This peer review discussion has been closed.
I've listed this article for peer review because I plan to work on this for FA once the
amphetamine FAC closes and I
finish editing this article and GA nominate it (I'll probably work on
ADD for GA as well). I'd just like some input from others on potential improvements to style, citations, and scope/coverage. I plan to use the feedback from this review as, more or less, a to-do list for when I'm ready to work on the article.
I just took a very quick glance, and think it is going to take a sustained effort to bring this article close to FA standards. Sometime since the last time I looked, some poorly sourced text calling
Tourette syndrome a "rare" (not) disorder crept in, and
tics were called "nervous" tics. The relationship between ADHD and TS is the subject of scores and scores of journal reviews, and is basically not covered here, and the contentious relationship isn't adequately covered in the faulty info from the NIH factsheet. There is scant coverage of the serious amount of information known about the neuropsych profile associated with ADHD, and the Treatment section is cursory at best. Prognosis also needs a lot more beef. To work this article up, someone needs to get hold of several dozen good reviews, and the article will need to depend on
summary style, with multiple sub-articles. "Rare" disorder, "nervous" tics ... the NIH has long had bad information on their factsheet pages, and this has been discussed several times at WT:MED-- ditch them-- there are so many high-quality secondary reviews that sources like that shouldn't be used.
SandyGeorgia (
Talk) 14:29, 18 January 2014 (UTC)reply
I expect to have my work cut out for me, but have a ton of relevant reviews and meta-analyses on ADHD or stimulants for ADHD that I plan to use from work on other articles.
Seppi333 (
Insert 2¢) 21:04, 18 January 2014 (UTC)reply
Notes (to self) by Seppi333 on potential sources for inclusion
Please add new comments/sections above this section.
Notes
Note to self:convert month and year to date
This section is mostly just for my convenience for reference and as a pre-formatted source list. I plan to use some/all of these later (this list will expand):
Relevant general material on ADHD or ADHD stimulants from
Amphetamine#medical
^Malenka RC, Nestler EJ, Hyman SE (2009). "???". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. ???.
ISBN9780071481274.
^Chavez B, Sopko MA, Ehret MJ, Paulino RE, Goldberg KR, Angstadt K, Bogart GT (June 2009). "An update on central nervous system stimulant formulations in children and adolescents with attention-deficit/hyperactivity disorder". Ann Pharmacother. 43 (6): 1084–1095.
doi:
10.1345/aph.1L523.
PMID19470858.
^Kidd PM (September 2007). "Omega-3 DHA and EPA for cognition, behavior, and mood: clinical findings and structural-functional synergies with cell membrane phospholipids". Altern Med Rev. 12 (3): 207–227.
PMID18072818.
^Brown CM, Austin DW (2011). "Autistic disorder and phospholipids: A review". Prostaglandins Leukot. Essent. Fatty Acids. 84 (1–2): 25–30.
doi:
10.1016/j.plefa.2010.09.007.
PMID20970971.
^Manor, I; Magen, A; Keidar, D; Rosen, S; Tasker, H; Cohen, T; Richter, Y; Zaaroor-Regev, D; Manor, Y; Weizman, A (Jul 2012). "The effect of phosphatidylserine containing Omega3 fatty-acids on attention-deficit hyperactivity disorder symptoms in children: a double-blind placebo-controlled trial, followed by an open-label extension". European psychiatry : the journal of the Association of European Psychiatrists. 27 (5): 335–342.
PMID21807480.{{
cite journal}}: CS1 maint: multiple names: authors list (
link)
^Vaisman N, Kaysar N, Zaruk-Adasha Y, Pelled D, Brichon G, Zwingelstein G, Bodennec J (May 2008). "Correlation between changes in blood fatty acid composition and visual sustained attention performance in children with inattention: effect of dietary n-3 fatty acids containing phospholipids". Am. J. Clin. Nutr. 87 (5): 1170–1180.
PMID18469236.
^Hirayama S, Terasawa K, Rabeler R, Hirayama T, Inoue T, Tatsumi Y, Purpura M, Jäger R (March 2013). "The effect of phosphatidylserine administration on memory and symptoms of attention-deficit hyperactivity disorder: a randomised, double-blind, placebo-controlled clinical trial". J Hum Nutr Diet.
doi:
10.1111/jhn.12090.
