Jaguar
Active member
- Joined
- May 5, 2007
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- 20,647
Stop being so accusatory. You really need to calm down.
Since I can't find any post where someone is flipping out, I guess a mod deleted it. Darn.
Stop being so accusatory. You really need to calm down.
For years, Murphy had suffered from severe depression that seemed untreatable—rounds of Effexor, Risperdal, Klonopin, Lithium, Cymbalta, Abilify, electroshock therapy and even an adorable new puppy failed to get her up out of bed. Then doctors offered her a new option, something called deep brain stimulation.
This is how Liss Murphy wound up with two 42-centimeter-long electrodes implanted deep within the white matter of her brain.
“My greatest hope the day of the surgery was that I would die on the table.â€
It worked. Murphy became one of the first people in world successfully treated for a psychiatric illness using deep brain stimulation, in which electronic neurostimulators are embedded deep within the brain to correct misfiring signals. Like Gage, the experience changed her, but for the better. She got out of bed, had a kid, and went back to work part-time after years of being able to barely leave the house.
In the current issue of Psychotherapy and Psychosomatics a new analysis discloses insights into the long term effects of antidepressant drugs. Major depressive disorder (MDD) is more often chronic or recurrent in clinical than in community samples. For example, perhaps 85 percent of patients but only 35 percent of persons in the community with MDD experience another depressive episode within 15 years. Nonetheless, active treatments including antidepressant medication or cognitive therapy reduce depressive symptoms and delay relapse compared to inactive controls. Follow-ups of treated and untreated persons in clinical trials have rarely exceeded 1-2 years, however.
The current analyses of a national sample with 9-year follow-ups clarified these possibilities. Using the same assessments for treated and untreated persons excluded the first possibility. Testing whether MDD severity and a wide range of demographic, psychosocial, and clinical variables accounted for long-term differences between treated and untreated persons estimated the second possibility, with remaining outcome differences more likely due to treatment. Twelve-month MDD prevalence at survey waves 1, 2, and 3 was 13.3, 10.5, and 9.9 percent, respectively. With MDD, 38.1 percent of participants received no treatment, 25.2 percent inadequate treatment including medication, 19.2 percent inadequate treatment without medication, 13.5 percent adequate treatment including medication, and 4.1 percent adequate treatment without medication during the past year.
Prior depressive status, treatment and their interaction, predicted subsequent depressive symptom levels. Among persons with major depressive disorder, symptoms were higher after inadequate treatment, adequate treatment, treatment without medication, or treatment including medication compared to no treatment, and symptoms were higher after treatment including medication versus treatment without medication. In addition, among persons with major depressive disorder, symptoms were higher after inadequate treatment, adequate treatment, or treatment including medication compared to no treatment, and symptoms were higher after treatment including medication versus treatment without medication.
These findings show that symptoms were more sharply elevated 9 years following treatment including medication than treatment without medication, and major depressive disorder severity plus other covariates did not account for increased depression after medication. Patient characteristics accounted for symptoms after treatment without medication, however. This pattern suggests possible long-term iatrogenic effects of antidepressants.
iatrogenic
adjective
relating to illness caused by medical examination or treatment.
An investigation published in the current issue of Psychotherapy and Psychosomatics indicates that mindfulness based cognitive therapy (MBCT) is most helpful when antidepressant drugs are not used.
Antidepressant medication (AD) is the most often used treatment for major depressive disorder (MDD), prescribed to an estimated 73.8% of the MDD patients in care in 2007. However, many patients with MDD who experience full symptomatic remission after AD treatment still have residual depressive symptoms, which have been associated with continued impaired functioning.
The sequential addition of psychotherapy to pharmacotherapy has therefore been considered, and shown, to offer a better possibility of improving long-term outcome in terms of reduced relapse/recurrence.
Dr. Bakker and colleagues explored this question in a randomized controlled trial of mindfulness-based cognitive therapy (MBCT) versus a waiting list control group (WLCG), based upon which it was previously shown that MBCT increases positive affect in people with residual depressive symptoms.
Their findings showed that sequentially adding psychotherapy to AD in the treatment of residual depressive symptoms seems beneficial in that it both decreases negative affects and increases positive affects. However, in terms of positive affects, the group that showed the largest increase were the participants without AD who received MBCT treatment. Since the generation of positive emotions is crucial in the initiation of a positive spiral towards recovery, long-term outcomes of this contingent inhibiting effect of AD on psychotherapy outcome in terms of positive affects will have to be investigated in more detail in experimental set-ups.
If these findings are replicated it would implicate that the sequential addition of psychotherapy to AD could be less efficient than discontinuing AD before/during receiving psychotherapy especially for improving long-term outcomes.
One traditional hypothesis of depression is that people who are depressed have a deficiency in monoamine neurotransmitters in the body, which leads to low levels of neurotransmitters like serotonin and norephinephrine in the brain. But growing evidence supports that at least some forms of depression may also be linked to ongoing low-grade inflammation in the body.
Previous studies have linked depression with higher level of inflammatory markers compared to people who are not depressed. When people are given proinflammatory cytokines, people experience more symptoms of depression and anxiety. Chronically higher levels of inflammation due to medical illnesses are also associated with higher rates of depression. Even brain imaging of people with depression show that their brain scans have increased neuroinflammation. When your body is in an inflammatory state fighting off the common cold or flu, you can experience symptoms overlapping with depression— disrupted sleep, depressed mood, fatigue, foggy-headedness, and impaired concentration.
A new study published in The Journal of Clinical Psychiatry supports the premise that increased inflammation may play a role in depression. The large study examined data from 14,275 people who were interviewed between 2007 and 2012 using the Patient Health Questionnaire (PHQ-9) to screen for depression and had blood samples drawn. They found that people who had depression had 46% higher levels of C-reactive protein (CRP), a marker of inflammatory disease, in their blood samples. The study was only able to establish an association between depression and inflammation but not causation, though it confirms the association of depression with high levels of inflammation as measured through CRP.
The theory that depression may be viewed as a psychoneuroimmunological disorder can also help explain why efforts to reduce chronic inflammation in the body also improves and helps prevent depression.
I Don’t Really Believe It, but I Say It to Patients Anyway
Psychiatrist Daniel Carlat is a practicing psychiatrist, a clinical instructor at Tufts University, and editor of The Carlat Psychiatry Report, which we have read for years. On July 13, 2010, he appeared on National Public Radio (NPR; Davies, 2010) to promote his book, Unhinged (2010), in which he describes psychiatry as a profession in crisis. Carlat had received some attention in The New York Times, candidly reporting his experience pitching venlafaxine(Effexor) to other doctors as a paid consultant for Wyeth. He found himself “tweaking and pruning the truth to stay positive about the product†and eventually resigned (Carlat, 2007).
We find that Carlat is unusually transparent, providing interesting insights into uncomfortable issues. Carlat was asked what we know about psychiatric medication. He responded:
What we don’t know, is we don’t know how the medications actually work in the brain. . . . I’ll often say something like the way Zoloft works, is, it increases the level of serotonin in your brain (or synapses, neurons), and, presumably, the reason you’re depressed or anxious is that you have some sort of a deficiency. And I say that [chuckles] not because I really believe it, because I know the evidence really isn’t there for us to understand the mechanism—I think I say that because patients want to know something. And they want to know that we as physicians have some basic understanding of what we’re doing when we’re prescribing medications. They certainly don’t want to know that a psychiatrist essentially has no idea how these medications work. (Davies, 2010)
This is surely a remarkable public admission.
I wouldn't be surprised if there were multiple causes of depression for different people. Meds might help some,but not other.