MEpedia - User contributions [en]

Eukaryotic initiation factor 2 alpha

2025-09-25T12:29:53Z

Notjusttired:gene, fix cat

{{stub}}
'''Eukaryotic initiation factor 2 alpha''' or '''eukaryotic translation initiation factor 2 α-subunit''' or '''α-subunit of eukaryotic initiation factor 2''' or '''EIF2S1''' or '''eIF2α''' is a multimeric protein. EIF2S1 is used to refer to both the eukaryotic initiation factor 2 alpha subunit protein and it's protein-encoding gene.<ref name="GeneCard" />

Eukaryotic initiation factor 2 alpha (EIF2S1) should not be confused with Eukaryotic Translation Initiation Factor 2A EIF2A, although both share the alias EIF2A.<ref name="P05198">{{Cite web|url=https://www.uniprot.org/uniprotkb/P05198/entry|title=P05198 {{!}} Eukaryotic translation initiation factor 2 subunit 1 {{!}} IF2A_HUMAN|website=UniProt|access-date=2025-09-25}}</ref><ref name="GeneCard">{{Cite web|url=https://www.genecards.org/cgi-bin/carddisp.pl?gene=EIF2A|title=EIF2A Gene {{!}} Eukaryotic Translation Initiation Factor 2A|date=2025-07-17|website=GeneCards|access-date=2025-09-25}}</ref><ref name="Komar2020">{{Cite journal|title=A Retrospective on eIF2A—and Not the Alpha Subunit of eIF2|date=2020-03-17|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC7139343/|journal=International Journal of Molecular Sciences|volume=21|issue=6|pages=2054|last=Komar|first=Anton A.|last2=Merrick|first2=William C.|language=en|doi=10.3390/ijms21062054|pmc=7139343|issn=1422-0067}}</ref>

==Function==

==ME/CFS==

==Notable studies==

==See also==
* [[Wiskott-Aldrich Syndrome Protein Family Member 3| WASF3]]
* [[Salubrinal]]

==Learn more==
* [https://www.genecards.org/cgi-bin/carddisp.pl?gene=EIF2S1 EIF2S1 Gene] - Gene Cards

==References==

[[Category:Biochemistry and cell biology]]
[[Category:Energy system]]
[[Category:Proteins]]
[[Category:Genes]]

Eukaryotic initiation factor 2 alpha

2025-09-25T09:44:05Z

Notjusttired:outline

{{stub}}
'''Eukaryotic initiation factor 2 alpha''' or '''eukaryotic translation initiation factor 2 α-subunit''' or '''α-subunit of eukaryotic initiation factor 2''' or '''EIF2S1''' or '''eIF2α''' is a multimeric protein.

Eukaryotic initiation factor 2 alpha should not be confused with the gene EIF2S1, which shares the alias EIF2A.<ref name="P05198">{{Cite web|url=https://www.uniprot.org/uniprotkb/P05198/entry|title=P05198 {{!}} Eukaryotic translation initiation factor 2 subunit 1 {{!}} IF2A_HUMAN|website=UniProt|access-date=2025-09-25}}</ref><ref name="GeneCard">{{Cite web|url=https://www.genecards.org/cgi-bin/carddisp.pl?gene=EIF2A|title=EIF2A Gene {{!}} Eukaryotic Translation Initiation Factor 2A|date=2025-07-17|website=GeneCards|access-date=2025-09-25}}</ref><ref name="Komar2020">{{Cite journal|title=A Retrospective on eIF2A—and Not the Alpha Subunit of eIF2|date=2020-03-17|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC7139343/|journal=International Journal of Molecular Sciences|volume=21|issue=6|pages=2054|last=Komar|first=Anton A.|last2=Merrick|first2=William C.|language=en|doi=10.3390/ijms21062054|pmc=7139343|issn=1422-0067}}</ref>

==Function==

==ME/CFS==

==Notable studies==

==See also==
* [[Wiskott-Aldrich Syndrome Protein Family Member 3| WASF3]]
* [[Salubrinal]]

==Learn more==

==References==

[[Category:Biochemistry and cell biology]]
[[Category:Energy production or transportation]]
[[Category:Proteins]]

Eukaryotic initiation factor 2 alpha

2025-09-25T09:42:53Z

Notjusttired:/* See also */ double redirect

{{stub}}
'''Eukaryotic initiation factor 2 alpha''' or '''eukaryotic translation initiation factor 2 α-subunit''' or '''α-subunit of eukaryotic initiation factor 2''' or '''EIF2S1''' or '''eIF2α''' is a multimeric protein.

Eukaryotic initiation factor 2 alpha should not be confused with the gene EIF2S1, which shares the alias EIF2A.<ref name="P05198">{{Cite web|url=https://www.uniprot.org/uniprotkb/P05198/entry|title=P05198 {{!}} Eukaryotic translation initiation factor 2 subunit 1 {{!}} IF2A_HUMAN|website=UniProt|access-date=2025-09-25}}</ref><ref name="GeneCard">{{Cite web|url=https://www.genecards.org/cgi-bin/carddisp.pl?gene=EIF2A|title=EIF2A Gene {{!}} Eukaryotic Translation Initiation Factor 2A|date=2025-07-17|website=GeneCards|access-date=2025-09-25}}</ref><ref name="Komar2020">{{Cite journal|title=A Retrospective on eIF2A—and Not the Alpha Subunit of eIF2|date=2020-03-17|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC7139343/|journal=International Journal of Molecular Sciences|volume=21|issue=6|pages=2054|last=Komar|first=Anton A.|last2=Merrick|first2=William C.|language=en|doi=10.3390/ijms21062054|pmc=7139343|issn=1422-0067}}</ref>

==Function==

==See also==
* [[Wiskott-Aldrich Syndrome Protein Family Member 3| WASF3]]
* [[Salubrinal]]

==Learn more==

==References==

[[Category:Biochemistry and cell biology]]
[[Category:Energy production or transportation]]
[[Category:Proteins]]

Eukaryotic initiation factor 2 alpha

2025-09-25T09:40:54Z

Notjusttired:refs expanded

{{stub}}
'''Eukaryotic initiation factor 2 alpha''' or '''eukaryotic translation initiation factor 2 α-subunit''' or '''α-subunit of eukaryotic initiation factor 2''' or '''EIF2S1''' or '''eIF2α''' is a multimeric protein.

Eukaryotic initiation factor 2 alpha should not be confused with the gene EIF2S1, which shares the alias EIF2A.<ref name="P05198">{{Cite web|url=https://www.uniprot.org/uniprotkb/P05198/entry|title=P05198 {{!}} Eukaryotic translation initiation factor 2 subunit 1 {{!}} IF2A_HUMAN|website=UniProt|access-date=2025-09-25}}</ref><ref name="GeneCard">{{Cite web|url=https://www.genecards.org/cgi-bin/carddisp.pl?gene=EIF2A|title=EIF2A Gene {{!}} Eukaryotic Translation Initiation Factor 2A|date=2025-07-17|website=GeneCards|access-date=2025-09-25}}</ref><ref name="Komar2020">{{Cite journal|title=A Retrospective on eIF2A—and Not the Alpha Subunit of eIF2|date=2020-03-17|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC7139343/|journal=International Journal of Molecular Sciences|volume=21|issue=6|pages=2054|last=Komar|first=Anton A.|last2=Merrick|first2=William C.|language=en|doi=10.3390/ijms21062054|pmc=7139343|issn=1422-0067}}</ref>

==Function==

==See also==
* [[WASF3]]
* [[Salubrinal]]

==Learn more==

==References==

[[Category:Biochemistry and cell biology]]
[[Category:Energy production or transportation]]
[[Category:Proteins]]

Eukaryotic initiation factor 2 alpha

2025-09-25T09:30:07Z

Notjusttired:EIF2A disambiguatio

{{stub}}
'''Eukaryotic initiation factor 2 alpha''' or '''eukaryotic translation initiation factor 2 α-subunit''' or '''α-subunit of eukaryotic initiation factor 2''' or '''EIF2S1''' or '''eIF2α''' is a multimeric protein.

Eukaryotic initiation factor 2 alpha should not be confused with the gene EIF2S1, which shares the alias EIF2A.<ref name="P05198">https://www.uniprot.org/uniprotkb/P05198/entry</ref><ref name="GeneCard">https://www.genecards.org/cgi-bin/carddisp.pl?gene=EIF2A</ref><ref name="Komar2020">https://www.mdpi.com/1422-0067/21/6/2054</ref>

==Function==

==See also==
* [[WASF3]]
* [[Salubrinal]]

==Learn more==

==References==

[[Category:Biochemistry and cell biology]]
[[Category:Energy production or transportation]]
[[Category:Proteins]]

Eukaryotic initiation factor 2 alpha

2025-09-25T09:03:49Z

Notjusttired:create

'''Eukaryotic initiation factor 2 alpha''' or '''eukaryotic translation initiation factor 2 α-subunit''' or eIF2α is a multimeric protein.

[[:Category:Proteins]]

EIF2α

2025-09-25T08:59:41Z

Notjusttired:c/e

#redirect [[Eukaryotic initiation factor 2 alpha]]
[[Category:Biochemistry and cell biology]]

EIF2α

2025-09-25T08:53:32Z

Notjusttired:fix

#redirect [[Eukaryotic translation initiation factor 2 alpha]]
[[Category:Biochemistry and cell biology]]

EIF2α

2025-09-25T08:31:07Z

Notjusttired:created page that turned out not to exist, not spelling glycine not glysine

<nowiki>#</nowiki>redirect [[Eukaryotic translation initiation factor 2 alpha]]

Wiskott-Aldrich Syndrome Protein Family Member 3

2025-09-25T08:27:20Z

Notjusttired:fix link

'''WASF3''' or '''WAVE3''' or '''Wiskott-Aldrich Syndrome Protein Family Member 3''' is a protein-encoding gene which has been implicated in [[chronic fatigue]] including the fatigue and [[exercise intolerance|exertion intolerance]] found in [[ME/CFS]] and [[Long COVID]].<ref name="Warrayat2025"/>

==Function ==
WASF3 possibly regulates [[brain]] [[cytokine]]s involved in the fatigue through the p38 MAPK regulatory pathway.<ref name="genecards">{{Cite web | url = https://www.genecards.org/cgi-bin/carddisp.pl?gene=WASF3 | title = WASF3 Gene - WASP Family Member 3 | website = Genecards | access-date = August 15, 2023}}</ref>

==ME/CFS==
In 2023, a [[Centers for Disease Control]] study by Wang et al. reported that over-expression of WASF3 may contribute to [[exercise intolerance]] in patients with ME/CFS.<ref name="Wang2023" />

A new, unlicensed and unapproved drug called [[salubrinal]] is being investigated as a potential treatment for ME/CFS and long-COVID because it appears to block or suppress WASF3 production.<ref name="Warrayat2025"/>

==Notable studies ==
*2025, Assessment of the therapeutic potential of salubrinal for ME/CFS and long-COVID<ref name="Warrayat2025">{{Cite journal|title=Assessment of the therapeutic potential of salubrinal for ME/CFS and long-COVID|date=May 2025|url=https://www.cell.com/trends/molecular-medicine/abstract/S1471-4914(24)00268-5|journal=Trends in Molecular Medicine|volume=31|issue=5|pages=466–478|last=Warrayat|first=Aseel|last2=Ali|first2=Ayah|last3=Waked|first3=Joulin|last4=Tocci|first4=Darcy|last5=Speth|first5=Robert C.|language=en|doi=10.1016/j.molmed.2024.10.001|issn=1471-4914}}</ref> - [https://www.cell.com/trends/molecular-medicine/abstract/S1471-4914(24)00268-5 (Abstract)]
*2023, WASF3 disrupts mitochondrial respiration and may mediate exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome<ref name="Wang2023">{{Cite journal|title=WASF3 disrupts mitochondrial respiration and may mediate exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome|date=2023-08-22|url=https://pnas.org/doi/10.1073/pnas.2302738120|journal=Proceedings of the National Academy of Sciences|volume=120|issue=34|pages=e2302738120|last=Wang|first=Ping-Yuan|last2=Ma|first2=Jin|last3=Kim|first3=Young-Chae|last4=Son|first4=Annie Y.|last5=Syed|first5=Abu Mohammad|last6=Liu|first6=Chengyu|last7=Mori|first7=Mateus P.|last8=Huffstutler|first8=Rebecca D.|last9=Stolinski|first9=JoEllyn L.|last10=Talagala|first10=S. Lalith|last11=Kang|first11=Ju-Gyeong|language=en|doi=10.1073/pnas.2302738120|issn=0027-8424}}</ref> - [https://www.pnas.org/doi/10.1073/pnas.2302738120 (Abstract)]
*2011, Meta analysis of Chronic Fatigue Syndrome through integration of clinical, gene expression, SNP and proteomic data<ref name="Pihur2011">{{Cite journal|title=Meta analysis of Chronic Fatigue Syndrome through integration of clinical, gene expression, SNP and proteomic data|date=2011-04-22|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089886/|journal=Bioinformation|volume=6|issue=3|pages=120–124|last=Pihur|first=Vasyl|last2=Datta|first2=Somnath|last3=Datta|first3=Susmita|pmc=3089886|pmid=21584188|issn=0973-2063}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089886/#fn-group-1title (Full text)]

==News and articles ==
* [https://www.science.org/content/article/protein-disrupts-cells-energy-centers-may-be-culprit-chronic-fatigue-syndrome A protein that disrupts cells’ energy centers may be a culprit in chronic fatigue syndrome] - Science

==See also==
* [[Salubrinal]]
* [[Mitochondria dysfunction]]
* [[Genetics of chronic fatigue syndrome]]

==Learn more==
* [https://www.genecards.org/cgi-bin/carddisp.pl?gene=WASF3 WASF3 - Genecards]

==References==
{{reflist}}

[[Category:Proteins]]
[[Category:Genes]]
[[Category:Mitochondria]]
[[Category:Biochemistry and cell biology]]

Protein Kinase R-like Endoplasmic Reticulum Kinase

2025-09-25T08:20:11Z

Notjusttired:stub

{{Stub}}
'''Protein Kinase R-like Endoplasmic Reticulum Kinase''' or '''PERK'''

==Function==

==ME/CFS==

==See also==
* [[Salubrinal]]

==Learn more==
*Outside articles: e.g. WebMD, Merck Manual, or ScienceDirect

== References ==
{{Reflist}}

[[Category:Enzymes]]
[[Category:Biochemistry and cell biology]]

Protein Kinase R-like Endoplasmic Reticulum Kinase

2025-09-25T08:18:09Z

Notjusttired:create

{{Stub}}
'''Protein Kinase R-like Endoplasmic Reticulum Kinase''' or '''PERK'''

== See also ==
* [[Salubrinal]]

== References ==
{{Reflist}}

[[Category:Enzymes]]
[[Category:Biochemistry and cell biology]]

Salubrinal

2025-09-24T22:08:51Z

Notjusttired:create

{{stub}}
'''Salubrinal''' is a new, unlicensed and unapproved drug which is being explored as a potential treatment for fatigue and extercise intolerance in [[ME/CFS]] and [[Long Covid]].<ref name="Warrayat2025"/>

Salubrinal suppresses production of the protein [[WASF3]], which has been implicated in [[fatigue]] and [[exercise intolerance]] in patients with ME/CFS.<ref name="Warrayat2025"/>

== Evidence ==

== Notable studies ==
*2025, Assessment of the therapeutic potential of salubrinal for ME/CFS and long-COVID<ref name="Warrayat2025">{{Cite journal|title=Assessment of the therapeutic potential of salubrinal for ME/CFS and long-COVID|date=May 2025|url=https://www.cell.com/trends/molecular-medicine/abstract/S1471-4914(24)00268-5|journal=Trends in Molecular Medicine|volume=31|issue=5|pages=466–478|last=Warrayat|first=Aseel|last2=Ali|first2=Ayah|last3=Waked|first3=Joulin|last4=Tocci|first4=Darcy|last5=Speth|first5=Robert C.|language=en|doi=10.1016/j.molmed.2024.10.001|issn=1471-4914}}</ref> - [https://www.cell.com/trends/molecular-medicine/abstract/S1471-4914(24)00268-5 (Abstract)]

== Clinicians ==

== Risks and safety ==

== Cost and availability ==

== See also ==
*[[WASF3]]

== Learn more ==


== References ==
{{reflist}}

Glycine

2025-09-24T22:02:14Z

Notjusttired:created page that turned out not to exist, not spelling glycine not glysine

{{stub}}
'''Glycine''' is a simple non-essential amino acid commonly found in food.

== Evidence ==

== Clinicians ==

== Risks and safety ==

== Cost and availability ==

== See also ==

== Learn more ==


== References ==
{{reflist}}

[[Category:Potential treatments]]
[[Category:Amino acids]]
[[Category:Supplements]]

Category:Potential treatments

2025-09-24T21:55:49Z

Notjusttired:page already exists Undo revision 244121 by AmberElkins (talk)

<div id="disclaimer">{{ambox|small=left|image=[[File:Information icon4.svg|20x20px|class=mbox-image mbox-text-small transparent|alt=Information icon]]|text='''Important Disclaimer:''' The following is a range of some of the interventions (including anecdotal) that have been used by patients to try to treat both individual symptoms and the disease as a whole, some of which have been researched and many which have not. The vast majority lack ANY reliable evidence of efficacy. Many carry significant side-effects and risks. This content is provided for information ONLY. MEpedia is not to be used to diagnose or treat any illness. Patients must consult a doctor before embarking on treatment. ''All potential treatments'' such as medications, over the counter (OTC) drugs and remedies, supplements, herbal remedies, and diets have side effects and possible interactions; discuss all potential treatments such as medications, OTC drugs and remedies, supplements, herbal remedies, and diets' side effects and possible interactions with with your doctor and pharmacist. '''Allergies:''' Make certain your doctor and pharmacist are aware of any and all allergies you have and past medication, OTC drugs and remedies, supplement, herbal remedy, and diets' allergies, side effects, or interactions you have had. '''Possible interactions:''' Inform your doctor and pharmacist of <u>all</u> current medications, OTC drugs and remedies, supplements, herbal remedies, and diets you currently use before using any new potential treatment such as a new medication, OTC drugs and remedies, supplement, herbal remedy, or diet. '''Pregnant and Lactating/Breastfeeding:''' If pregnant or lactating/breastfeeding, consult a doctor and pharmacist before taking any potential treatment such as a medication, OTC drugs and remedies, supplement, herbal remedy, or diet as they can negatively impact the fetus or baby causing birth defects, addiction, and injury.}}</div>

The following are potential treatments for [[myalgic encephalomyelitis]] (ME) and [[chronic fatigue syndrome]] (CFS), [[ME/CFS]], and other illnesses, diseases, and conditions like [[fibromyalgia]], [[sleep dysfunction]], [[depression]], etc., found on MEpedia.

==Please expand these stub pages==
{{StubPagesInCategory|Potential treatments|mode=inline}}

==Please create pages for==
<div style="column-count:3">
*[[Acamprosate]]
*[[Acetazolamide]] (carbonic anhydrase inhibitor)
*[[Acupressure]]
*[[Adalimumab]]
*[[Adrafinil]]
*[[Alpha ketoglutarate]] (supplement)
*[[Alpha linolenic acid]] (omega 3 PUFA)
*[[Alteplase]]
*[[Amisulpride]] (low dose)
*[[Amygdala retraining]] (The Amygdala Retraining Program)
*[[Anakinra]]
*[[Aniracetam]]
*[[Antifungal]]
*[[ANS rewire]] brain re-wiring/brain training
*[[Antihistamine]]
*[[Aprepitant]]
*[[Armodafinil]]
*[[Aromatherapy]]
*[[Aszopiclone]] (hypnotic)
*[[Atenolol]] (beta blocker)
*[[Atomoxetine]] (CNS stimulant)
*[[Atorvastatin]]
*[[Azithromycin]] (antibiotic)

*[[Bach remedies]]
*[[Baclofen]]
*[[Baricitinib]]<ref>[https://www.medsci.ox.ac.uk/news/recovery-trial-shows-baricitinib-reduces-deaths-in-patients-hospitalised-with-covid-19 1]</ref> - immunosuppressant, Janus kinase (JAK) inhibitor
*[[Beta blocker]]s
*[[Beta-carotene]] (vitamin; supplement)
*[[Betaine HCL]] (supplement)
*[[Beta-alanine]] (β-Alanine or b-alanine)
*[[Biaxin]] (antibiotic)
*[[Bilberry]] (plant source; supplement)
*[[Biofeedback]]
*[[Bone Marrow Concentrate Therapy]] (BMC)
*[[Borage seed oil]] (essential fatty acid)
*[[Botulinum toxin A]]
*[[Botulinum toxin B]]
*[[Bromocriptine]]
*[[Buphenine]]
*[[Butyric acid]] (supplement)
*[[Buvicaine]]

*[[Calcitonin]]
*[[Calcium channel blocker]]
*[[Captopril]]
*[[Carbamazepine]]
*[[Carisoprodol]]
*[[CELLFOOD]]
*[[Central nervous system stimulant]]
*[[Chemical avoidance]]
*[[Chiropractic]]
*[[Chlorphenamine]] (Chlorpheniramine)
*[[Chlorpheniramine maleate]] (antihistamine)
*[[Chlorzoxazone]]
*[[Cholinesterase inhibitors]]
*[[Cidofovir]] (antiviral)
*[[Clarithromycin]]
*[[Clonidine]]
*[[Colloidal silver]] (mineral)
*[[Competitive plasticity]] ([[Moskowitz approach]])
*[[Corticosteroid pulse therapy]]
*[[Cranial osteopathy]]
*[[Craniosacral massage]]
*[[Cyclobenzaprine]] (muscle relaxant)
*[[Cycloserine]]
*[[Cyproheptadine]]
*[[Dantrolene]]
*[[Darifenacin]]
*[[Desiprimine]] (trycyclic antidepressant)
*[[Desmopressin]]
*[[Detoxification]]
*[[Dexedrine]] (CNS stimulant)
*[[Dextromethorphan]] (expectorant, sometimes used with quinidine)
*[[Dextropropoxyphene]] (Propoxyphene)
*[[Dicycloverine]] (Dicyclomine)
*[[Diflucan]] (antifungal)
*[[Digestive enzymes]] (supplement)
*[[Dihydroergotamine]]
*[[Disopyramide]]
*[[Diroex]]
*[[Donepezil]]
*[[Dosulepin]] (Dothiepin)
*[[Doxycycline]] (antibiotic)
*[[Dronabinol]]

*[[Emotional Freedom Technique]]
*[[Enalapril]]
*[[Enoxaparin]]
*[[Ephedrine]] (vasoconstrictor)
*[[Epoetin]]
*[[Epoetin alfa]] (glycoprotein)
*[[Erdosteine]]
*[[Ergoloid]]
*[[Ergotamine]] (vasoconstrictor)
*[[Erythropoietin]] (hormone)
*[[Esomeprazole]]
*[[Eszopiclone]]
*[[Etanercept]]
*[[Eterocoxib]]
*[[Etilefrine]]
*[[Etodolac]]
*[[Felbamate]]
*[[Fentanyl]] (opioid)
*[[Flavocoxid]]
*[[Flavoxate]]
*[[Flaxseed oil]] (omega 3 PUFA, linseed oil)
*[[Flupirtine]]
*[[Flurbiprofen]]
*[[Fluvastatin]]
*[[Fluvoxamine]]
*[[Folinic acid]] (Leucovorin)
*[[FOS]] (fructooligosaccharides; supplement)
*[[Foscarnet]] (antiviral)
*[[Furazolidone]] (antibacterial)

*[[Gabitril]] (anticonvulsant)
*[[Galantamine]] (supplement)
*[[Galantine]]
*[[Gamma globulin]] (blood plasma protein)
*[[Glucosamine sulfate]] (supplement)
*[[Glyceryl trinitrate]]
*[[Granisetron]]
*[[Grape seed extract]] (flavonoid)
*[[Greens powder]]s (supplement)
*[[Growth hormone]] (hormone)
*[[Guaifenesin]] (expectorant)

*[[Histame]] (supplement)
*[[Homeopathy]]
*[[Hydralazine]]
*[[Hydrochlorothiazide]]
*[[Hydromorphone]]
*[[Hydrotherapy]]
*[[Hyoscyamine]]
*[[Hypnosis]]
*[[Hypnotic]] sleep medication

*[[Immunoglobulin]] -[[Subcutaneous immunoglobulin]]/sub-cutaneous immunoglobulin / subcutaneous immune globulin (SCIG)
*[[Immunoglobulin replacement therapy]]
*[[Inclined bed therapy]]
*Idebenone
*[[Indometacin]] NSAID
*[[Infliximab]]
*[[Inosine]] (supplement)
*[[Intramuscular vitamin B12]]
*[[Intravenous saline]]
*[[Intravenous vitamin C]]
*[[Isometric exercise]]
*[[Isoxsuprine]]
*[[Ivabradine]]
*[[Ketamine]]
*[[Ketoconazole]]
*[[Labetalol]]
*[[Lamivudine]] (antiviral)
*[[Lamotrigine]]
*[[Lecithin]]
*[[Levetiracetam]]
*[[Levodopa and Carbidopa]]
*[[Levofolinic acid]] (Levoleucovorin)
*[[Levomefolic acid]] (L-5-MTHF)
*[[Lidocaine]], [[Intranasal lidocaine]], [[Intravenous lidocaine]], [[Topical lidocaine]], [[Topical lidocaine and prilocaine]]
*[[Liothyronine]]
*[[Lisdexamphetamine]]
*[[Losartan]]
*[[Lovastatin]]
*[[Low-level laser therapy]]
*Low- dose immunotherapy (LDI)
*[[Luteolin]] (flavonoid)
*[[Lymphatic drainage]]

*[[Mabilone]]
*[[Massage]]
*[[Meclofenoxate]]
*[[Memantine]]
*[[Metaxalone]]
*[[Methadone]] (analgesic)
*[[Methocarbamol]]
*[[Methyldopa]] (antihypertensive)
*[[Metoprolol]]
*[[Metronidazole]] (antibiotic)
*[[Mexiletine]]
*[[Mianserin]]
*[[Midodrine]] (anti-hypotensive; vasoconstrictor)
*[[Mind-Body Reset]] (see Advertising Standards Association ruling)
*[[Minocycline]] (antibiotic)
*[[Misoprostol]] (synthetic prostaglandin analogue)
*[[Moclobemide]]
*[[Monolaurin]] (supplement)
*[[Montelukast]]
*[[Moskowitz approach]] ([[competitive plasticity]])
*[[Moxifloxacin]] (antibiotic)
*[[Moxonidine]]
*[[Mycobacterium vaccae]]
*[[Mycophenolate]]
*[[Myer's cocktail]]
*[[Myofascial release]]