PMID23495677.
^Manor I, Magen A, Keidar D, Rosen S, Tasker H, Cohen T, Richter Y, Zaaroor-Regev D, Manor Y, Weizman A (July 2012). "The effect of phosphatidylserine containing Omega3 fatty-acids on attention-deficit hyperactivity disorder symptoms in children: a double-blind placebo-controlled trial, followed by an open-label extension". Eur. Psychiatry. 27 (5): 335–342.
doi:
10.1016/j.eurpsy.2011.05.004.
PMID21807480.
^See the first three sources in the next section (expand the collapse tab)
Every primary source in this paragraph could be replaced with one of the following 3 reviews:[1][2][3]
In individuals with ADHD, there is significant evidence that
phenethylamine (PEA) – an endogenous amphetamine homologue with analogous dopaminergic
pharmacodynamics[4][5] – metabolism is reduced compared to healthy individuals.[6][7][8] It is well documented that urinary excretion of PEA increases following administration of amphetamine and
methylphenidate, and that urinary excretion of these drugs is highly correlated with urinary excretion of PEA;[9][10][11]moreover, studies on rodents show that brain PEA biosynthesis and metabolism greatly increases following amphetamine administration at therapeutic doses.[12][13] There is also evidence that pharmacological depletion of PEA blocks the stimulant effects of amphetamine, suggesting that endogenous PEA plays an important role in mediating the effects of amphetamines.[14][15](Note to self: Update the text of the struck-out clauses to current evidence on humans from these reviews)
References
^Berry, MD (Jan 2007). "The potential of trace amines and their receptors for treating neurological and psychiatric diseases". Reviews on recent clinical trials. 2 (1): 3–19.
PMID18473983. changes in trace amines, in particular PE [phenethylamine], have been identified as a possible factor for the onset of attention deficit/hyperactivity disorder (ADHD) [5, 27, 43, 78].
^Miller, GM (Jan 2011). "The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity". Journal of neurochemistry. 116 (2): 164–176.
PMID21073468. TAARs as potential drug targets for the treatment of psychiatric disorders The dysregulation of TA levels has been linked to several diseases, which highlights the corresponding members of the TAAR family as potential targets for drug development. In this article, we focus on the relevance of TAs and their receptors to nervous system-related disorders, namely schizophrenia and depression; however, TAs have also been linked to other diseases such as migraine, attention deficit hyperactivity disorder, substance abuse and eating disorders [7,8,36]. ... b-PEA has been referred to as the body's 'endogenous amphetamine' [39] ... More direct evidence has been obtained recently for a role of trace amines in ADHD. Urinary PE levels have been reported to be decreased in ADHD patients in comparison to both controls and patients with autism [103-105]. Evidence for a decrease in PE levels in the brain of ADHD patients has also recently been reported [4]. In addition, decreases in the urine and plasma levels of the PE metabolite phenylacetic acid and the precursors phenylalanine and tyrosine have been reported along with decreases in plasma tyramine [103].
^Nielsen, JA (7 Nov 1983). "Differential effects of d-amphetamine, beta-phenylethylamine, cocaine and methylphenidate on the rate of dopamine synthesis in terminals of nigrostriatal and mesolimbic neurons and on the efflux of dopamine metabolites into cerebroventricular perfusates of rats". Life sciences. 33 (19): 1899–907.
doi:
10.1016/0024-3205(83)90674-4.
PMID6645784. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Parker, EM (Apr 1988). "Comparative effects of amphetamine, phenylethylamine and related drugs on dopamine efflux, dopamine uptake and mazindol binding". The Journal of pharmacology and experimental therapeutics. 245 (1): 199–210.
PMID3129549. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Matsuishi, T (May 1999). "[Neurochemical and neurotransmitter studies in patients with learning disabilities]". No to hattatsu. Brain and development. 31 (3): 245–8.
PMID10355264. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Kusaga, A (May 2002). "[Decreased beta-phenylethylamine in urine of children with attention deficit hyperactivity disorder and autistic disorder]". No to hattatsu. Brain and development. 34 (3): 243–8.
