases of postpartum mental health concerns received attention in the media and brought about dialogue on ways to address and understand more on postpartum mental health. Andrea Yates, a former nurse, became pregnant for the first time in 1976. After giving birth to five children in the coming years, she suffered severe depression and had many depressive episodes. This led to her believing that her children needed to be saved, and that by killing them, she could rescue their eternal souls. She drowned her children one by one over the course of an hour, by holding their heads under water in their family bathtub. When called into trial, she felt that she had saved her children rather than harming them and that this action would contribute to defeating Satan.

This was one of the first public and notable cases of postpartum psychosis, which helped create dialogue on women's mental health after childbirth. The court found that Yates’ was experiencing mental illness concerns, and the trial started the conversation of mental illness in cases of murder and whether or not it would lessen the sentence or not. It also started a dialogue on women going against “maternal instinct” after childbirth and what maternal instinct was truly defined by.

Yates' case brought wide media attention to the problem of filicide, or the murder of children by their parents. Throughout history, both men and women have perpetrated this act, but study of maternal filicide is more extensive.

 

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.