*[[Naphazoline]]
*[[Narcotic]]s (analgesics)
*[[Nefazodone]]
*[[Nefopam]]
*[[Neomycin]] (antibiotic)
*[[Neurotropin]]
*[[Nicardipin]] (calcium channel blocker)
*[[Nicergoline]]
*[[Nifedipine]] (calcium channel blocker)
*[[Nilvadipine]]
*[[Nitazoxanide]] (antiparasitic; antiviral)
*[[Nitroglycerin]] (nitrate)
*[[Nizoral]] (antifungal)
*[[Nystatin]] (antifungal)

*[[Octreotide]] (vasoconstrictor)
*[[Oestrogen]] (hormone)
*[[Oestrogen and progesterone]] (hormone)
*[[Olanzapine]]
*[[Olmesartan]]
*[[Omeprazole]]
*[[Ornidazole]] (antibiotic)
*[[Orphenadrine]]
*[[Osteopathy]]
*[[Oxcarbazepine]]
*[[Oxybutynin]]
*[[Oxycodone]] (opioid)

*[[Parenteral magnesium]]
*[[Pegademase]]
*[[Pemoline]] (CNS stimulant)
*[[Pentazocine]]
*[[Pentosan polysulfate]]
*[[Pentoxifylline]] (Oxpentifylline)
*[[Pethidine]] (Meperidine)
*[[Phenalzine]] (MAOI antidepressant)
*[[Phenazopyridine]]
*[[Phenelzine]]
*[[Phentermine]] (CNS stimulant)
*[[Phenytoin]]
*[[Physiotherapy]]
*[[Pindolol]]
*[[Pioglitazone]]
*[[Piracetam]] (supplement)
*[[Piroxicam]]
*[[Pituitary hormone replacement therapy]]
*[[Pizotifen]]
*[[Polyethylene glycol]] (PEG, inactive ingredient)
*[[Prazosin]]
*[[Prednisolone]]
*[[Probenecid]]
*[[Probioplex]] (whey product; supplement)
*[[Propranolol]] (beta blocker)
*[[Protriptyline]]
*[[Pseudoephedrine]] (vasoconstrictor)
*[[Pycnogenol]] (flavonoid)
*[[Pyritinol]]

*[[Rabeprazole]]
*[[Raloxifene]]
*[[Ramelteon]] (hypnotic)
*[[Rasagiline]]
*[[Reboxetine]] (Edronax, NRI antidepressant)
*[[Reflexology]]
*[[Regenerative injection treatment]] (RIT)
*[[Rifampin]] (antibiotic)
*[[Riluzole]]
*[[Risperidone]] (antipsychotic)
*[[Ropinirole]]
*[[Rosiglitazone]]
*[[Royal jelly]] (supplement)

*[[Sambucol]] (supplement)
*[[S-ketamine]] ([[ketamine]])
*[[Sarapin]]
*[[Sativex]] (Tetrahydrocannabinol and cannabidiol)
*[[Schisandra]]
*[[Scopolamine]] (Hyoscine)
*[[Secnidazole]]
*[[Selegiline]]
*[[Shiatsu]]
*[[Sibutramine]]
*[[Sildenafil]] ([[Viagra]])
*[[Simvastatin]]
*[[Sizofiran]]
*[[Solifenacin]]
*[[Spironolactone]]
*[[Sporanox]] (antifungal)
*[[Staphylococcus toxoid]]
*[[Streptokinase]]
*[[Stress reduction]]
*[[Sulbutiamine]]
*[[Sulpiride]]
*[[Sumatriptan]] (analgesic)

*[[Tacrine]]
*[[Tadalafil]]
*[[Tamsulosin]]
*[[Transcutaneous Electrical Nerve Stimulation]] (TENS)
*[[Thalidomide]]
*[[Theaflavin]] (flavonoid, black tea)
*[[Theophylline]] (vasoconstrictor)
*[[Thearubigins]] (flavonoid, black tea)
*[[Thiocolchicoside]]
*[[Thymalfasin]]
*[[Thyroxine and liothyronine]]
*[[Tiagabine]]
*[[Tianeptine]]
*[[Tinidazole]] (antiparasitic)
*[[Tizanidine]]
*[[Tocotrienol]]s (vitamin; supplement)
*[[Tolterodine]]
*[[Topiramate]] (Topamax, for migraine)
*[[Triazolam]]
*[[Tropisetron]]
*[[Trospium]]
*[[Undenatured whey]] (whey product; supplement)
*[[Urised]] (Uriseptic)
*[[Urokinase]]
*[[Valsartan]]
*[[Vegan/non-whey protein powders with amino acid complex]] (supplement)
*[[VegEPA]] (supplement)
*[[Verapimil]] (calcium channel blocker)
*[[Vigabatrin]]
*Vinpocetine
*[[Yohimbine]] (vasoconstrictor)
*[[Zaleplon]]
*[[Ziprasidone]]
*[[Zithromax]] (antibiotic)
*[[Zolpidem]] (hypnotic)
*[[Zonisamide]]
</div>

(remove any blue links from this section)

==Sources==

*[https://mecfsroadmap.altervista.org Chronic Fatigue Syndrome - A Roadmap for Testing and Treatment]
*Reviving the Broken Marionette: Treatments for CFS/ME and Fibromyalgia. Maija Haavisto. (2008)
*Chronic Fatigue Syndrome: A Treatment Guide, 2nd Edition (eBook). Erica Verrillo. (2012)
*[http://www.fiikus.net/?cfstreatment Fiikus - Medications I've tried for CFS/ME]
*[http://www.fiikus.net/?cfssupplements Fiikus - Supplement, diets and other OTC treatments I've tried for CFS/ME]
*[http://www.cfs-healing.info/database.htm CFS-Healing - Database]
*[http://www.storiesoutloud.co.uk/supplementsme/pollresultsall.py?sort=good_votes#id_pollresults ME/CFS supplements poll results] - Storiesoutloud
*[http://www.prohealth.com/me-cfs/me-chronic-fatigue-syndrome-treatment-overview.cfm ProHealth - ME/CFS Treatments]
*[https://web.archive.org/web/20180104051326/http://curetogether.com/chronic%20fatigue%20syndrome/ig/treatment-effectiveness-vs-popularity CureTogether - 203 Chronic Fatigue Syndrome Treatments Compared]
<references />

Wiskott-Aldrich Syndrome Protein Family Member 3

2025-09-24T21:51:54Z

Notjusttired:/* Notable studies */ ref format

'''WASF3''' or '''WAVE3''' or '''Wiskott-Aldrich Syndrome Protein Family Member 3''' is a protein-encoding gene which has been implicated in [[chronic fatigue]] including the fatigue and [[exercise intolerance|exertion intolerance]] found in [[ME/CFS]] and [Long COVID]].<ref name="Warrayat2025"/>

==Function ==
WASF3 possibly regulates [[brain]] [[cytokine]]s involved in the fatigue through the p38 MAPK regulatory pathway.<ref name="genecards">{{Cite web | url = https://www.genecards.org/cgi-bin/carddisp.pl?gene=WASF3 | title = WASF3 Gene - WASP Family Member 3 | website = Genecards | access-date = August 15, 2023}}</ref>

==ME/CFS==
In 2023, a [[Centers for Disease Control]] study by Wang et al. reported that over-expression of WASF3 may contribute to [[exercise intolerance]] in patients with ME/CFS.<ref name="Wang2023" />

A new, unlicensed and unapproved drug called [[salubrinal]] is being investigated as a potential treatment for ME/CFS and long-COVID because it appears to block or suppress WASF3 production.<ref name="Warrayat2025"/>

==Notable studies ==
*2025, Assessment of the therapeutic potential of salubrinal for ME/CFS and long-COVID<ref name="Warrayat2025">{{Cite journal|title=Assessment of the therapeutic potential of salubrinal for ME/CFS and long-COVID|date=May 2025|url=https://www.cell.com/trends/molecular-medicine/abstract/S1471-4914(24)00268-5|journal=Trends in Molecular Medicine|volume=31|issue=5|pages=466–478|last=Warrayat|first=Aseel|last2=Ali|first2=Ayah|last3=Waked|first3=Joulin|last4=Tocci|first4=Darcy|last5=Speth|first5=Robert C.|language=en|doi=10.1016/j.molmed.2024.10.001|issn=1471-4914}}</ref> - [https://www.cell.com/trends/molecular-medicine/abstract/S1471-4914(24)00268-5 (Abstract)]
*2023, WASF3 disrupts mitochondrial respiration and may mediate exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome<ref name="Wang2023">{{Cite journal|title=WASF3 disrupts mitochondrial respiration and may mediate exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome|date=2023-08-22|url=https://pnas.org/doi/10.1073/pnas.2302738120|journal=Proceedings of the National Academy of Sciences|volume=120|issue=34|pages=e2302738120|last=Wang|first=Ping-Yuan|last2=Ma|first2=Jin|last3=Kim|first3=Young-Chae|last4=Son|first4=Annie Y.|last5=Syed|first5=Abu Mohammad|last6=Liu|first6=Chengyu|last7=Mori|first7=Mateus P.|last8=Huffstutler|first8=Rebecca D.|last9=Stolinski|first9=JoEllyn L.|last10=Talagala|first10=S. Lalith|last11=Kang|first11=Ju-Gyeong|language=en|doi=10.1073/pnas.2302738120|issn=0027-8424}}</ref> - [https://www.pnas.org/doi/10.1073/pnas.2302738120 (Abstract)]
*2011, Meta analysis of Chronic Fatigue Syndrome through integration of clinical, gene expression, SNP and proteomic data<ref name="Pihur2011">{{Cite journal|title=Meta analysis of Chronic Fatigue Syndrome through integration of clinical, gene expression, SNP and proteomic data|date=2011-04-22|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089886/|journal=Bioinformation|volume=6|issue=3|pages=120–124|last=Pihur|first=Vasyl|last2=Datta|first2=Somnath|last3=Datta|first3=Susmita|pmc=3089886|pmid=21584188|issn=0973-2063}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089886/#fn-group-1title (Full text)]

==News and articles ==
* [https://www.science.org/content/article/protein-disrupts-cells-energy-centers-may-be-culprit-chronic-fatigue-syndrome A protein that disrupts cells’ energy centers may be a culprit in chronic fatigue syndrome] - Science

==See also==
* [[Salubrinal]]
* [[Mitochondria dysfunction]]
* [[Genetics of chronic fatigue syndrome]]

==Learn more==
* [https://www.genecards.org/cgi-bin/carddisp.pl?gene=WASF3 WASF3 - Genecards]

==References==
{{reflist}}

[[Category:Proteins]]
[[Category:Genes]]
[[Category:Mitochondria]]
[[Category:Biochemistry and cell biology]]

Wiskott-Aldrich Syndrome Protein Family Member 3

2025-09-24T21:48:51Z

Notjusttired:expand to link to Salubrina

'''WASF3''' or '''WAVE3''' or '''Wiskott-Aldrich Syndrome Protein Family Member 3''' is a protein-encoding gene which has been implicated in [[chronic fatigue]] including the fatigue and [[exercise intolerance|exertion intolerance]] found in [[ME/CFS]] and [Long COVID]].<ref name="Warrayat2025"/>

==Function ==
WASF3 possibly regulates [[brain]] [[cytokine]]s involved in the fatigue through the p38 MAPK regulatory pathway.<ref name="genecards">{{Cite web | url = https://www.genecards.org/cgi-bin/carddisp.pl?gene=WASF3 | title = WASF3 Gene - WASP Family Member 3 | website = Genecards | access-date = August 15, 2023}}</ref>

==ME/CFS==
In 2023, a [[Centers for Disease Control]] study by Wang et al. reported that over-expression of WASF3 may contribute to [[exercise intolerance]] in patients with ME/CFS.<ref name="Wang2023" />

A new, unlicensed and unapproved drug called [[salubrinal]] is being investigated as a potential treatment for ME/CFS and long-COVID because it appears to block or suppress WASF3 production.<ref name="Warrayat2025"/>

==Notable studies ==
*2025, Assessment of the therapeutic potential of salubrinal for ME/CFS and long-COVID<ref name="Warrayat2025">https://www.cell.com/trends/molecular-medicine/abstract/S1471-4914(24)00268-5</ref>[https://www.cell.com/trends/molecular-medicine/abstract/S1471-4914(24)00268-5 (Full text)]
*2023, WASF3 disrupts mitochondrial respiration and may mediate exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome<ref name="Wang2023">{{Cite journal|title=WASF3 disrupts mitochondrial respiration and may mediate exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome|date=2023-08-22|url=https://pnas.org/doi/10.1073/pnas.2302738120|journal=Proceedings of the National Academy of Sciences|volume=120|issue=34|pages=e2302738120|last=Wang|first=Ping-Yuan|last2=Ma|first2=Jin|last3=Kim|first3=Young-Chae|last4=Son|first4=Annie Y.|last5=Syed|first5=Abu Mohammad|last6=Liu|first6=Chengyu|last7=Mori|first7=Mateus P.|last8=Huffstutler|first8=Rebecca D.|last9=Stolinski|first9=JoEllyn L.|last10=Talagala|first10=S. Lalith|last11=Kang|first11=Ju-Gyeong|language=en|doi=10.1073/pnas.2302738120|issn=0027-8424}}</ref> - [https://www.pnas.org/doi/10.1073/pnas.2302738120 (Abstract)]
*2011, Meta analysis of Chronic Fatigue Syndrome through integration of clinical, gene expression, SNP and proteomic data<ref name="Pihur2011">{{Cite journal|title=Meta analysis of Chronic Fatigue Syndrome through integration of clinical, gene expression, SNP and proteomic data|date=2011-04-22|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089886/|journal=Bioinformation|volume=6|issue=3|pages=120–124|last=Pihur|first=Vasyl|last2=Datta|first2=Somnath|last3=Datta|first3=Susmita|pmc=3089886|pmid=21584188|issn=0973-2063}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089886/#fn-group-1title (Full text)]

==News and articles ==
* [https://www.science.org/content/article/protein-disrupts-cells-energy-centers-may-be-culprit-chronic-fatigue-syndrome A protein that disrupts cells’ energy centers may be a culprit in chronic fatigue syndrome] - Science

==See also==
* [[Salubrinal]]
* [[Mitochondria dysfunction]]
* [[Genetics of chronic fatigue syndrome]]

==Learn more==
* [https://www.genecards.org/cgi-bin/carddisp.pl?gene=WASF3 WASF3 - Genecards]

==References==
{{reflist}}

[[Category:Proteins]]
[[Category:Genes]]
[[Category:Mitochondria]]
[[Category:Biochemistry and cell biology]]

Wiskott-Aldrich Syndrome Protein Family Member 3

2025-09-24T21:42:16Z

Notjusttired:/* Notable studies */ add

'''WASF3''' or '''WAVE3''' or '''Wiskott-Aldrich Syndrome Protein Family Member 3''' is a protein-encoding gene which has been implicated in [[chronic fatigue]] including the fatigue and [[exercise intolerance|exertion intolerance]] found in [[ME/CFS]].

==Function ==
WASF3 possibly regulates [[brain]] cytokines involved in the fatigue through the p38 MAPK regulatory pathway.<ref name="genecards">{{Cite web | url = https://www.genecards.org/cgi-bin/carddisp.pl?gene=WASF3 | title = WASF3 Gene - WASP Family Member 3 | website = Genecards | access-date = August 15, 2023}}</ref>

==ME/CFS==
In 2023, a [[Centers for Disease Control]] study by Wang et al. reported that over-expression of WASF3 may contribute to exercise intolerance in patients with ME/CFS.<ref name="Wang2023" />

==Notable studies ==
*2025, Assessment of the therapeutic potential of salubrinal for ME/CFS and long-COVID<ref name="Warrayat2025">https://www.cell.com/trends/molecular-medicine/abstract/S1471-4914(24)00268-5</ref>[https://www.cell.com/trends/molecular-medicine/abstract/S1471-4914(24)00268-5 (Full text)]
*2023, WASF3 disrupts mitochondrial respiration and may mediate exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome<ref name="Wang2023">{{Cite journal|title=WASF3 disrupts mitochondrial respiration and may mediate exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome|date=2023-08-22|url=https://pnas.org/doi/10.1073/pnas.2302738120|journal=Proceedings of the National Academy of Sciences|volume=120|issue=34|pages=e2302738120|last=Wang|first=Ping-Yuan|last2=Ma|first2=Jin|last3=Kim|first3=Young-Chae|last4=Son|first4=Annie Y.|last5=Syed|first5=Abu Mohammad|last6=Liu|first6=Chengyu|last7=Mori|first7=Mateus P.|last8=Huffstutler|first8=Rebecca D.|last9=Stolinski|first9=JoEllyn L.|last10=Talagala|first10=S. Lalith|last11=Kang|first11=Ju-Gyeong|language=en|doi=10.1073/pnas.2302738120|issn=0027-8424}}</ref> - [https://www.pnas.org/doi/10.1073/pnas.2302738120 (Abstract)]
*2011, Meta analysis of Chronic Fatigue Syndrome through integration of clinical, gene expression, SNP and proteomic data<ref name="Pihur2011">{{Cite journal|title=Meta analysis of Chronic Fatigue Syndrome through integration of clinical, gene expression, SNP and proteomic data|date=2011-04-22|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089886/|journal=Bioinformation|volume=6|issue=3|pages=120–124|last=Pihur|first=Vasyl|last2=Datta|first2=Somnath|last3=Datta|first3=Susmita|pmc=3089886|pmid=21584188|issn=0973-2063}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089886/#fn-group-1title (Full text)]

==News and articles ==
* [https://www.science.org/content/article/protein-disrupts-cells-energy-centers-may-be-culprit-chronic-fatigue-syndrome?fbclid=IwAR3l6y8l0siDc8lWWLj8CbmrTD_P1ruMkIY4uZS8Kvv690QplWKS6gX6AVg A protein that disrupts cells’ energy centers may be a culprit in chronic fatigue syndrome] - Science

==See also==
* [[Mitochondria dysfunction]]
* [[Genetics of chronic fatigue syndrome]]

==Learn more==
* [https://www.genecards.org/cgi-bin/carddisp.pl?gene=WASF3 WASF3 - Genecards]

==References==
{{reflist}}

[[Category:Proteins]]
[[Category:Genes]]
[[Category:Mitochondria]]
[[Category:Biochemistry and cell biology]]

Carbonic anhydrase 10

2025-08-06T20:58:11Z

Notjusttired:create

{{stub}}
'''Carbonic anhydrase 10''' or '''CA10'''

[[Category:Genes]]

DecodeME

2025-08-06T20:52:51Z

Notjusttired:its notable studies, not publications

[[File:DecodeME_logo.png|border|frameless|250px|right|class=white|alt=Decode ME logo]]
'''DecodeME''' is a UK-based genome-wide association study (GWAS), investigating the DNA of people with [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]], in comparison to healthy controls.<ref>{{Cite web|url=https://www.decodeme.org.uk/the-science/|title=The Science Behind the DNA Study|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref> DecodeME is also known as the '''ME/CFS Biomedical Partnership''', and is a collaboration between researchers, people with ME/CFS, their carers and the general public.<ref>{{Cite web|url=https://www.decodeme.org.uk/about-us/|title=About the ME/CFS Biomedical Partnership|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

DecodeME is the largest ever study investigating biological differences in people with ME/CFS. It seeks to find genetic factors that may help to determine the [[causes]] of ME/CFS and guide treatment development.<ref name="Announce25MEGroup">{{Cite web | url = https://25megroup.org/wp-content/uploads/2020/06/£3.2m-funding-for-DecodeME-largest-ever-DNA-study-of-ME.pdf | title=Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study | last = 25% ME Group|first = | authorlink = | date = Jun 23, 2020 | website = [[25 Percent ME Group|25% ME Group]]| archive-url = | archive-date = |url-status = | access-date=2020-06-23}}</ref>

==Funding==
UK's Medical Research Council and the National Institute for Health Research have provided £3.2 million to fund the DecodeME study.<ref>{{Cite web|url=https://www.decodeme.org.uk/decodeme-dna-study-awarded-3m-funding/|title=Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study|last=Support|first=Itineris|date=2020-06-22|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

== Patient criteria ==
DecodeME used questionnaires to screen patients. Participants must have been diagnosed with ME/CFS by a health professional. They must fullfill the [[National Academy of Medicine]] (NAM) criteria (formerly called Institute of Medicine) or the 2003 [[Canadian Consensus Criteria|Canadian Consensus criteria]] (CCC), both of which require [[post-exertional malaise]], and must be at least 16 years of age.

Participants with any other diagnoses which could cause chronic fatigue were excluded.

DecodeME planned to recruit at least 20,000 people with ME/CFS which began before the 2019 [[COVID-19|COVID]] pandemic and 5,000 whose ME/CFS arose after infection with the [[Severe acute respiratory syndrome coronavirus 2|SARS-CoV-2]] virus.<ref>{{Cite journal|title=DecodeME: community recruitment for a large genetics study of myalgic encephalomyelitis / chronic fatigue syndrome|date=2022-07-19|url=https://doi.org/10.1186/s12883-022-02763-6|journal=BMC Neurology|volume=22|issue=1|pages=269|last=Devereux-Cooke|first=Andy|last2=Leary|first2=Sian|last3=McGrath|first3=Simon J.|last4=Northwood|first4=Emma|last5=Redshaw|first5=Anna|last6=Shepherd|first6=Charles|last7=Stacey|first7=Pippa|last8=Tripp|first8=Claire|last9=Wilson|first9=Jim|last10=Mar|first10=Margaret|last11=Boobyer|first11=Danielle|doi=10.1186/s12883-022-02763-6|pmc=PMC9294749|pmid=35854226|issn=1471-2377}}</ref>

Participation was limited to those living in the [[United Kingdom]].<ref>{{Cite web|url=https://www.decodeme.org.uk/faqs/can-people-from-outside-the-uk-participate/|title=Can people from outside the UK participate?|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

==Partners==
The UK charities involved as partners are [[Action for ME]] and [[Forward-ME]]. The other partners are the Medical Research Council Human Genetics Unit, and the UK's National Institute for Health Research.<ref name="website">{{Cite web | url = https://www.decodeme.org.uk/ | title = Get Involved | last = DecodeME|website=DecodeME|language=en-GB|access-date=2020-06-23}}</ref>

==Timeline==
*Jul 2020, DecodeME website launched, patients able to sign-up for news and give contact details, study recruitment planned to start on Mar 2021.<ref name="Webinar2020">{{Cite web | url = https://www.decodeme.org.uk/join-our-webinar/ | title = Join our webinar Q&A | date = 2020-07-02 | last = |website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>
*26 Aug 2020, Official start expected in "very early 2021".<ref name="early2021">{{Cite web | title = About the ME/CFS Biomedical Partnership | last = DecodeME|first = | authorlink = | date = 2020-07-16 | website = DecodeME | url=https://www.decodeme.org.uk/faqs/ |archive-url=https://web.archive.org/web/20200716170315/https://www.decodeme.org.uk/faqs/|url-status=dead|archive-date=2020-07-16|quote=This is a fantastic start but we have a huge amount to do before we open recruitment. We’re aiming for 40,000 sign-ups by the time recruitment begins in March 2021 to give us the best chance of having at least 20,000 people taking part in the study.<br>Over the last few months, we have been working hard in preparation for the project officially starting next month.}}</ref>
*Nov 2021, Announcement that recruitment has been delayed until 2022, and will start with a small invited group first.<ref name="jan2022launch">{{Cite web | url = https://www.decodeme.org.uk/update-decodeme-to-launch-in-january-2022/ | title = Update: DecodeME to launch in January 2022 | date =2021-11-11 | last = DecodeME|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>
*Nov 2020, DecodeME announces that [[London School of Hygiene and Tropical Medicine]] will no longer be involved. Co-Principle Investigator Dr [[Luis Nacul]] of LSHTM will no longer be an investigator, and Dr [[Eliana Lacerda]] wil no longer be on the Trial Management Group.<ref name="LSHTM">{{Cite web | url = https://www.decodeme.org.uk/partnership-update/ | title = Partnership update | date = 2020-11-30 | last = DecodeME|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref><ref name="about-2020">{{Cite web | url = https://www.decodeme.org.uk/about-us/ | title = About the ME/CFS Biomedical Partnership | last = DecodeME|first = | authorlink = |website=DecodeME|archive-url=http://web.archive.org/web/20200716192716/https://www.decodeme.org.uk/about-us/|archive-date=2020-07-16|url-status=dead|access-date=2021-11-13}}</ref>
*2021, Beyond the scenes update states that data will be analyzed by Thermo Fisher, first set due back by end of 2022. Data will takes months to analyze, possibly some by "halfway through 2023". Funding has been increased to add an extra 5000 people to the study who got ME/CFS following [[COVID-19|Covid]].<ref name="bindthescenes">{{Cite web | url = https://www.decodeme.org.uk/webinar-recording-transcript-why-patient-involvement-is-crucial/ | title = Why patient involvement is crucial | date = 2021 | last = |website=DecodeME|language=en-GB|access-date=2022-03-26}}</ref>
*14 Jun 2021, Ethics approval granted.<ref>{{Cite web|url=https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/decodeme/|title=DecodeME|website=Health Research Authority|language=en-GB|access-date=2024-06-05}}</ref><ref name="EthicsREC">{{Cite web | date = Jun 14, 2021 | title = DecodeME | url = https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/decodeme/|website=[[Health Research Authority]]|access-date=2022-03-26}}</ref>
*Jan 2022, Announcement that phase 1 due to begin on Jan 31st with 50 [[severe and very severe ME]] patients, plus 500 randomly selected participants who registered online.<ref name="BlogJan2022">{{Cite web | url = https://www.decodeme.org.uk/great-news-decodeme-opens-for-first-participants-this-month/ | title = Great news! DecodeME opens for first participants this month | date = Jan 2022 | website = DecodeME|language=en-GB|access-date=2022-03-26}}</ref>
*Mar 2024, Due to operational challenges, the study's deadline was extended by one year, to August 2025.<ref>{{Cite web|url=https://www.decodeme.org.uk/study-extension/|title=DecodeME completion date extended to August 2025|last=Connolly|first=Anne|date=2024-03-07|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>
*Apr 2024, DecodeME announces process to share questionnaire and genetic data with eligible researchers not affiliated with the study.<ref>{{Cite web|url=https://www.decodeme.org.uk/data-access/|title=DecodeME launches data access process|last=Connolly|first=Anne|date=2024-04-29|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

