Postpartum depressive disorder is a spectrum of depressive disorders that typically includes postpartum blues, postpartum depression, and postpartum psychosis.[45] Postpartum blues is by far the most common type, with an estimated prevalence ranging from 30% to 85%.[38,46] This relatively mild emotional disturbance is characterized by mild depressive symptoms such as mood liability, depression, irritability, tearfulness, generalized anxiety, increased sensitivity to criticism, fatigue, and disruptions in sleep and appetite.
These relatively benign and transient symptoms typically peak on the fourth or fifth day after delivery and remit by the tenth postpartum day. Although symptoms are time-limited and require little intervention, approximately 20% of women will develop MD in the first postpartum year.[46] DSM-IV defines postpartum depression (PPD) as a major depressive episode that occurs within 4 weeks of delivery.
PPD is relatively common, with an estimated prevalence rate ranging from 10% to 16% during the 6 to 12 weeks after delivery.[38,45,47-49] Residual depressive symptoms may persist up to 1 to 2 years.[47] These rates are very similar to the rates of depression observed in nonpuerperal women (that is, in women who have not just given birth). Because the symptom profile of PPD resembles that of a major depressive episode experienced at other times in life, the same DSM-IV criteria for MD apply to the diagnosis of PPD. The most reliable predictors of PPD are a prior history of MD (postpartum or nonpuerperal) and an absence of social support.
These two factors can double the risk of developing PPD.[50] Prior PPD was associated with a 50% to 62% increased risk of subsequent postpartum episodes, and prior nonpuerperal MD was associated with a 30% risk of subsequent postpartum episodes.[45,47,48] Risk factors for PPD are shown in Table 6. Comorbid psychiatric illnesses, such as anxiety and obsessive compulsive disorder, are also prevalent in women with PPD.
Three hypotheses have been proposed to explain the predominance of MD in women: the artifact hypothesis, the biological hypothesis, and the psychosocial hypothesis.[14,15] As its name implies, the artifact hypothesis proposes that the greater prevalence of depression in women is the result of an artifact — specifically, the higher likelihood of women versus men to report symptoms of MD and to more frequently seek psychiatric care.
Biologically, the hypothalamic-pituitary-adrenal (HPA) axis is the part of the nervous system that regulates levels of cortisol and other hormones in the stress responses of both males and females. Some researchers have suggested that women are more likely to have a dysregulated HPA stress response. This dysregulation may consequently make females more prone to becoming depressed in response to stress.
Shadick and colleagues (1999) studied the neurologic and musculoskeletal sequelae of Lyme disease in a cohort from Nantucket Island, Massachusetts. They identified 353 persons, 186 of whom met the Centers for Disease Control and Prevention (CDC) criteria for prior Lyme disease and 167 of whom did not. An appropriate control group was also studied. The patients’ medical history, physical examination, psychometric testing, and serology testing were extensively reviewed.
The safety of aspartame, a product that the FDA refused to approve for more than eight years because of the seizures and brain tumors it produced in animals, continues to be questioned. In 1981, after years of denial, the FDA finally approved the use of aspartame in dry goods. Since then it has been approved as an ingredient in every type of food product including baked goods. It is currently sold under the brand names: NutraSweet, Equal, and Spoonful. It appears on ingredient labels as aspartame.
Background Patients with chronic fatigue syndrome (CFS) and depressive illness share many, but not all, features. Aims To test the hypothesis that patients with CFS have abnormal cerebral perfusion, that differs from that in patients with depressive illness. Method We recruited 30 patients with CFS who were not depressed, 12 depressed patients and 15 healthy volunteers. Regional cerebral perfusion at rest was assessed using region of interest (ROI) and voxel-based statistical parametric mapping (SPM) techniques. Results On SPM analysis there was increased perfusion in the right thalamus, pallidum and putamen in patients with CFS and in those with depressive illness.
“The essence of our study is that at a time of day when we know that light has no effect [on the circadian clock], serotonin will shift the clock,” Turek told Psychiatric News. “If we give light and serotonin [an agonist] at the same time, [light] blocks the effect of serotonin. If light can alter the way that neural tissue, the brain of a hamster, can respond to exogenous serotonergic stimulation, it raises the hypothesis that light may alter the way the brain is responding to serotonin in the brain.” It is clear that light impulses have a direct impact on the brain through the “optic nerves” into the suprachiasmatic nucleus of the hypothalamus, said Turek.