PMID12030014.
^Kusaga, A (Sep 2002). "Increased urine phenylethylamine after methylphenidate treatment in children with ADHD". Annals of neurology. 52 (3): 372–4.
doi:
10.1002/ana.10302.
PMID12205654. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Zametkin, AJ (Mar 1985). "Stimulants, urinary catecholamines, and indoleamines in hyperactivity. A comparison of methylphenidate and dextroamphetamine". Archives of general psychiatry. 42 (3): 251–5.
doi:
10.1001/archpsyc.1985.01790260045005.
PMID2579615. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Zametkin, AJ (Sep 1984). "Urinary phenethylamine response to d-amphetamine in 12 boys with attention deficit disorder". The American journal of psychiatry. 141 (9): 1055–8.
PMID6380319. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Karoum, F (Sep–Oct 1997). "Effects of the administration of amphetamine, either alone or in combination with reserpine or cocaine, on regional brain beta-phenylethylamine and dopamine release". American journal of therapeutics. 4 (9–10): 333–42.
doi:
10.1097/00045391-199709000-00009.
PMID10423628. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Borison, RL (Nov 1974 15). "Biosynthesis of brain 2-phenylethylamine: influence of decarboxylase inhibitors and D-amphetamine". Life sciences. 15 (10): 1837–48.
doi:
10.1016/0024-3205(74)90185-4.
PMID4620995. {{
cite journal}}: Check date values in: |date= (
help); Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Borison, RL (15 Oct 1975). "Brain 2-phenylethylamine as a major mediator for the central actions of amphetamine and methylphenidate". Life sciences. 17 (8): 1331–43.
doi:
10.1016/0024-3205(75)90147-2.
PMID1196013. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Hirano, M (Dec 1989). "[beta-Phenylethylamine and amphetamine: similar aspects in their behavioropharmacological and neurochemical characteristics]". Yakubutsu, seishin, kodo = Japanese journal of psychopharmacology. 9 (4): 335–48.
PMID2698018. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
This peer review discussion has been closed.
I've listed this article for peer review because I plan to work on this for FA once the
amphetamine FAC closes and I
finish editing this article and GA nominate it (I'll probably work on
ADD for GA as well). I'd just like some input from others on potential improvements to style, citations, and scope/coverage. I plan to use the feedback from this review as, more or less, a to-do list for when I'm ready to work on the article.
I just took a very quick glance, and think it is going to take a sustained effort to bring this article close to FA standards. Sometime since the last time I looked, some poorly sourced text calling
Tourette syndrome a "rare" (not) disorder crept in, and
tics were called "nervous" tics. The relationship between ADHD and TS is the subject of scores and scores of journal reviews, and is basically not covered here, and the contentious relationship isn't adequately covered in the faulty info from the NIH factsheet. There is scant coverage of the serious amount of information known about the neuropsych profile associated with ADHD, and the Treatment section is cursory at best. Prognosis also needs a lot more beef. To work this article up, someone needs to get hold of several dozen good reviews, and the article will need to depend on
summary style, with multiple sub-articles. "Rare" disorder, "nervous" tics ... the NIH has long had bad information on their factsheet pages, and this has been discussed several times at WT:MED-- ditch them-- there are so many high-quality secondary reviews that sources like that shouldn't be used.
SandyGeorgia (
Talk) 14:29, 18 January 2014 (UTC)reply
I expect to have my work cut out for me, but have a ton of relevant reviews and meta-analyses on ADHD or stimulants for ADHD that I plan to use from work on other articles.
Seppi333 (
Insert 2¢) 21:04, 18 January 2014 (UTC)reply
Notes (to self) by Seppi333 on potential sources for inclusion
Please add new comments/sections above this section.
Notes
Note to self:convert month and year to date
This section is mostly just for my convenience for reference and as a pre-formatted source list. I plan to use some/all of these later (this list will expand):
Relevant general material on ADHD or ADHD stimulants from
Amphetamine#medical
^Malenka RC, Nestler EJ, Hyman SE (2009). "???". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. ???.
ISBN9780071481274.
