SSRI's May Worsen PTSD Symptoms.

[Ema]

The Food and Drug Administration has already approved a drug called agomelatine that blocks this type of serotonin receptor (5-HT2C) and is used as an antidepressant.

Such a drug might also be useful to treat patients who already suffer from PTSD. These patients' traumatic memories are already consolidated, but some research has shown that when memories are recalled, there is a window of time during which they can be altered and reconsolidated. It may be possible to weaken these memories by using serotonin-blocking drugs to interfere with the reconsolidation process, says Goosens, who plans to begin testing that possibility in animals.

The findings also suggest that the antidepressant Prozac and other selective serotonin reuptake inhibitors (SSRIs), which are commonly given to PTSD patients, likely do not help and may actually worsen their symptoms. Prozac enhances the effects of serotonin by prolonging its exposure to brain cells. While this often helps those suffering from depression, "There's no biological evidence to support the use of SSRIs for PTSD," Goosens says.

"The consolidation of traumatic memories requires this serotonergic cascade and we want to block it, not enhance it," she adds. "This study suggests we should rethink the use of SSRIs in PTSD and also be very careful about how they are used, particularly when somebody is recently traumatized and their memories are still being consolidated, or when a patient is undergoing cognitive behavior therapy where they're recalling the memory of the trauma and the memory is going through the process of reconsolidation."


Story Source:

The above post is reprinted from materials provided by Massachusetts Institute of Technology. Note: Materials may be edited for content and length.

Journal Reference:

1. Michael V. Baratta, Suhasa B. Kodandaramaiah, Patrick E. Monahan, Junmei Yao, Michael D. Weber, Pei-Ann Lin, Barbara Gisabella, Natalie Petrossian, Jose Amat, Kyungman Kim, Aimei Yang, Craig R. Forest, Edward S. Boyden, Ki A. Goosens. Stress enables reinforcement-elicited serotonergic consolidation of fear memory. Biological Psychiatry, 2015; DOI: 10.1016/j.biopsych.2015.06.025

 

[JaimeS]

Hmm, I wonder what this implies about the memories of PWME - who are documented to have higher than usual levels of serotonin in the brain in general.

-J

 

[Ema]

Hmm, I wonder what this implies about the memories of PWME - who are documented to have higher than usual levels of serotonin in the brain in general.

-J

Do you have a link to the research showing higher than usual serotonin levels?

I thought there was still some uncertainty...and it was more about upregulated receptors than absolute serotonin levels.

Experts are split, however, as to whether serotonin levels are high or low in people with chronic fatigue syndrome (CFS or ME/CFS). Some studies show that the problem in ME/CFS may lie in low serotonin-receptor activity, which could mean that the brain isn't using serotonin properly, even if plenty is available. A newer study suggests a possible autoimmune reaction to serotonin.

http://chronicfatigue.about.com/od/treatingfmscfs/a/serotonin.htm

 

[JaimeS]

Definitely could be true for some of us, @Ema . I think that if we are making antibodies to serotonin (as about 2/3 of us seem to, according to the study cited below) then that could account for increased receptor sensitivity. But I know I've also seen studies that say that serotonin, while decreased in the blood, is increased in the CSF. (I can't find it, but maybe someone else remembers? If so, I will cite it below.) Blood serotonin doesn't really tell us much about uptake in the CNS. When I got my blood serotonin and urine serotonin measured, my doctor said that my urine serotonin was more indicative of the system's serotonin.

In receptor sensitivity or overabundance in the brain, selective serotonin blockers may end up being helpful.

Antibodies to serotonin:

Maes, M., Ringel, K., Kubera, M., Anderson, G., Morris, G., Galecki, P., Geffard, M. (2013). In myalgic encephalomyelitis/chronic fatigue syndrome, increased autoimmune activity against 5-HT is associated with immuno-inflammatory pathways and bacterial translocation. Journal of Affective Disorders, 150(2):223-30.

Elevated serotonin in PWME in the CSF:

??? Does anyone else recall where this was?

About 1/3 of PWME benefit from selective serotonin blockers:

Späth, M., Welzel, D., Färber, L. (2000). Treatment of chronic fatigue syndrome with 5-HT3 receptor antagonists-- preliminary results. Scandanavian Journal of Rheumatology Supplemental, 113:72-7.

Increased receptor sensitivity:

Bakheit, A. M., Behan, P. O., Dinan, T. G., Gray, C. E., & O’Keane, V. (1992). Possible upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome. BMJ : British Medical Journal, 304(6833), 1010–1012.

Cleare, A. J., Bearn, J., Allain, T., McGregor, S., Wessley, S., Murray, R.M., O'Keane, V. (1995). Contrasting neuroendocrine responses in depression and chronic fatigue syndrome. Journal of Affective Disorders. 34(4):283-9.

Demitrack, M.A., Gold, P.W., Dale, J.K., Krahn, D.D., Kling, M.A., Straus, S.E. (1992). Plasma and cerebrospinal fluid monoamine metabolism in patients with chronic fatigue syndrome: preliminary findings. Biological psychiatry, 32(12):1065-77.

Sharpe, M., Hawton, K., Clements, A., & Cowen, P. J. (1997). Increased brain serotonin function in men with chronic fatigue syndrome. BMJ : British Medical Journal, 315(7101), 164–165.

On a personal note, when I was tested for serotonin, my blood serotonin was quite low; the urine was dead-center normal. My doc told me that what I had was not a serotonin imbalance (the neuro at Mayo) because the urine serotonin was a much more valid indicator of serotonin in the system.

I've since wondered if low blood serotonin coupled with normal urine excretion implies a high level in the CNS. Unless I am peeing away my serotonin at a greater rate than I am producing it (!) and will eventually have zero serotonin (!!), logically that 'extra' serotonin must be somewhere.

All hypotheses, of course...

-J