Pharmacological Treatment

A number of studies have pointed out that Postpartum Depression (PPD) is essentially the same as Major Depression (MDD) and, therefore, benefits from pharmacological treatment with antidepressant medication, but very few studies have conducted randomized controlled trails comparing different medication and placebos.¹ In general, pharmacological treatment of MDD has proven to be just as effective as psychological interventions.² However, the adverse effects on breastfeeding and infant well-being remain largely unknowns and medication has to be prescribed with caution.^{1, 2} An extensive review by Fitelson and associated¹ outlines several open studies that have established fluoxamine, sertraline, bupropion, nefazodone and venlafaxine as effective pharmacological treatment for PPD. Yet, the validity and generalizability of these studies is limited by small sample sizes (4 to 15 participants) and tainted by pharmacological companies’ sponsorship. In  cases where patients have responded well to a particular antidepressant in the past, experts advise practitioners to choose the same medication for the treatment of PPD.^1,3

Pharmacological Treatment as a Preventative Measure

There is some evidence that pharmacological treatment can have preventative properties as well. A randomized placebo-controlled pilot study by Wisner and colleagues (2004)⁴ has shown that sertraline treatment started shortly after delivery prevented women with history of PPD from experiencing another episode. Yet, these results remain inconclusive and more research is needed to establish the role of antidepressants in PPD prevention.

Pharmacological Treatment’s Effect on the Child

The major concerns surrounding pharmacological treatment of PPD revolve around its effect of lactation, breastfeeding and infant well-being.¹ Infants are particularly vulnerable to the effects of medication, due to their immature blood-brain barrier, hepatic and renal systems and still developing neurological systems and brain structures.⁵ Still, research on the effects of antidepressants on the baby through maternal breastfeeding is very limited and largely contains of small studies with questionable external validity, and isolated case studies.¹ Some researchers have deducted that sertraline and paroxetine, among the Selective Serotonin Reuptake Inhibitors, are least likely to be detected in the infant’s system and adverse effects have rarely been observed.⁵ In comparison, citalopram and fluoxetine, appear to be more readily transmitted through breast milk. Their effects range from sleep changes in the infant to more serious respiratory, gastrointestinal problems and even seizures.⁵ In addition, antidepressants in infants have been correlated with increased plasma levels.¹ Although the observed effects among infants have been of mild to moderate severity and have remitted after the mother discontinued medication use, there are no guarantees there will be no effects in the long run. In addition, research has not determined whether lack of clinically significant amounts of antidepressants in the baby’s system actually means the child is not affected in any way.¹ These concerns suggest the need for further research, including more longitudinal studies.

Why Medication May Not be The Best Option

The benefits of breastfeeding have been extensively studied and firmly established by prominent organizations, such as the World Health Organization, the American Academy of Family Practitioners and the American Academy of Pediatrics, all of which recommend breastfeeding for at least six months after birth.^6,7,8 Considering this, most clinicians recommend non-pharmacological treatment for cases of mild or moderate depression, especially since these can be just as effective, but without the risk of side effects.¹ Yet, if pharmacological treatment is initiated, experts suggest that the baby’s pediatrician is immediately informed and begins to routinely examine for possible exposure and monitor any changes of sleeping and feeding patterns, sedation, irritability and other signs of drug toxicity1.^1,9

Research has demonstrated the effectiveness of psychological and psychosocial treatments of PPT, which also bypass the risk of side effects and infant drug toxicity.^{1, 10}

Interpersonal Therapy

Interpersonal therapy (IPT) has been suggested as effective psychological treatment for PPD and women who received IPT had a significant decrease in PPD symptomatology.¹¹ The typical course of IPT lasts for 12 to 20 weeks and focuses on four main interpersonal problem areas: role transition, role dispute, interpersonal deficits and grief. Clients are encouraged to transform their problematic interpersonal approaches into more healthy and adaptive ones, which is expected to improve the mother-infant and  mother-partner relationships and help the new mother for the upcoming transition back to work.¹¹ It has been further established that a group format of IPT may have benefits compared to individual therapy, as it increases social support, helps new mothers improve their interpersonal skills, allows for realization of the normality of the symptoms and issues and reduces the stigma associated with PPD.¹