==Results==
Initial results showed that the following genes were significantly more common in ME/CFS patients than in the general population:
*[[ARFGEF2]]
*[[Butyrophilin subfamily 2 member A2|BTN2A2]]
*[[Carbonic anhydrase 10|CA10]]
*[[FBXL4]]
*[[OLFM4]]
*[[RABGAP1L]]<ref name="PontingPreprint2025"/>

==Criticism==

==Investigators==
*[[Chris Ponting]] - Principle investigator
*[[Sonya Chowdhury]] - Co-investigator (PPI), CEO of Action for ME

== Patient and Public Involvement Steering Group ==
* [[Sonya Chowdhury]], [[Action for ME]] CEO, co-investigator (PPI) on the DecodeME Trial Management Group, founding charity member of the [[UK CFS/ME Research Collaborative]] (CMRC)
* [[Andrew Devereux-Cooke|Andy Devereux-Cooke]], co-founder of the [[Science for ME]]
* [[Margaret of Mar, 31st Countess of Mar]], representing [[Forward-ME]]
* [[Jim Wilson]], parent and carer, Associate Member of the [[CMRC]], and former Convenor of the CMRC Patient Advisory Group
* [[Emma Northwood]], [[ME Association]]
* [[Sian Leary]], advocate with Sheffield ME & Fibromyalgia Group, the [[ME/CFS Priority Setting Partnership]] (PSP) and [[MEActionUK]]
* [[Claire Tripp]], parent and carer involved with [[MEActionUK]]<ref name="about">{{Cite web | url = https://www.decodeme.org.uk/about-us/ | title = About the ME/CFS Biomedical Partnership|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>

==Trial management group==
* Professor [[Chris Ponting]], Principal investigator
* [[Sonya Chowdhury]], [[Action for ME]] CEO, co-investigator (PPI)<ref name="about" />
* [[Andrew Devereux-Cooke|Andy Devereux-Cooke]], from the PPI<ref name="about" />

== Science Advisory Board ==
* Professor [[Stephen Holgate]]
* Professor [[Martin Tobin]]
* Professor [[Julia Newton]]
* Professor [[Brian Hughes]]
* Professor [[Benedicte Alexandra Lie]]<ref name="about" />

==Notable studies==
* 2023, Typing myalgic encephalomyelitis by infection at onset: A DecodeME study.<ref name="Bretherick2023">{{Cite journal|title=Typing myalgic encephalomyelitis by infection at onset: A DecodeME study|date=2023-08-21|url=https://openresearch.nihr.ac.uk/articles/3-20/v4|journal=NIHR Open Research|volume=3|pages=20|last=Bretherick|first=Andrew D.|author-link=Andrew Bretherick|last2=McGrath|first2=Simon J.|author-link2=Simon McGrath|last3=Devereux-Cooke|first3=Andy|author-link3=Andy Devereux-Cooke|last4=Leary|first4=Sian|author-link4=Sian Leary|last5=Northwood|first5=Emma|last6=Redshaw|first6=Anna|last7=Stacey|first7=Pippa|last8=Tripp|first8=Claire|last9=Wilson|first9=Jim|last10=Chowdhury|first10=Sonya|author-link10=Sonya Chowdhury|last11=Lewis|first11=Isabel|language=en|doi=10.3310/nihropenres.13421.4|issn=2633-4402}}</ref> - [https://openresearch.nihr.ac.uk/articles/3-20/v4 (Full text)]

* 2025, Initial findings from the DecodeME genome-wide association study of myalgic encephalomyelitis/chronic fatigue syndrome<ref name="PontingPreprint2025">https://www.research.ed.ac.uk/en/publications/initial-findings-from-the-decodeme-genome-wide-association-study-</ref> [https://www.research.ed.ac.uk/en/publications/initial-findings-from-the-decodeme-genome-wide-association-study- (Full text, pre-print)]

==News and articles==
* Jun 2020, [https://www.theguardian.com/society/2020/jun/23/uk-to-launch-genetic-study-chronic-fatigue-syndrome-cfs UK to launch genetic study of Chronic Fatigue Syndrome] - The Guardian
* Jun 2020, [https://www.thetimes.co.uk/article/chronic-fatigue-syndrome-search-for-genetic-clues-kfclg0qh6? Chronic Fatigue Syndrome - search for genetic clues] - The Times
* Jun 2020, [https://25megroup.org/wp-content/uploads/2020/06/%C2%A33.2m-funding-for-DecodeME-largest-ever-DNA-study-of-ME.pdf Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study] - [[25 Percent ME Group|25% ME Group]]
* Jun 2020, [https://www.meaction.net/2020/06/23/3-2million-granted-for-largest-me-cfs-dna-study-ever/ £3.2 million for largest ME/CFS DNA study ever] - #MEAction
* Jun 2020, [https://www.meresearch.org.uk/decodeme-the-largest-ever-me-cfs-dna-study/ DecodeME – the largest ever ME/CFS DNA study] - ME Research UK

== Webinars ==
* 18 Dec 2020, [https://www.youtube.com/watch?v=z7lXOYQnyH4 DecodeME Winter Webinar]<ref>{{Citation | title = DecodeME Winter Webinar |url =https://www.youtube.com/watch?v=z7lXOYQnyH4|language=en|access-date=2021-05-12}}</ref>
* 14 Apr 2021, [https://www.youtube.com/watch?v=ASDXDhgYHyY DecodeME April Webinar]<ref>{{Citation | title = DecodeME April Webinar |url =https://www.youtube.com/watch?v=ASDXDhgYHyY|language=en|access-date=2021-05-12}}</ref>

==Online presence==
*[https://www.decodeme.org.uk/ Website]
*[https://www.facebook.com/decodeMEstudy Facebook]
*[https://twitter.com/decodeMEstudy Twitter]

==See also==
*[[Chris Ponting]]
*[[Andrew Devereux-Cooke]]
*[[Action for ME]]
*[[ME/CFS Gene Study]]

==Learn more==
*[https://www.decodeme.org.uk/faqs/ FAQs - DecodeME]
*[https://www.ukbiobank.ac.uk/2020/02/using-uk-biobank-data-to-investigate-the-biomolecular-and-genetic-bases-to-myalgic-encephalomyelitis-me-cfs/ UK Biobank genetic and biomolecular ME/CFS study]

==References==
{{reflist}}

[[Category:Research initiatives]]
[[Category:British research initiatives]]

Category:Stub pages last edited in 2024

2025-08-06T20:49:54Z

Notjusttired:created

{{NOINDEX}}{{hiddencat}}{{empty category}}{{tracking category}}

Stubs last edited in 2024

Category:Stub pages last edited in 2025

2025-08-06T20:48:40Z

Notjusttired:create

{{NOINDEX}}

{{hiddencat}}
{{empty category}}
{{tracking category}}

Stubs last edited in 2025

[[Category:Stubs]]

Butyrophilin subfamily 2 member A2

2025-08-06T20:46:59Z

Notjusttired:stub

{{stub}}
'''Butyrophilin subfamily 2 member A2''' or '''BTN2A2''' is a protein encoding gene that may be linked to [[myalgic encephalomyelitis/chronic fatigue syndrome|ME/CFS]].<ref name ="PontingPreprint2025"/><ref name="genecards">{{Cite web|access-date=2025-08-06 | url = https://www.genecards.org/cgi-bin/carddisp.pl?gene=BTN2A2 | title = Butyrophilin subfamily 2 member A2 Gene card
| website = Gene cards}}</ref >

==Function ==

==ME/CFS ==
The first publication from the [[DecodeME]] gene study looked for common genes that were found significantly more in ME/CFS patients of European ancestry than in healthy people of European ancestry. BTN2A2 was one of the top genes significantly more common in patients.<ref name="PontingPreprint2025" />

== Notable studies ==
* 2025, Initial findings from the DecodeME genome-wide association study of myalgic encephalomyelitis/chronic fatigue syndrome-<ref name="PontingPreprint2025">https://www.research.ed.ac.uk/en/publications/initial-findings-from-the-decodeme-genome-wide-association-study</ref> [https://www.research.ed.ac.uk/en/publications/initial-findings-from-the-decodeme-genome-wide-association-study- (Full text, pre-print)]

==See also ==
*[[DecodeME]]
*[[Genetics of chronic fatigue syndrome]]
*[[Innate immune system]]
*[[Nervous system]]

==Learn more ==
* Aug 6, 2025, [https://www.decodeme.org.uk/initial-dna-results/ Initial DecodeME DNA Results] - DecodeME
*[https://www.genecards.org/cgi-bin/carddisp.pl?gene=BTN2A2 BTN2A2 - Genecards]

==References ==

[[Category:Genes]]
[[Category:Biochemistry and cell biology]]

DecodeME

2025-08-06T20:41:13Z

Notjusttired:/* Notable studies */ tidy

[[File:DecodeME_logo.png|border|frameless|250px|right|class=white|alt=Decode ME logo]]
'''DecodeME''' is a UK-based genome-wide association study (GWAS), investigating the DNA of people with [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]], in comparison to healthy controls.<ref>{{Cite web|url=https://www.decodeme.org.uk/the-science/|title=The Science Behind the DNA Study|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref> DecodeME is also known as the '''ME/CFS Biomedical Partnership''', and is a collaboration between researchers, people with ME/CFS, their carers and the general public.<ref>{{Cite web|url=https://www.decodeme.org.uk/about-us/|title=About the ME/CFS Biomedical Partnership|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

DecodeME is the largest ever study investigating biological differences in people with ME/CFS. It seeks to find genetic factors that may help to determine the [[causes]] of ME/CFS and guide treatment development.<ref name="Announce25MEGroup">{{Cite web | url = https://25megroup.org/wp-content/uploads/2020/06/£3.2m-funding-for-DecodeME-largest-ever-DNA-study-of-ME.pdf | title=Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study | last = 25% ME Group|first = | authorlink = | date = Jun 23, 2020 | website = [[25 Percent ME Group|25% ME Group]]| archive-url = | archive-date = |url-status = | access-date=2020-06-23}}</ref>

==Funding==
UK's Medical Research Council and the National Institute for Health Research have provided £3.2 million to fund the DecodeME study.<ref>{{Cite web|url=https://www.decodeme.org.uk/decodeme-dna-study-awarded-3m-funding/|title=Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study|last=Support|first=Itineris|date=2020-06-22|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

== Patient criteria ==
DecodeME used questionnaires to screen patients. Participants must have been diagnosed with ME/CFS by a health professional. They must fullfill the [[National Academy of Medicine]] (NAM) criteria (formerly called Institute of Medicine) or the 2003 [[Canadian Consensus Criteria|Canadian Consensus criteria]] (CCC), both of which require [[post-exertional malaise]], and must be at least 16 years of age.

Participants with any other diagnoses which could cause chronic fatigue were excluded.

DecodeME planned to recruit at least 20,000 people with ME/CFS which began before the 2019 [[COVID-19|COVID]] pandemic and 5,000 whose ME/CFS arose after infection with the [[Severe acute respiratory syndrome coronavirus 2|SARS-CoV-2]] virus.<ref>{{Cite journal|title=DecodeME: community recruitment for a large genetics study of myalgic encephalomyelitis / chronic fatigue syndrome|date=2022-07-19|url=https://doi.org/10.1186/s12883-022-02763-6|journal=BMC Neurology|volume=22|issue=1|pages=269|last=Devereux-Cooke|first=Andy|last2=Leary|first2=Sian|last3=McGrath|first3=Simon J.|last4=Northwood|first4=Emma|last5=Redshaw|first5=Anna|last6=Shepherd|first6=Charles|last7=Stacey|first7=Pippa|last8=Tripp|first8=Claire|last9=Wilson|first9=Jim|last10=Mar|first10=Margaret|last11=Boobyer|first11=Danielle|doi=10.1186/s12883-022-02763-6|pmc=PMC9294749|pmid=35854226|issn=1471-2377}}</ref>

Participation was limited to those living in the [[United Kingdom]].<ref>{{Cite web|url=https://www.decodeme.org.uk/faqs/can-people-from-outside-the-uk-participate/|title=Can people from outside the UK participate?|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

==Partners==
The UK charities involved as partners are [[Action for ME]] and [[Forward-ME]]. The other partners are the Medical Research Council Human Genetics Unit, and the UK's National Institute for Health Research.<ref name="website">{{Cite web | url = https://www.decodeme.org.uk/ | title = Get Involved | last = DecodeME|website=DecodeME|language=en-GB|access-date=2020-06-23}}</ref>

==Timeline==
*Jul 2020, DecodeME website launched, patients able to sign-up for news and give contact details, study recruitment planned to start on Mar 2021.<ref name="Webinar2020">{{Cite web | url = https://www.decodeme.org.uk/join-our-webinar/ | title = Join our webinar Q&A | date = 2020-07-02 | last = |website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>
*26 Aug 2020, Official start expected in "very early 2021".<ref name="early2021">{{Cite web | title = About the ME/CFS Biomedical Partnership | last = DecodeME|first = | authorlink = | date = 2020-07-16 | website = DecodeME | url=https://www.decodeme.org.uk/faqs/ |archive-url=https://web.archive.org/web/20200716170315/https://www.decodeme.org.uk/faqs/|url-status=dead|archive-date=2020-07-16|quote=This is a fantastic start but we have a huge amount to do before we open recruitment. We’re aiming for 40,000 sign-ups by the time recruitment begins in March 2021 to give us the best chance of having at least 20,000 people taking part in the study.<br>Over the last few months, we have been working hard in preparation for the project officially starting next month.}}</ref>
*Nov 2021, Announcement that recruitment has been delayed until 2022, and will start with a small invited group first.<ref name="jan2022launch">{{Cite web | url = https://www.decodeme.org.uk/update-decodeme-to-launch-in-january-2022/ | title = Update: DecodeME to launch in January 2022 | date =2021-11-11 | last = DecodeME|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>
*Nov 2020, DecodeME announces that [[London School of Hygiene and Tropical Medicine]] will no longer be involved. Co-Principle Investigator Dr [[Luis Nacul]] of LSHTM will no longer be an investigator, and Dr [[Eliana Lacerda]] wil no longer be on the Trial Management Group.<ref name="LSHTM">{{Cite web | url = https://www.decodeme.org.uk/partnership-update/ | title = Partnership update | date = 2020-11-30 | last = DecodeME|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref><ref name="about-2020">{{Cite web | url = https://www.decodeme.org.uk/about-us/ | title = About the ME/CFS Biomedical Partnership | last = DecodeME|first = | authorlink = |website=DecodeME|archive-url=http://web.archive.org/web/20200716192716/https://www.decodeme.org.uk/about-us/|archive-date=2020-07-16|url-status=dead|access-date=2021-11-13}}</ref>
*2021, Beyond the scenes update states that data will be analyzed by Thermo Fisher, first set due back by end of 2022. Data will takes months to analyze, possibly some by "halfway through 2023". Funding has been increased to add an extra 5000 people to the study who got ME/CFS following [[COVID-19|Covid]].<ref name="bindthescenes">{{Cite web | url = https://www.decodeme.org.uk/webinar-recording-transcript-why-patient-involvement-is-crucial/ | title = Why patient involvement is crucial | date = 2021 | last = |website=DecodeME|language=en-GB|access-date=2022-03-26}}</ref>
*14 Jun 2021, Ethics approval granted.<ref>{{Cite web|url=https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/decodeme/|title=DecodeME|website=Health Research Authority|language=en-GB|access-date=2024-06-05}}</ref><ref name="EthicsREC">{{Cite web | date = Jun 14, 2021 | title = DecodeME | url = https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/decodeme/|website=[[Health Research Authority]]|access-date=2022-03-26}}</ref>
*Jan 2022, Announcement that phase 1 due to begin on Jan 31st with 50 [[severe and very severe ME]] patients, plus 500 randomly selected participants who registered online.<ref name="BlogJan2022">{{Cite web | url = https://www.decodeme.org.uk/great-news-decodeme-opens-for-first-participants-this-month/ | title = Great news! DecodeME opens for first participants this month | date = Jan 2022 | website = DecodeME|language=en-GB|access-date=2022-03-26}}</ref>
*Mar 2024, Due to operational challenges, the study's deadline was extended by one year, to August 2025.<ref>{{Cite web|url=https://www.decodeme.org.uk/study-extension/|title=DecodeME completion date extended to August 2025|last=Connolly|first=Anne|date=2024-03-07|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>
*Apr 2024, DecodeME announces process to share questionnaire and genetic data with eligible researchers not affiliated with the study.<ref>{{Cite web|url=https://www.decodeme.org.uk/data-access/|title=DecodeME launches data access process|last=Connolly|first=Anne|date=2024-04-29|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

==Results==
Initial results showed that the following genes were significantly more common in ME/CFS patients than in the general population:
*[[ARFGEF2]]
*[[Butyrophilin subfamily 2 member A2|BTN2A2]]
*[[Carbonic anhydrase 10|CA10]]
*[[FBXL4]]
*[[OLFM4]]
*[[RABGAP1L]]<ref name="PontingPreprint2025"/>

==Criticism==

== Notable studies ==
* 2025, Initial findings from the DecodeME genome-wide association study of myalgic encephalomyelitis/chronic fatigue syndrome<ref name="PontingPreprint2025">https://www.research.ed.ac.uk/en/publications/initial-findings-from-the-decodeme-genome-wide-association-study-</ref> [https://www.research.ed.ac.uk/en/publications/initial-findings-from-the-decodeme-genome-wide-association-study- (Full text, pre-print)]

==Investigators==
*[[Chris Ponting]] - Principle investigator
*[[Sonya Chowdhury]] - Co-investigator (PPI), CEO of Action for ME

== Patient and Public Involvement Steering Group ==
* [[Sonya Chowdhury]], [[Action for ME]] CEO, co-investigator (PPI) on the DecodeME Trial Management Group, founding charity member of the [[UK CFS/ME Research Collaborative]] (CMRC)
* [[Andrew Devereux-Cooke|Andy Devereux-Cooke]], co-founder of the [[Science for ME]]
* [[Margaret of Mar, 31st Countess of Mar]], representing [[Forward-ME]]
* [[Jim Wilson]], parent and carer, Associate Member of the [[CMRC]], and former Convenor of the CMRC Patient Advisory Group
* [[Emma Northwood]], [[ME Association]]
* [[Sian Leary]], advocate with Sheffield ME & Fibromyalgia Group, the [[ME/CFS Priority Setting Partnership]] (PSP) and [[MEActionUK]]
* [[Claire Tripp]], parent and carer involved with [[MEActionUK]]<ref name="about">{{Cite web | url = https://www.decodeme.org.uk/about-us/ | title = About the ME/CFS Biomedical Partnership|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>

==Trial management group==
* Professor [[Chris Ponting]], Principal investigator
* [[Sonya Chowdhury]], [[Action for ME]] CEO, co-investigator (PPI)<ref name="about" />
* [[Andrew Devereux-Cooke|Andy Devereux-Cooke]], from the PPI<ref name="about" />

== Science Advisory Board ==
* Professor [[Stephen Holgate]]
* Professor [[Martin Tobin]]
* Professor [[Julia Newton]]
* Professor [[Brian Hughes]]
* Professor [[Benedicte Alexandra Lie]]<ref name="about" />

==Publications==
* 2023, Typing myalgic encephalomyelitis by infection at onset: A DecodeME study.<ref name="Bretherick2023">{{Cite journal|title=Typing myalgic encephalomyelitis by infection at onset: A DecodeME study|date=2023-08-21|url=https://openresearch.nihr.ac.uk/articles/3-20/v4|journal=NIHR Open Research|volume=3|pages=20|last=Bretherick|first=Andrew D.|author-link=Andrew Bretherick|last2=McGrath|first2=Simon J.|author-link2=Simon McGrath|last3=Devereux-Cooke|first3=Andy|author-link3=Andy Devereux-Cooke|last4=Leary|first4=Sian|author-link4=Sian Leary|last5=Northwood|first5=Emma|last6=Redshaw|first6=Anna|last7=Stacey|first7=Pippa|last8=Tripp|first8=Claire|last9=Wilson|first9=Jim|last10=Chowdhury|first10=Sonya|author-link10=Sonya Chowdhury|last11=Lewis|first11=Isabel|language=en|doi=10.3310/nihropenres.13421.4|issn=2633-4402}}</ref> - [https://openresearch.nihr.ac.uk/articles/3-20/v4 (Full text)]

==News and articles==
* Jun 2020, [https://www.theguardian.com/society/2020/jun/23/uk-to-launch-genetic-study-chronic-fatigue-syndrome-cfs UK to launch genetic study of Chronic Fatigue Syndrome] - The Guardian
* Jun 2020, [https://www.thetimes.co.uk/article/chronic-fatigue-syndrome-search-for-genetic-clues-kfclg0qh6? Chronic Fatigue Syndrome - search for genetic clues] - The Times
* Jun 2020, [https://25megroup.org/wp-content/uploads/2020/06/%C2%A33.2m-funding-for-DecodeME-largest-ever-DNA-study-of-ME.pdf Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study] - [[25 Percent ME Group|25% ME Group]]
* Jun 2020, [https://www.meaction.net/2020/06/23/3-2million-granted-for-largest-me-cfs-dna-study-ever/ £3.2 million for largest ME/CFS DNA study ever] - #MEAction
* Jun 2020, [https://www.meresearch.org.uk/decodeme-the-largest-ever-me-cfs-dna-study/ DecodeME – the largest ever ME/CFS DNA study] - ME Research UK

== Webinars ==
* 18 Dec 2020, [https://www.youtube.com/watch?v=z7lXOYQnyH4 DecodeME Winter Webinar]<ref>{{Citation | title = DecodeME Winter Webinar |url =https://www.youtube.com/watch?v=z7lXOYQnyH4|language=en|access-date=2021-05-12}}</ref>
* 14 Apr 2021, [https://www.youtube.com/watch?v=ASDXDhgYHyY DecodeME April Webinar]<ref>{{Citation | title = DecodeME April Webinar |url =https://www.youtube.com/watch?v=ASDXDhgYHyY|language=en|access-date=2021-05-12}}</ref>

==Online presence==
*[https://www.decodeme.org.uk/ Website]
*[https://www.facebook.com/decodeMEstudy Facebook]
*[https://twitter.com/decodeMEstudy Twitter]

==See also==
*[[Chris Ponting]]
*[[Andrew Devereux-Cooke]]
*[[Action for ME]]
*[[ME/CFS Gene Study]]

==Learn more==
*[https://www.decodeme.org.uk/faqs/ FAQs - DecodeME]
*[https://www.ukbiobank.ac.uk/2020/02/using-uk-biobank-data-to-investigate-the-biomolecular-and-genetic-bases-to-myalgic-encephalomyelitis-me-cfs/ UK Biobank genetic and biomolecular ME/CFS study]

==References==
{{reflist}}

[[Category:Research initiatives]]
[[Category:British research initiatives]]

DecodeME

2025-08-06T20:40:16Z

Notjusttired:studies

[[File:DecodeME_logo.png|border|frameless|250px|right|class=white|alt=Decode ME logo]]
'''DecodeME''' is a UK-based genome-wide association study (GWAS), investigating the DNA of people with [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]], in comparison to healthy controls.<ref>{{Cite web|url=https://www.decodeme.org.uk/the-science/|title=The Science Behind the DNA Study|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref> DecodeME is also known as the '''ME/CFS Biomedical Partnership''', and is a collaboration between researchers, people with ME/CFS, their carers and the general public.<ref>{{Cite web|url=https://www.decodeme.org.uk/about-us/|title=About the ME/CFS Biomedical Partnership|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

DecodeME is the largest ever study investigating biological differences in people with ME/CFS. It seeks to find genetic factors that may help to determine the [[causes]] of ME/CFS and guide treatment development.<ref name="Announce25MEGroup">{{Cite web | url = https://25megroup.org/wp-content/uploads/2020/06/£3.2m-funding-for-DecodeME-largest-ever-DNA-study-of-ME.pdf | title=Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study | last = 25% ME Group|first = | authorlink = | date = Jun 23, 2020 | website = [[25 Percent ME Group|25% ME Group]]| archive-url = | archive-date = |url-status = | access-date=2020-06-23}}</ref>

==Funding==
UK's Medical Research Council and the National Institute for Health Research have provided £3.2 million to fund the DecodeME study.<ref>{{Cite web|url=https://www.decodeme.org.uk/decodeme-dna-study-awarded-3m-funding/|title=Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study|last=Support|first=Itineris|date=2020-06-22|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

== Patient criteria ==
DecodeME used questionnaires to screen patients. Participants must have been diagnosed with ME/CFS by a health professional. They must fullfill the [[National Academy of Medicine]] (NAM) criteria (formerly called Institute of Medicine) or the 2003 [[Canadian Consensus Criteria|Canadian Consensus criteria]] (CCC), both of which require [[post-exertional malaise]], and must be at least 16 years of age.

Participants with any other diagnoses which could cause chronic fatigue were excluded.

