Talk:Antidepressants: Difference between revisions

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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~~ ==

== Major types ==

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

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

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* Tricyclic antidepressants ('''TCAs''')

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

==Types of antidepressants==

===Serotonergics===

====Serotonin reuptake inhibitors====

[[Dextromethorphan]]<ref>http://www.sciencedirect.com/science/article/pii/S0306987711000545</ref>

Because dextromethorphan can show similar antidepressant effects to ketamine in low doses (compared to common recreational doses), it is possible that dextromethorphan could be a possible treatment for treatment-resistant and severe depression. Many users of dextromethorphan claim that they do not feel any depression within a week of using dextromethorphan.{{citation needed}} It has a very similar mechanism of action to SSRIs. It is also useful for anxiety.

====Selective serotonin reuptake inhibitors ([[SSRIs]])====

:Selective serotonin reuptake inhibitors are believed to increase the level of extracellular [[serotonin]], therefore allowing more serotonin to be in the brain. The reason SSRIs are used for depression is that the serotonin hypothesis, one of the most commonly accepted theories for depression, states that low serotonin in the brain causes depression. SSRIs are the most commonly prescribed antidepressant, and the most commonly prescribed anxiolytic for children. They are also the first-line treatment for panic disorder, not benzodiazepines like lorazepam and alprazolam.

====Selective serotonin reuptake enhancers (SSREs)====

====[[Serotonin-norepinephrine reuptake inhibitors]] (SNRIs)====

====Serotonin modulators and stimulators (SMSes)====

====Serotonin antagonists and reuptake inhibitors (SARIs)====

====Serotonin releasing agents (SRAs)====

These agents work by directly increasing the amount of serotonin in the brain. Substances such as [[cocaine]] and [[MDMA]] can do this, but both are addictive and tolerance quickly builds to each. Additionally, the MDMA "comedown" can produce weeks to months of a low mood and motivation if the user "rolls" (doses) frequently and suddenly stops.

===Norepinephrine reuptake inhibitors (NRIs)===

NRIs are believed to increase the level of extracellular [[norepinephrine]], therefore allowing more of it to be in the brain. Controversy has been sparked over the effectiveness of reboxetine, an NRI sold as Trintellix. <ref>"Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis." Multiple authors (2009) https://www.researchgate.net/profile/Andrea_Cipriani/publication/23967068_Comparative_efficacy_and_acceptability_of_12_new-generation_antidepressants_A_multiple-treatments_meta-analysis/links/00b7d5278b5bed4c17000000.pdf</ref>

===Norepinephrine-dopamine reuptake inhibitors (NDRIs)===

NDRIs are believed to increase the level of extracellular [[norepinephrine]] and [[dopamine]], therefore allowing more of these to be in the brain. Agents such as bupropion (Wellbutrin) have been found effective for MDD with little direct effect on serotonin, and therefore it can be hypothesized that other agents are effective for it. Bupropion and other NDRIs are also effective for depression with fatigue or sleepiness.

===Tricyclic antidepressants (TCAs)===

===Tetracyclic antidepressants (TeCAs)===

===Monoamine oxidase inhibitors ([[MAOI]]s)===

MAOIs are usually prescribed when no other antidepressants are helping. This is because MAOIs require diet changes and have a very large amount of side effects.<ref>http://www.mayoclinic.org/diseases-conditions/depression/in-depth/maois/art-20043992</ref>

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

==Psychedelics for treating depression==

===[[Psilocybin mushrooms]] ("Magic mushrooms")===

===[[Ketamine]]===

In clinical studies, ketamine has proven to be an extremely effective and fast acting antidepressant at low doses (compared to common recreational doses).<ref>https://www.nimh.nih.gov/about/strategic-planning-reports/highlights/highlight-ketamine-a-new-and-faster-path-to-treating-depression.shtml</ref> It has become increasingly common for doctors to prescribe ketamine for treatment-resistant and severe depression.