Cognitive behavioral Therapy

Cognitive Behavioral Therapy (CBT) is another therapeutic modality that has proven no be beneficial in the treatment of depression, including PPD.^1,12,13 The main focus in CBT is to help clients modify their distorted cognitive patterns and negative thinking and initiate behavioral changes that will enhance their coping and reduce distress.^13,14 Fitelson and associates¹ have reviewed a study where only six sessions of CBT correlated with significant decrease of depressive symptoms in postpartum women. A pilot study by Cho and colleagues (2008)¹³ has examined antenatal CBT as a way of primary prevention. The intervention incorporated classic CBT components for treatment of depression and components aiming at enhancing marital relationship and communication. Their CBT intervention proved effective in reducing automatic negative thoughts, marital dissatisfaction and communication dissatisfaction. This individual CBT intervention not only improved well-being during pregnancy, but also during the postpartum period. The authors’ conclusion is that individually-tailored CBT intervention is more effective than a group format. However, if group sessions are the only option, helping professionals should avoid issues around personal fatigue, the condition of the unborn baby and dissatisfaction from partner.¹³ One key hypothesis in these studies is that interventions  that improve the quality of the marital relationship have great preventative power for PDD, as they increase both actual and perceived support.

Person-Centered Therapy

Person-centered counseling, also referred to as non-directive counseling, has also shown to decrease depressive symptoms in postpartum women in a number of randomized controlled studies.¹

Social Support

Lack of adequate social support is among the first risk factors for PPD, therefore peer and partner support groups have received a lot of attention among researchers.¹ Dennis (2003)¹⁵ has studied the effects of mother-to-mother support over telephone communication and has observed the beneficial effects of this approach. In fact, the severity of depressive symptoms was significantly reduced in eight weeks. Additionally, women who have been identified as high risk for developing PPD were involved in telephone-based peer support over 12 weeks and were later recorded to have lower incidence of PPD when compared to a control group. This gives hope that these noninvasive and cost-effective therapeutic approaches can also serve as preventative measures.

Alternative Therapies

Interesting research by Field and colleagues (1996)¹⁶ has shown that teaching new mothers to massage their infant reduces irritability and sleep problems in the baby, while leading to reduced depression in the mother. This massage therapy is a relatively simplistic techniques with potential to greatly benefit both the mother, child and their interaction. Findings like these increase our hopes that researchers will establish new methods of prevention and treatment which can transform the prevalence rates of PPD among new mothers.

References:

A previous article already introduced some of the symptoms and risks of Postpartum Depression (PPD), but I would still like to emphasize the profound effects of this disorder. In this particular stage of life, depression does not only hurt the new mother, but poses threat for the well-being of the baby as well. In other words, It could be an ailment for two. This makes the need for timely and adequate help even more compelling.

Beyond the emotional and psychological suffering experienced by women with PPD, there are multiple negative effects for the infant. Women who experience more severe or prolonged PPD symptoms are more likely to develop insecure attachment to their infants and perceive their baby in a negative way, unable to enjoy the bonding and joy reported by healthy mothers.¹  A body of research shows that children of depressed mothers tend to receive lower scores on measures of intellectual and motor development when compared to children born to non-depressed mothers. These babies also tend to be fussier  and of more difficult temperament.¹  Another unfortunate consequence is that children of depressed mothers typically react poorly to stress, show poorer academic performance, delayed development of self-regulation, low self-esteem, lack of social competence and multiple behavioral problems.²

At least one study³ has shown that infants born to depressed mothers experience significant sleep disturbance in the developmental period between two weeks and the first six months of life. The difference is compelling when compared to infants of non-depressed mothers. This is especially troubling since it is known that this initial phase of life is a critical developmental period for sleep-wake cycles, melatonin and temperature rhythms.³

Depressed mothers tend to be more irritable and hostile towards their child, interacting with either intrusive, controlling and over-stimulating style or with withdrawn, passive and under-stimulating style.⁴ Neither of those extremes is beneficial for infant development. In comparison with healthy mothers, mothers with PPD touch their babies less frequently and more often do it in a negative, harmful way. Depressed mothers also have different vocal behavior, more negative affect and engage in less baby talk. Overall, they spend less time playing with the child or reading, talking, and touching. This contributes to creating an inadequate environment for the developing infant, which is deprived of mother-child bonding, synchrony and enrichment activities. Additionally, depressed mothers are less likely to begin breastfeeding and even when they do, they are more likely to discontinue in around 4 to 16 weeks.⁴

Women with PPD are more likely to start smoking or abuse alcohol and illicit substances which can further exacerbate the severity of their symptoms and the negative effect on the child. Further, these mother are at greater risk for experiencing physical, emotional or sexual abuse.⁵

References:

