Depression, a painful and lonely state

All of us have experienced depression during one time or another. Sadness is quite normal when we are hurt or when our expectations are not met. The sadness we feel during those times drift away after some time and we get back to our lives. Nevertheless, persistent depression is precarious and should not be left untreated. Time and effort is needed to cure it. The most commonly found symptoms of depression are hatred towards self, fear of failure, anxiety, lack of interest in any kind of activities and insecurity. The negative feelings sometimes get so intense, the person starts harboring suicidal thoughts.


If someone you love is in depression, it is for the person’s family and friends to extend a helping hand to the person so that he can regain balance of life. The task can be quite a task as you will need extreme patience and extra effort to motivate the suffering person. However, there are ways to help your friend in need.


Lending a patient ear- Lending a patient ear is the best help you can do to your loved one during her or his time of difficulty. Try to find out the cause of his trouble and encourage him to pour out his thoughts to you. Assure him your help and understanding. Very often, the person might keep him contained without sharing the cause of his trouble. A good friend should make him open up his mind.


Instilling positive feelings- Avoid using a negative tone when you talk to the person in depression, and avoid criticisms. It will only add to his or her misery. Talk to him about the importance of leading a positive life and instill optimistic views in the person’s mind. Raise his confidence level by ensuring that every problem has a solution and difficult times are only temporary. Counsel him not to worry if things do not work out the way he expected, as sometimes better prospective may be awaiting us.


Be there for your loved one or friend- Ensure that your friend does not stay back alone and brood in corridors. Take him with you for movies, shopping, or for walks. Get him to speak, share, laugh and socialize. Getting him to join in an activity club will help him keep engaged. Though he will be reluctant to do anything, make him take part in things he once loved. Compliments help to gain back confidence.


Protect him from using harmful things- Individuals in depression have a tendency to use drugs and other harmful products as it gives them temporary relief.  Use of too much anti-depressant is also observed in mentally disturbed people. Ensure your friend does not fall victim to such unhealthy habits.


Get help- Clinical depression or severe depression can be cured only through medical procedures like cognitive behavioral therapy, talk therapy, psychotherapy and expert counseling. Take him to a doctor at the earliest.


Depression needs some time to get cured. Encouraging the depressed person to stay active will speed the process of recovery.






Post partum depression

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.

Etiologies of depression

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.


The artifact hypothesis takes into account gender differences in symptom reporting and help-seeking behavior as well as cultural and diagnostic biases. The biological hypothesis attributes the sex difference in the prevalence of MD to the frequent shifts in reproductive hormone levels in women.[14,16] Biological theories have proposed differences in brain structure and function between men and women, including neurotransmitter, neuroendocrine, and circadian rhythms, as well as genetic factors and reproductive function.[15] Hormonal influences on depressive episodes, related to reproductive events such as pre-menses, pregnancy, postpartum, and menopause, have been observed in some women. A change in estrogen status, such as the estrogen deficiency of menopause, can lead to modulation of serotonergic function and increase the risk of depression for women.


The psychosocial hypothesis emphasizes that women, in general, have a lower socioeconomic status and are more prone to stressful life events, victimization, and maladaptive coping styles, all of which may contribute to their higher risk of MD.[14,15] Chronic stressful life events can modulate neurotransmitter activity, contributing to a biological basis of depression. Additionally, major depressive episodes can be triggered by season of the year.


Women have been shown to be more susceptible than men to developing a seasonal pattern to their depression, with a female-to-male ratio for seasonal affective disorder of greater than 3 to 1.[18] The gender/sex difference in the lifetime prevalence of MD thus appears to result from many interacting factors. These factors may contribute to the diverse subtypes of depression that occur in women and the varied presentations observed in clinical practice.

Why women are more depressed?

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.


Adolescent females and adults also appear more likely than their male counterparts to cope with stress inwardly rather than relieving themselves of the distress outwardly, research shows. Depression can and should be treated with psychotherapy, medication when appropriate, or changes in the affected person’s environment, Nolen-Hoeksema said. “Fortunately, depression can be reduced by targeting several different biological, social or psychological problems a woman might have,” she added.


