Niacin: Difference between revisions
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====Other adverse effects==== | ====Other adverse effects==== | ||
High doses of niacin can also cause niacin [[maculopathy]], a thickening of the [[macula]] and [[retina]], which leads to blurred vision and blindness. This maculopathy is reversible after niacin intake ceases.<ref>{{cite journal |vauthors=Domanico D, Verboschi F, Altimari S, Zompatori L, Vingolo EM |title=Ocular Effects of Niacin: A Review of the Literature |journal=Med Hypothesis Discov Innov Ophthalmol |volume=4 |issue=2 |pages=64–71 |date=2015 |pmid=26060832 |pmc=4458328 }}</ref> Niaspan, the slow-release product, has been associated with a reduction in platelet content and a modest increase in prothrombin time.<ref name=Niaspan /> | High doses of niacin can also cause niacin [[maculopathy]], a thickening of the [[macula]] and [[retina]], which leads to blurred vision and blindness. This maculopathy is reversible after niacin intake ceases.<ref>{{cite journal |vauthors=Domanico D, Verboschi F, Altimari S, Zompatori L, Vingolo EM |title=Ocular Effects of Niacin: A Review of the Literature |journal=Med Hypothesis Discov Innov Ophthalmol |volume=4 |issue=2 |pages=64–71 |date=2015 |pmid=26060832 |pmc=4458328 }}</ref> Niaspan, the slow-release product, has been associated with a reduction in platelet content and a modest increase in prothrombin time.<ref name=Niaspan /> | ||
==In schizophenia== | |||
In 1954, researchers [[Abram Hoffer]] and [[Humphry Osmond]] claimed that adrenochrome is a [[neurotoxin|neurotoxic]], [[psychotomimetic]] substance and may play a role in [[schizophrenia]] and other mental illnesses.<ref name="pmid13152519">{{cite journal | last1 = Hoffer | first1 = Abram | author-link1 = Abram Hoffer | last2 = Osmond | first2 = Humphrey | author-link2 = Humphry Osmond | first3 = John | last3 = Smythies| author-link3 = John Raymond Smythies | title = Schizophrenia: A New Approach. II. Result of a Year's Research | journal = [[British Journal of Psychiatry|The Journal of Mental Science]] | volume = 100 | issue = 418 | pages = 29–45 | date = January 1954 | pmid = 13152519 | doi = 10.1192/bjp.100.418.29 | eissn = 1472-1465 | issn = 0007-1250 | lccn = 89649366 | oclc = 1537306 | s2cid = 42531852 | df = dmy-all }}</ref> | |||
In what Hoffer called the "adrenochrome hypothesis",<ref name="Hoffer2">{{cite journal | last1 = Hoffer | first1 = Abram | author-link1 = Abram Hoffer | last2 = Osmond | first2 = Humphrey | author-link2 = Humphry Osmond | title = The Adrenochrome Hypothesis and Psychiatry | url = http://www.orthomolecular.org/library/jom/1999/articles/1999-v14n01-p049.shtml | access-date = 2024-03-15 | journal = [[The Journal of Orthomolecular Medicine]] | volume = 14 | issue = 1 | date = First Quarter 1999 | pages = 49–62 | archive-url = https://web.archive.org/web/20240220043758/http://www.orthomolecular.org/library/jom/1999/articles/1999-v14n01-p049.shtml | archive-date = 2024-02-20 | url-status = live | issn = 0834-4825 | oclc = 15726974 | s2cid = 41468628 | df = dmy-all}}</ref> he and Osmond in 1967 speculated that [[Megavitamin therapy|megadoses]] of [[vitamin C]] and [[niacin (nutrient)|niacin]] could cure schizophrenia by reducing brain adrenochrome.