DecodeME planned to recruit at least 20,000 people with ME/CFS which began before the 2019 [[COVID-19|COVID]] pandemic and 5,000 whose ME/CFS arose after infection with the [[Severe acute respiratory syndrome coronavirus 2|SARS-CoV-2]] virus.<ref>{{Cite journal|title=DecodeME: community recruitment for a large genetics study of myalgic encephalomyelitis / chronic fatigue syndrome|date=2022-07-19|url=https://doi.org/10.1186/s12883-022-02763-6|journal=BMC Neurology|volume=22|issue=1|pages=269|last=Devereux-Cooke|first=Andy|last2=Leary|first2=Sian|last3=McGrath|first3=Simon J.|last4=Northwood|first4=Emma|last5=Redshaw|first5=Anna|last6=Shepherd|first6=Charles|last7=Stacey|first7=Pippa|last8=Tripp|first8=Claire|last9=Wilson|first9=Jim|last10=Mar|first10=Margaret|last11=Boobyer|first11=Danielle|doi=10.1186/s12883-022-02763-6|pmc=PMC9294749|pmid=35854226|issn=1471-2377}}</ref>

Participation was limited to those living in the [[United Kingdom]].<ref>{{Cite web|url=https://www.decodeme.org.uk/faqs/can-people-from-outside-the-uk-participate/|title=Can people from outside the UK participate?|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

==Partners==
The UK charities involved as partners are [[Action for ME]] and [[Forward-ME]]. The other partners are the Medical Research Council Human Genetics Unit, and the UK's National Institute for Health Research.<ref name="website">{{Cite web | url = https://www.decodeme.org.uk/ | title = Get Involved | last = DecodeME|website=DecodeME|language=en-GB|access-date=2020-06-23}}</ref>

==Timeline==
*Jul 2020, DecodeME website launched, patients able to sign-up for news and give contact details, study recruitment planned to start on Mar 2021.<ref name="Webinar2020">{{Cite web | url = https://www.decodeme.org.uk/join-our-webinar/ | title = Join our webinar Q&A | date = 2020-07-02 | last = |website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>
*26 Aug 2020, Official start expected in "very early 2021".<ref name="early2021">{{Cite web | title = About the ME/CFS Biomedical Partnership | last = DecodeME|first = | authorlink = | date = 2020-07-16 | website = DecodeME | url=https://www.decodeme.org.uk/faqs/ |archive-url=https://web.archive.org/web/20200716170315/https://www.decodeme.org.uk/faqs/|url-status=dead|archive-date=2020-07-16|quote=This is a fantastic start but we have a huge amount to do before we open recruitment. We’re aiming for 40,000 sign-ups by the time recruitment begins in March 2021 to give us the best chance of having at least 20,000 people taking part in the study.<br>Over the last few months, we have been working hard in preparation for the project officially starting next month.}}</ref>
*Nov 2021, Announcement that recruitment has been delayed until 2022, and will start with a small invited group first.<ref name="jan2022launch">{{Cite web | url = https://www.decodeme.org.uk/update-decodeme-to-launch-in-january-2022/ | title = Update: DecodeME to launch in January 2022 | date =2021-11-11 | last = DecodeME|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>
*Nov 2020, DecodeME announces that [[London School of Hygiene and Tropical Medicine]] will no longer be involved. Co-Principle Investigator Dr [[Luis Nacul]] of LSHTM will no longer be an investigator, and Dr [[Eliana Lacerda]] wil no longer be on the Trial Management Group.<ref name="LSHTM">{{Cite web | url = https://www.decodeme.org.uk/partnership-update/ | title = Partnership update | date = 2020-11-30 | last = DecodeME|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref><ref name="about-2020">{{Cite web | url = https://www.decodeme.org.uk/about-us/ | title = About the ME/CFS Biomedical Partnership | last = DecodeME|first = | authorlink = |website=DecodeME|archive-url=http://web.archive.org/web/20200716192716/https://www.decodeme.org.uk/about-us/|archive-date=2020-07-16|url-status=dead|access-date=2021-11-13}}</ref>
*2021, Beyond the scenes update states that data will be analyzed by Thermo Fisher, first set due back by end of 2022. Data will takes months to analyze, possibly some by "halfway through 2023". Funding has been increased to add an extra 5000 people to the study who got ME/CFS following [[COVID-19|Covid]].<ref name="bindthescenes">{{Cite web | url = https://www.decodeme.org.uk/webinar-recording-transcript-why-patient-involvement-is-crucial/ | title = Why patient involvement is crucial | date = 2021 | last = |website=DecodeME|language=en-GB|access-date=2022-03-26}}</ref>
*14 Jun 2021, Ethics approval granted.<ref>{{Cite web|url=https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/decodeme/|title=DecodeME|website=Health Research Authority|language=en-GB|access-date=2024-06-05}}</ref><ref name="EthicsREC">{{Cite web | date = Jun 14, 2021 | title = DecodeME | url = https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/decodeme/|website=[[Health Research Authority]]|access-date=2022-03-26}}</ref>
*Jan 2022, Announcement that phase 1 due to begin on Jan 31st with 50 [[severe and very severe ME]] patients, plus 500 randomly selected participants who registered online.<ref name="BlogJan2022">{{Cite web | url = https://www.decodeme.org.uk/great-news-decodeme-opens-for-first-participants-this-month/ | title = Great news! DecodeME opens for first participants this month | date = Jan 2022 | website = DecodeME|language=en-GB|access-date=2022-03-26}}</ref>
*Mar 2024, Due to operational challenges, the study's deadline was extended by one year, to August 2025.<ref>{{Cite web|url=https://www.decodeme.org.uk/study-extension/|title=DecodeME completion date extended to August 2025|last=Connolly|first=Anne|date=2024-03-07|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>
*Apr 2024, DecodeME announces process to share questionnaire and genetic data with eligible researchers not affiliated with the study.<ref>{{Cite web|url=https://www.decodeme.org.uk/data-access/|title=DecodeME launches data access process|last=Connolly|first=Anne|date=2024-04-29|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

==Results==
Initial results showed that the following genes were significantly more common in ME/CFS patients than in the general population:
*[[ARFGEF2]]
*[[Butyrophilin subfamily 2 member A2|BTN2A2]]
*[[Carbonic anhydrase 10|CA10]]
*[[FBXL4]]
*[[OLFM4]]
*[[RABGAP1L]]<ref name="PontingPreprint2025"/>

==Criticism==

== Notable studies ==
* 2025, Initial findings from the DecodeME genome-wide association study of myalgic encephalomyelitis/chronic fatigue syndrome-<ref name="PontingPreprint2025">https://www.research.ed.ac.uk/en/publications/initial-findings-from-the-decodeme-genome-wide-association-study-</ref> [https://www.research.ed.ac.uk/en/publications/initial-findings-from-the-decodeme-genome-wide-association-study- (Full text, pre-print)]

==Investigators==
*[[Chris Ponting]] - Principle investigator
*[[Sonya Chowdhury]] - Co-investigator (PPI), CEO of Action for ME

== Patient and Public Involvement Steering Group ==
* [[Sonya Chowdhury]], [[Action for ME]] CEO, co-investigator (PPI) on the DecodeME Trial Management Group, founding charity member of the [[UK CFS/ME Research Collaborative]] (CMRC)
* [[Andrew Devereux-Cooke|Andy Devereux-Cooke]], co-founder of the [[Science for ME]]
* [[Margaret of Mar, 31st Countess of Mar]], representing [[Forward-ME]]
* [[Jim Wilson]], parent and carer, Associate Member of the [[CMRC]], and former Convenor of the CMRC Patient Advisory Group
* [[Emma Northwood]], [[ME Association]]
* [[Sian Leary]], advocate with Sheffield ME & Fibromyalgia Group, the [[ME/CFS Priority Setting Partnership]] (PSP) and [[MEActionUK]]
* [[Claire Tripp]], parent and carer involved with [[MEActionUK]]<ref name="about">{{Cite web | url = https://www.decodeme.org.uk/about-us/ | title = About the ME/CFS Biomedical Partnership|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>

==Trial management group==
* Professor [[Chris Ponting]], Principal investigator
* [[Sonya Chowdhury]], [[Action for ME]] CEO, co-investigator (PPI)<ref name="about" />
* [[Andrew Devereux-Cooke|Andy Devereux-Cooke]], from the PPI<ref name="about" />

== Science Advisory Board ==
* Professor [[Stephen Holgate]]
* Professor [[Martin Tobin]]
* Professor [[Julia Newton]]
* Professor [[Brian Hughes]]
* Professor [[Benedicte Alexandra Lie]]<ref name="about" />

==Publications==
* 2023, Typing myalgic encephalomyelitis by infection at onset: A DecodeME study.<ref name="Bretherick2023">{{Cite journal|title=Typing myalgic encephalomyelitis by infection at onset: A DecodeME study|date=2023-08-21|url=https://openresearch.nihr.ac.uk/articles/3-20/v4|journal=NIHR Open Research|volume=3|pages=20|last=Bretherick|first=Andrew D.|author-link=Andrew Bretherick|last2=McGrath|first2=Simon J.|author-link2=Simon McGrath|last3=Devereux-Cooke|first3=Andy|author-link3=Andy Devereux-Cooke|last4=Leary|first4=Sian|author-link4=Sian Leary|last5=Northwood|first5=Emma|last6=Redshaw|first6=Anna|last7=Stacey|first7=Pippa|last8=Tripp|first8=Claire|last9=Wilson|first9=Jim|last10=Chowdhury|first10=Sonya|author-link10=Sonya Chowdhury|last11=Lewis|first11=Isabel|language=en|doi=10.3310/nihropenres.13421.4|issn=2633-4402}}</ref> - [https://openresearch.nihr.ac.uk/articles/3-20/v4 (Full text)]

==News and articles==
* Jun 2020, [https://www.theguardian.com/society/2020/jun/23/uk-to-launch-genetic-study-chronic-fatigue-syndrome-cfs UK to launch genetic study of Chronic Fatigue Syndrome] - The Guardian
* Jun 2020, [https://www.thetimes.co.uk/article/chronic-fatigue-syndrome-search-for-genetic-clues-kfclg0qh6? Chronic Fatigue Syndrome - search for genetic clues] - The Times
* Jun 2020, [https://25megroup.org/wp-content/uploads/2020/06/%C2%A33.2m-funding-for-DecodeME-largest-ever-DNA-study-of-ME.pdf Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study] - [[25 Percent ME Group|25% ME Group]]
* Jun 2020, [https://www.meaction.net/2020/06/23/3-2million-granted-for-largest-me-cfs-dna-study-ever/ £3.2 million for largest ME/CFS DNA study ever] - #MEAction
* Jun 2020, [https://www.meresearch.org.uk/decodeme-the-largest-ever-me-cfs-dna-study/ DecodeME – the largest ever ME/CFS DNA study] - ME Research UK

== Webinars ==
* 18 Dec 2020, [https://www.youtube.com/watch?v=z7lXOYQnyH4 DecodeME Winter Webinar]<ref>{{Citation | title = DecodeME Winter Webinar |url =https://www.youtube.com/watch?v=z7lXOYQnyH4|language=en|access-date=2021-05-12}}</ref>
* 14 Apr 2021, [https://www.youtube.com/watch?v=ASDXDhgYHyY DecodeME April Webinar]<ref>{{Citation | title = DecodeME April Webinar |url =https://www.youtube.com/watch?v=ASDXDhgYHyY|language=en|access-date=2021-05-12}}</ref>

==Online presence==
*[https://www.decodeme.org.uk/ Website]
*[https://www.facebook.com/decodeMEstudy Facebook]
*[https://twitter.com/decodeMEstudy Twitter]

==See also==
*[[Chris Ponting]]
*[[Andrew Devereux-Cooke]]
*[[Action for ME]]
*[[ME/CFS Gene Study]]

==Learn more==
*[https://www.decodeme.org.uk/faqs/ FAQs - DecodeME]
*[https://www.ukbiobank.ac.uk/2020/02/using-uk-biobank-data-to-investigate-the-biomolecular-and-genetic-bases-to-myalgic-encephalomyelitis-me-cfs/ UK Biobank genetic and biomolecular ME/CFS study]

==References==
{{reflist}}

[[Category:Research initiatives]]
[[Category:British research initiatives]]

DecodeME

2025-08-06T20:38:57Z

Notjusttired:/* Results */ initial genes

[[File:DecodeME_logo.png|border|frameless|250px|right|class=white|alt=Decode ME logo]]
'''DecodeME''' is a UK-based genome-wide association study (GWAS), investigating the DNA of people with [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]], in comparison to healthy controls.<ref>{{Cite web|url=https://www.decodeme.org.uk/the-science/|title=The Science Behind the DNA Study|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref> DecodeME is also known as the '''ME/CFS Biomedical Partnership''', and is a collaboration between researchers, people with ME/CFS, their carers and the general public.<ref>{{Cite web|url=https://www.decodeme.org.uk/about-us/|title=About the ME/CFS Biomedical Partnership|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

DecodeME is the largest ever study investigating biological differences in people with ME/CFS. It seeks to find genetic factors that may help to determine the [[causes]] of ME/CFS and guide treatment development.<ref name="Announce25MEGroup">{{Cite web | url = https://25megroup.org/wp-content/uploads/2020/06/£3.2m-funding-for-DecodeME-largest-ever-DNA-study-of-ME.pdf | title=Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study | last = 25% ME Group|first = | authorlink = | date = Jun 23, 2020 | website = [[25 Percent ME Group|25% ME Group]]| archive-url = | archive-date = |url-status = | access-date=2020-06-23}}</ref>

==Funding==
UK's Medical Research Council and the National Institute for Health Research have provided £3.2 million to fund the DecodeME study.<ref>{{Cite web|url=https://www.decodeme.org.uk/decodeme-dna-study-awarded-3m-funding/|title=Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study|last=Support|first=Itineris|date=2020-06-22|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

== Patient criteria ==
DecodeME used questionnaires to screen patients. Participants must have been diagnosed with ME/CFS by a health professional. They must fullfill the [[National Academy of Medicine]] (NAM) criteria (formerly called Institute of Medicine) or the 2003 [[Canadian Consensus Criteria|Canadian Consensus criteria]] (CCC), both of which require [[post-exertional malaise]], and must be at least 16 years of age.

Participants with any other diagnoses which could cause chronic fatigue were excluded.

DecodeME planned to recruit at least 20,000 people with ME/CFS which began before the 2019 [[COVID-19|COVID]] pandemic and 5,000 whose ME/CFS arose after infection with the [[Severe acute respiratory syndrome coronavirus 2|SARS-CoV-2]] virus.<ref>{{Cite journal|title=DecodeME: community recruitment for a large genetics study of myalgic encephalomyelitis / chronic fatigue syndrome|date=2022-07-19|url=https://doi.org/10.1186/s12883-022-02763-6|journal=BMC Neurology|volume=22|issue=1|pages=269|last=Devereux-Cooke|first=Andy|last2=Leary|first2=Sian|last3=McGrath|first3=Simon J.|last4=Northwood|first4=Emma|last5=Redshaw|first5=Anna|last6=Shepherd|first6=Charles|last7=Stacey|first7=Pippa|last8=Tripp|first8=Claire|last9=Wilson|first9=Jim|last10=Mar|first10=Margaret|last11=Boobyer|first11=Danielle|doi=10.1186/s12883-022-02763-6|pmc=PMC9294749|pmid=35854226|issn=1471-2377}}</ref>

Participation was limited to those living in the [[United Kingdom]].<ref>{{Cite web|url=https://www.decodeme.org.uk/faqs/can-people-from-outside-the-uk-participate/|title=Can people from outside the UK participate?|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

==Partners==
The UK charities involved as partners are [[Action for ME]] and [[Forward-ME]]. The other partners are the Medical Research Council Human Genetics Unit, and the UK's National Institute for Health Research.<ref name="website">{{Cite web | url = https://www.decodeme.org.uk/ | title = Get Involved | last = DecodeME|website=DecodeME|language=en-GB|access-date=2020-06-23}}</ref>

==Timeline==
*Jul 2020, DecodeME website launched, patients able to sign-up for news and give contact details, study recruitment planned to start on Mar 2021.<ref name="Webinar2020">{{Cite web | url = https://www.decodeme.org.uk/join-our-webinar/ | title = Join our webinar Q&A | date = 2020-07-02 | last = |website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>
*26 Aug 2020, Official start expected in "very early 2021".<ref name="early2021">{{Cite web | title = About the ME/CFS Biomedical Partnership | last = DecodeME|first = | authorlink = | date = 2020-07-16 | website = DecodeME | url=https://www.decodeme.org.uk/faqs/ |archive-url=https://web.archive.org/web/20200716170315/https://www.decodeme.org.uk/faqs/|url-status=dead|archive-date=2020-07-16|quote=This is a fantastic start but we have a huge amount to do before we open recruitment. We’re aiming for 40,000 sign-ups by the time recruitment begins in March 2021 to give us the best chance of having at least 20,000 people taking part in the study.<br>Over the last few months, we have been working hard in preparation for the project officially starting next month.}}</ref>
*Nov 2021, Announcement that recruitment has been delayed until 2022, and will start with a small invited group first.<ref name="jan2022launch">{{Cite web | url = https://www.decodeme.org.uk/update-decodeme-to-launch-in-january-2022/ | title = Update: DecodeME to launch in January 2022 | date =2021-11-11 | last = DecodeME|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>
*Nov 2020, DecodeME announces that [[London School of Hygiene and Tropical Medicine]] will no longer be involved. Co-Principle Investigator Dr [[Luis Nacul]] of LSHTM will no longer be an investigator, and Dr [[Eliana Lacerda]] wil no longer be on the Trial Management Group.<ref name="LSHTM">{{Cite web | url = https://www.decodeme.org.uk/partnership-update/ | title = Partnership update | date = 2020-11-30 | last = DecodeME|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref><ref name="about-2020">{{Cite web | url = https://www.decodeme.org.uk/about-us/ | title = About the ME/CFS Biomedical Partnership | last = DecodeME|first = | authorlink = |website=DecodeME|archive-url=http://web.archive.org/web/20200716192716/https://www.decodeme.org.uk/about-us/|archive-date=2020-07-16|url-status=dead|access-date=2021-11-13}}</ref>
*2021, Beyond the scenes update states that data will be analyzed by Thermo Fisher, first set due back by end of 2022. Data will takes months to analyze, possibly some by "halfway through 2023". Funding has been increased to add an extra 5000 people to the study who got ME/CFS following [[COVID-19|Covid]].<ref name="bindthescenes">{{Cite web | url = https://www.decodeme.org.uk/webinar-recording-transcript-why-patient-involvement-is-crucial/ | title = Why patient involvement is crucial | date = 2021 | last = |website=DecodeME|language=en-GB|access-date=2022-03-26}}</ref>
*14 Jun 2021, Ethics approval granted.<ref>{{Cite web|url=https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/decodeme/|title=DecodeME|website=Health Research Authority|language=en-GB|access-date=2024-06-05}}</ref><ref name="EthicsREC">{{Cite web | date = Jun 14, 2021 | title = DecodeME | url = https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/decodeme/|website=[[Health Research Authority]]|access-date=2022-03-26}}</ref>
*Jan 2022, Announcement that phase 1 due to begin on Jan 31st with 50 [[severe and very severe ME]] patients, plus 500 randomly selected participants who registered online.<ref name="BlogJan2022">{{Cite web | url = https://www.decodeme.org.uk/great-news-decodeme-opens-for-first-participants-this-month/ | title = Great news! DecodeME opens for first participants this month | date = Jan 2022 | website = DecodeME|language=en-GB|access-date=2022-03-26}}</ref>
*Mar 2024, Due to operational challenges, the study's deadline was extended by one year, to August 2025.<ref>{{Cite web|url=https://www.decodeme.org.uk/study-extension/|title=DecodeME completion date extended to August 2025|last=Connolly|first=Anne|date=2024-03-07|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>
*Apr 2024, DecodeME announces process to share questionnaire and genetic data with eligible researchers not affiliated with the study.<ref>{{Cite web|url=https://www.decodeme.org.uk/data-access/|title=DecodeME launches data access process|last=Connolly|first=Anne|date=2024-04-29|website=DecodeME|language=en-GB|access-date=2024-06-05}}</ref>

==Results==
Initial results showed that the following genes were significantly more common in ME/CFS patients than in the general population:
*[[ARFGEF2]]
*[[Butyrophilin subfamily 2 member A2|BTN2A2]]
*[[Carbonic anhydrase 10|CA10]]
*[[FBXL4]]
*[[OLFM4]]
*[[RABGAP1L]]<ref name="PontingPreprint2025"/>

==Criticism==

==Investigators==
*[[Chris Ponting]] - Principle investigator
*[[Sonya Chowdhury]] - Co-investigator (PPI), CEO of Action for ME

== Patient and Public Involvement Steering Group ==
* [[Sonya Chowdhury]], [[Action for ME]] CEO, co-investigator (PPI) on the DecodeME Trial Management Group, founding charity member of the [[UK CFS/ME Research Collaborative]] (CMRC)
* [[Andrew Devereux-Cooke|Andy Devereux-Cooke]], co-founder of the [[Science for ME]]
* [[Margaret of Mar, 31st Countess of Mar]], representing [[Forward-ME]]
* [[Jim Wilson]], parent and carer, Associate Member of the [[CMRC]], and former Convenor of the CMRC Patient Advisory Group
* [[Emma Northwood]], [[ME Association]]
* [[Sian Leary]], advocate with Sheffield ME & Fibromyalgia Group, the [[ME/CFS Priority Setting Partnership]] (PSP) and [[MEActionUK]]
* [[Claire Tripp]], parent and carer involved with [[MEActionUK]]<ref name="about">{{Cite web | url = https://www.decodeme.org.uk/about-us/ | title = About the ME/CFS Biomedical Partnership|website=DecodeME|language=en-GB|access-date=2021-11-13}}</ref>

==Trial management group==
* Professor [[Chris Ponting]], Principal investigator
* [[Sonya Chowdhury]], [[Action for ME]] CEO, co-investigator (PPI)<ref name="about" />
* [[Andrew Devereux-Cooke|Andy Devereux-Cooke]], from the PPI<ref name="about" />

== Science Advisory Board ==
* Professor [[Stephen Holgate]]
* Professor [[Martin Tobin]]
* Professor [[Julia Newton]]
* Professor [[Brian Hughes]]
* Professor [[Benedicte Alexandra Lie]]<ref name="about" />

==Publications==
* 2023, Typing myalgic encephalomyelitis by infection at onset: A DecodeME study.<ref name="Bretherick2023">{{Cite journal|title=Typing myalgic encephalomyelitis by infection at onset: A DecodeME study|date=2023-08-21|url=https://openresearch.nihr.ac.uk/articles/3-20/v4|journal=NIHR Open Research|volume=3|pages=20|last=Bretherick|first=Andrew D.|author-link=Andrew Bretherick|last2=McGrath|first2=Simon J.|author-link2=Simon McGrath|last3=Devereux-Cooke|first3=Andy|author-link3=Andy Devereux-Cooke|last4=Leary|first4=Sian|author-link4=Sian Leary|last5=Northwood|first5=Emma|last6=Redshaw|first6=Anna|last7=Stacey|first7=Pippa|last8=Tripp|first8=Claire|last9=Wilson|first9=Jim|last10=Chowdhury|first10=Sonya|author-link10=Sonya Chowdhury|last11=Lewis|first11=Isabel|language=en|doi=10.3310/nihropenres.13421.4|issn=2633-4402}}</ref> - [https://openresearch.nihr.ac.uk/articles/3-20/v4 (Full text)]

==News and articles==
* Jun 2020, [https://www.theguardian.com/society/2020/jun/23/uk-to-launch-genetic-study-chronic-fatigue-syndrome-cfs UK to launch genetic study of Chronic Fatigue Syndrome] - The Guardian
* Jun 2020, [https://www.thetimes.co.uk/article/chronic-fatigue-syndrome-search-for-genetic-clues-kfclg0qh6? Chronic Fatigue Syndrome - search for genetic clues] - The Times
* Jun 2020, [https://25megroup.org/wp-content/uploads/2020/06/%C2%A33.2m-funding-for-DecodeME-largest-ever-DNA-study-of-ME.pdf Patients, scientists and advocates celebrate £3.2m funding for DecodeME, the largest ever ME/CFS DNA study] - [[25 Percent ME Group|25% ME Group]]
* Jun 2020, [https://www.meaction.net/2020/06/23/3-2million-granted-for-largest-me-cfs-dna-study-ever/ £3.2 million for largest ME/CFS DNA study ever] - #MEAction
* Jun 2020, [https://www.meresearch.org.uk/decodeme-the-largest-ever-me-cfs-dna-study/ DecodeME – the largest ever ME/CFS DNA study] - ME Research UK

== Webinars ==
* 18 Dec 2020, [https://www.youtube.com/watch?v=z7lXOYQnyH4 DecodeME Winter Webinar]<ref>{{Citation | title = DecodeME Winter Webinar |url =https://www.youtube.com/watch?v=z7lXOYQnyH4|language=en|access-date=2021-05-12}}</ref>
* 14 Apr 2021, [https://www.youtube.com/watch?v=ASDXDhgYHyY DecodeME April Webinar]<ref>{{Citation | title = DecodeME April Webinar |url =https://www.youtube.com/watch?v=ASDXDhgYHyY|language=en|access-date=2021-05-12}}</ref>

==Online presence==
*[https://www.decodeme.org.uk/ Website]
*[https://www.facebook.com/decodeMEstudy Facebook]
*[https://twitter.com/decodeMEstudy Twitter]

==See also==
*[[Chris Ponting]]
*[[Andrew Devereux-Cooke]]
*[[Action for ME]]
*[[ME/CFS Gene Study]]

==Learn more==
*[https://www.decodeme.org.uk/faqs/ FAQs - DecodeME]
*[https://www.ukbiobank.ac.uk/2020/02/using-uk-biobank-data-to-investigate-the-biomolecular-and-genetic-bases-to-myalgic-encephalomyelitis-me-cfs/ UK Biobank genetic and biomolecular ME/CFS study]

==References==
{{reflist}}

[[Category:Research initiatives]]
[[Category:British research initiatives]]

CA10

2025-08-06T20:29:12Z

Notjusttired:create

#REDIRECT [[Carbonic anhydrase 10]]

[[Category:Genes]]

FBXL4

2025-08-06T20:27:54Z

Notjusttired:create

#REDIRECT [[F-box and leucine rich repeat protein 4]]

[[Category:Genes]]

ARFGEF2

2025-08-06T20:25:17Z

Notjusttired:create

#REDIRECT [[ARF guanine nucleotide exchange factor 2]]

[[Category:Genes]]

RABGAP1L

2025-08-06T20:21:29Z

Notjusttired:create

#REDIRECT [[RAB GTPase Activating Protein 1 Like]]

[[Category:Genes]]

OLFM4

2025-08-06T20:19:14Z

Notjusttired:created

#REDIRECT [[Olfactomedin 4]]

[[Category:Genes]]

BTN2A2

2025-08-06T20:14:40Z

Notjusttired:create

#REDIRECT [[Butyrophilin subfamily 2 member A2]]

[[Category:Genes]]

SYNGAP1

2025-08-06T20:11:20Z

Notjusttired:fix

#REDIRECT [[Synaptic Ras GTPase Activating Protein 1]]

[[Category:Genes]]

SYNGAP1

2025-08-06T20:10:20Z

Notjusttired:fix

[[#REDIRECT Synaptic Ras GTPase Activating Protein 1]]

[[Category:Genes]]

SYNGAP1

2025-08-06T20:03:44Z

Notjusttired:create

#REDIRECT [[Synaptic Ras GTPase Activating Protein 1]]

[[Category:Genes]]