^Chavez B, Sopko MA, Ehret MJ, Paulino RE, Goldberg KR, Angstadt K, Bogart GT (June 2009). "An update on central nervous system stimulant formulations in children and adolescents with attention-deficit/hyperactivity disorder". Ann Pharmacother. 43 (6): 1084–1095.
doi:
10.1345/aph.1L523.
PMID19470858.
^Kidd PM (September 2007). "Omega-3 DHA and EPA for cognition, behavior, and mood: clinical findings and structural-functional synergies with cell membrane phospholipids". Altern Med Rev. 12 (3): 207–227.
PMID18072818.
^Brown CM, Austin DW (2011). "Autistic disorder and phospholipids: A review". Prostaglandins Leukot. Essent. Fatty Acids. 84 (1–2): 25–30.
doi:
10.1016/j.plefa.2010.09.007.
PMID20970971.
^Manor, I; Magen, A; Keidar, D; Rosen, S; Tasker, H; Cohen, T; Richter, Y; Zaaroor-Regev, D; Manor, Y; Weizman, A (Jul 2012). "The effect of phosphatidylserine containing Omega3 fatty-acids on attention-deficit hyperactivity disorder symptoms in children: a double-blind placebo-controlled trial, followed by an open-label extension". European psychiatry : the journal of the Association of European Psychiatrists. 27 (5): 335–342.
PMID21807480.{{
cite journal}}: CS1 maint: multiple names: authors list (
link)
^Vaisman N, Kaysar N, Zaruk-Adasha Y, Pelled D, Brichon G, Zwingelstein G, Bodennec J (May 2008). "Correlation between changes in blood fatty acid composition and visual sustained attention performance in children with inattention: effect of dietary n-3 fatty acids containing phospholipids". Am. J. Clin. Nutr. 87 (5): 1170–1180.
PMID18469236.
^Hirayama S, Terasawa K, Rabeler R, Hirayama T, Inoue T, Tatsumi Y, Purpura M, Jäger R (March 2013). "The effect of phosphatidylserine administration on memory and symptoms of attention-deficit hyperactivity disorder: a randomised, double-blind, placebo-controlled clinical trial". J Hum Nutr Diet.
doi:
10.1111/jhn.12090.
PMID23495677.
^Manor I, Magen A, Keidar D, Rosen S, Tasker H, Cohen T, Richter Y, Zaaroor-Regev D, Manor Y, Weizman A (July 2012). "The effect of phosphatidylserine containing Omega3 fatty-acids on attention-deficit hyperactivity disorder symptoms in children: a double-blind placebo-controlled trial, followed by an open-label extension". Eur. Psychiatry. 27 (5): 335–342.
doi:
10.1016/j.eurpsy.2011.05.004.
PMID21807480.
^See the first three sources in the next section (expand the collapse tab)
Every primary source in this paragraph could be replaced with one of the following 3 reviews:[1][2][3]
In individuals with ADHD, there is significant evidence that
phenethylamine (PEA) – an endogenous amphetamine homologue with analogous dopaminergic
pharmacodynamics[4][5] – metabolism is reduced compared to healthy individuals.[6][7][8] It is well documented that urinary excretion of PEA increases following administration of amphetamine and
methylphenidate, and that urinary excretion of these drugs is highly correlated with urinary excretion of PEA;[9][10][11]moreover, studies on rodents show that brain PEA biosynthesis and metabolism greatly increases following amphetamine administration at therapeutic doses.[12][13] There is also evidence that pharmacological depletion of PEA blocks the stimulant effects of amphetamine, suggesting that endogenous PEA plays an important role in mediating the effects of amphetamines.[14][15](Note to self: Update the text of the struck-out clauses to current evidence on humans from these reviews)
References
^Berry, MD (Jan 2007). "The potential of trace amines and their receptors for treating neurological and psychiatric diseases". Reviews on recent clinical trials. 2 (1): 3–19.
PMID18473983. changes in trace amines, in particular PE [phenethylamine], have been identified as a possible factor for the onset of attention deficit/hyperactivity disorder (ADHD) [5, 27, 43, 78].
^Miller, GM (Jan 2011). "The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity". Journal of neurochemistry. 116 (2): 164–176.
