Are SS/NRIs appropriate in any situation?

[Barbarannamated]

IF antidepressants are used, are SS/NRIs ever an appropriate choice? Friend who is Peer Specialist is training in geropsych now and asked me. I know they effect bone density, so increased risk of fractures.

[Altostrata]

Good question. I moved it here because Introductions is only for individual personal topics. I guess we can use this forum for debate and speculation, too.

 

My personal opinion is that newer generation SSRIs, SNRIs, etc. should not be used at all. They are too strong for the human nervous system.

 

In older people, they definitely should not be used, as they increase risk of osteoporosis, diabetes, stroke, etc. -- an older person doesn't need any more risk of those.

 

(Also see Prozac for the elderly 'could be dangerous' about a recent paper in the British Medical Journal, 2011 Antidepressant use and risk of adverse outcomes in older people )

 

Robert Whitaker points out they are beneficial used short-term in acute situations. How an acute situation might be defined, I don't know.

[Barbarannamated]

I was wondering that exact thing when I perused the literature for Viibyd. It struck me that the trials lasted 8 weeks max and prescribing info states that it may take 4-6 weeks to notice improvement. I know that is typical for class, it just jumped out at me. Concerning that they are calling this a SPARI--Serotonin partial agonist and reuptake inhibitor. Sounds like alot of serotonin.

[solida]

After all we know now and the terrible withdrawal we have to endure I just wonder how it comes that in spite of everything soooooo many people have a very good result with SSRIS?????????

 

I know a lot of poeple who take them for years,even stop them take them again or switch without any side effects.

 

 

solida

[Altostrata]

solida, we don't know what the rate of withdrawal syndrome is, or indeed if "most" people switch them with no side effects.

 

This is the problem with anecdotal information. We hear what we hear and that forms our opinion.

 

Yes, perhaps most people quit antidepressants with minor difficulty. But we don't know how large the group is that has difficulty. Is it 10%? Is it 20%?

 

Even if it was 10%, it would still be a highly significant number. In clinical trials, if an severe adverse event occurred in even 1%, the FDA would consider that highly significant.

[alexjuice]

I don't know to be honest.

 

My therapist tells me she was suicidal her entire life with depression and anxiety. She claims effexor literally saved her life, took the gun barrel out of her mouth. She currently takes 150 a day. I don't argue or dispute her belief. Though, of course I doubt it and I worry about her health.

 

That said, I guess I don't feel it's my place to tell her she is wrong. If she really was suicidally, hopelessly miserable, nonresponsive to therapy and other medication but has enjoyed a sustained fulfilling life with acceptable side effects since starting Effexor, well, then I suppose she should get to choose for herself whether to continue or not.

 

What is critical, though, is that the status quo be overturned. Patients need to be fully informed of the risks in more somber way. Doctors need to adopt a more critical posture when evaluating pharmaceutical claims and they need to communicate complexity and uncertainty to patients -- enough with the NAMI cartoons. Sadly, this may not be realistic.

 

Alex.i

[Altostrata]

Exactly. Maybe the risk of diabetes etc. is acceptable to her.

[Baxter]

And the side effects. There are always side effects.

[meistersinger]

I was wondering that exact thing when I perused the literature for Viibyd. It struck me that the trials lasted 8 weeks max and prescribing info states that it may take 4-6 weeks to notice improvement. I know that is typical for class, it just jumped out at me. Concerning that they are calling this a SPARI--Serotonin partial agonist and reuptake inhibitor. Sounds like alot of serotonin.

 

6 to 8 weeks my @$$!!!! After that amount of time I started feeling all the side effects.

 

Incidentally, I was put on antidepressants because I started hearing voices to kill myself, as well as to get a real f^^^^^^ job, go f^^^ yourself, as well as the entire score of Mahler's 8th Symphony. (Wait.. all the top calibre musicians are supposed to hear entire scores in their head!)

[meistersinger]

I don't know to be honest.

 

My therapist tells me she was suicidal her entire life with depression and anxiety. She claims effexor literally saved her life, took the gun barrel out of her mouth. She currently takes 150 a day. I don't argue or dispute her belief. Though, of course I doubt it and I worry about her health.

 

That said, I guess I don't feel it's my place to tell her she is wrong. If she really was suicidally, hopelessly miserable, nonresponsive to therapy and other medication but has enjoyed a sustained fulfilling life with acceptable side effects since starting Effexor, well, then I suppose she should get to choose for herself whether to continue or not.

 

What is critical, though, is that the status quo be overturned. Patients need to be fully informed of the risks in more somber way. Doctors need to adopt a more critical posture when evaluating pharmaceutical claims and they need to communicate complexity and uncertainty to patients -- enough with the NAMI cartoons. Sadly, this may not be realistic.