<ref name="hallucinogens">{{cite book | last1 = Hoffer | first1 = Abram | author-link1 = Abram Hoffer | last2 = Osmond | first2 = Humphrey | author-link2 = Humphry Osmond | date = 1968-01-01 | title = The Hallucinogens | url = https://archive.org/details/hallucinogens0000hoff/ | url-access = registration | language = en | edition = First | publisher = [[Academic Press]] | isbn = 978-0123518507 | lccn = 66030086 | oclc = 332437 | ol = OL35255701M | access-date = 2024-03-15 | via = [[Internet Archive]] | quote= | quote-page= | quote-pages= | df = dmy-all}}</ref><ref name=hoffer94>{{cite journal | vauthors = Hoffer A | date = 1994 | title = Schizophrenia: An Evolutionary Defense Against Severe Stress | journal = Journal of Orthomolecular Medicine | volume = 9 | issue = 4 | pages = 205–2221 | url = http://orthomolecular.org/library/jom/1994/pdf/1994-v09n04-p205.pdf }}</ref> | |||
The treatment of schizophrenia with such potent anti-oxidants is highly contested. In 1973, the [[American Psychiatric Association]] reported methodological flaws in Hoffer's work on niacin as a schizophrenia treatment and referred to follow-up studies that did not confirm any benefits of the treatment.<ref name="APA">{{cite web | vauthors = Lipton MA, Ban TA, Kane FJ, Levine J, Mosher LR, Wittenborn R | title = Task Force Report on Megavitamin and Orthomolecular Therapy in Psychiatry | publisher = American Psychiatric Association | year = 1973 | url = https://www.old.quackwatch.org/01QuackeryRelatedTopics/apa_megavitamin.pdf | access-date = 7 September 2020 | archive-date = 23 February 2021 | archive-url = https://web.archive.org/web/20210223194022/https://www.old.quackwatch.org/01QuackeryRelatedTopics/apa_megavitamin.pdf | url-status = dead }}</ref> Multiple additional studies in the United States,<ref name="ArchGenPsy">{{cite journal | doi = 10.1001/archpsyc.1973.01750330010002 |vauthors=Wittenborn JR, Weber ES, Brown M | title = Niacin in the Long-Term Treatment of Schizophrenia | journal = Archives of General Psychiatry | year = 1973 | volume = 28 | issue = 3 | pages = 308–315 | pmid = 4569673 | url = http://archpsyc.ama-assn.org/cgi/content/abstract/28/3/308}}</ref> Canada,<ref name="SZ Bull">{{cite journal | vauthors = Ban TA, Lehmann HE | title = Nicotinic Acid in the Treatment of Schizophrenia: A Summary Report | journal = Schizophrenia Bulletin | year = 1970 | volume = 1 | issue = 3 | pages = 5–7 | doi = 10.1093/schbul/1.3.5 | doi-access = free }}</ref> and Australia<ref name="ANZJP">{{cite journal |vauthors=Vaughan K, McConaghy N | s2cid = 38857700 | title = Megavitamin and dietary treatment in schizophrenia: a randomised, controlled trial | journal = Australian and New Zealand Journal of Psychiatry | year = 1999 | volume = 33 | issue = 1 | pages = 84–88 | pmid = 10197889 | doi =10.1046/j.1440-1614.1999.00527.x}}</ref> similarly failed to find benefits of megavitamin therapy to treat [[History of schizophrenia|schizophrenia]]. | |||
The adrenochrome theory of schizophrenia waned, despite some evidence that it may be [[psychotomimetic]], as adrenochrome was not detectable in people with schizophrenia.{{citation needed|date=March 2021}} | |||
In the early 2000s, interest was renewed by the discovery that adrenochrome may be produced normally as an intermediate in the formation of [[neuromelanin]].<ref name=Smythies /> This finding may be significant because adrenochrome is detoxified at least partially by [[glutathione-S-transferase]]. Some studies have found genetic defects in the gene for this enzyme.<ref>{{cite book | vauthors = Smythies J | veditors = Smythies J |title=Disorders of Synaptic Plasticity and Schizophrenia |date=2004 |publisher=Elsevier Academic Press |isbn=978-0-12-366860-8 |pages=xv |edition=1st}}</ref> | |||
==Pharmacology== | ==Pharmacology== |