PMID21073468. TAARs as potential drug targets for the treatment of psychiatric disorders The dysregulation of TA levels has been linked to several diseases, which highlights the corresponding members of the TAAR family as potential targets for drug development. In this article, we focus on the relevance of TAs and their receptors to nervous system-related disorders, namely schizophrenia and depression; however, TAs have also been linked to other diseases such as migraine, attention deficit hyperactivity disorder, substance abuse and eating disorders [7,8,36]. ... b-PEA has been referred to as the body's 'endogenous amphetamine' [39] ... More direct evidence has been obtained recently for a role of trace amines in ADHD. Urinary PE levels have been reported to be decreased in ADHD patients in comparison to both controls and patients with autism [103-105]. Evidence for a decrease in PE levels in the brain of ADHD patients has also recently been reported [4]. In addition, decreases in the urine and plasma levels of the PE metabolite phenylacetic acid and the precursors phenylalanine and tyrosine have been reported along with decreases in plasma tyramine [103].
^Nielsen, JA (7 Nov 1983). "Differential effects of d-amphetamine, beta-phenylethylamine, cocaine and methylphenidate on the rate of dopamine synthesis in terminals of nigrostriatal and mesolimbic neurons and on the efflux of dopamine metabolites into cerebroventricular perfusates of rats". Life sciences. 33 (19): 1899–907.
doi:
10.1016/0024-3205(83)90674-4.
PMID6645784. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Parker, EM (Apr 1988). "Comparative effects of amphetamine, phenylethylamine and related drugs on dopamine efflux, dopamine uptake and mazindol binding". The Journal of pharmacology and experimental therapeutics. 245 (1): 199–210.
PMID3129549. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Matsuishi, T (May 1999). "[Neurochemical and neurotransmitter studies in patients with learning disabilities]". No to hattatsu. Brain and development. 31 (3): 245–8.
PMID10355264. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Kusaga, A (May 2002). "[Decreased beta-phenylethylamine in urine of children with attention deficit hyperactivity disorder and autistic disorder]". No to hattatsu. Brain and development. 34 (3): 243–8.
PMID12030014.
^Kusaga, A (Sep 2002). "Increased urine phenylethylamine after methylphenidate treatment in children with ADHD". Annals of neurology. 52 (3): 372–4.
doi:
10.1002/ana.10302.
PMID12205654. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Zametkin, AJ (Mar 1985). "Stimulants, urinary catecholamines, and indoleamines in hyperactivity. A comparison of methylphenidate and dextroamphetamine". Archives of general psychiatry. 42 (3): 251–5.
doi:
10.1001/archpsyc.1985.01790260045005.
PMID2579615. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Zametkin, AJ (Sep 1984). "Urinary phenethylamine response to d-amphetamine in 12 boys with attention deficit disorder". The American journal of psychiatry. 141 (9): 1055–8.
PMID6380319. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Karoum, F (Sep–Oct 1997). "Effects of the administration of amphetamine, either alone or in combination with reserpine or cocaine, on regional brain beta-phenylethylamine and dopamine release". American journal of therapeutics. 4 (9–10): 333–42.
doi:
10.1097/00045391-199709000-00009.
PMID10423628. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Borison, RL (Nov 1974 15). "Biosynthesis of brain 2-phenylethylamine: influence of decarboxylase inhibitors and D-amphetamine". Life sciences. 15 (10): 1837–48.
doi:
10.1016/0024-3205(74)90185-4.
PMID4620995. {{
cite journal}}: Check date values in: |date= (
help); Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Borison, RL (15 Oct 1975). "Brain 2-phenylethylamine as a major mediator for the central actions of amphetamine and methylphenidate". Life sciences. 17 (8): 1331–43.
doi:
10.1016/0024-3205(75)90147-2.
PMID1196013. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
^Hirano, M (Dec 1989). "[beta-Phenylethylamine and amphetamine: similar aspects in their behavioropharmacological and neurochemical characteristics]". Yakubutsu, seishin, kodo = Japanese journal of psychopharmacology. 9 (4): 335–48.
PMID2698018. {{
cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (
help)