1. Cho, H. J., Kwon, J. H., & Lee, J. J. (2008). Antenatal cognitive-behavioral therapy for prevention of postpartum depression: a pilot study. Yonsei Medical Journal, 49(4), 553-562.   2. Goodman, S. H. & Gotlib, I. H. (1999). Risk for psychopathology in the children of depressed mothers: a developmental model for understanding mechanisms of transmission. Psychological Review, 106(3), 458-490.   3. Armitage, R., Flynn, H., Hoffmann, R., Vazquez, D., Lopez, J., & Marcus, S. (2009). Early developmental changes in sleep in infants: the impact of maternal depression. Sleep, 32(5), 693-696.   4. Field, T. (2010). Postpartum depression effects on early interactions, parenting and safety practices: a review. Infant Behavioral development, 33(1), 1. doi:10.1016/j.infbeh.2009.10.005.   5. Fitelson, E., Kim, S., Baker, A. S., & Leight, K. (2011). Treatment of postpartum depression:clinical, psychological and pharmacological options. International Journal of Women’s Health, 3, 1-14.

Postpartum Depression (PPD): A Psychological Disorder

Postpartum Depression (PPD) is a fairly common complication of childbirth and often accompanies the postpartum period, leading to psychological suffering for the mother, negative effects on the infant and strained family relationships.¹

Pregnancy, childbirth and the postpartum period involve intense emotional experiences for most women and are characterized by a major developmental transition, physical and psychological demands, body image changes, as well as psychosocial changes, all within a short period of time.² Sadly, psychiatric disorders are the leading cause of maternal deaths, very often through suicide.¹

Women with PPD suffer from depressive mood and profound sadness, frequent crying, insomnia, lack of appetite, fatigue, lack of motivation, low self-esteem, perceived inability to cope, suicidal ideation as well as multiple physical complaints.^3,4

Some researchers attempt to conceptualize PPD as a complicated maternal identity formation, where the new mother is unable to achieve a sense of maternal competence and incorporate her new psychosocial role.³ In other words, there is a dominating American middle-class perspective on mothering, which expects an intense child-centered parenting that is both economically and emotionally demanding. Yet, we often fail to appreciate the largely diverse population of the United States in the context of child rearing. Thus, mothers who may not fit the middle-class American script may feel like a failure and begin to experience growing maternal incompetence, diminished self-efficacy, self-esteem and increased distress. All of these may be contributing to the onset of PPD.³

Why is this Disorder Often Undiagnosed?

Women diagnosed with PPD often describe themselves as “bad mothers” and report intense feelings of guilt and shame.^{3, p.374}  This gives us an idea about the social stigma associated with PPD and would partly explain why most women do not seek professional help and remain undiagnosed and untreated. That is why helping professionals need to put every effort into promoting psycho-education and establishing PPD as a diagnosable, treatable disorder, so that no mother and her child remain in suffering. In fact, researchers point out that some women may experience the diagnosis of PPD as a relief, helping them accept their symptoms and reduce their personal feelings of guilt, self-blame and shame.³

How Common Is The Disorder?

The estimated prevalence rate of PPD is about 13%, with higher incidence among teenage mothers.⁵ A study of women in Sweden has shown depressive symptoms in around 17% of pregnant women during the late stages of pregnancy and in 13% of new mothers.⁶ Other studies have found prevalence rates of 14% in both early pregnancy and during the first year after delivery.^{Rubertsson cited in 6}

Such prevalence rates pinpoint PPD as a serious public health issue that affects not only mothers, but also their children and other family members.

Risk Factors

Many life events and psychological factors have been identified as risk factors for PPD. Among these, anxiety and depression during pregnancy have shown to be strong predictors for the onset of PPD.⁷ Many studies have also established low socioeconomic status as a strong risk factor.^3,6 Obese pregnant women are also at higher risk of developing PPD.⁷

Postpartum depression might be more common than you have imagined. It is not as common as “baby blues” also referred to as “postpartum blues” that affect about 75% of new mothers within the first ten days after delivery.^8,9 PPD’s symptoms are more serious and longer lasting than those of postpartum blues. Still, if your wife, partner, or friend is experiencing such profound sadness, you should not underestimate the possible seriousness of the issue. Pay close attention to the symptoms and provide support and understanding. (An article on prevention and treatment will be posted soon).