What the hell do ANY of you bitches have to be depressed about in our matriarchal society? Especially you adolescent bitches? Don’t you know that “sisterhood is powerful”? Don’t you see how society panders to you at the expense of males? Don’t you know that “there’s never been a better time to be a girl”? Go out and play soccer or something. But actually, I would rather that you simply remained depressed. MAN, it makes my day to find out how unhappy females are! I never thought that I would ever have occasion to say this Women who “attempt suicide” are expecting to get sympathy and attention for themselves whereas a man who suicides generally does so to spare others any trouble over him.


Finally, don’t commit a Pargism by confusing higher rates of *reporting* depression with higher rates of depression. In fact, people who suffer but _cannot express it_ are suffering more deeply. They need more help, not less. Isn’t it bad therapy to identify _only_ the woman as a victim? Yes. But it’s good politics. Why? Singling out the woman allows us to make her feel special. But special as what? Special as a victim.

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Help for my depressed daughter

Emily felt equally helpless when her parents were each struck down by illness. In 1997 her mother, who is 60 this month, was seriously ill after contracting amoebic dysentery while filming in Zimbabwe and the following year her father, now aged 69, had a major heart attack. ‘When Mum was really ill I think she realized for the first time exactly what I had been going through. She was so fatigued she wondered if she would ever get better again and I felt terrible because I couldn’t help her,’ says Emily.


‘It was a real strain for Dad supporting us both, and then when he had his heart attack, it was a terrible shock.’ However, no matter how much she loved her parents, Emily knew subconsciously that her depression was somehow linked to the protective, cotton wool existence her mother and father had lovingly built around her. ‘It was me who decided to go into hospital that last time, as an in-patient rather than an outpatient, although I don’t think I even admitted to myself the real reason,’ says Emily, who insisted she made her own way there by taxi.


‘I was scared about going in there because I thought it would be full of loonies, but the minute I arrived I felt wonderful. They put me on a ward with girls my own age and for the first time in years I felt like my own person – independent. It was almost as if I’d left home to go to college, it was very exciting. Every day I was doing art and drama therapy, assertiveness training, and taking part in discussion groups. ‘I remember one Sunday the father of one of the girls smuggled in a copy of The Blair Witch Project and we sat around on bean bags being scared out of our wits.


It felt like one of those adolescent sleep-over parties. It was something I’d never experienced before and it was so liberating. From the moment I went into hospital I felt phobic about going home. It wasnt that I didn’t love my parents, I loved them enormously, but our house held so many unhappy memories for me. At home I felt like a little vulnerable china doll and I didn’t want to feel like that anymore’.

Long-Term Outcomes of Depression

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.


Patients with past Lyme disease had a higher prevalence of memory impairment, joint pain, and fatigue than did age-matched controls. Because pain and fatigue affect functional status scores, these patients had poorer scores than controls (i.e., in the 25th percentile of age-matched controls). Patients with past Lyme disease had more knee, hip, and proximal interphalangeal joint pain on motion. Knee swelling was also more common in patients. Neurocognitive testing was normal, yielding the same results for patients and controls. Patients with persistent symptoms were more likely to have had a longer delay between disease onset and antimicrobial therapy.


In summary, approximately one-third of patients with prior Lyme disease had persistent symptoms of memory loss, joint pain, and fatigue but did not have objective findings on neurocognitive testing, were not depressed, did not have fibromyalgia on examination, and had minimal objective joint findings. Seltzer and colleagues (2000) performed a longitudinal cohort study of patients diagnosed with Lyme disease 1-11 years earlier. The patients were interviewed and underwent functional status testing, quality of life surveys, and assessment by CES-D (a tool to diagnose depression, for adults only). A total of 445 adults and 233 children were included. Patients were diagnosed with Lyme disease a median of 51 months (range, 15 to 135 months) before this study.