===[[LSD]]===

== Adverse effects ==

@@ Line 19: / Line 19: @@
 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 ==
+== Major types ==
 * [[Selective serotonin reuptake inhibitor]]s ('''SSRIs''')
 * [[Serotonin–norepinephrine reuptake inhibitor]]s ('''SNRIs''')
@@ Line 26: / Line 26: @@
 * Tricyclic antidepressants ('''TCAs''')
 * Tetracyclic antidepressants ('''TeCAs''')
+==Types of antidepressants==
+===Serotonergics===
+====Serotonin reuptake inhibitors====
+[[Dextromethorphan]]<ref>http://www.sciencedirect.com/science/article/pii/S0306987711000545</ref>
+Because dextromethorphan can show similar antidepressant effects to ketamine in low doses (compared to common recreational doses), it is possible that dextromethorphan could be a possible treatment for treatment-resistant and severe depression. Many users of dextromethorphan claim that they do not feel any depression within a week of using dextromethorphan.{{citation needed}} It has a very similar mechanism of action to SSRIs. It is also useful for anxiety.
+====Selective serotonin reuptake inhibitors ([[SSRIs]])====
+:Selective serotonin reuptake inhibitors are believed to increase the level of extracellular [[serotonin]], therefore allowing more serotonin to be in the brain. The reason SSRIs are used for depression is that the serotonin hypothesis, one of the most commonly accepted theories for depression, states that low serotonin in the brain causes depression. SSRIs are the most commonly prescribed antidepressant, and the most commonly prescribed anxiolytic for children. They are also the first-line treatment for panic disorder, not benzodiazepines like lorazepam and alprazolam.
+====Selective serotonin reuptake enhancers (SSREs)====
+====[[Serotonin-norepinephrine reuptake inhibitors]] (SNRIs)====
+====Serotonin modulators and stimulators (SMSes)====
+====Serotonin antagonists and reuptake inhibitors (SARIs)====
+====Serotonin releasing agents (SRAs)====
+These agents work by directly increasing the amount of serotonin in the brain. Substances such as [[cocaine]] and [[MDMA]] can do this, but both are addictive and tolerance quickly builds to each. Additionally, the MDMA "comedown" can produce weeks to months of a low mood and motivation if the user "rolls" (doses) frequently and suddenly stops.
+===Norepinephrine reuptake inhibitors (NRIs)===
+NRIs are believed to increase the level of extracellular [[norepinephrine]], therefore allowing more of it to be in the brain. Controversy has been sparked over the effectiveness of reboxetine, an NRI sold as Trintellix. <ref>"Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis." Multiple authors (2009) https://www.researchgate.net/profile/Andrea_Cipriani/publication/23967068_Comparative_efficacy_and_acceptability_of_12_new-generation_antidepressants_A_multiple-treatments_meta-analysis/links/00b7d5278b5bed4c17000000.pdf</ref>
+===Norepinephrine-dopamine reuptake inhibitors (NDRIs)===
+NDRIs are believed to increase the level of extracellular [[norepinephrine]] and [[dopamine]], therefore allowing more of these to be in the brain. Agents such as bupropion (Wellbutrin) have been found effective for MDD with little direct effect on serotonin, and therefore it can be hypothesized that other agents are effective for it. Bupropion and other NDRIs are also effective for depression with fatigue or sleepiness.
+===Tricyclic antidepressants (TCAs)===
+===Tetracyclic antidepressants (TeCAs)===
+===Monoamine oxidase inhibitors ([[MAOI]]s)===
+MAOIs are usually prescribed when no other antidepressants are helping. This is because MAOIs require diet changes and have a very large amount of side effects.<ref>http://www.mayoclinic.org/diseases-conditions/depression/in-depth/maois/art-20043992</ref>
+===Reversible monoamine oxidase A inhibitors ('''rMAO-AI''')===
+==Psychedelics for treating depression==
+===[[Psilocybin mushrooms]] ("Magic mushrooms")===
+===[[Ketamine]]===
+In clinical studies, ketamine has proven to be an extremely effective and fast acting antidepressant at low doses (compared to common recreational doses).<ref>https://www.nimh.nih.gov/about/strategic-planning-reports/highlights/highlight-ketamine-a-new-and-faster-path-to-treating-depression.shtml</ref> It has become increasingly common for doctors to prescribe ketamine for treatment-resistant and severe depression.
+===[[LSD]]===
+{{citation needed}}
 == Adverse effects ==