 

Alex.i

 

An English professor I had as a freshman in college was very mentally ill. I saw her melt down in class. For her, her psychologist was heavy into Jung, which worked for her.

 

I also worked with a girl who told me she could go from 0 to ***** in .3 seconds (and I saw her do it, several times. I thought I cycled through moods quickly. This was another reason I was put on antidepressants, especially when I melted down and cycled in my GP's office during a followup appointment for diabetes.) Again, what may work for me now may not work for me in the future. Now that managed care has thoroughly screwed up the works, who knows if I'll ever be right.

[meistersinger]

http://discovermagazine.com/2001/jul/cover

 

 

 

"I think you have to accept that there's a structural change in your brain when you take drugs like Prozac."

 

And this was published in 2001

[meistersinger]

http://www.wellnessresources.com/studies/effectiveness_of_ssri_antidepressants_reduced_by_anti-inflammatory_drugs

 

This was on a commercial site hawking the owner's business

 

Antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) are attenuated by antiinflammatory drugs in mice and humans

 

Antiinflammatory drugs achieve their therapeutic actions at least in part by regulation of cytokine formation. A “cytokine hypothesis” of depression is supported by the observation that depressed individuals have elevated plasma levels of certain cytokines compared with healthy controls. Here we investigated a possible interaction between antidepressant agents and antiinflammatory agents on antidepressant-induced behaviors and on p11, a biochemical marker of depressive-like states and antidepressant responses. We found that widely used antiinflammatory drugs antagonize both biochemical and behavioral responses to selective serotonin reuptake inhibitors (SSRIs). In contrast to the levels detected in serum, we found that frontal cortical levels of certain cytokines (e.g., TNFα and IFNγ) were increased by serotonergic antidepressants and that these effects were inhibited by antiinflammatory agents. The antagonistic effect of antiinflammatory agents on antidepressant-induced behaviors was confirmed by analysis of a dataset from a large-scale real-world human study, “sequenced treatment alternatives to relieve depression” (STAR*D), underscoring the clinical significance of our findings. Our data indicate that clinicians should carefully balance the therapeutic benefits of antiinflammatory agents versus the potentially negative consequences of antagonizing the therapeutic efficacy of antidepressant agents in patients suffering from depression.

[Altostrata]

From http://discovermagazine.com/2001/jul/cover

 

The Serotonin Surprise

by Gary Greenberg From the July 2001 issue; published online July 1, 2001

 

Glenmullen has long suspected that drugs that alter serotonin metabolism cause profound changes in the brain. He bases his suspicion on a body of research during the last 20 years by scientists investigating another class of drugs that includes MDMA (Ecstasy) as well as fenfluramine, the diet drug recently removed from the market because of its association with heart valve problems. These drugs do more than just block serotonin reuptake; they primarily stimulate the release of large quantities of serotonin from nerve endings into the brain. The resulting flood is thought to cause the mind-altering effects of MDMA. And that flood, some scientists argue, leaves brain damage in its wake. When monkeys and rats are given high doses of serotonin releasers--up to 40 times the dose that people generally take--the microscopic architecture of their brains looks different from normal brains. The nerve fibers (axons) that carry serotonin to the target cells seem to change their shape and diminish in number--effects some scientists claim are properly understood as brain damage.

 

Glenmullen is convinced these results raise questions about other serotonergic drugs like Prozac, and a recent study has only increased his concern. Research conducted by neurologist Madhu Kalia at Jefferson Medical College in Philadelphia and scientists at the Centers for Disease Control and Prevention showed that the rats given very high doses (up to 100 times the human dose, by body weight) of Prozac and Zoloft contained the same kinds of brain abnormalities--neurons with swollen or kinked tips--as rats who were given high doses of serotonin releasers.

 

Jim O'Callaghan, a Centers for Disease Control neuroscientist and a coauthor of the study, doesn't think the results indicate that Prozac causes brain damage. To the contrary, he and his team believe that neither serotonin enhancers nor serotonin releasers are properly understood as neurotoxic. According to O'Callaghan, the point of the study was to show that even a drug like Prozac, which virtually no one claims is neurotoxic, can produce some of the same abnormalities as the serotonin releasers. Other scientists, in his view, have been too quick to "deduce what they think is going on in the [nerve] fibers" from two pieces of data: The serotonin releasers deplete serotonin, and the microphotographs of brains exposed to high doses of these drugs look abnormal. O'Callaghan believes that scientists should rethink their definition of neurotoxicity, because high doses of Prozac and Zoloft, which do not deplete serotonin, cause the same transient abnormalities as do high doses of drugs such as MDMA. (Blair Austin, a spokesperson for Eli Lilly, producer of Prozac, points out that the abnormalities have not been linked to any physiological result. Moreover, he says, based on the high dosage and other conditions of the study, "the findings are only of minor toxicological importance and pose no risk to human safety.")