Almost 71 percent believed that they were cured, 20 percent were unsure and stated that they did not feel sure that Lyme disease was curable, and 9 percent (15 percent of adults and 5 percent of children) believed that they were not cured. Those who believed they were cured had fewer comorbid conditions. The proportion of patients who thought they were cured was higher in the group who met the CDC criteria for Lyme disease than in the group who did not meet these criteria (75 percent vs. 63 percent). Although 69 percent of patients reported various symptoms or trouble with the activities of daily living, only 19 percent attributed these difficulties to Lyme disease. The majority believed that these symptoms were due to normal aging or to comorbid conditions.


Patients who did not meet the case definition for Lyme disease had more symptoms and trouble with activities of daily living than those who did meet the definition. Patients who did not meet the case definition were somewhat less likely to have been treated with antimicrobial agents for Lyme disease. In summary, 64 percent of the patients met the case definition for Lyme disease, and few of these patients had residual symptoms or trouble with activities of daily living secondary to prior Lyme.


The frequency of these symptoms was similar to the frequency in the control group. Of patients who did not meet the case definition, three-quarters had nonspecific symptoms such as fatigue, arthralgias, and trouble formulating ideas. The authors concluded that many of these patients probably did not have Lyme disease.

Depression can be an allergy to a medicine

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.



Food labels must also contain warnings because of the phenylalanine content in aspartame (2% of the population with the genetic disorder phenylketonuria cannot metabolize this chemical). Since FDA approval a significant portion of the population has become hooked on sugar-free products that contain aspartame. Many Americans are consuming upwards of 3 diet sodas a day, fooling themselves into thinking they are doing a favor for their body by drinking sugarfree, calorie free beverages.


Aspartame consists of three chemicals; it is 50% phenylalanine, 40% aspartic acid, and 10% methanol or wood alcohol. Diketopiperazine (DKP) is a by-product of aspartame metabolism. Ingesting high amounts of the amino acid phenylalanine results in a phenylalanine build up in the brain. This buildup potentially decreases the amount of serotonin in the brain, resulting in depression and mood disorders. Excessive buildup may result in brain damage. The phenylalanine content in aspartame breaks down into DKP, a brain tumor agent.


Aspartic acid is an amino acid and when digested in its free from it elevates the blood plasma concentration of aspartate and glutamate. This excess allows a high concentration of calcium into the cells which invites free radicals thereby destroying neurons. Aspartate and glutamate are referred to as “excitotoxins,” since they essentially “excite” or stimulate the neurons to death. High aspartic acid consumption directly leads to neurological damage. Once the methanol in aspartame is ingested it converts to formaldehyde (a deadly neurotoxin) and then formic acid (a toxic metabolite) and causes metabolic acidosis. This is referred to as methanol toxicity.


Multiple studies which conducted experiments on rats came to the conclusion that consumption of aspartame leads to the formation of formaldehyde adducts (chemical addition products) which accumulate in tissue proteins and nucleic acids. A February 1994 Department of Health and Human Services report documented more than 90 symptoms of aspartame poisoning include fibromyalgia symptoms, depression, shooting pains, numbness in your legs, dizziness, joint pain, memory loss, slurred speech, headaches, vision loss, and anxiety attacks.

Clinical implications of depression

Thalamic output on the cerebral cortex is modulated in response to levels of sleep and wakefulness (Steriade & Contreras, 1995), and recent work has demonstrated its relevance to general attention and vigilance (Kinomura et al, 1996; Roland, 1996) and to the discrimination of painful stimuli (Lenz et al, 1995). Some authors have proposed a dynamic role for the thalamus in modulating information transmission to the cortex (Sherman & Guillery, 1996). Others have suggested a crucial role for the thalamus in the modulation of motor and cognitive coordination (Roland, 1996).


Importantly for CFS, the lateral ventral nucleus of the thalamus receives input from muscle afferents and the cerebellum that provide critical information about motor state. There is an intriguing overlap between these sensorimotor functions and the core symptoms reported in CFS. Thalamic overactivity in CFS (and depression) may, therefore, reflect increased attention to motor and cognitive tasks, with previously automatic tasks requiring higher levels of vigilance and thereby becoming effortful.


