Talk:Antidepressants: Difference between revisions

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The major classes of antidepressants are the [[selective serotonin reuptake inhibitor]]s ('''SSRIs'''), [[serotonin–norepinephrine reuptake inhibitors]] ('''SNRIs'''), [[MAOI|monoamine oxidase inhibitors]] ('''MAOIs'''), reversible monoamine oxidase A inhibitors ('''rMAO-A inhibitors'''), tetracyclic antidepressants ('''TeCAs'''), and noradrenergic and specific serotonergic antidepressant ('''NaSSAs'''). Herbal substances such as '''St. John's wort''' is also sometimes used in the treatment of depression<ref>Linde, K., Kriston, L., Rucker, G., Jamil, S., Schumann, I., Meissner, K., . . . Schneider, A. (2015). '''''Efficacy and Acceptability of Pharmacological Treatments for Depressive Disorders in Primary Care: Systematic Review and Network Meta-Analysis.''''' ''The Annals of Family Medicine'', 13(1), 69-79. doi:10.1370/afm.1687</ref><ref>Linde, K., Berner, M. M., & Kriston, L. (2008). St John's wort for major depression. ''Cochrane Database of Systematic Reviews''. doi:10.1002/14651858.cd000448.pub3</ref>

~~== Major Types ==~~

* [[Selective serotonin reuptake inhibitor]]s ('''SSRIs''')

* [[Serotonin–norepinephrine reuptake inhibitor]]s ('''SNRIs''')

* Reversible monoamine oxidase A inhibitors ('''rMAO-AI''')

* Monoamine oxidase inhibitors ('''MAOIs''')

* Tetracyclic antidepressants ('''TeCAs''')

~~== Pharmacology ==~~

~~{{stub}}~~

The earliest and probably most widely accepted scientific theory of antidepressant action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the [[monoamine neurotransmitter]]s (namely [[serotonin]], [[norepinephrine]] and [[dopamine]]).<ref name = GG /> It was originally proposed based on the observation that certain hydrazine anti-tuberculosis agents produce antidepressant effects, which was later linked to their inhibitory effects on [[monoamine oxidase]], the enzyme that catalyses the breakdown of the monoamine neurotransmitters.<ref name = GG /> All currently marketed antidepressants have the monoamine hypothesis as their theoretical basis, with the possible exception of agomelatine which acts on a dual [[Melatonin|melatonergic]]-[[Serotonin|serotonergic]] pathway.<ref name = GG /> Despite the success of the monoamine hypothesis it has a number of limitations: for one, all monoaminergic antidepressants have a delayed onset of action of at least a week; and secondly, there are a sizeable portion (>40%) of depressed patients that do not adequately respond to monoaminergic antidepressants.<ref name="Infl">{{cite journal |vauthors=Maes M, Yirmyia R, Noraberg J, Brene S, Hibbeln J, Perini G, Kubera M, Bob P, Lerer B, Maj M | title = The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression | journal = Metabolic Brain Disease | volume = 24 | issue = 1 | pages = 27–53 | date = March 2009 | pmid = 19085093 | doi = 10.1007/s11011-008-9118-1 }}</ref><ref name="glut">{{cite journal |vauthors=Sanacora G, Treccani G, Popoli M | title = Towards a glutamate hypothesis of depression: an emerging frontier of neuropsychopharmacology for mood disorders | journal = Neuropharmacology | volume = 62 | issue = 1 | pages = 63–77 | date = January 2012 | pmid = 21827775 | doi = 10.1016/j.neuropharm.2011.07.036 | pmc=3205453}}</ref> A number of alternative hypotheses have been proposed, including the glutamate, neurogenic, [[Epigenetics|epigenetic]], cortisol hypersecretion and inflammatory hypotheses.<ref name = Infl /><ref name = glut /><ref name="Epig">{{cite journal |vauthors=Menke A, Klengel T, Binder EB | title = Epigenetics, depression and antidepressant treatment | journal = Current Pharmaceutical Design | volume = 18 | issue = 36 | pages = 5879–5889 | year = 2012 | pmid = 22681167 | doi = 10.2174/138161212803523590 }}</ref><ref name="Epig2">{{cite journal |vauthors=Vialou V, Feng J, Robison AJ, Nestler EJ | title = Epigenetic mechanisms of depression and antidepressant action | journal = Annual Review of Pharmacology and Toxicology | volume = 53 | issue = 1 | pages = 59–87 | date = January 2013 | pmid = 23020296 | doi = 10.1146/annurev-pharmtox-010611-134540 }}</ref>