References:

1. Bick, D. & Howard, L. (2010). When should women be screened for postnatal depression? Expert Reviews of Neurotherapeutics, 10(2), 151-154.    2. Clark, A., Skouteris, H., Wertheim, E. H., Paxton, S. J., & Milgrom J. (2009). The relationship between depression and body dissatisfaction across pregnancy and the postpartum. Journal of Health Psychology, 14(1), 27-35.   3. Abrams, L. S. & Curran, L. (2011). Maternal identity negotiations among low-income women with symptoms of postpartum depression. Qualitative Health Research, 21(3), 373-385.   4. Cho, H. J., Kwon, J. H., & Lee, J. J. (2008). Antenatal cognitive-behavioral therapy for prevention of postpartum depression: a pilot study. Yonsei Medical Journal, 49(4), 553-562.   5. O’Hara, M. W. & Swain, A. M. (1996). Rates and risks of postpartum depression: a meta-analysis. International Review of Psychiatry, 8, 37-54.   6. Claesson, I., Josefsson, A., & Sydsjo, G. (2010). Prevalence of anxiety and depressive symptoms among obese pregnant and postpartum women: an intervention study.  BioMed Central Public Health, 10, 766-776.   8. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Fourth Edition, Text Revision. Washington, DC, American Psychiatric Association, 2000.

Prozak (fluoxetine) is among the Selective Serotonin Reuptake Inhibitors (SSRIs), aka. second-generation antidepressants. As all SSRIs, Prozak blocks the reuptake transporter for serotonin, preventing it from being taken back to the axon terminal. Since this transporter is blocked, serotonin remains in the synaptic cleft for long periods, continuing to have its effect on the postsynaptic neuron. Although this effect takes place very quickly, depression symptoms take long periods to be alleviated. This phenomenon is not fully understood, but it’s interesting to note that Prozak increases the production of new neurons in the hippocampus – a limbic structure that is very vulnerable to stress-induced damage. Therefore, it is suspected that this renewal in the hippocampus is exactly the reason behind this antidepressant’s effect.

Symptoms of Major Depression

Feelings of helplessness and hopelessness; sadness; loss of interest and pleasure (from food and/ or sex) – anhedonia; may be accompanied by significant weight loss or gain (sometimes hyperphagia); insomnia or hypersomnia (middle of the night awakening, early morning awakening); fatigue, general loss of energy; having hard time concentrating. People with depressive symptoms are indecisive, have low self-esteem; pessimism; disturbance of body rhythms; suicidal tendencies are common.

Evidence for genetic predisposition for Depression

Although the impact of genes varies, depending on the type of depression, there is a correlation. Depression tends to run in families. That is why adopted children, resembling their real parents’ genes may have depression in spite of living in a cheerful, lively atmosphere. One is at risk of depression if one has close relatives who have had severe early-onset depression, especially if that relative is a female. However, no single gene has been identified to have a strong link with that mood disorder. So, obviously, depression depends on a combination of genes and environmental factors.

Are males or females more vulnerable to depression? What is the role of hormones?

Depression is much more common in women, in all cultures. For sure, hormonal changes can trigger an episode of depression, but this correlation does not necessarily imply causation, as some women are more vulnerable than others. Still, the reason why women suffer depression more often is not clearly identified.

What is the role of traumatic experiences for episodes of depression?

Stress is a typical trigger for an episode of depression, as it causes the release of cortisol that prepares the body for action and, in the long run, exhausts the body. A lot of women experience postpartum depression, after giving birth and some of them enter a more serious, long lasting depressed condition. However, giving birth itself does not cause depression as many of the women have already suffered previous onsets. Thus, traumatic experiences may trigger an episode of major depression, but do not cause the disorder.

What are the patterns of hemispheric dominance with happy moods in normal people? How do they differ from patterns in depressed people?

Happy mood is generally related with increased activity in the left prefrontal cortex. Depressed people, however, have decreased activity in that area, whereas it is increased in the right prefrontal cortex. Also, many people who have had damage to the left hemisphere become seriously depressed. Fewer become depressed after damage to the right hemisphere. And sometimes, people with right hemisphere damage become manic.

What is Borna disease? What evidence links it to depression?

Borna disease was first noticed in European farm animals. It affects behavior, causing frantic activity or inactivity. In severe cases, the disease can be fatal. As many other viruses, Borna disease can be passed between humans and other species. However, the effect is different in humans. In an experiment/ survey, in all 12 cases of people with Borna disease, those same people had either major depression or bipolar disorder.

What are 3 groups of antidepressants? How does each of them exerts its effects?

Tricyclics prevent the presynaptic neuron from reabsorbing catecholamines or serotonin after they have been released. Thus, the neurotransmitters remain in the synaptic cleft longer, continuing to stimulate the postsynaptic cell. They inhibit the reuptake of NE and dopamine. However, tricyclic also block certain receptor which may lead to side effect.

Selective serotonin reuptake inhibitor (SSRIs) block the reuptake of serotonin by the presynaptic terminal (in a way, those are similar to tricyclics). SSRIs have little and only mild side effects. Still, sometimes, they may cause nervousness and, thus, are not recommended for people suffering anxiety.