Autism spectrum disorder

2025-08-06T20:02:25Z

Notjusttired:link to gene page /* Genes Related to Neuron Function */

'''Autism spectrum disorder (ASD)''' is a developmental disorder, meaning it affects how an individual develops mentally and physically. As of 2020, the CDC estimates 1 in 36 children have an autism diagnosis.<ref>{{Cite web|url=https://www.cdc.gov/autism/data-research/index.html|title=Data and Statistics on Autism Spectrum Disorder|last=CDC|date=2024-07-19|website=Autism Spectrum Disorder (ASD)|language=en-us|access-date=2025-01-25}}</ref>

== Causes ==
A 2017 Swedish study suggests autism is 83% heritable.<ref>{{Cite journal|title=The Heritability of Autism Spectrum Disorder|date=2017-09-26|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5818813/|journal=JAMA|volume=318|issue=12|pages=1182–1184|last=Sandin|first=Sven|last2=Lichtenstein|first2=Paul|last3=Kuja-Halkola|first3=Ralf|last4=Hultman|first4=Christina|last5=Larsson|first5=Henrik|last6=Reichenberg|first6=Abraham|doi=10.1001/jama.2017.12141|pmc=5818813|pmid=28973605|issn=0098-7484}}</ref> In other words, most cases of autism are caused by genes inherited from one's parents. There are up to 1,000 genes that can potentially be involved in developing autism.<ref>{{Cite journal|title=The Emerging Picture of Autism Spectrum Disorder: Genetics and Pathology|date=2015|url=https://www.annualreviews.org/content/journals/10.1146/annurev-pathol-012414-040405#right-ref-B9|journal=Annual Reviews|volume=10|pages=111-144|last=Chen|first=Jason|last2=Penagarikano|first2=Olga|last3=Belgard|first3=T. Grant|last4=Swarup|first4=Vivek|last5=Geschwind|first5=Daniel}}</ref>

Some prenatal environmental triggers are also linked with autism, including (but not limited to):

* Prenatal infection with viruses such as measles and rubella. It's unclear whether a fetus' development changes due to direct interference from the virus or influence from the mother's activated immune system.<ref>{{Cite journal|title=Association between Viral Infections and Risk of Autistic Disorder: An Overview|date=2021-03-10|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7999368/|journal=International Journal of Environmental Research and Public Health|volume=18|issue=6|pages=2817|last=Shuid|first=Ahmad Naqib|last2=Jayusman|first2=Putri Ayu|last3=Shuid|first3=Nazrun|last4=Ismail|first4=Juriza|last5=Kamal Nor|first5=Norazlin|last6=Mohamed|first6=Isa Naina|doi=10.3390/ijerph18062817|pmc=7999368|pmid=33802042|issn=1661-7827}}</ref>
* Prenatal exposure to the the insecticide dichlorodiphenyltrichloroethane (DDT).<ref>{{Cite journal|title=Association of Maternal Insecticide Levels With Autism in Offspring From a National Birth Cohort|date=2018-11-01|url=https://pubmed.ncbi.nlm.nih.gov/30111184/|journal=The American Journal of Psychiatry|volume=175|issue=11|pages=1094–1101|last=Brown|first=Alan S.|last2=Cheslack-Postava|first2=Keely|last3=Rantakokko|first3=Panu|last4=Kiviranta|first4=Hannu|last5=Hinkka-Yli-Salomäki|first5=Susanna|last6=McKeague|first6=Ian W.|last7=Surcel|first7=Heljä-Marja|last8=Sourander|first8=Andre|doi=10.1176/appi.ajp.2018.17101129|pmc=6377859|pmid=30111184|issn=1535-7228}}</ref>
* Maternal exposure to traffic-related air pollution. More specifically, mothers living within 309 meters (~3.5 football fields) of a freeway during the third trimester are more likely to have autistic babies.<ref>{{Cite journal|title=Residential proximity to freeways and autism in the CHARGE study|date=2011-06|url=https://pubmed.ncbi.nlm.nih.gov/21156395/|journal=Environmental Health Perspectives|volume=119|issue=6|pages=873–877|last=Volk|first=Heather E.|last2=Hertz-Picciotto|first2=Irva|last3=Delwiche|first3=Lora|last4=Lurmann|first4=Fred|last5=McConnell|first5=Rob|doi=10.1289/ehp.1002835|pmc=3114825|pmid=21156395|issn=1552-9924}}</ref>

It's important to note that environmental triggers generally do not cause autism by themselves.<ref>{{Cite web|url=https://www.niehs.nih.gov/health/topics/conditions/autism|title=Autism|website=National Institute of Environmental Health Sciences|language=en|access-date=2025-01-25}}</ref> Rather, they cause changes that are thought to overlap with a child's pre-existing genetic risk factors - tipping the scales, so to speak.

There is little to no evidence that individuals can develop autism after birth.<ref name=":0">{{Cite web|url=https://medschool.ucla.edu/news-article/is-autism-genetic|title=Is Autism Genetic?|date=2024-04-10|website=UCLA Medical School|language=en|access-date=2025-01-26}}</ref> Research repeatedly demonstrates no connection between autism and childhood vaccination.<ref>{{Cite journal|title=The myth of vaccination and autism spectrum|date=January 2022|url=https://www.sciencedirect.com/science/article/pii/S1090379821002312|journal=European Journal of Paediatric Neurology|volume=36|pages=151-158|last=Gabis|first=Lydia|last2=Attia|first2=Odelia|last3=Goldman|first3=Mia|last4=Barak|first4=Noy|last5=Tefera|first5=Paula|last6=Shefer|first6=Shahar}}</ref>

== Similarities to ME/CFS ==

====== Symptoms ======
People with autism can develop many of the same symptoms as ME/CFS, including:<ref name="Bileviciute Ljungar, 2018" />

* [[Brain fog]]
* Fatigue, especially after stressful situations
* [[Irritable bowel syndrome]] (IBS)<ref>{{Cite journal|title=Gastrointestinal issues and Autism Spectrum Disorder|date=2020-7|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8608248/|journal=Child and adolescent psychiatric clinics of North America|volume=29|issue=3|pages=501–513|last=Madra|first=Moneek|last2=Ringel|first2=Roey|last3=Margolis|first3=Kara G.|doi=10.1016/j.chc.2020.02.005|pmc=8608248|pmid=32471598|issn=1056-4993}}</ref>
* Sensory sensitivity
* Sleep disturbances

====== Genes Related to Neuron Function ======
A 2025 preprint study linked ME/CFS to dysfunction in genes that control synaptic function (e.g., [[Synaptic Ras GTPase Activating Protein 1|SYNGAP1]]).<ref>{{Cite web|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC12047926|title=Dissecting the genetic complexity of myalgic encephalomyelitis/chronic fatigue syndrome via deep learning-powered genome analysis|last=Zhang|first=Sai|last2=Jahanbani|first2=Fereshteh|date=2025-04-16|website=pmc.ncbi.nlm.nih.gov|language=en|doi=10.1101/2025.04.15.25325899|access-date=2025-08-03|last3=Chander|first3=Varuna|last4=Kjellberg|first4=Martin|last5=Liu|first5=Menghui|last6=Glass|first6=Katherine A.|last7=Iu|first7=David S.|last8=Ahmed|first8=Faraz|last9=Li|first9=Han}}</ref> Mutations in these genes affect how your brain cells communicate. Prior research has also linked these genes to differences in autistic brain development.<ref>{{Cite journal|title=SYNGAP1: Mind the Gap|date=2016-02-15|url=https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2016.00032/full|journal=Frontiers in Cellular Neuroscience|volume=10|last=Nallathambi|first=Jeyabalan,|last2=P.|first2=Clement, James|language=English|doi=10.3389/fncel.2016.00032/full|issn=1662-5102}}</ref>

====== Cellular Metabolism ======
Autism and ME/CFS have similar alterations to their cellular metabolism. However, there are distinct differences between the conditions.
{| class="wikitable"
|'''Topic'''
|'''Summary'''
|'''ME/CFS'''
|'''ASD'''
|-
|'''Lactate Levels'''
|People with ME/CFD and autism both have high [[lactate]] levels in the blood. However, the conditions for high lactate levels differ.
|Lactate levels rise after exercise.<ref>{{Cite journal|title=Abnormal blood lactate accumulation during repeated exercise testing in myalgic encephalomyelitis/chronic fatigue syndrome|date=2019-06|url=https://pubmed.ncbi.nlm.nih.gov/31161646/|journal=Physiological Reports|volume=7|issue=11|pages=e14138|last=Lien|first=Katarina|last2=Johansen|first2=Bjørn|last3=Veierød|first3=Marit B.|last4=Haslestad|first4=Annicke S.|last5=Bøhn|first5=Siv K.|last6=Melsom|first6=Morten N.|last7=Kardel|first7=Kristin R.|last8=Iversen|first8=Per O.|doi=10.14814/phy2.14138|pmc=6546966|pmid=31161646|issn=2051-817X}}</ref> A subgroup of people who have heightened blood lactate levels while resting are more likely to have PEM'''.<ref>{{Cite journal|title=Elevated blood lactate in resting conditions correlate with post-exertional malaise severity in patients with Myalgic encephalomyelitis/Chronic fatigue syndrome|date=2019-12-11|url=https://www.nature.com/articles/s41598-019-55473-4|journal=Scientific Reports|volume=9|issue=1|pages=18817|last=Ghali|first=Alaa|last2=Lacout|first2=Carole|last3=Ghali|first3=Maria|last4=Gury|first4=Aline|last5=Beucher|first5=Anne-Berengere|last6=Lozac’h|first6=Pierre|last7=Lavigne|first7=Christian|last8=Urbanski|first8=Geoffrey|language=en|doi=10.1038/s41598-019-55473-4|issn=2045-2322}}</ref>'''

|Some autistic kids have high lactate levels at rest.<ref>{{Cite journal|title=Mitochondrial Disease in Autism Spectrum Disorder Patients: A Cohort Analysis|date=2008-11-26|url=https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0003815|journal=PLOS ONE|volume=3|issue=11|pages=e3815|last=Weissman|first=Jacqueline R.|last2=Kelley|first2=Richard I.|last3=Bauman|first3=Margaret L.|last4=Cohen|first4=Bruce H.|last5=Murray|first5=Katherine F.|last6=Mitchell|first6=Rebecca L.|last7=Kern|first7=Rebecca L.|last8=Natowicz|first8=Marvin R.|language=en|doi=10.1371/journal.pone.0003815|issn=1932-6203}}</ref><ref>{{Cite journal|title=Mitochondrial dysfunction in autism spectrum disorders: a population-based study|date=Feb 13, 2007|url=https://onlinelibrary.wiley.com/doi/10.1111/j.1469-8749.2005.tb01113.x|journal=Developmental Medicine and Child Neurology|volume=47|issue=3|pages=185-189|last=Oliveira|first=G|last2=Diogo|first2=L|last3=Grazina|first3=M|last4=Garcia|first4=P}}</ref>

|-
|'''mtDNA'''
|Mutations in [[mitochondrial DNA]] (mtDNA) can cause fatigue. This issue is much more prevalent in autism than ME/CFS.

|A large, multi-national study found mutations in mtDNA are not any more common in the ME/CFS population than in the general public.<ref>{{Cite journal|title=MtDNA population variation in Myalgic encephalomyelitis/Chronic fatigue syndrome in two populations: a study of mildly deleterious variants|date=2019-02-27|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6393470/|journal=Scientific Reports|volume=9|pages=2914|last=Venter|first=Marianne|last2=Tomas|first2=Cara|last3=Pienaar|first3=Ilse S.|last4=Strassheim|first4=Victoria|last5=Erasmus|first5=Elardus|last6=Ng|first6=Wan-Fai|last7=Howell|first7=Neil|last8=Newton|first8=Julia L.|last9=Van der Westhuizen|first9=Francois H.|last10=Elson|first10=Joanna L.|doi=10.1038/s41598-019-39060-1|pmc=6393470|pmid=30814539|issn=2045-2322}}</ref>

|Up to 5% of autistic children may have mitochondrial disease caused by mtDNA mutations, a rate MUCH higher than that of the general public.<ref>{{Cite journal|title=Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis|date=2012-03|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3285768/|journal=Molecular Psychiatry|volume=17|issue=3|pages=290–314|last=Rossignol|first=D A|last2=Frye|first2=R E|doi=10.1038/mp.2010.136|pmc=3285768|pmid=21263444|issn=1359-4184}}</ref> The most common genes involved are:

* 3397A>G (complex I)
* 4295A>G (tRNA)
* 3243A>G MELAS × 2, POLG × 2, LHON × 2
* 3243A>G × 2
* G8363A (tRNA)
* G10406A (tRNA)

|-
|'''Mitochondrial dysfunction in skeletal muscle'''
|Both conditions have mitochondrial dysfunction in skeletal muscle. The dysfunction in ME/CFS seems to be more structural. Meanwhile, the dysfunction in autism is more related to a part of [[cellular respiration]] called the electron transport chain (ETC). ETC has 5 stages called complexes, labeled I through V.
|Within ME/CFS patients, the subsarcolemmal mitochondria have fewer cristae (folds), which may affect the production of certain chemicals.<ref name=":2">{{Cite journal|title=Functional and Morphological Differences of Muscle Mitochondria in Chronic Fatigue Syndrome and Post-COVID Syndrome|date=2024-01-30|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10855807/|journal=International Journal of Molecular Sciences|volume=25|issue=3|pages=1675|last=Bizjak|first=Daniel Alexander|last2=Ohmayer|first2=Birgit|last3=Buhl|first3=Jasmine Leonike|last4=Schneider|first4=Elisabeth Marion|last5=Walther|first5=Paul|last6=Calzia|first6=Enrico|last7=Jerg|first7=Achim|last8=Matits|first8=Lynn|last9=Steinacker|first9=Jürgen Michael|doi=10.3390/ijms25031675|pmid=38338957|issn=1422-0067}}</ref> Subsarcolemmal mitochondria are thought to be involved in fatty acid oxidation, insulin signaling, and [[glucose]] transport.<ref>{{Cite journal|title=Deficiency of Subsarcolemmal Mitochondria in Obesity and Type 2 Diabetes|date=Jan 1, 2005|url=https://diabetesjournals.org/diabetes/article/54/1/8/14686/Deficiency-of-Subsarcolemmal-Mitochondria-in|journal=Diabetes|volume=54|issue=1|pages=8-14|last=Ritov|first=Vladimir|last2=Menshikova|first2=Elizabeth|last3=He|first3=Jing|last4=Ferrell|first4=Robert}}</ref>

There aren't significant changes in complex I-IV in the ETC.<ref name=":2" /><ref>{{Cite journal|title=Mitochondrial complex activity in permeabilised cells of chronic fatigue syndrome patients using two cell types|date=2019|url=https://pubmed.ncbi.nlm.nih.gov/30847260/|journal=PeerJ|volume=7|pages=e6500|last=Tomas|first=Cara|last2=Brown|first2=Audrey E.|last3=Newton|first3=Julia L.|last4=Elson|first4=Joanna L.|doi=10.7717/peerj.6500|pmc=6398432|pmid=30847260|issn=2167-8359}}</ref>

|In a 2008 study, 4 out of 23 children who had quadriceps muscle biopsies showed structural abnormalities in their mitochondria.<ref name=":3">{{Cite journal|title=Mitochondrial Disease in Autism Spectrum Disorder Patients: A Cohort Analysis|date=2008-11-26|url=https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0003815|journal=PLOS ONE|volume=3|issue=11|pages=e3815|last=Weissman|first=Jacqueline R.|last2=Kelley|first2=Richard I.|last3=Bauman|first3=Margaret L.|last4=Cohen|first4=Bruce H.|last5=Murray|first5=Katherine F.|last6=Mitchell|first6=Rebecca L.|last7=Kern|first7=Rebecca L.|last8=Natowicz|first8=Marvin R.|language=en|doi=10.1371/journal.pone.0003815|issn=1932-6203}}</ref> The type of abnormality wasn't listed.

The same study found 65% of participants had a defect in the first part of ETC, called complex I. The middle stage, complex III, was affected in 20% of patients.<ref name=":3" /> Smaller studies have had similar findings.<ref>{{Cite journal|title=Evidence of Mitochondrial Dysfunction in Autism: Biochemical Links, Genetic-Based Associations, and Non-Energy-Related Mechanisms|date=May 29, 2017|url=https://onlinelibrary.wiley.com/doi/10.1155/2017/4314025|journal=Oxidative Medicine and Cellular Longevity|last=Griffiths|first=Keren|last2=Levy|first2=Richard}}</ref>
|-
|'''Mitochondrial dysfunction in lymphocytes'''
|Research suggests both ME/CFS and ASD individuals may have altered ETC processes in their immune cells. In certain people, it seems Complex V is underactive, while other parts of the ETC process become hyperactive to compensate.
|Lymphoblastoid cell lines (LCLs) are actively replicating [[B cell|B cells]] cultured outside the body. The LCLs derived from ME/CFS patients have an inefficient Complex V. It seems as though the rest of the ETC is constantly upregulated to compensate. Yet when extra ATP is needed, such as during exercise, the mitochondria can't deliver because they're already working at full capacity.<ref>{{Cite journal|title=An Isolated Complex V Inefficiency and Dysregulated Mitochondrial Function in Immortalized Lymphocytes from ME/CFS Patients|date=2020-02-06|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7036826/|journal=International Journal of Molecular Sciences|volume=21|issue=3|pages=1074|last=Missailidis|first=Daniel|last2=Annesley|first2=Sarah J.|last3=Allan|first3=Claire Y.|last4=Sanislav|first4=Oana|last5=Lidbury|first5=Brett A.|last6=Lewis|first6=Donald P.|last7=Fisher|first7=Paul R.|doi=10.3390/ijms21031074|pmc=7036826|pmid=32041178|issn=1422-0067}}</ref>
|Within LCLs derived from autistic people, mitochondria are more vulnerable to [[oxidative stress]]. This seems to be driven by alterations to [[glutathione]] metabolism.<ref>{{Cite journal|title=Oxidative stress induces mitochondrial dysfunction in a subset of autistic lymphoblastoid cell lines|date=2014-04|url=https://www.nature.com/articles/tp201415|journal=Translational Psychiatry|volume=4|issue=4|pages=e377–e377|last=Rose|first=S.|last2=Frye|first2=R. E.|last3=Slattery|first3=J.|last4=Wynne|first4=R.|last5=Tippett|first5=M.|last6=Melnyk|first6=S.|last7=James|first7=S. J.|language=en|doi=10.1038/tp.2014.15|issn=2158-3188}}</ref> The study authors believe these changes are related to overactivity in Complex IV found in a previous study.<ref>{{Cite journal|title=Autistic disorder with complex IV overactivity: A new mitochondrial syndrome|date=2011-12|url=http://www.thieme-connect.de/DOI/DOI?10.3233/JPN-2011-0507|journal=Journal of Pediatric Neurology|volume=09|issue=4|pages=427–434|last=Frye|first=Richard E.|last2=Naviaux|first2=Robert K.|language=en|doi=10.3233/JPN-2011-0507|issn=1304-2580}}</ref>
A 2010 study looked at peripheral blood lymphocytes, which are immune cells taken directly from the blood. Six out of 10 patients had low activity in Complex I. Four of those six also had deficiencies in Complex V.<ref>{{Cite journal|title=Mitochondrial Dysfunction in Autism|date=2010-12-01|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3915058/|journal=JAMA : the journal of the American Medical Association|volume=304|issue=21|pages=2389–2396|last=Giulivi|first=Cecilia|last2=Zhang|first2=Yi-Fan|last3=Omanska-Klusek|first3=Alicja|last4=Ross-Inta|first4=Catherine|last5=Wong|first5=Sarah|last6=Hertz-Picciotto|first6=Irva|last7=Tassone|first7=Flora|last8=Pessah|first8=Isaac N.|doi=10.1001/jama.2010.1706|pmc=3915058|pmid=21119085|issn=0098-7484}}</ref>

|}

== Autistic Burnout ==

====== Autistic Burnout Symptoms ======
Autistic burnout is a phenomenon characterized by:<ref>{{Cite journal|title=“Having All of Your Internal Resources Exhausted Beyond Measure and Being Left with No Clean-Up Crew”: Defining Autistic Burnout|date=2020-06-01|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7313636/|journal=Autism in Adulthood|volume=2|issue=2|pages=132–143|last=Raymaker|first=Dora M.|last2=Teo|first2=Alan R.|last3=Steckler|first3=Nicole A.|last4=Lentz|first4=Brandy|last5=Scharer|first5=Mirah|last6=Delos Santos|first6=Austin|last7=Kapp|first7=Steven K.|last8=Hunter|first8=Morrigan|last9=Joyce|first9=Andee|last10=Nicolaidis|first10=Christina|doi=10.1089/aut.2019.0079|pmc=7313636|pmid=32851204|issn=2573-9581}}</ref>

* '''Severe exhaustion:''' Physical and mental fatigue can impact employment, relationships, and self-care. Similar to [[post-exertional malaise]], the fatigue can worsen after straining oneself mentally or physically. However, physical triggers generally involve sensory sensitivities rather than exercise.
* '''Reduced tolerance to stimulus:''' Individuals may be more sensitive to noise, light, and other sensory stimuli. They may also have more trouble regulating their emotions than they used to. Some may grow extremely dependent on routines in order to self-regulate.
* '''Loss of skills:''' Individuals may have difficulty with executive functions like following plans and making decisions. They also may have trouble speaking or remembering common vocabulary. These skills can often return after the burnout episode, but not always to the level they were before.

====== Autistic Burnout Diagnosis ======
The term "autistic burnout" was coined around 2005 and reached mainstream awareness around 2018.<ref>{{Cite journal|title=What Is Autistic Burnout? A Thematic Analysis of Posts on Two Online Platforms|date=2022-03-01|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8992925/|journal=Autism in Adulthood: Challenges and Management|volume=4|issue=1|pages=52–65|last=Mantzalas|first=Jane|last2=Richdale|first2=Amanda L.|last3=Adikari|first3=Achini|last4=Lowe|first4=Jennifer|last5=Dissanayake|first5=Cheryl|doi=10.1089/aut.2021.0021|pmc=8992925|pmid=36605565|issn=2573-9581}}</ref> Some research may also call it "autistic regression."<ref>{{Cite journal|title=Prevalence and Age of Onset of Regression in Children with Autism Spectrum Disorder: A Systematic Review and Meta-analytical Update|date=2021-03|url=https://pubmed.ncbi.nlm.nih.gov/33491292/|journal=Autism Research: Official Journal of the International Society for Autism Research|volume=14|issue=3|pages=582–598|last=Tan|first=Christine|last2=Frewer|first2=Veronica|last3=Cox|first3=Georgina|last4=Williams|first4=Katrina|last5=Ure|first5=Alexandra|doi=10.1002/aur.2463|pmid=33491292|issn=1939-3806}}</ref> However, neither of these names are an official diagnosis.

There is no official test for autistic burnout. However, a 2024 study found the AASPIRE Autistic Burnout Measure (ABM) is a valid measure of autistic burnout.<ref>{{Cite journal|title=Measuring and validating autistic burnout|date=Apr, 25, 2024|url=https://onlinelibrary.wiley.com/doi/10.1002/aur.3129|journal=Autism Research|volume=17|issue=7|pages=1417-1449|last=Mantzalas|first=Jane|last2=Richdale|first2=Amanda|last3=Li|first3=Xia|last4=Dissanayake|first4=Cheryl}}</ref> (Validity means the test accurately captures the concept it claims to measure.)

