2 replies to this topic

[agwoodliffe]

This is in connection with one of my earlier posts.
It has been long thought that cytokines like TNF-a and IFNy positively modulate depressive symptoms. I have attached a scientific study that suggests the opposite.

Extremely confusing.

All I can say is, watch out if you're taking anti-inflammatory drugs like Paracetemol.

Attached Files

•  PNAS-2011-Warner-Schmidt-1104836108.pdf   1.06MB   10 downloads

[nowayout]

Paracetamol (acetaminophen for U.S. readers) is an analgesic but is not much of an anti-inflammatory. It is not considered an NSAID. It is actually supposedly good for existential depression and anxiety (as per a study or two) but I have never felt any benefit from it. It is liver-toxic, though, so it should be used with care.

[chemicalambrosia]

Because p11 has been shown to be both
necessary and sufficient for behavioral antidepressant responses
(7 –9) and IBU potently inhibited antidepressant-induced
increases in p11 (Fig. 2 B), we examined the possibility that IBU
might inhibit the behavioral response to antidepressant drugs.
We tested various classes of antidepressants including SSRIs
(citalopram and fl uoxetine), TCAs (imipramine and de-sipramine), a MAOI (tranylcypromine), and an atypical antidepressant (bupropion) in two well-established mouse models of depression: the tail suspension test (TST) and the forced swim
test (FST). All antidepressants tested signi fi cantly reduced im-mobility time in both the TST [Fig. 4A, interaction antidepressant × NSAID: F
(4, 95)= 6.11,P < 0.001] and the FST [Fig. 4B,
interaction antidepressant × NSAID: F(6, 106)
= 5.07,P < 0.001].IBU significantly attenuated the antidepressant-like effects of
SSRIs in both tests (Fig. 4 A and B). IBU was less effective in
altering the behavioral response to TCAs and failed to alter the
behavioral response to other classes of antidepressant drugs
= 5.07,P < 0.001].
IBU significantly attenuated the antidepressant-like effects of
SSRIs in both tests (Fig. 4 A and B). IBU was less effective in
altering the behavioral response to TCAs and failed to alter the
behavioral response to other classes of antidepressant drugs."

NSAIDs have been reported to increase the efficacy of some
antidepressant treatments, but those reports focus on tricyclic or
noradrenergic antidepressants (30) and not SSRIs. Our data
indicate that the antagonism by NSAIDs of antidepressant
responses is specific for serotonergic antidepressants. It is important to emphasize that the interaction between antidepressants and ant-inflammatory agents appears to be specific to the
efficacy of SSRIs and not a general effect on all classes of anti-depressants. Furthermore, there is no evidence from our studies
that NSAID administration alone has any effect on depressive-like states.

This is the study cited as reference 30:
http://www.ncbi.nlm....pubmed/16491133

The study pretty strongly suggests that SSRI medications are unlikely to work as well when combined with common pain killers. However, other types of antidepressants may be boosted by using anti-inflammatories(per the other study, and lack of interaction in this study). Interesting and useful stuff. It doesn't invalidate what I've been doing, taking tianeptine as well as curcumin,

Paracetamol (acetaminophen for U.S. readers) is an analgesic but is not much of an anti-inflammatory. It is not considered an NSAID. It is actually supposedly good for existential depression and anxiety (as per a study or two) but I have never felt any benefit from it. It is liver-toxic, though, so it should be used with care.

Even though it acknowledges acetaminophen as an analgesic, it still blocked the effects of the SSRI in this study:

To examine the specificity of the effect of IBU on SSRI-induced behavioral changes, we tested the effect of three different NSAIDs and an analgesic on the behavioral response to
citalopram. Mice were treated with IBU (1 mg/mL), naproxen (2
mg/mL), acetylsalicylic acid (3 mg/mL), or acetaminophen (3 mg/
mL) in their drinking water for 5–7 d and received a single injection of citalopram (20 mg/kg, i.p.) or saline before testing in
the TST or FST. All of the drugs tested significantly blocked the
antidepressant effect of citalopram on immobility time i n both tests
(F ig. 4 C and D) c ompared with m ice t hat received citalopram
alone [TST interacti on a ntidepressant × NSAID: F
(6, 129)
=3.25,
P < 0.01; FST interaction antidepressant × NSA ID :F
(6, 106)
=5.07,
P < 0.005].

Sorry for formatting, the copy-paste from .pdf isn't working too well for me.