== Clinical Guidelines for Diagnosis and Prescription ==

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The guidelines further note that antidepressant treatment should be used in combination with psychosocial interventions in most cases, should be continued for at least six months to reduce the risk of relapse, and that SSRIs are typically better tolerated than other antidepressants.<ref>http://www.nice.org.uk/guidance/cg90/chapter/key-priorities-for-implementation | Depression in adults: The treatment and management of depression in adults (National Institute for Health and Care Excellence)</ref>

== Pharmacology ==

The earliest and probably most widely accepted scientific theory of antidepressant action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the [[monoamine neurotransmitter]]s (namely [[serotonin]], [[norepinephrine]] and [[dopamine]]).<ref name = GG /> It was originally proposed based on the observation that certain hydrazine anti-tuberculosis agents produce antidepressant effects, which was later linked to their inhibitory effects on [[monoamine oxidase]], the enzyme that catalyses the breakdown of the monoamine neurotransmitters.<ref name = GG /> All currently marketed antidepressants have the monoamine hypothesis as their theoretical basis, with the possible exception of agomelatine which acts on a dual [[Melatonin|melatonergic]]-[[Serotonin|serotonergic]] pathway.<ref name = GG /> Despite the success of the monoamine hypothesis it has a number of limitations: for one, all monoaminergic antidepressants have a delayed onset of action of at least a week; and secondly, there are a sizeable portion (>40%) of depressed patients that do not adequately respond to monoaminergic antidepressants.<ref name="Infl">{{cite journal |vauthors=Maes M, Yirmyia R, Noraberg J, Brene S, Hibbeln J, Perini G, Kubera M, Bob P, Lerer B, Maj M | title = The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression | journal = Metabolic Brain Disease | volume = 24 | issue = 1 | pages = 27–53 | date = March 2009 | pmid = 19085093 | doi = 10.1007/s11011-008-9118-1 }}</ref><ref name="glut">{{cite journal |vauthors=Sanacora G, Treccani G, Popoli M | title = Towards a glutamate hypothesis of depression: an emerging frontier of neuropsychopharmacology for mood disorders | journal = Neuropharmacology | volume = 62 | issue = 1 | pages = 63–77 | date = January 2012 | pmid = 21827775 | doi = 10.1016/j.neuropharm.2011.07.036 | pmc=3205453}}</ref> A number of alternative hypotheses have been proposed, including the glutamate, neurogenic, [[Epigenetics|epigenetic]], cortisol hypersecretion and inflammatory hypotheses.<ref name = Infl /><ref name = glut /><ref name="Epig">{{cite journal |vauthors=Menke A, Klengel T, Binder EB | title = Epigenetics, depression and antidepressant treatment | journal = Current Pharmaceutical Design | volume = 18 | issue = 36 | pages = 5879–5889 | year = 2012 | pmid = 22681167 | doi = 10.2174/138161212803523590 }}</ref><ref name="Epig2">{{cite journal |vauthors=Vialou V, Feng J, Robison AJ, Nestler EJ | title = Epigenetic mechanisms of depression and antidepressant action | journal = Annual Review of Pharmacology and Toxicology | volume = 53 | issue = 1 | pages = 59–87 | date = January 2013 | pmid = 23020296 | doi = 10.1146/annurev-pharmtox-010611-134540 }}</ref>

== Major Types ==

* [[Selective serotonin reuptake inhibitor]]s ('''SSRIs''')

* [[Serotonin–norepinephrine reuptake inhibitor]]s ('''SNRIs''')

* Reversible monoamine oxidase A inhibitors ('''rMAO-AI''')

* Monoamine oxidase inhibitors ('''MAOIs''')

* Tetracyclic antidepressants ('''TeCAs''')