While some symptoms of autistic burnout do overlap with depression criteria, the two conditions are distinct. Autistic people experiencing burnout can still experience the full range of emotions and find joy in special interests. While low mood is common, it's not the defining feature of burnout. Similar to post-exertional malaise, rest is considered the primary method of recovery for an autistic burnout episode. <ref name=":1">{{Cite journal|title=Defining autistic burnout through experts by lived experience: Grounded Delphi method investigating #AutisticBurnout|date=Jun 4, 2021|url=https://journals.sagepub.com/doi/10.1177/13623613211019858|journal=Autism|volume=25|issue=8|last=Higgins|first=Julianne|last2=Arnold|first2=Samuel|last3=Weise|first3=Janelle|last4=Pellicano|first4=Elizabeth|last5=Trollor|first5=Jullian}}</ref>

==Notable studies==
*2024 - A genome-wide association study suggests autism has a "shared genetic architecture" with fatigue, multi-site pain, and IBS. However, it's too early to say whether there is a causal relationship.<ref>{{Cite journal|title=Shared genetic architecture and causality between autism spectrum disorder and irritable bowel syndrome, multisite pain, and fatigue|date=2024-11-23|url=https://www.nature.com/articles/s41398-024-03184-4|journal=Translational Psychiatry|volume=14|issue=1|pages=1–9|last=Li|first=Yiran|last2=Xie|first2=Tian|last3=Vos|first3=Melissa|last4=Snieder|first4=Harold|last5=Hartman|first5=Catharina A.|language=en|doi=10.1038/s41398-024-03184-4|pmc=11585586|pmid=39580447|issn=2158-3188}}</ref>
*2024 - Children with autistic traits are 78% more likely to have chronic disabling fatigue by the time they reach 18. The link between autism and fatigue held true even when researchers controlled for depressive symptoms. The study authors said this link was likely mediated by higher levels of the inflammatory cytokine [[Interleukin 6|IL-6]].
*2022 - In a study of 973 autistic adults, 21% had a formal diagnosis of one or more [[Central sensitization|central sensitivity syndromes]] (CSS). These included [[fibromyalgia]], ME/CFS, IBS, [[Restless legs syndrome|restless leg syndrome]], and temperomandibular joint disorder. In addition, 60% of participants met the clinical cut-off for a CSS on the Central Sensitization Inventory.
*2018 - Patients with [[chronic fatigue syndrome]] do not score higher on the Autism Spectrum Quotient (a test measuring autistic traits) than healthy controls.<ref name="Bileviciute Ljungar, 2018" /> [http://www.diva-portal.org/smash/record.jsf?pid=diva2%3A1190903&dswid=7740 (Abstract)]

==References==
<references>
<ref name="Bileviciute Ljungar, 2018">
{{Citation | last1 = Bileviciute Ljungar | first1 = Indre | author-link1 = Indre Bileviciute Ljungar | last2 = Maroti | first2 = Daniel | author-link2 = | last3 = Bejerot | first3 = Susanne | author-link3 = | title = Patients with chronic fatigue syndrome do not score higher on the Autism-apectrum quotient than healthy controls: comparison with autism spectrum disorder | journal = Scandinavian Journal of Psychology | volume = | issue = | page = | date = 2018 | pmid = | doi = | url = http://www.diva-portal.org/smash/record.jsf?pid=diva2%3A1190903&dswid=7740 }}</ref>
</references>

[[Category:Diagnoses]]

Lucinda Bateman

2025-06-29T22:40:22Z

Notjusttired:/* Clinic location */ c/e

[[File:LucindaBateman.jpeg|right]]
'''Lucinda Bateman''' (Cindy Bateman), MD, is an [[ME/CFS]] physician and researcher. She founded and is Chief Medical Officer of the [[Bateman Horne Center]] of Excellence for ME/CFS and Fibromyalgia in Salt Lake City, Utah.<ref>https://batemanhornecenter.org/</ref>

Dr. Bateman was one of the authors of the 2011 case definition, [[International Consensus Criteria]],<ref>{{Cite journal|last = Carruthers | first = Bruce M. | authorlink = Bruce Carruthers | last2 = van de Sande | first2 = Marjorie I. | authorlink2 = Marjorie van de Sande | last3 = De Meirleir | first3 = Kenny L. | authorlink3 = Kenny De Meirleir | last4 = Klimas | first4 = Nancy G. | author-link4 = Nancy Klimas | last5 = Broderick | first5 = Gordon | author-link5 = Gordon Broderick | last6 = Mitchell | first6 = Terry | authorlink6 = Terry Mitchell | last7 = Staines | first7 = Donald | author-link7 = Donald Staines | last8 = Powles | first8 = A.C. Peter | authorlink8 = A C Peter Powles | last9 = Speight | first9 = Nigel | authorlink9 = Nigel Speight | last10 = Vallings | first10 = Rosamund | authorlink10 = Rosamund Vallings | last11 = Bateman | first11 = Lucinda | authorlink11 = Lucinda Bateman | last12 = Baumgarten-Austrheim | first12 = Barbara | authorlink12 = Barbara Baumgarten-Austrheim | last13 = Bell | first13 = David | author-link13 = David Bell | last14 = Carlo-Stella | first14 = Nicoletta | author-link14 = Nicoletta Carlo-Stella | last15 = Chia | first15 = John | author-link15 = John Chia | last16 = Darragh | first16 = Austin | author-link16 = Austin Darragh | last17 = Jo | first17 = Daehyun | author-link17 = Daehyun Jo | last18 = Lewis | first18 = Donald | author-link18 = Donald Lewis | last19 = Light | first19 = Alan | author-link19 = Alan Light | last20 = Marshall-Gradisnik | first20 = Sonya | author-link20 = Sonya Marshall-Gradisnik | last21 = Mena | first21 = Ismael | author-link21 = Ismael Mena | last22 = Mikovits | first22 = Judy | author-link22 = Judy Mikovits | last23 = Miwa | first23 = Kunihisa | author-link23 = Kunihisa Miwa | last24 = Murovska | first24 = Modra | author-link24 = Modra Murovska | last25 = Pall | first25 = Martin | author-link25 = Martin Pall | last26 = Stevens | first26 = Staci | author-link26 = Staci Stevens | date = 2011-08-22 | title=Myalgic encephalomyelitis: International Consensus Criteria|url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2796.2011.02428.x|journal=Journal of Internal Medicine|language=en|volume=270|issue=4 | pages = 327–338|doi=10.1111/j.1365-2796.2011.02428.x|issn=0954-6820|pmc=3427890|pmid=21777306|via=}}</ref> and was one of the experts on the "Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome" that was convened for the 2015 [[Institute of Medicine report]].<ref>{{Cite book | title = Biographical Sketches of Committee Members, Consultants, and Staff|language=en | url =https://www.ncbi.nlm.nih.gov/books/NBK284904/ | date = 2015-02-10|publisher=National Academies Press (US)|last = Syndrome | first = Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue | last2 = Populations | first2 = Board on the Health of Select | last3 = Medicine | first3 = Institute of}}</ref>

[[Suzanne Vernon]], PhD, the Research Liaison at [[Bateman Horne Center]] of Excellence works closely with Dr. Bateman on [[ME/CFS]] and [[fibromyalgia]] research.<ref>https://batemanhornecenter.org/suzanne-d-vernon-phd/</ref>

==Awards==
*2016, Rudy Perpich Senior Lectureship Award, presented to a distinguished [[Chronic fatigue syndrome|CFS]]/[[fibromyalgia|FMS]] scientist, physician or healthcare worker awarded by [[International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis]]<ref>{{Cite web|url=https://www.iacfsme.org/iacfs-me-awardees | title = IACFS/ME Awardees|website=
IACFS/ME|access-date=2020-04-23}}</ref>

==Boards and committees==

===CFSAC committee===
Dr. Bateman was a voting member of the [[Health and Human Services]]'s [[Chronic Fatigue Syndrome Advisory Committee]] for the terms 12/01/05 to 12/01/08<ref name="Nov, 2006" /> & 01/03/06 to 01/03/10<ref name="Spring, 2009" /> and was serving the term 12/13/2017 to Sep 2020 when the committee was dissolved by HHS.<ref>https://www.hhs.gov/ash/advisory-committees/cfsac/about-cfsac/roster/index.html</ref>

=== Journal editoral board ===
Dr. Bateman serves on the editorial board of the journal, [[Fatigue: Biomedicine, Health & Behavior]].<ref>{{Cite web|url=https://www.tandfonline.com/action/journalInformation?show=editorialBoard&journalCode=rftg20& | title = Fatigue: Biomedicine, Health & Behavior | website = tandfonline.com|access-date=2019-11-01}}</ref>

===ME/CFS Common Data Elements (CDE) Project===
Member of the Pain Working Group of the Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Common Data Element (CDE) Project sponsored by the [[National Institute of Neurological Disorders and Stroke]] and the [[Centers for Disease Control and Prevention]].<ref>{{Cite web|url=https://www.commondataelements.ninds.nih.gov/Myalgic%20Encephalomyelitis/Chronic%20Fatigue%20Syndrome#pane-138 | title = Complete Myalgic Encephalomyelitis/Chronic Fatigue Syndrome CDE Roster | last = | first = | authorlink = | date = | website = NIH|archive-url=|archive-date=|url-status=|access-date=2019-10-11}}</ref>

==Advocacy==

===Open letter to ''The Lancet''===
Two [[open letter to the Lancet | open letters to the editor of ''The Lancet'']] urged the editor to commission a fully independent review of the [[PACE trial]], which the journal had published in 2011. In 2016, Dr. Bateman, along with 41 colleagues in the [[ME/CFS]] field, signed the second letter.
*10 February 2016, [http://www.virology.ws/2016/02/10/open-letter-lancet-again/ An open letter to The Lancet, again - Virology blog]

=== Editorials ===
* Aug 2019, Editorial: Advances in ME/CFS Research and Clinical Care<ref>{{Cite journal | last = Friedman | first = Kenneth | authorlink = Kenneth Friedman | last2 = Bateman | first2 = Lucinda | authorlink2 = Lucinda Bateman | last3 = Bested | first3 = Alison C. | authorlink3 = Alison Bested | last4 = Nahle | first4 = Zaher | authorlink4 = Zaher Nahle | date = Aug 2019 | title = Editorial: Advances in ME/CFS Research and Clinical Care|url=https://www.frontiersin.org/articles/10.3389/fped.2019.00370/full|journal=Frontiers in Pediatrics|volume=|issue=|pages=|doi=10.3389/fped.2019.00370|pmc=|pmid=|access-date=|quote=|via=}}</ref> - [https://www.frontiersin.org/articles/10.3389/fped.2019.00370/full (Partial text)]

==Research studies==
*2005, A team approach to treating [[Chronic fatigue syndrome|CFS]]: Matching best medical practices to phases of illness.<ref>Fennell, P. A., & Bateman, L. (2005). "A team approach to treating CFS: Matching best medical practices to phases of illness." ''CFS Research Review'', Summer.</ref>
*2010, Severity of symptom flare after moderate [[exercise]] is linked to [[cytokine]] activity in [[chronic fatigue syndrome]]<ref>White, A.T., Light, A.R., Hughen, R.W., Bateman, L., Martins, T.B., Hill, H.R., and Light, K.C. (2010) Severity of symptom flare after moderate exercise is linked to cytokine activity in chronic fatigue syndrome. ''Psychophysiology'', 47(4):615-24. doi: 10.1111./j.1469-8986.2010.00978.x</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4378647/ (Full Text)]
*2011, Absence of [[XMRV]] retrovirus and other murine leukemia virus-related viruses in patients with [[chronic fatigue syndrome]]<ref>{{Cite journal|last = Shin | first = Clifford H. | last2 = Bateman | first2 = Lucinda | authorlink2 = Lucinda Bateman | last3 = Schlaberg | first3 = Robert | last4 = Bunker | first4 = Ashley M. | last5 = Leonard | first5 = Christopher J. | last6 = Hughen | first6 = Ronald W. | last7 = Light | first7 = Alan R. | authorlink7 = Alan Light | last8 = Light | first8 = Kathleen C | authorlink8 = Kathleen Light | last9 = Singh | first9 = Ila R. | date = Jul 2011 | title = Absence of XMRV retrovirus and other murine leukemia virus-related viruses in patients with chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3126563/|journal=Journal of Virology|volume=85|issue=14 | pages = 7195-202|doi=10.1128/JVI.00693-11|via=}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3126563/ (Full Text)]
*2011, Evidence for a heritable predisposition to [[Chronic Fatigue Syndrome]]<ref name="Albright, 2011" /> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3128000/ (Full Text)]
*2012, A double-blind, placebo-controlled, randomized, clinical trial of the TLR-3 agonist [[rintatolimod]] in severe cases of chronic fatigue syndrome<ref name="Strayer, 2012" /> - [http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0031334 (Full Text)]
*2012, A Multicenter Blinded Analysis Indicates No Association between [[ME/CFS|Chronic Fatigue Syndrome/Myalgic Encephalomyelitis]] and either [[Xenotropic murine leukemia virus-related virus|Xenotropic Murine Leukemia Virus-Related Virus]] or Polytropic Murine Leukemia Virus<ref name="Alter, et al, 2012" /> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3448165/ (Full Text)]
*2012, Gene expression alterations at baseline and following moderate [[exercise]] in patients with [[Chronic Fatigue Syndrome]] and [[Fibromyalgia]] Syndrome<ref name="Light, 2012" /> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175315/ (Full Text)]
*2013, Differing [[leukocyte]] gene expression profiles associated with fatigue in patients with prostate cancer versus [[chronic fatigue syndrome]]<ref>{{Cite journal|last = Light | first = Kathleen C. | authorlink = Kathleen Light | last2 = Agarwal | first2 = Neeraj | authorlink2 = | last3 = Iacob | first3 = Eli | authorlink3 = | last4 = White | first4 = Andrea T. | authorlink4 = | last5 = Kinney | first5 = Anita Y. | authorlink5 = | last6 = VanHaitsma | first6 = Timothy A. | authorlink6 = | last7 = Aizad | first7 = Hannah | last8 = Hughen | first8 = Ronald W. | last9 = Bateman | first9 = Lucinda | authorlink9 = Lucinda Bateman | date = Dec 2013 | title = Differing leukocyte gene expression profiles associated with fatigue in patients with prostate cancer versus chronic fatigue syndrome|url=https://linkinghub.elsevier.com/retrieve/pii/S0306453013002977|journal=Psychoneuroendocrinology|language=en|volume=38|issue=12|pages=2983–2995|doi=10.1016/j.psyneuen.2013.08.008|pmc = 3848711|pmid=24054763|access-date=|quote=|via=}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3848711/ (Full Text)]
*2014, No association found between the detection of either [[xenotropic murine leukemia virus-related virus]] or polytropic murine leukemia virus and [[chronic fatigue syndrome]] in a blinded, multi-site, prospective study by the establishment and use of the [[SolveCFS BioBank & Patient Registry|SolveCFS BioBank]]<ref>{{Cite journal|last = Irlbeck|first = David M. | last2 = Vernon | first2 = Suzanne D. | authorlink2 = Suzanne Vernon | last3 = McCleary | first3 = K. Kimberly | authorlink3 = Kim McCleary | last4 = Bateman | first4 = Lucinda | authorlink4 = Lucinda Bateman | last5 = Klimas | first5 = Nancy G. | authorlink5 = Nancy Klimas | last6 = Lapp | first6 = Charles W. | authorlink6 = Charles Lapp | last7 = Peterson | first7 = Daniel L. | authorlink7 = Daniel Peterson | last8 = Brown | first8 = James R. | last9 = Remlinger | first9 = Katja S.| date = 2014 | title = No association found between the detection of either xenotropic murine leukemia virus-related virus or polytropic murine leukemia virus and chronic fatigue syndrome in a blinded, multi-site, prospective study by the establishment and use of the SolveCFS BioBank | url =https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4236736/|journal=BMC Research Notes|volume=7 | pages = 461|doi=10.1186/1756-0500-7-461|via= | last10 = Wilfret | last11 = Gerondelis | first11 = Peter | first10 = David A.}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4236736/ (Full Text)]
*2015, Findings from a clinical and laboratory database developed for discovery of pathogenic mechanisms in [[ME/CFS|myalgic encephalomyelitis/chronic fatigue syndrome]]<ref name="KlimasNG, 2015" /> - [http://www.tandfonline.com/doi/full/10.1080/21641846.2015.1023652 (Abstract)]
*2015, [[Chronic fatigue syndrome]] and co-morbid and consequent conditions: evidence from a multi-site clinical epidemiology study<ref name="BatemanL, 2015" /> - [http://www.tandfonline.com/doi/full/10.1080/21641846.2014.978109 (Abstract)]
* 2015, Distinct plasma immune signatures in ME/CFS are present early in the course of illness<ref>{{Cite journal | last1 = Hornig | first1 = M | authorlink = Mady Hornig | last2 = Montoya | first2 = JG | authorlink2 = Jose Montoya | last3 = Klimas | first3 = NG | authorlink3 = Nancy Klimas | last4 = Levine | first4 = SM | authorlink4 = Susan Levine | last5 = Felsenstein | first5 = D | authorlink5 = Donna Felsenstein | last6 = Bateman | first6 = L | authorlink6=Lucinda Bateman | last7 = Peterson | first7 = DL | authorlink7 = Daniel Peterson | last8 = Gottschalk | first8 = CG | authorlink8 = Gunnar Gottschalk | last9 = Schultz|first9 = AF | authorlink9=Andrew Schultz | last10 = Che | first10 = X | authorlink10=Xiaoyu Che | last11 = Eddy | first11 = ML | authorlink11=Meredith Eddy | last12 = Komaroff | first12 = AL | authorlink12=Anthony Komaroff | last13 = Lipkin | first13 = WI | authorlink13 = Ian Lipkin | title = Distinct plasma immune signatures in ME/CFS are present early in the course of illness|journal=Science Advances|volume=1|issue=1 | page = | date = 2015 | pmid = |doi =10.1126/sciadv.1400121 | url = http://advances.sciencemag.org/content/1/1/e1400121.full}}</ref> - [https://advances.sciencemag.org/content/1/1/e1400121 (Full text)]
*2016, Treatment of [[postural orthostatic tachycardia syndrome]] and management of [[ME/CFS|myalgic encephalomyelitis/chronic fatigue syndrome]] following suspected West Nile virus infection<ref name="Baldwin, 2016" /> - [http://www.tandfonline.com/doi/full/10.1080/21641846.2016.1247971 (Abstract)]
*2017, Multi-Site Clinical Assessment of [[ME/CFS|Myalgic Encephalomyelitis/Chronic Fatigue Syndrome]] (MCAM): Design and Implementation of a Prospective/Retrospective Rolling Cohort Study<ref name="Unger, 2017" /> - [https://www.ncbi.nlm.nih.gov/pubmed/28338983 (Abstract)]
*2017, Multi-Site Clinical Assessment of [[ME/CFS|Myalgic Encephalomyelitis/Chronic Fatigue Syndrome]] (MCAM): Design and Implementation of a Prospective/Retrospective Rolling Cohort Study<ref name="Unger, 2017" /> - [https://www.ncbi.nlm.nih.gov/pubmed/28338983 (Abstract)]
*2017, Fecal metagenomic profiles in subgroups of patients with [[ME/CFS|myalgic encephalomyelitis/chronic fatigue syndrome]]<ref name="Nagy-Szakal, 2017" /> - [https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-017-0261-y (Full Text)]
*2018, KPAX002 as a treatment for [[ME/CFS|Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)]]: A prospective, randomized trial<ref name="Montoya, 2018" /> - [http://www.ijcem.com/files/ijcem0065685.pdf (Full Text)]
*2018, Insights into [[ME/CFS|myalgic encephalomyelitis/chronic fatigue syndrome]] phenotypes through comprehensive [[metabolomics]]<ref name="Nagy-Szakal, 2018" /> - [https://www.nature.com/articles/s41598-018-28477-9.pdf (Full Text)]
*2019, Estimating Prevalence, Demographics, and Costs of ME/CFS Using Large Scale Medical Claims Data and Machine Learning<ref>{{Cite journal | last = Proskauer | first = Charmian | authorlink = Charmian Proskauer | last2 = Rowe | first2 = Peter C. | authorlink2 = Peter Rowe | last3 = Lapp | first3 = Charles W. | authorlink3 = Charles Lapp | last4 = DeMaria | first4 = Alfred Jr | authorlink4 = | last5 = Bateman | first5 = Lucinda | authorlink5 = Lucinda Bateman | last6 = Attewell | first6 = John R. | last7 = Proskauer | first7 = Daniel | last8 = Kiernicki | first8 = David J. | last9 = Adebayo | first9 = Seyi | date = 2019 | title=Estimating Prevalence, Demographics, and Costs of ME/CFS Using Large Scale Medical Claims Data and Machine Learning | url =https://www.frontiersin.org/articles/10.3389/fped.2018.00412/full|journal=Frontiers in Pediatrics|language=English|volume=6|issue=|pages=|doi=10.3389/fped.2018.00412|issn=2296-2360|pmc=|pmid=30671425|quote=|via=}}</ref> - [https://www.frontiersin.org/articles/10.3389/fped.2018.00412/full (Full text)]
* Aug 2019, Editorial: Advances in ME/CFS Research and Clinical Care<ref>{{Cite journal | last = Friedman | first = Kenneth | authorlink = Kenneth Friedman | last2 = Bateman | first2 = Lucinda | authorlink2 = Lucinda Bateman | last3 = Bested | first3 = Alison C. | authorlink3 = Alison Bested | last4 = Nahle | first4 = Zaher | authorlink4 = Zaher Nahle | date = Aug 2019 | title = Editorial: Advances in ME/CFS Research and Clinical Care|url=https://www.frontiersin.org/articles/10.3389/fped.2019.00370/full|journal=Frontiers in Pediatrics|volume=|issue=|pages=|doi=10.3389/fped.2019.00370|pmc=|pmid=|access-date=|quote=|via=}}</ref> - [https://www.frontiersin.org/articles/10.3389/fped.2019.00370/full (Full text)]
* 2019, Pilot assessment of low NK cell-mediated ADCC and FCGR3A genetics in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): Based on inclusion of family members without ME/CFS as controls, low ADCC is unsuitable as a diagnostic biomarker<ref>{{Cite journal|last = Sung|first = Alexander P. | authorlink = | last2 = Tang | first2 = Jennifer J-J | authorlink2 = | last3 = Guglielmo | first3 = Michael J | authorlink3 = | last4 = Smith-Gagen | first4 = Julie | authorlink4 = | last5 = Bateman | first5 = Lucinda | authorlink5 = Lucinda Bateman | last6 = Redelman | first6 = Doug D. | authorlink6 = | last7 = Hudig | first7 = Dorothy | date = 2019-12-27 | title = Pilot assessment of low NK cell-mediated ADCC and FCGR3A genetics in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): Based on inclusion of family members without ME/CFS as controls, low ADCC is unsuitable as a diagnostic biomarker |url =http://medrxiv.org/lookup/doi/10.1101/2019.12.20.19015438|journal=MedRxIV|language=en|volume=|issue=|pages=|doi=10.1101/2019.12.20.19015438|pmc=|pmid=|access-date=|quote=|via=}}</ref> - [https://www.medrxiv.org/content/10.1101/2019.12.20.19015438v1 (Abstract)]
* 2019, Perturbation of effector and regulatory [[T cell]] subsets in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)<ref>{{Cite journal | last = Karhan | first = Ece | last2 = Gunter | first2 = Courtney L | last3 = Ravanmehr | first3 = Vida | last4 = Horne | first4 = Meghan | last5 = Kozhaya | first5 = Lina | last6 = Renzullo | first6 = Stephanie | last7 = Placek | first7 = Lindsey | last8 = George | first8 = Joshy | last9 = Robinson | first9 = Peter N | last10 = Vernon | first10 = Suzanne D. | authorlink10 = Suzanne Vernon | last11 = Bateman | first11 = Lucinda | authorlink11 = Lucinda Bateman | last12 = Unutmaz | first12 = Derya | authorlink12 = Derya Unutmaz | date = 2019-12-26 | title = Perturbation of effector and regulatory T cell subsets in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)|journal=biorxiv|url=http://biorxiv.org/lookup/doi/10.1101/2019.12.23.887505|language=en|doi=10.1101/2019.12.23.887505}}</ref> - [https://www.biorxiv.org/content/10.1101/2019.12.23.887505v1.full (Full text)]
*2020, Hemodynamics during the 10-minute NASA Lean Test: evidence of circulatory decompensation in a subset of ME/CFS patients<ref>{{Cite journal|last = Lee | first = Jihyun | authorlink = | last2 = Vernon | first2 = Suzanne D. | authorlink2 = Suzanne Vernon | last3 = Jeys | first3 = Patricia | authorlink3 = | last4 = Ali | first4 = Weam | authorlink4 = | last5 = Campos | first5 = Andrea | authorlink5 = | last6 = Unutmaz | first6 = Derya | authorlink6 = Derya Unutmaz | last7 = Yellman | first7 = Brayden | last8 = Bateman | first8 = Lucinda | authorlink8 = Lucinda Bateman | date = Dec 2020 | title = Hemodynamics during the 10-minute NASA Lean Test: evidence of circulatory decompensation in a subset of ME/CFS patients|url=https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-020-02481-y|journal=Journal of Translational Medicine|language=en|volume=18|issue=1 | pages = 314|doi=10.1186/s12967-020-02481-y|issn=1479-5876|pmc = 7429890|pmid=32799889|access-date=|quote=|via=}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7429890/ (Full text)]
*2021, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Essentials of Diagnosis and Management<ref name="Essentials2021">{{Cite journal | title = Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Essentials of Diagnosis and Management | date = 2021-11-01|url=https://www.sciencedirect.com/science/article/pii/S0025619621005139|journal=Mayo Clinic Proceedings|volume=96|issue=11|pages=2861–2878|last = Bateman | first = Lucinda | authorlink = Lucinda Bateman | last2 = Bested | first2 = Alison C. | authorlink2 = Alison Bested | last3 = Bonilla | first3 = Hector F. | authorlink3 = Hector Bonilla | last4 = Chheda | first4 = Bela V. | authorlink4 = Bela Chheda | last5 = Chu | first5 = Lily | authorlink5 = Lily Chu | last6 = Curtin | first6 = Jennifer M. | authorlink6 = | last7 = Dempsey | first7 = Tania T. | last8 = Dimmock | first8 = Mary E. | authorlink8 = Mary Dimmock | last9 = Dowell | first9 = Theresa G. | last10 = Felsenstein | first10 = Donna | last11 = Kaufman | first11 = David L. | authorlink11 = David Kaufman|language=en|doi=10.1016/j.mayocp.2021.07.004|pmc=|pmid=|access-date=|issn=0025-6196|quote=|via=}}</ref> - [https://www.sciencedirect.com/science/article/pii/S0025619621005139 (Full text)]

==Clinic location==
[https://batemanhornecenter.org/ The Bateman Horne Center]

24 S. 1100 E., Suite 205

Salt Lake City, Utah 84102

<nowiki>Tel: 1-801-359-7400
</nowiki>

==Talks and interviews==
*Sep 9, 2014, [http://www.fcclinic.com/SLEEP%20research%20CDC%20talk%20090914%20final.pdf ''Can ME/CFS and FM Research Help You Sleep?'']
*2015, [[Spoonie Radio]] Episode 10 Guest - Dr. Lucinda Bateman - [http://www.drcourtneycraig.com/blog/2015/5/6/spoonie-radio-ep-10-dr-lucinda-bateman Podcast and Full Text Transcript]
*2016, [https://www.youtube.com/watch?v=ru8o-n-u_Ts Simple But Effective Tools for Management of ME/CFS and FM - Lucinda Bateman, MD]
*2016, [https://www.youtube.com/watch?v=kXTt_JFDQ5w&feature=em-subs_digest BHC Wings to Fly - Dr. Bateman]
*2016, [http://iacfsme.org/Conferences/2016-Fort-Lauderdale/Agenda/Professional-Agenda.aspx 12th International IACFS/ME Biennial Clinical and Research Conference, Emerging Science and Clinical Care, Paper presentation:''Synergy Trial for CFS – a phase 2 study of low-dose methylphenidate plus mitochondrial support'']
*May 3-5, 2018, [[ME/CFS Canadian Collaborative Team Conference]] - Speech title: ''Objective Diagnosis of ME/CFS''<ref>{{Cite web|url=https://fourwaves-sots.s3.amazonaws.com/static/media/uploads/5FFGG5h0kBRlJTgexdugaQ%3D%3D/2018/04/24/me_cfs_final-program.pdf | title=ME/CFS Canadian Collaborative Team Conference program|last = | first = | authorlink = | date = | website = |archive-url=|archive-date=|url-status=|access-date=2019-03-06}}</ref>
*Oct 23, 2021, [https://youtu.be/goPzV8U8MNU Clinical Perspective and Impact of Long Covid]

==Webinars ==

'''Science to patients / Wetenschap voor patienten'''

*2015, [https://youtu.be/1TogkD07tHA 68. Introduction and diagnosis / intriductie en diagnose - Dr. Lucinda Bateman]
*2015, [https://youtu.be/HiiLYbCzfIM 69. Autoimmunity in ME/cfs / Auto-immuniteit bij ME/cvs - Dr. Lucinda Bateman]
*2015, [https://youtu.be/la3HQtoJWzE 70. Neuroinflammation and ME/cfs / Neuro-inflammatie en ME/cvs - Dr. Lucinda Bateman]
*2015, [https://youtu.be/OZ39Jy9Z9QI 71. ME/cfs and the Brain/ ME/cvs en de hersenen - Dr. Lucinda Bateman]
*2015, [https://youtu.be/F1PP21TmUPs 72. Gene-expression and exercise / gen-expressie en inspanning - Dr. Lucinda Bateman]
*2015, [https://youtu.be/p70hBlLgtaI 73. FAQs part 1 / Veel gestelde vragen deel 1 - Dr. Lucinda Bateman]
*2015, [https://youtu.be/QuXO8RCjyWQ 74. FAQs part 2 / Veel gestelde vragen deel 2 - Dr. Lucinda Bateman]

'''Solve ME/CFS Initiative'''

*[https://www.youtube.com/watch?v=359XmpNBHM8 Apr 17, 2015 "Will SEID Diagnostic Criteria Improve Diagnosis and Treatment?"]
*[https://www.youtube.com/watch?v=w4OEGOCw3Dg&feature=youtu.be Nov 14, 2014 "Can ME CFS and Fibromyalgia Research Help You Sleep?"]