Many similar disturbances and symptoms are evident in depression, but we found that prefrontal perfusion distinguishes the disorders. This is in keeping with our findings, in the same group of patients, that patients with depression have similar motor but more profound cognitive deficits than patients with CFS (Lawrie et al, 2000). These important similarities and differences in the patterns of cerebral perfusion between patients with depression and those with CFS may, therefore, be associated with their similar but different clinical presentations.


Clinical Implications and Limitations CLINICAL IMPLICATIONS The patterns of cerebral perfusion in chronic fatigue syndrome (CFS) and in depression show important similarities and differences. Biological disturbance in CFS is not limited to those with comorbid depressive symptoms. These changes are quantitative rather than qualitative — single-photon emission computerised tomography has (as yet) no role in the clinical diagnosis of CFS.

Cerebral perfusion in chronic fatigue syndrome and depression

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.


CFS patients also had increased perfusion in the left thalamus. Depressed patients differed from those with CFS in having relatively less perfusion of the left prefrontal cortex. The results were similar on ROI analysis. Conclusions Abnormal cerebral perfusion patterns in CFS subjects who are not depressed are similar but not identical to those in patients with depressive illness. Thalamic overactivity may be a correlate of increased attention to activity in CFS and depression; reduced prefrontal perfusion in depression may be associated with the greater neuropsychological deficits in that disorder.


INTRODUCTION Chronic fatigue syndrome (CFS) is characterised by incapacitating fatigue of at least 6 months’ duration, that is made worse by relatively minor exertion. Although depressive or anxiety disorders have been diagnosed in up to two-thirds of CFS sufferers, the nature of the relationship between CFS and depression remains uncertain (Kendell, 1991). One way to identify similarities and differences between CFS and depressive illness is to study their biological correlates thorough the use of neuroimaging techniques. Functional imaging studies have yielded inconsistent results to date. Most of the single-photon emission computerised tomography (SPECT) studies have reported areas of cerebral hypoperfusion, either global (Ichise et al, 1992; Schwartz et al, 1994) or localized (Costa et al, 1995; Goldstein et al, 1995). However, others have reported no significant cerebral perfusion differences compared with healthy (Peterson et al, 1994) and/or depressed (Fischler et al, 1996) controls.


These inconsistencies may be explained in terms of (a) patient selection (as most of the studies have not explicitly excluded confounding psychopathology), and (b) different scanning methodology — most studies to date have used relatively subjective, non-standardized techniques for reporting statistical abnormalities of cerebral perfusion.


In this paper, we present a comparison between patients with CFS who do not have a concurrent depressive illness, patients with major depressive disorders (both groups diagnosed with standardized criteria) and healthy volunteers. The results are from high-resolution single-photon emission tomography, with both region of interest (ROI) and vowel-based statistical parametric mapping (SPM) analysis of the effects of diagnosis on perfusion.

Studies on the effect of serotonin in depression patients

“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.


“That light information is somehow able to synchronize the endogenous neuroclock” from within the suprachiasmatic nucleus. Light is effective in treating SAD, observed Turek, yet understanding of its actions remains rudimentary. Similarly, there is but imprecise understanding of how serotonin-enhancing drugs like Prozac (fluoxetine) and Zoloft (sertraline) exert their effects, Turek observed. While they inhibit reuptake of serotonin at the receptor, “we don’t know how that translates into alleviating depression. We need to begin to address physiological mechanisms here.”


So it was logical to ask whether light would affect serotonergic function, he added. Norman Rosenthal, M.D., chief of the Section on Environmental Psychiatry at the National Institute of Mental Health (NIMH), spoke with Psychiatric News from Tromso, where he was chairing the SAD conference. “I think what the Turek article does is indicate interaction between light and a serotonergic drug in an animal model.


It’s not the first time in animals that light and serotonin have somehow been connected with each other.” Earlier work has shown that light exposure alters the firing rate of serotonergic neurons in rats. Another study found that the amount of light influences the concentration of serotonin in the rat brain.