== Adverse effects ==

@@ Line 2: / Line 2: @@
 The major classes of antidepressants are the [[selective serotonin reuptake inhibitor]]s ('''SSRIs'''), [[serotonin–norepinephrine reuptake inhibitors]] ('''SNRIs'''), [[MAOI|monoamine oxidase inhibitors]] ('''MAOIs'''), reversible monoamine oxidase A inhibitors ('''rMAO-A inhibitors'''), tetracyclic antidepressants ('''TeCAs'''), and noradrenergic and specific serotonergic antidepressant ('''NaSSAs'''). Herbal substances such as '''St. John's wort''' is also sometimes used in the treatment of depression<ref>Linde, K., Kriston, L., Rucker, G., Jamil, S., Schumann, I., Meissner, K., . . . Schneider, A. (2015). '''''Efficacy and Acceptability of Pharmacological Treatments for Depressive Disorders in Primary Care: Systematic Review and Network Meta-Analysis.''''' ''The Annals of Family Medicine'', 13(1), 69-79. doi:10.1370/afm.1687</ref><ref>Linde, K., Berner, M. M., & Kriston, L. (2008). St John's wort for major depression. ''Cochrane Database of Systematic Reviews''. doi:10.1002/14651858.cd000448.pub3</ref>
-== Major Types ==
-* [[Selective serotonin reuptake inhibitor]]s ('''SSRIs''')
-* [[Serotonin–norepinephrine reuptake inhibitor]]s ('''SNRIs''')
-* Reversible monoamine oxidase A inhibitors ('''rMAO-AI''')
-* Monoamine oxidase inhibitors ('''MAOIs''')
-* Tetracyclic antidepressants ('''TeCAs''')
-== Pharmacology ==
-{{stub}}
-The earliest and probably most widely accepted scientific theory of antidepressant action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the [[monoamine neurotransmitter]]s (namely [[serotonin]], [[norepinephrine]] and [[dopamine]]).<ref name = GG /> It was originally proposed based on the observation that certain hydrazine anti-tuberculosis agents produce antidepressant effects, which was later linked to their inhibitory effects on [[monoamine oxidase]], the enzyme that catalyses the breakdown of the monoamine neurotransmitters.<ref name = GG /> All currently marketed antidepressants have the monoamine hypothesis as their theoretical basis, with the possible exception of agomelatine which acts on a dual [[Melatonin|melatonergic]]-[[Serotonin|serotonergic]] pathway.<ref name = GG /> Despite the success of the monoamine hypothesis it has a number of limitations: for one, all monoaminergic antidepressants have a delayed onset of action of at least a week; and secondly, there are a sizeable portion (>40%) of depressed patients that do not adequately respond to monoaminergic antidepressants.<ref name="Infl">{{cite journal |vauthors=Maes M, Yirmyia R, Noraberg J, Brene S, Hibbeln J, Perini G, Kubera M, Bob P, Lerer B, Maj M | title = The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression | journal = Metabolic Brain Disease | volume = 24 | issue = 1 | pages = 27–53 | date = March 2009 | pmid = 19085093 | doi = 10.1007/s11011-008-9118-1 }}</ref><ref name="glut">{{cite journal |vauthors=Sanacora G, Treccani G, Popoli M | title = Towards a glutamate hypothesis of depression: an emerging frontier of neuropsychopharmacology for mood disorders | journal = Neuropharmacology | volume = 62 | issue = 1 | pages = 63–77 | date = January 2012 | pmid = 21827775 | doi = 10.1016/j.neuropharm.2011.07.036 | pmc=3205453}}</ref>  A number of alternative hypotheses have been proposed, including the glutamate, neurogenic, [[Epigenetics|epigenetic]], cortisol hypersecretion and inflammatory hypotheses.<ref name = Infl /><ref name = glut /><ref name="Epig">{{cite journal |vauthors=Menke A, Klengel T, Binder EB | title = Epigenetics, depression and antidepressant treatment | journal = Current Pharmaceutical Design | volume = 18 | issue = 36 | pages = 5879–5889 | year = 2012 | pmid = 22681167 | doi = 10.2174/138161212803523590 }}</ref><ref name="Epig2">{{cite journal |vauthors=Vialou V, Feng J, Robison AJ, Nestler EJ | title = Epigenetic mechanisms of depression and antidepressant action | journal = Annual Review of Pharmacology and Toxicology | volume = 53 | issue = 1 | pages = 59–87 | date = January 2013 | pmid = 23020296 | doi = 10.1146/annurev-pharmtox-010611-134540 }}</ref>