==Blog posts==
*October 17, 2016, [http://solvecfs.org/pearls-of-wisdom-from-an-mecfs-physician-part-1/ Pearls of Wisdom from an ME/CFS Physician, part 1]
*October 17, 2016, [http://solvecfs.org/pearls-of-wisdom-from-an-mecfs-physician-part-2/ Pearls of Wisdom from an ME/CFS Physician, part 2]
*October 17, 2016, [http://solvecfs.org/pearls-of-wisdom-from-a-cfs-physician-part-3/ Pearls of Wisdom from a CFS Physician, part 3]

==Online presence==
*[https://www.ncbi.nlm.nih.gov/pubmed/?term=Bateman+Lucinda%5BAuthor%5D PubMed - Lucinda Bateman]
*[https://twitter.com/LBatemanMD Twitter]
*[https://www.facebook.com/lucinda.bateman.1?fref=ts Facebook]
*[https://batemanhornecenter.org/ Website - Bateman Horne Center]
*[https://www.youtube.com/user/OFFERUtah YouTube]

==See also==
*[[Bateman Horne Center]]
*[[Suzanne Vernon]]
==Learn more==
*[http://www.cortjohnson.org/chronic-fatigue-syndrome-mecfs-doctor-resource-center/dr-lucinda-bateman/ Cort Johnson - Lucinda Bateman profile]
*[https://batemanhornecenter.org/drlucindabateman/ Lucinda Bateman]

==References==
<references>
<ref name="Albright, 2011">{{Citation | last1 = Albright | first1 = Frederick | authorlink1 = | last2 = Light | first2 = Kathleen | authorlink2 = Kathleen Light | last3 = Light | first3 = Alan | authorlink3 = Alan Light | last4 = Bateman | first4 = Lucinda | authorlink4 = Lucinda Bateman | last5 = Cannon-Albright | first5 = Lisa A | authorlink5 = | title = Evidence for a heritable predisposition to Chronic Fatigue Syndrome | journal = BMC Neurology | volume = 11 | issue = 62 | page = | date = 2011 | doi = 10.1186/1471-2377-11-62 }}</ref>
<ref name="Alter, et al, 2012">{{Citation | last1 = Alter | first1 = Harvey J. | authorlink1 = | last2 = Mikovits | first2 = Judy A. | authorlink2 = Judy Mikovits | last3 = Switzer | first3 = William M. | authorlink3 = | last4 = Ruscetti | first4 = Francis W. | authorlink4 = | last5 = Lo | first5 = Shyh-Ching | authorlink5 = | last6 = Klimas | first6 = Nancy | authorlink6 = Nancy Klimas | last7 = Komaroff | first7 = Anthony L. | authorlink7 = Anthony Komaroff | last8 = Montoya | first8 = Jose G. | authorlink8 = Jose Montoya | last9 =Bateman | first9 = Lucinda | authorlink9 = Lucinda Bateman | last10 = Levine | first10 = Susan | authorlink10 = Susan Levine | last11 = Peterson | first11 = Daniel | authorlink11 = Daniel Peterson | last12 = Levin | first12 = Bruce | authorlink12 = Bruce Levin | last13 = Hanson | first13 = Maureen R. | authorlink13 = Maureen Hanson | last14 = Genfi | first14 = Afia | authorlink14 = | last15 = Bhat | first15 = Meera | authorlink15 = | last16 = Zheng | first16 = HaoQiang | authorlink16 = | last17 = Wang | first17 = Richard | authorlink17 = | last18 = Li | first18 = Bingjie | authorlink18 = | last19 = Hung | first19 = Guo-Chiuan | authorlink19 = | last20 = Lee | first20 = Li Ling | authorlink20 = | last21 = Sameroff | first21 = Stephen | authorlink21 = | last22 = Heneine | first22 = Walid | authorlink22 = | last23 = Coffin | first23 = John | authorlink23 = | last24 = Hornig | first24 = Mady | authorlink24 = Mady Hornig | last25 = Lipkin | first25 = W. Ian | authorlink25 = Ian Lipkin | title = A Multicenter Blinded Analysis Indicates No Association between Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and either Xenotropic Murine Leukemia Virus-Related Virus or Polytropic Murine Leukemia Virus | journal = mBio | volume = 3 | issue = 5 | page = e00266–12 | date = 2012 | pmid = | doi = 10.1128/mBio.00266-12 }}</ref>
<ref name="Baldwin, 2016">{{Citation | last1 = Baldwin | first1 = Nicole L. | authorlink1 = | last2 = Murray | first2 = Kristy O. | authorlink2 = | last3 = Garcia | first3 = Melissa N. | authorlink3 = | last4 = Bateman | first4 = Lucinda | authorlink4 = Lucinda Bateman | title = Treatment of postural orthostatic tachycardia syndrome and management of myalgic encephalomyelitis/chronic fatigue syndrome following suspected West Nile virus infection | journal = Fatigue: Biomedicine, Health & Behavior | volume = 4 | issue = 4 | page = 226-236 | date = 2016 | doi = 10.1080/21641846.2016.1247971 }}</ref>
<ref name="BatemanL, 2015">{{Citation | last1 = Bateman | first1 = L. | authorlink1 = Lucinda Bateman | last2 = Darakjy | first2 = S. | authorlink2 = | last3 = Klimas | first3 = N. | authorlink3 = Nancy Klimas | last4 = Peterson | first4 = D. | authorlink4 = Daniel Peterson | last5 = Levine | first5 = S.M. | authorlink5 = Susan Levine | last6 = Allen | first6 = A. | authorlink6 = | last7 = Carlson | first7 = S.A. | authorlink7 = | last8 = Balbin | first8 = E.G. | authorlink8 = Elizabeth Balbin | last9 = Gottschalk | first9 = G. | authorlink9 = Gunnar Gottschalk | last10 = March | first10 = D. | authorlink10 = | title = Chronic fatigue syndrome and co-morbid and consequent conditions: evidence from a multi-site clinical epidemiology study | journal = Fatigue: Biomedicine, Health & Behavior | volume = 3 | issue = 1 | page = 1-15 | date = 2015 | pmid = | doi = 10.1080/21641846.2014.978109 }}</ref>
<ref name="KlimasNG, 2015">{{Citation | last1 = Klimas | first1 = N.G. | authorlink1 = Nancy Klimas | last2 = Ironson | first2 = G. | authorlink2 = | last3 = Carter | first3 = A. | authorlink3 = | last4 = Balbin | first4 = E. | authorlink4 = Elizabeth Balbin | last5 = Bateman | first5 = L. | authorlink5 = Lucinda Bateman | last6 =Felsenstein | first6 = D. | authorlink6 = Donna Felsenstein | last7 = Levine | first7 = S. | authorlink7 = Susan Levine | last8 = Peterson | first8 = D. | authorlink8 = Daniel Peterson | last9 =Chiu | first9 = K. | authorlink9 = | last10 = Allen | first10 = A. | authorlink10 = | last11 = Cunningham | first11 = K. | authorlink11 = | last12 = Gottschalk | first12 = C.G. | authorlink12 = Gunnar Gottschalk | last13 = Fletcher | first13 = M | authorlink13 = Mary Ann Fletcher | last14 = Hornig | first14 = M. | authorlink14 = Mady Hornig | last15 = Canning | first15 = C. | authorlink15 =| last16 = Komaroff | first16 = A.L. | authorlink16 = Anthony Komaroff | title = Findings from a clinical and laboratory database developed for discovery of pathogenic mechanisms in myalgic encephalomyelitis/chronic fatigue syndrome | journal = Fatigue: Biomedicine, Health & Behavior | volume = 3 | issue = 2 | page = 75-96 | date = 2015 | pmid = | doi = 10.1080/21641846.2015.1023652 }}</ref>
<ref name="Light, 2012">{{Citation | last1 = Light | first1 = Alan R | authorlink1 = Alan Light | last2 = Bateman | first2 = Lucinda | authorlink2 = Lucinda Bateman | last3 = Jo | first3 = Daehyun | authorlink3 = Daehyun Jo | last4 = Hughen | first4 = RW | authorlink4 = | last5 = Vanhaitsma | first5 = TA | authorlink5 = | last6 = White | first6 = AT | authorlink6 = | last7 = Light | first7 = Kathleen | authorlink7 = Kathleen Light | title = Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome and Fibromyalgia Syndrome | journal = Journal of Internal Medicine | volume = 271 | issue = 1 | page = 64-81 | date = 2012 | pmid = | doi = 10.1111/j.1365-2796.2011.02405.x }}</ref>
<ref name="Montoya, 2018">{{Citation | last1 = Montoya | first1 = Jose G | authorlink1 = Jose Montoya | last2 = Anderson | first2 = Jill N | authorlink2 = | last3 = Adolphs | first3 = Danya L | authorlink3 = | last4 = Bateman | first4 = Lucinda| authorlink4 = Lucinda Bateman | last5 = Klimas | first5 = Nancy | authorlink5 = Nancy Klimas | last6 = Levine | first6 = Susan M | authorlink6 = Susan Levine | last7 = Garvert | first7 = Donn W | authorlink7 = | last8 = Kaiser | first8 = Jon D | authorlink8 = Jon Kaiser | title = KPAX002 as a treatment for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A prospective, randomized trial | journal = International Journal of Clinical and Experimental Medicine | volume = 11 | issue = 3 | page = 2890-2900 | date = 2018 | pmid = | doi = | url = http://www.ijcem.com/files/ijcem0065685.pdf }}</ref>
<ref name="Nagy-Szakal, 2017">{{Citation | last1 = Nagy-Szakal | first1 = Dorottya | authorlink1 = Dorottya Nagy-Szakal | last2 = Williams | first2 = Brent L. | authorlink2 = | last3 = Mishra | first3 = Nischay | authorlink3 = | last4 = Che | first4 = Xiaoyu | authorlink4 = | last5 = Lee | first5 = Bohyun | authorlink5 = | last6 = Bateman | first6 = Lucinda | authorlink6 = Lucinda Bateman | last7 = Klimas | first7 = Nancy G. | authorlink7 = Nancy Klimas | last8 = Komaroff | first8 = Anthony L. | authorlink8 = Anthony Komaroff | last9 = Levine | first9 = Susan | authorlink9 = Susan Levine | last10 = Montoya | first10 = Jose G. | authorlink10 = Jose Montoya | last11 = Peterson | first11 = Daniel L. | authorlink11 = Daniel Peterson | last12 = Ramanan | first12 = Devi | authorlink12 = | last13 = Jain | first13 = Komal | authorlink13 = | last14 = Eddy | first14 = Meredith L. | authorlink14 = | last15 = Hornig | first15 = Mady | authorlink15 = Mady Hornig | last16 = Lipkin | first16 = W. Ian | authorlink16 = Ian Lipkin | title = Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome | journal = Microbiome | volume = 5 | issue = 44 | page = | date = 2017 | pmid = | doi = 10.1186/s40168-017-0261-y }}</ref>
<ref name="Nagy-Szakal, 2018">{{Citation | last1 = Nagy-Szakal | first1 = Dorottya | authorlink1 = Dorottya Nagy-Szakal | last2 = Barupal | first2 = Dinesh K. | authorlink2 = | last3 = Lee | first3 = Bohyun | authorlink3 = | last4 = Che | first4 = Xiaoyu | authorlink4 = | last5 = Williams | first5 = Brent L. | authorlink5 = | last6 = Kahn | first6 = Ellie J. R. | authorlink6 = | last7 = Ukaigwe | first7 = Joy E. | authorlink7 = | last8 = Bateman | first8 = Lucinda | authorlink8 = Lucinda Bateman | last9 = Klimas | first9 = Nancy G. | authorlink9 = Nancy Klimas | last10 = Komaroff | first10 = Anthony L. | authorlink10 = Anthony Komaroff | last11 = Levine | first11 = Susan | authorlink11 = Susan Levine | last12 = Montoya | first12 = Jose G. | authorlink12 = Jose Montoya | last13 = Peterson | first13 = Daniel L. | authorlink13 = Daniel Peterson | last14 = Levin | first14 = Bruce | authorlink14 = Bruce Levin | last15 = Hornig | first15 = Mady | authorlink15 = Mady Hornig | last16 = Fiehn | first16 = Oliver | authorlink16 = | last17 = Lipkin | first17 = W. Ian | authorlink17 = Ian Lipkin | title = Insights into myalgic encephalomyelitis/chronic fatigue syndrome phenotypes through comprehensive metabolomics | journal = Scientific Reports | volume = 8 | issue = 1 | page = 10056 | date = 2018 | pmid = | doi = 10.1038/s41598-018-28477-9 }}</ref>
<ref name="Nov, 2006">{{citation | author = HHS.gov | title = Nov 20 & 21, 2006 CFSAC Meeting
| type = Minutes | date = 2006 | url = http://wayback.archive-it.org/3919/20140324192930/http://www.hhs.gov/advcomcfs/meetings/minutes/cfsac061120min_pdf.pdf }}</ref>
<ref name="Spring, 2009">{{citation | author = HHS.gov | title = May 27 & 28, 2009 CFSAC Meeting
| type = Roster | date = 2009 | url = http://wayback.archive-it.org/3919/20140324192913/http://www.hhs.gov/advcomcfs/meetings/minutes/cfsac052709min.pdf }}</ref>
<ref name="Strayer, 2012">{{Citation | last1 = Strayer | first1 = DR | authorlink1 = David Strayer | last2 = Carter | first2 = WA | authorlink2 = William Carter | last3 = Stouch | first3 = BC | authorlink3 = | last4 = Stevens | first4 = SR | authorlink4 = Staci Stevens | last5 = Bateman | first5 = L | authorlink5 = Lucinda Bateman | last6 = Cimoch | first6 = PJ | authorlink6 = | last7 = Lapp | first7 = CW | authorlink7 = Charles Lapp | last8 = Peterson | first8 = DL | authorlink8 = Daniel Peterson | last9 =Chronic Fatigue Syndrome AMP-516 Study Group | authorlink9 = | last10 = Mitchell | first10 = WM | authorlink10 = William Mitchell | title = A double-blind, placebo-controlled, randomized, clinical trial of the TLR-3 agonist rintatolimod in severe cases of chronic fatigue syndrome. | journal = PLoS One | volume = 7 | issue = 3 | page = e31334 | date = 2012 | pmid = 22431963 | doi = 10.1371/journal.pone.0031334 }}</ref>
<ref name="Unger, 2017">{{Citation | last1 = Unger | first1 = Elizabeth R. | authorlink1 = Elizabeth Unger | last2 = Lin | first2 = Jin-Mann S. | authorlink2 = Jin-Mann Sally Lin | last3 = Tian | first3 = Hao | authorlink3 = | last4 = Natelson | first4 = Benjamin H | authorlink4 = Benjamin Natelson | last5 = Lange | first5 = Gudrun | authorlink5 = Gudrun Lange | last6 = Vu | first6 = Diana | authorlink6 = | last7 = Blate | first7 = Michelle | authorlink7 = | last8 = Klimas | first8 = Nancy G. | authorlink8 = Nancy Klimas | last9 =Balbin | first9 = Elizabeth G. | authorlink9 = Elizabeth Balbin | last10 = Bateman | first10 = Lucinda | authorlink10 = Lucinda Bateman | last11 = Allen | first11 = Ali | authorlink11 = | last12 = Lapp | first12 = Charles W. | authorlink12 = Charles Lapp | last13 = Springs | first13 = Wendy | authorlink13 = | last14 = Kogelnik | first14 = Andreas M. | authorlink14 = Andreas Kogelnik | last15 = Phan | first15 = Catrina C. | authorlink15 = | last16 = Danver | first16 = Joan | authorlink16 = | last17 = Podell | first17 = Richard N. | authorlink17 = Richard Podell | last18 = Fitzpatrick | first18 = Trisha | authorlink18 = | last19 = Peterson | first19 = Daniel L. | authorlink19 = Daniel Peterson | last20 = Gottschalk | first20 = C. Gunnar | authorlink20 = Gunnar Gottschalk | last21 = Rajeevan | first21 = Mangalathu S. | authorlink21 = Mangalathu Rajeevan | last22 = MCAM Study Group | title = Multi-Site Clinical Assessment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (MCAM): Design and Implementation of a Prospective/Retrospective Rolling Cohort Study. | journal = American Journal of Epidemiology | volume = 1-10 | issue = | page = | date = 2017 | pmid = | doi = 10.1093/aje/kwx029 }}</ref>
</references>

[[Category:Researchers]]
[[Category:US researchers]]
[[Category:Clinicians]]
[[Category:American clinicians]]
[[Category:Utah clinicians]]
[[Category:Psychological paradigm critics]]
[[Category:PACE trial critics]]
[[Category:CFSAC members]]
[[Category:Institute of Medicine report committee members]]

Hypoxia

2025-06-26T17:44:00Z

Notjusttired:fix

'''Hypoxia''' is a condition in which the body or a region of the body is deprived of adequate oxygen supply at the tissue level. Hypoxia may be classified as either ''generalized'', affecting the whole body, or ''local'', affecting a region of the body.

Hypoxia can be caused by insufficient blood supply or by inflammation<ref>{{Cite journal|title=Inflammatory Hypoxia: Role of Hypoxia-Inducible Factor|date=2005-02-19|url=https://www.tandfonline.com/doi/full/10.4161/cc.4.2.1407|journal=Cell Cycle|volume=4|issue=2|pages=255–257|last=Karhausen|first=Jörn|last2=Haase|first2=Volker H.|last3=Colgan|first3=Sean P.|language=en|doi=10.4161/cc.4.2.1407|issn=1538-4101}}</ref>.

Hypoxia at altitude iscaused by pressure gradient difference between the atmospheric oxygen and the oxygen in the lungs, or the oxygen in the lungs and the oxygen in other parts of the body. Hypoxia is frequently experienced as altitude sickness.

=== In ME/CFS ===

Several findings in [[Myalgic encephalomyelitis]] suggest that patients might be experiencing local or global hypoxia. For example, many studies have found reduced blood flow to the [[heart]]<ref>{{Cite journal | last = Patrick Neary|first = J. | last2 = Roberts | first2 = Andy D.W. | last3 = Leavins | first3 = Nina | last4 = Harrison | first4 = Michael F. | last5 = Croll | first5 = James C. | last6 = Sexsmith | first6 = James R. | date = Nov 2008 | title = Prefrontal cortex oxygenation during incremental exercise in chronic fatigue syndrome|url=https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1475-097X.2008.00822.x|journal=Clinical Physiology and Functional Imaging|volume=28|issue=6 | pages = 364–372|doi=10.1111/j.1475-097x.2008.00822.x|issn=1475-0961}}</ref><ref>{{Cite journal | last = Peterson | first = PK | last2 = Sirr | first2 = SA | last3 = Grammith | first3 = FC | last4 = Schenck | first4 = CH | last5 = Pheley | first5 = AM | last6 = Hu | first6 = S | last7 = Chao | first7 = C C | date = Mar 1994 | title = Effects of mild exercise on cytokines and cerebral blood flow in chronic fatigue syndrome patients.|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC368231/|journal=Clinical and Diagnostic Laboratory Immunology|volume=1|issue=2|pages=222–226|issn=1071-412X|pmid=7496949}}</ref>, [[Cerebral hypoperfusion]] (reduced blood flow to the brain) in ME/CFS,<ref name="Natelson, 2017">{{Cite journal | last1 = Natelson | first1 =Benjamin | author-link1 = Benjamin Natelson | last2 = Mao | first2 = Xiangling | author-link2 = | last3 = Stegner | first3 = Aaron J | author-link3 = | last4 = Lange | first4 = Gudrun | author-link4 = Gudrun Lange | last5 = Vu | first5 = Diana| author-link5 = | last6 = Blate | first6 = Michelle| author-link6 = | last7 = Kang | first7 = Guoxin | author-link7 = | last8 = Soto | first8 = Eli | author-link8 = | last9 = Kapusuz | first9 = Tolga| author-link9 = | last10 = Shungu | first10 = Dikoma C | author-link10 = | title = Multimodal and simultaneous assessments of brain and spinal fluid abnormalities in chronic fatigue syndrome and the effects of psychiatric comorbidity | journal = Journal of the Neurological Sciences | volume = 375 | issue = | page = 411-416 | date = 2017 | pmid = | pmc = PMC5393352 | url = https://www.ncbi.nlm.nih.gov/pmc/articles/pmc5393352/ | doi = 10.1016/j.jns.2017.02.046}}</ref><ref name="Costa1995">{{Cite journal | last = Costa | first = D.C. | last2 = Tannock | first2 = C. | last3 = Brostoff | first3 = J. | date = Nov 1995 | title = Brainstem perfusion is impaired in chronic fatigue syndrome | url =https://www.ncbi.nlm.nih.gov/pubmed/8542261 | journal = QJM: monthly journal of the Association of Physicians | volume = 88 | issue = 11 | pages = 767–773|issn=1460-2725|pmid=8542261}}</ref><ref name="Barnden2011">{{Cite journal | last = Barnden | first = Leighton R. | last2 = Crouch | first2 = Benjamin | last3 = Kwiatek | first3 = Richard | last4 = Burnet | first4 = Richard | last5 = Mernone | first5 = Anacleto | last6 = Chryssidis | first6 = Steve | last7 = Scroop | first7 = Garry | last8 = Fante | first8 = Peter Del | date = 2011 | title = A brain MRI study of chronic fatigue syndrome: evidence of brainstem dysfunction and altered homeostasis |url =https://onlinelibrary.wiley.com/doi/abs/10.1002/nbm.1692 | journal = NMR in Biomedicine|language=en | volume = 24 | issue = 10 | pages = 1302–1312|doi=10.1002/nbm.1692|issn=1099-1492|pmc=4369126|pmid=21560176}}</ref><ref name="Biswal2011">{{Cite journal | last = Biswal | first = Bharat | last2 = Kunwar | first2 = Pratap | last3 = Natelson | first3 = Benjamin H. | date = 2011-02-15 | title = Cerebral blood flow is reduced in chronic fatigue syndrome as assessed by arterial spin labeling | url =http://www.sciencedirect.com/science/article/pii/S0022510X10005666 | journal = Journal of the Neurological Sciences | volume = 301 | issue = 1 | pages = 9–11|doi=10.1016/j.jns.2010.11.018|issn=0022-510X}}</ref><ref name="Yoshiuchi2006">{{Cite journal | last = Yoshiuchi | first = Kazuhiro | last2 = Farkas | first2 = Jeffrey | last3 = Natelson | first3 = Benjamin H. | date = 2006 | title = Patients with chronic fatigue syndrome have reduced absolute cortical blood flow | url =https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1475-097X.2006.00649.x | journal = Clinical Physiology and Functional Imaging|language=en | volume = 26 | issue = 2 | pages = 83–86|doi=10.1111/j.1475-097X.2006.00649.x|issn=1475-097X}}</ref><ref>{{Cite journal | last = Freedman | first = M. | last2 = Kirsh | first2 = J.C. | last3 = Gray | first3 = B. | last4 = Chung | first4 = D.G. | last5 = Abbey | first5 = S.E. | last6 = Salit | first6 = I.E. | last7 = Ichise | first7 = M. | date = Oct 1992 | title = Assessment of regional cerebral perfusion by 99Tcm-HMPAO SPECT in chronic fatigue syndrome. | url = http://europepmc.org/abstract/med/1491843 | journal = Nuclear medicine communications | volume = 13 | issue = 10 | pages = 767–772|issn=0143-3636|pmid=1491843}}</ref><ref>{{Cite journal | last = Chao | first = C.C. | last2 = Hu | first2 = S. | last3 = Pheley | first3 = A.M. | last4 = Schenck | first4 = C.H. | last5 = Grammith | first5 = F.C. | last6 = Sirr | first6 = S.A. | last7 = Peterson | first7 = P.K. | date = 1994-03-01 | title = Effects of mild exercise on cytokines and cerebral blood flow in chronic fatigue syndrome patients. | url = https://cvi.asm.org/content/1/2/222 | journal = Clinical and Diagnostic Laboratory Immunology|language=en | volume = 1 | issue = 2 | pages = 222–226|issn=1071-412X|pmid=7496949}}</ref><ref>{{Cite journal | last = Lange | first = Gudrun | last2 = Wang | first2 = Samuel | last3 = DeLuca | first3 = John | last4 = Natelson | first4 = Benjamin H. | date = 1998-09-28 | title = Neuroimaging in chronic fatigue syndrome | url =http://www.sciencedirect.com/science/article/pii/S0002934398001752 | journal = The American Journal of Medicine | volume = 105 | issue = 3, Supplement 1 | pages = 50S–53S|doi=10.1016/S0002-9343(98)00175-2|issn=0002-9343}}</ref>, even in the absence of [[postural orthostatic tachycardia]] or [[Neurally mediated hypotension|neurally-mediated hypotension]]; cerebral hypo-metabolism (reduced metabolic activity in the brain)<ref>{{Cite journal | title = Observer independent analysis of cerebral glucose metabolism in patients with chronic fatigue syndrome | url =https://jnnp.bmj.com/content/74/7/922 | journal = Journal of Neurology, Neurosurgery & Psychiatry | date = 2003-07-01|issn=0022-3050|pmid=12810781 | pages = 922–928 | volume = 74 | issue = 7|doi=10.1136/jnnp.74.7.922|language=en | first = P. | last = Bartenstein | first2 = U.T. | last2 = Egle | first3 = M. | last3 = Schreckenberger | first4 = J. | last4 = Hardt | first5 = W.A. | last5 = Nix | first6 = T. | last6 = Siessmeier}}</ref><ref>{{Cite journal | last = Tirelli | first = Umberto | last2 = Chierichetti | first2 = Franca | last3 = Tavio | first3 = Marcello | last4 = Simonelli | first4 = Cecilia | last5 = Bianchin | first5 = Gianluigi | last6 = Zanco | first6 = Pierluigi | last7 = Ferlin | first7 = Giorgio | date = 1998-09-28 | title = Brain positron emission tomography (PET) in chronic fatigue syndrome: preliminary data | url = http://www.sciencedirect.com/science/article/pii/S000293439800179X | journal = The American Journal of Medicine | volume = 105 | issue = 3, Supplement 1 | pages = 54S–58S|doi=10.1016/S0002-9343(98)00179-X|issn=0002-9343}}</ref>; as well as elevated [[Lactic acid]] in the brain<ref name="Natelson, 20172">{{Cite journal | last1 = Natelson | first1 =Benjamin | author-link1 = Benjamin Natelson | last2 = Mao | first2 = Xiangling | author-link2 = | last3 = Stegner | first3 = Aaron J | author-link3 = | last4 = Lange | first4 = Gudrun | author-link4 = Gudrun Lange | last5 = Vu | first5 = Diana| author-link5 = | last6 = Blate | first6 = Michelle| author-link6 = | last7 = Kang | first7 = Guoxin | author-link7 = | last8 = Soto | first8 = Eli | author-link8 = | last9 = Kapusuz | first9 = Tolga| author-link9 = | last10 = Shungu | first10 = Dikoma C | author-link10 = | title = Multimodal and simultaneous assessments of brain and spinal fluid abnormalities in chronic fatigue syndrome and the effects of psychiatric comorbidity | journal = Journal of the Neurological Sciences | volume = 375 | issue = | page = 411-416 | date = 2017 | pmid = | pmc = PMC5393352 | url = https://www.ncbi.nlm.nih.gov/pmc/articles/pmc5393352/ | doi = 10.1016/j.jns.2017.02.046}}</ref> and blood<ref name=":0">{{Cite journal | last = Ghali | first = Alaa | last2 = Lacout | first2 = Carole | last3 = Ghali | first3 = Maria | last4 = Gury | first4 = Aline | last5 = Beucher | first5 = Anne-Berengere | last6 = Lozac’h | first6 = Pierre | last7 = Lavigne | first7 = Christian | last8 = Urbanski | first8 = Geoffrey | date = 2019-12-11 | title = Elevated blood lactate in resting conditions correlate with post-exertional malaise severity in patients with Myalgic encephalomyelitis/Chronic fatigue syndrome|url=https://www.nature.com/articles/s41598-019-55473-4|journal=Scientific Reports|language=en|volume=9|issue=1|pages=1–9|doi=10.1038/s41598-019-55473-4|issn=2045-2322}}</ref>. Peripheral endothelial dysfunction has also been found.<ref name="endothelial2020">{{Cite journal | last = Scherbakov|first = Nadja | authorlink = | last2 = Szklarski | first2 = Marvin | author-link2 = | last3 = Hartwig | first3 = Jelka | author-link3 = | last4 = Sotzny | first4 = Franziska | author-link4 = Franziska Sotzny | last5 = Lorenz | first5 = Sebastian | author-link5 = | last6 = Meyer | first6 = Antje | authorlink6 = Antje Meyer | last7 = Grabowski | first7 = Patricia | last8 = Doehner | first8 = Wolfram | last9 = Scheibenbogen | first9 = Carmen | authorlink9 = Carmen Scheibenbogen | date = 2020 | title=Peripheral endothelial dysfunction in myalgic encephalomyelitis/chronic fatigue syndrome|url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ehf2.12633|journal=ESC Heart Failure|language=en|volume=7|issue=3|pages=1064–1071|doi=10.1002/ehf2.12633|issn=2055-5822|pmc = 7261521|pmid=32154656|access-date=|quote=|via=}}</ref>