Monoamine oxidase inhibitors (MAOIs) block the enzyme monoamine oxidase, which has the function to metabolize catacholamines and serotonin into an inactive form. O, when this enzyme I blocked, the amount of those neurotransmitters in the presynaptic terminal and the cleft increases. However, MAOIs tend to affect blood pressure, which can be very dangerous and, in general, are very dangerous in the long run, although they tend to work within a few days.

Why does Prozac/ fluoxetine preferred over tricyclics and the monoamine oxidase inhibitors?

It almost no side effects (sometimes mild nausea, headache, or nervousness, very rarely people react with having Serotonin fever). Also, there is almost no risk of over dosage. In addition, it takes only within 2 – 4 weeks to work and, in the short term, causes loss of weight, which is, generally desired by people.

What are atypical antidepressants? For whom are they used?

This is a miscallaneous group of drugs that have the antidepressant effect, but very little side effects. They are being prescribed to people who did not respond to the other drugs. Some atypical antidepressants are bupropion (inhibiting the reuptake of DA and sometime NE, but not 5HT), venlafaxin (mostly inhibit the reuptake of serotonin, and lightly of DA and NE).

How effective is St. John’s wort? Which class of antidepressants produces similar effect? What is one potential problem?

St. John’ wort is an herb that works like the selective serotonin reuptake inhibitors. However, it efficacy I not yet accurately determined, a different studies how different results (some suggest it is more effective that SSRIs, some claim it is equal to them, others that it is not effective at all). One potential dangerous side effect is that St. John’s wort increases the production of the liver enzyme that breaks don toxins, also medicines. Thus, it decreases the effectiveness of many medicines that may be vital. Another problem is, that it is cheaper that drugs and can be taken without prescription, which hides risk of inappropriate use and dosage.

Explain the problem of time course effects on neurotransmitters and depressive symptoms. What are some delayed effects of antidepressants?

Antidepressant drugs, in general, have delayed effects that limit the excitation of the postsynaptic cell, decreasing the sensitivity or the receptors on the postsynaptic cell. They also affect autoreceptors (the negative feedback receptors on the presynaptic terminals). Also, Prozac, for example, causes gain of weight hen used for a long time.

What neurotrophin is produced as a result of repeated use of antidepressants? In which brain areas is it produced?

Brain-derived neurotrophic factor is produced that aid the growth, survival and connections between the neurons. The cerebral cortex and the hippocampus.

How is electroconvulsive therapy (ECT) applied today? How is this an improvement over practices in the 1950s?

In the 1950, ECT was widely used without patients’ consent, being tried on many people in mental hospitals. Today, however, ECT is used only with informed consent for patients who do not respond to other antidepressant drugs. During ECT, the patient is under general anesthesia, with muscles being blocked. Thus, the process is not painful and the risk of injury is minimized. A common side effect is that the patient has a loss of memory for that particular time hen ECT has taken place.

For which two groups of patient is ECT most often used?

ECT is used with people ho do not respond to other antidepressant drugs and with people ho have severe depression and suicidal tendencies, who need fast results and betterments (may be the difference between life and death).

What are the advantages and disadvantages of ECT?

Advantage is that it is the most effective treatment available nowadays and gives very fast results. Some disadvantages are that it may cause prolonged convulsion that can be fatal. Also, ECT should be applied over long periods of time and, as people lose memory of that time, it may, eventually, cause amnesia. Often, the case is that, after ECT treatment, patients enter another episode of depression within 6 months.

What are the effects of ECT on neurotransmitter receptors? What newer treatment is similar to ECT?

ECT stimulates the production of additional dopamine (types D1 and D2 receptors) and decreases the number of norepinephrine receptors.

How does the onset of REM sleep differ in depressed people, compared in non-depressed? How may this be related to body temperature cycles?

People with mood disorders also suffer some disorder of the biological rhythms. Depressed people have troubles sleeping and people who have sleep problems are more likely to get depressed, so it is a two way street. After going to sleep, most non-depressed people enter REM sleep after about 80-90 minutes and the amount of REM sleep is increased in the second half of the night. Depressed people, however, enter REM phase of sleep after about 45 minutes after going to bed. Also, the have trouble staying asleep and feel drowsy the next day.

What change in sleeping schedules has been found to alleviate depression? How long do the benefits last?

Surprisingly, sleep deprivation improves the condition of depressed people, relieving the symptoms of the disorder. Yet, this is not a solution as sleep deprivation is dangerous in the long run. Both antidepressant drugs and sleep deprivation decrease the amount of REM sleep. So, there is something about that stage of sleep that may be a hidden cure for depression, but researchers are not certain yet.