 == Clinical Guidelines for Diagnosis and Prescription ==
@@ Line 24: / Line 13: @@
 The guidelines further note that antidepressant treatment should be used in combination with psychosocial interventions in most cases, should be continued for at least six months to reduce the risk of relapse, and that SSRIs are typically better tolerated than other antidepressants.<ref>http://www.nice.org.uk/guidance/cg90/chapter/key-priorities-for-implementation | Depression in adults: The treatment and management of depression in adults (National Institute for Health and Care Excellence)</ref>
+== Pharmacology ==
+{{stub}}
+The earliest and probably most widely accepted scientific theory of antidepressant action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the [[monoamine neurotransmitter]]s (namely [[serotonin]], [[norepinephrine]] and [[dopamine]]).<ref name = GG /> It was originally proposed based on the observation that certain hydrazine anti-tuberculosis agents produce antidepressant effects, which was later linked to their inhibitory effects on [[monoamine oxidase]], the enzyme that catalyses the breakdown of the monoamine neurotransmitters.<ref name = GG /> All currently marketed antidepressants have the monoamine hypothesis as their theoretical basis, with the possible exception of agomelatine which acts on a dual [[Melatonin|melatonergic]]-[[Serotonin|serotonergic]] pathway.<ref name = GG /> Despite the success of the monoamine hypothesis it has a number of limitations: for one, all monoaminergic antidepressants have a delayed onset of action of at least a week; and secondly, there are a sizeable portion (>40%) of depressed patients that do not adequately respond to monoaminergic antidepressants.<ref name="Infl">{{cite journal |vauthors=Maes M, Yirmyia R, Noraberg J, Brene S, Hibbeln J, Perini G, Kubera M, Bob P, Lerer B, Maj M | title = The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression | journal = Metabolic Brain Disease | volume = 24 | issue = 1 | pages = 27–53 | date = March 2009 | pmid = 19085093 | doi = 10.1007/s11011-008-9118-1 }}</ref><ref name="glut">{{cite journal |vauthors=Sanacora G, Treccani G, Popoli M | title = Towards a glutamate hypothesis of depression: an emerging frontier of neuropsychopharmacology for mood disorders | journal = Neuropharmacology | volume = 62 | issue = 1 | pages = 63–77 | date = January 2012 | pmid = 21827775 | doi = 10.1016/j.neuropharm.2011.07.036 | pmc=3205453}}</ref>  A number of alternative hypotheses have been proposed, including the glutamate, neurogenic, [[Epigenetics|epigenetic]], cortisol hypersecretion and inflammatory hypotheses.<ref name = Infl /><ref name = glut /><ref name="Epig">{{cite journal |vauthors=Menke A, Klengel T, Binder EB | title = Epigenetics, depression and antidepressant treatment | journal = Current Pharmaceutical Design | volume = 18 | issue = 36 | pages = 5879–5889 | year = 2012 | pmid = 22681167 | doi = 10.2174/138161212803523590 }}</ref><ref name="Epig2">{{cite journal |vauthors=Vialou V, Feng J, Robison AJ, Nestler EJ | title = Epigenetic mechanisms of depression and antidepressant action | journal = Annual Review of Pharmacology and Toxicology | volume = 53 | issue = 1 | pages = 59–87 | date = January 2013 | pmid = 23020296 | doi = 10.1146/annurev-pharmtox-010611-134540 }}</ref>
+== Major Types ==
+* [[Selective serotonin reuptake inhibitor]]s ('''SSRIs''')
+* [[Serotonin–norepinephrine reuptake inhibitor]]s ('''SNRIs''')
+* Reversible monoamine oxidase A inhibitors ('''rMAO-AI''')
+* Monoamine oxidase inhibitors ('''MAOIs''')
+* Tetracyclic antidepressants ('''TeCAs''')
 == Adverse effects ==