Elevated [[WASF3]] was found in one case study. WASF3 can be elevated in other conditions where hypoxia is a mechanism, such as cancer<ref>{{Cite journal|title=HIF1A induces expression of the WASF3 metastasis-associated gene under hypoxic conditions|date=2012-09-15|url=https://onlinelibrary.wiley.com/doi/10.1002/ijc.27631|journal=International Journal of Cancer|volume=131|issue=6|pages=E905–E915|last=Ghoshal|first=Pushpankur|last2=Teng|first2=Yong|last3=Lesoon|first3=Leslie Ann|last4=Cowell|first4=John K.|language=en|doi=10.1002/ijc.27631|pmc=PMC3629704|pmid=22581642}}</ref><ref>{{Cite journal|title=Targeting WASF3 Signaling in Metastatic Cancer|date=2021|url=https://www.mdpi.com/1422-0067/22/2/836|journal=International Journal of Molecular Sciences|volume=22|issue=2|pages=836|last=Loveless|first=Reid|last2=Teng|first2=Yong|language=en|doi=10.3390/ijms22020836|pmc=7830529|pmid=33467681|issn=1422-0067}}</ref>, and in animal models<ref>{{Cite journal|title=Comparative transcriptome analysis of the swimbladder reveals expression signatures in response to low oxygen stress in channel catfish, Ictalurus punctatus|date=2018-08-01|url=https://www.physiology.org/doi/10.1152/physiolgenomics.00125.2017|journal=Physiological Genomics|volume=50|issue=8|pages=636–647|last=Yang|first=Yujia|last2=Fu|first2=Qiang|last3=Wang|first3=Xiaozhu|last4=Liu|first4=Yang|last5=Zeng|first5=Qifan|last6=Li|first6=Yun|last7=Gao|first7=Sen|last8=Bao|first8=Lisui|last9=Liu|first9=Shikai|last10=Gao|first10=Dongya|last11=Dunham|first11=Rex|language=en|doi=10.1152/physiolgenomics.00125.2017|issn=1094-8341}}</ref><ref>{{Cite journal|title=Hypoxia-related gene expression in porcine skeletal muscle tissues at different altitude|date=2015-09-01|url=https://doi.org/10.4238/2015.September.28.10|journal=Genetics and molecular research|volume=14|issue=3|pages=11587–11593|last=Zhang|first=J|last2=Chen|first2=L|last3=Long|first3=K R|last4=Mu|first4=Z P|doi=10.4238/2015.september.28.10|pmid=26436399|issn=1676-5680}}</ref>. [[Natural killer cell]] function<ref name="Barker1994">{{Cite journal | last1 = Barker | first1 = Edward | authorlink1 = | last2 = Fujimura | first2 = Sue F. | authorlink2 = | last3 = Fadem | first3 = Mitchell B. | authorlink3 = | last4 = Landay | first4 = Alan L. | authorlink4 = | last5 = Levy | first5 = Jay A. | authorlink5 = Jay Levy | title = Immunologic Abnormalities Associated with Chronic Fatigue Syndrome | journal = Clin Infect Dis. | date = 1994 | volume = 18 | issue = Suppl 1 | pages = S136-S141 | doi = 10.1093/clinids/18.Supplement_1.S136 | url = http://cid.oxfordjournals.org/content/18/Supplement_1/S136.short }}</ref><ref name="WhitesideTL1998">{{citation | last1 = Whiteside | first1 = TL | last2 = Friberg | first2 = D | title = Natural killer cells and natural killer cell activity in chronic fatigue syndrome. | journal = Am J Med | date = 1998 | volume= 105 | issue= 3A | pages = 27S-34S | pmid = 9790479 | doi= }}</ref><ref name="BrenuEW2014">{{Cite journal | last1 = Brenu | first1 = EW | authorlink1 = Ekua Brenu | last2 = Huth | first2 = TK | authorlink2 = Teilah Huth | last3 = Hardcastle | first3 = SL | authorlink3 = Sharni Hardcastle | last4 = Fuller | first4 = K | authorlink4 = | last5 = Kaur | first5 = M | authorlink5 = | last6 = Johnston | first6 = S | authorlink6 = | last7 = Ramos | first7 = S | authorlink7 = Sandra Ramos | last8 = Staines | first8 = D | authorlink8 = Donald Staines | last9 =Marshall-Gradisnik | first9 = S | authorlink9 = Sonya Marshall-Gradisnik | title = The Role of adaptive and innate immune cells in chronic fatigue syndrome/myalgic encephalomyelitis | journal = International Immunology | date = 2014 | volume = 26 | issue = 4 | pages = 233-42 | pmid = 24343819 | doi = 10.1093/intimm/dxt068 }}</ref><ref name="FletcherMA2002">{{citation | last1 = Fletcher | first1 = Mary Ann | authorlink1 = Mary Ann Fletcher | last2 = Maher | first2 = Kevin J | authorlink2 = | last3 = Klimas | first3 = Nancy | authorlink3 = Nancy Klimas | title = Natural killer cell function in chronic fatigue syndrome | journal = Clinical and Applied Immunology Reviews | volume = 2 | issue = 2 | date = April 2002 | pages = 129–139 | doi = 10.1016/S1529-1049(01)00047-2 | url = http://www.sciencedirect.com/science/article/pii/S1529104901000472 }}</ref><ref name="BrenuEW2012">{{citation | last1 = Brenu | first1 = Ekua W | authorlink1 = Ekua Brenu | last2 = van Driel | first2 = Mieke L | authorlink2 = | last3 = Staines | first3 = Donald R | authorlink3 = Donald Staines | last4 = Ashton | first4 = Kevin J | authorlink4 = | last5 = Hardcastle | first5 = Sharni L | authorlink5 = Sharni Hardcastle | last6 = Keane | first6 = James | authorlink6 = | last7 = Tajouri | first7 = Lotti | authorlink7 = | last8 = Peterson | first8 = Daniel | authorlink8 = Daniel Peterson | last9 =Ramos | first9 = Sandra B | authorlink9 = Sandra Ramos | last10 = Marshall-Gradisnik | first10 = Sonya M | authorlink10 = Sonya Marshall-Gradisnik | title = Longitudinal investigation of natural killer cells and cytokines in chronic fatigue syndrome/myalgic encephalomyelitis | journal = Journal of Translational Medicine | date = 2012 | volume = 10 | issue = | pages = 88 | doi = 10.1186/1479-5876-10-88 | url = http://www.translational-medicine.com/content/10/1/88 }}</ref>, lower in ME/CFS patients, is also reduced in conditions of hypoxia.<ref>{{Cite journal|title=NK Cells Under Hypoxia: The Two Faces of Vascularization in Tumor and Pregnancy|date=2022|url=https://www.frontiersin.org/articles/10.3389/fimmu.2022.924775|journal=Frontiers in Immunology|volume=13|last=Garcés-Lázaro|first=Irene|last2=Kotzur|first2=Rebecca|last3=Cerwenka|first3=Adelheid|last4=Mandelboim|first4=Ofer|doi=10.3389/fimmu.2022.924775/full|issn=1664-3224}}</ref> [[Mast cell|Mast cells]], increased in ME/CFS patients, can create conditions similar to hypoxia while conversely, systemic hypoxia causes mast cell deganulation.<ref>{{Cite journal|title=Mast cells mediate the microvascular inflammatory response to systemic hypoxia|date=2003-01-01|url=https://www.physiology.org/doi/10.1152/japplphysiol.00637.2002|journal=Journal of Applied Physiology|volume=94|issue=1|pages=325–334|last=Steiner|first=Dawn R. S.|last2=Gonzalez|first2=Norberto C.|last3=Wood|first3=John G.|language=en|doi=10.1152/japplphysiol.00637.2002|issn=8750-7587}}</ref>

Preliminary data from the [[UK ME/CFS biobank]] show an association between increased risk of ME/CFS and a gene variant that encodes for a subunit of [[prolyl 4-hydroxylase]] subunit alpha 1 (P4HA1), which encodes for [[procollagen-proline dioxygenase]], an enzyme involved in the production of collagen. P4HA1 also plays a role in the regulation of [[energy metabolism]] via downregulation of [[pyruvate dehydrogenase]] during [[hypoxia]].<ref>{{Cite journal|title=Therapeutic inhibition of prolyl hydroxylase domain-containing enzymes in surgery: putative applications and challenges|date=Jan 2015|url=https://www.dovepress.com/therapeutic-inhibition-of-prolyl-hydroxylase-domain-containing-enzymes-peer-reviewed-fulltext-article-HP|journal=Hypoxia|volume=3|pages=1|last=Schneider|first=Martin|last2=Harnoss|first2=Jonathan Michael|last3=Strowitzki|first3=Moritz J.|last4=Radhakrishnan|first4=Praveen|last5=Platzer|first5=Lisa|last6=Harnoss|first6=Julian Camill|last7=Hank|first7=Thomas|last8=Cai|first8=Jun|last9=Ulrich|first9=Alexis|language=English|doi=10.2147/HP.S60872|issn=2324-1128}}</ref>

[[Creatine]], elevated in #MECFS patients<ref>{{Cite journal | last = Albrecht | first = Robert | date = March 21, 1964 | title = Epidemic Neuromyasthenia Outbreak in a Convent in New York State|url=https://www.ncbi.nlm.nih.gov/pubmed/14100144|journal=Journal of the American Medical Association|volume=187 | pages = 904-907|via=}}</ref>, is protective against hypoxia<ref>{{Cite journal|title=Exogenous creatine delays anoxic depolarization and protects from hypoxic damage: dose–effect relationship|date=1999-01-16|url=https://www.sciencedirect.com/science/article/pii/S0006899398011317|journal=Brain Research|volume=816|issue=1|pages=124–130|last=Balestrino|first=Maurizio|last2=Rebaudo|first2=Renata|last3=Lunardi|first3=Gianluigi|doi=10.1016/S0006-8993(98)01131-7|issn=0006-8993}}</ref>.

Hypoxia can induce mitochondrial damage and dysfunction<ref>{{Cite journal|title=Hypoxia–reoxygenation-induced mitochondrial damage and apoptosis in human endothelial cells are inhibited by vitamin C|date=2005-05-15|url=https://www.sciencedirect.com/science/article/pii/S0891584905000353|journal=Free Radical Biology and Medicine|volume=38|issue=10|pages=1311–1322|last=Dhar-Mascareño|first=Manya|last2=Cárcamo|first2=Juan M.|last3=Golde|first3=David W.|doi=10.1016/j.freeradbiomed.2005.01.017|issn=0891-5849}}</ref>, which has been found in ME/CFS patients<ref>{{Cite journal | last = Behan | first = W. M.H. | last2 = More | first2 = I.A.R. | last3 = Behan | first3 = P.O. | date = Dec 1991 | title = Mitochondrial abnormalities in the postviral fatigue syndrome|url=https://link.springer.com/article/10.1007/BF00294431|journal=Acta Neuropathologica|language=en|volume=83|issue=1 | pages = 61–65|doi=10.1007/bf00294431|issn=0001-6322}}</ref><ref name=":02">{{Cite journal | date = 1996-04-19 | title = Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome|url=https://www.sciencedirect.com/science/article/abs/pii/0304394096125593|journal=Neuroscience Letters|language=en|volume=208|issue=2|pages=117–120|doi=10.1016/0304-3940(96)12559-3|issn=0304-3940}}</ref>.

=== In Long COVID ===

=== In mast cell activation syndrome ===

==Learn more==

*[http://science.sciencemag.org/content/352/6281/54 Hypoxia as a therapy for mitochondrial disease]

==See also==

== References ==
*[[Hyperbaric oxygen therapy]]

Abortive infection theory of ME/CFS

2025-06-26T17:40:13Z

Notjusttired:fix refs

[[A Martin Lerner|Dr A Martin Lerner]] developed a remarkable theory regarding the cause of myalgic encephalomyelitis / chronic fatigue syndrome: Dr Lerner posited that herpesvirus-associated ME/CFS is caused not by normal '''productive''' infections with herpesviruses, but is caused by herpesviruses in an unusual mode of infection called an '''abortive''' infection. An '''abortive''' infection is one in which a virus enters a cell, but is unable to replicate fully within that cell, and so does not produce any new viral particles (virions) inside the cell.

Abortive infections are typically created when a virus enters a cell which does not possess an internal environment that facilitates the virus to replicate itself and create new virions — such cells are called '''non-permissive''' (their internal environment does not permit the virus to reproduce).

In abortive infections, although the virus cannot fully reproduce itself with non-permissive cells, the virus is constantly trying to do so, and in its persistent attempts to replicate, it synthesises many viral proteins inside the cell; these proteins may then lead to cellular dysfunction or have other adverse effects.

Dr Lerner hypothesized that herpesvirus-associated ME/CFS is caused when herpesviruses inadvertently enter non-permissive cells, and thereby create chronic abortive herpesvirus infections.

== Definition of an Abortive Infection ==
Definition of terms:<ref>{{Cite book|title=Multiplication|date=1996|url=http://www.ncbi.nlm.nih.gov/books/NBK8181/|last=Roizman|first=Bernard|isbn=978-0-9631172-1-2|location=Galveston (TX)|publisher=University of Texas Medical Branch at Galveston|editor-last=Baron|editor-first=Samuel|pmid=21413311}}</ref>

'''Permissive cell''' — this is a cell that a virus can break into, circumvent any cellular defenses, and fully replicate itself. In permissive cells, a virus will enter the cell, reproduce itself many thousands of times, and these new virions will then burst out of the cell by lysis usually, killing the cell in the process, with the virions escaping and going off to infect more cells.

'''Non-permissive cell''' — this is a cell that does not support replication of a virus. This may because the cell does not possess the internal factors or environment that the virus requires for full replication, and in which case, once in the non-permissive cell, the virus may start producing some of its proteins, but is not able to produce and assemble all the proteins necessary to manufacture duplicate virions. So no new virions are created.

'''Semi-permissive cell''' — this similar to a non-permissive cell, except that a small yield of new virions may be produced.

'''Productive infection''' — this is where a virus enters a permissive cell and successfully completes its replication cycle, reproducing itself typically thousands of times, and then usually bursting out of the cell by lysis. This is the normal viral replication cycle in a cell.

'''Abortive infection''' — this is where a virus enters cell but cannot successfully complete its replication cycle. Abortive infections can occur when a virus enters a non-permissive host cell, or when the virus itself is defective, and so cannot replicate properly.

== Abortive Infections Are Not Latent Infections ==
Abortive infections are not to be confused with latent infections, which are a different phenomenon. Productive infections and abortive infections are both active ongoing infections, whereas a latent viral infection is usually dormant and inactive. But note that while productive infections produce lots of new viral particles, abortive infections do not create any new viral particles, but nevertheless are ongoing infections within the infected cells.

Latent infections are where the virus has stopped replicating for a period of time, and hides inside a cell waiting for the right opportunity to reawaken from latency and start replicating again (usually at a moment of immune weakness, to maximize its success). Latency is the viral strategy of "running away in order to live to fight another day". An example of latency is the cold sore virus (herpes simplex virus), which stays in a latent state for months or years in the cells around the lips, but every now and then springs back to life, creating a cold sore.

Latent infections only exist in permissive cells (since in a non-permissive cell, a virus can never replicate, and thus a latent virus could never later spring back to life, which would defeat the purpose of latency). So a latent infection is where a virus in a permissive cell has itself switched off its replication for the time being. Whereas in an abortive infection in a non-permissive cell, the virus can never fully replicate itself.

One example of an abortive infections is in HIV: more than 95% of CD4 T-cells dying after infection with HIV are not productively infected; instead, these cells harbor an abortive infection, which leads to cell death.<ref>{{Cite journal|title=Abortive HIV Infection Mediates CD4 T-Cell Depletion and Inflammation in Human Lymphoid Tissue|date=2010-11-24|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026834/|journal=Cell|volume=143|issue=5|pages=789–801|last=Doitsh|first=Gilad|last2=Cavrois|first2=Marielle|last3=Lassen|first3=Kara G.|last4=Zepeda|first4=Orlando|last5=Yang|first5=Zhiyuan|last6=Santiago|first6=Mario L.|last7=Hebbeler|first7=Andrew M.|last8=Greene|first8=Warner C.|doi=10.1016/j.cell.2010.11.001|pmc=3026834|pmid=21111238|issn=0092-8674}}</ref>

Abortive infections however are not well studied, because they are normally considered to be of little biological importance. But Dr Lerner thought otherwise, and postulated that abortive infections were the etiological basis of ME/CFS.

== Dr A Martin Lerner's Abortive Infection Theory of ME/CFS ==
Dr Lerner explains his abortive infection theory of ME/CFS in his 2011 paper: <blockquote>We propose that ME/CFS patients have nonpermissive herpesvirus (EBV, HCMV, HHV6) replication, expressing immediate-early (IE) gene products, which induce host cell dysregulation and host cell apoptosis<ref>{{Cite journal|title=A paradigm linking herpesvirus immediate-early gene expression apoptosis and myalgic encephalomyelitis chronic fatigue syndrome|date=2011|url=http://www.dovepress.com/a-paradigm-linking-herpesvirus-immediate-early-gene-expression-apoptos-peer-reviewed-article-VAAT|journal=Virus Adaptation and Treatment|pages=19|last=Lerner|first=Martin|language=en|doi=10.2147/VAAT.S15105|issn=1179-1624}}</ref></blockquote>By "non-permissive herpesvirus replication," Dr Lerner means an abortive herpesvirus infection in non-permissive cells. Note that Dr Lerner often refers to abortive infections as "non-permissive infections", although strictly speaking, the term non-permissive refers to cells, not to infections (cells in which abortive infections can arise). Dr Lerner says in the same paper that:<blockquote>EBV ME/CFS subset patients also have uniquely elevated serum antibody titers to the nonstructural gene products EBV-specific DNase and DNA polymerase. These elevated EBV-specific serum antibody titers are also present in patients with EBV-related malignancies, Burkitt’s lymphoma, and nasopharyngeal carcinoma, but are not present in patients with infectious mononucleosis or in healthy individuals.</blockquote>So ME/CFS patients are producing antibodies to nonstructural proteins made by viruses. This might be because in abortive infections, there may be higher levels of nonstructural proteins, and a lack of structural viral capsid proteins (since in abortive infections, full virions are not constructed).

Dr Lerner says that the diffuse and restricted component of Epstein-Barr virus (EBV) early antigen (EA) indicates abortive EBV viral infection.<ref>{{Cite web|archive-date=2014-01-04|url=http://www.treatmentcenterforcfs.com/links/documents/AMLEBVReviewPressRelease9.23.10.pdf|url-status=dead|archive-url=http://hive.web/20140104024937/http://www.treatmentcenterforcfs.com/links/documents/AMLEBVReviewPressRelease9.23.10.pdf|title=Causal Relationship Identified Between Epstein Barr Virus and Chronic Fatigue Syndrome. Press release September 23, 2010.|last=Lerner|first=A Martin}}</ref> In his 2012 paper, Dr Lerner finds that in 106 ME/CFS patients with herpesvirus infections, 81% had elevated early antibodies, to EBV early antigen (diffuse).

Dr Lerner also found antibodies to deoxyuridine triphosphatase (dUTPase) from EBV and EBV DNA polymerase.<ref>{{Cite journal|title=Abortive lytic Epstein-Barr virus replication in tonsil-B lymphocytes in infectious mononucleosis and a subset of the chronic fatigue syndrome|date=2012|url=http://www.dovepress.com/abortive-lytic-epsteinndashbarr-virus-replication-in-tonsil-b-lymphocy-peer-reviewed-article-VAAT|journal=Virus Adaptation and Treatment|pages=85|last=Lerner|first=Martin|last2=Beqaj|first2=Safedin|language=en|doi=10.2147/VAAT.S36540|issn=1179-1624}}</ref> dUTPase is a viral enzyme produced in both productive and abortive infections. EBV-encoded dUTPase has been shown to induce sickness behavior symptoms (which are similar to ME/CFS symptoms).<ref>{{Cite journal|title=Epstein-Barr virus-encoded dUTPase modulates immune function and induces sickness behavior in mice|date=2004|url=https://pubmed.ncbi.nlm.nih.gov/15368518/|journal=Journal of Medical Virology|volume=74|issue=3|pages=442–448|last=Padgett|first=David A.|last2=Hotchkiss|first2=Andrew K.|last3=Pyter|first3=Leah M.|last4=Nelson|first4=Randy J.|last5=Yang|first5=Eric|last6=Yeh|first6=Peir-En|last7=Litsky|first7=Monica|last8=Williams|first8=Marshall|last9=Glaser|first9=Ronald|doi=10.1002/jmv.20196|pmid=15368518|issn=0146-6615}}</ref>

In his 2008 paper on [[cytomegalovirus]] in ME/CFS,<ref>{{Cite journal|title=Immunoassay with cytomegalovirus early antigens from gene products p52 and CM2 (UL44 and UL57) detects active infection in patients with chronic fatigue syndrome|date=2008|url=https://pubmed.ncbi.nlm.nih.gov/18037660/|journal=Journal of Clinical Pathology|volume=61|issue=5|pages=623–626|last=Beqaj|first=S. H.|last2=Lerner|first2=A. M.|last3=Fitzgerald|first3=J. T.|doi=10.1136/jcp.2007.050633|pmid=18037660|issn=1472-4146}}</ref> Dr Lerner says that:<blockquote>The p52, CM2 recombinant IgM assay to early human cytomegalovirus (HCMV) antigens is diagnostic of abortive HCMV infection.</blockquote><blockquote>These results confirm our previous findings that p52 and CM2 serum antibodies are specific in diagnosis of HCMV abortive infection in CFS patients similar to those infected with EBV.

In that study, p52 and CM2 HCMV IgM serum antibody titres were present in this HCMV subset of CFS patients, but not in control non-CFS patients. In turn, the presence of p52 and CM2 antibodies to p52 and CM2 non-structural antigens may account for difficulties in detecting HCMV DNA in blood or cardiac biopsies in these CFS patients, consistent with the paradigm of incomplete or abortive viral multiplication.

Abortive viral multiplication in immunocompetent CFS patients may be unique</blockquote>A team at Ohio State University have also discovered that antibodies to herpesvirus dUTPase are more common in ME/CFS patients: they found 31% to 53% of ME/CFS patients have high levels of antibodies to the dUTPase protein produced by EBV, HHV-6 and VZV.<ref>{{Cite journal|title=Myalgic encephalomyelitis/chronic fatigue syndrome and gulf war illness patients exhibit increased humoral responses to the herpesviruses-encoded dUTPase: Implications in disease pathophysiology|date=2017|url=https://pubmed.ncbi.nlm.nih.gov/28303641/|journal=Journal of Medical Virology|volume=89|issue=9|pages=1636–1645|last=Halpin|first=Peter|last2=Williams|first2=Marshall Vance|last3=Klimas|first3=Nancy G.|last4=Fletcher|first4=Mary Ann|last5=Barnes|first5=Zachary|last6=Ariza|first6=Maria Eugenia|doi=10.1002/jmv.24810|pmc=5513753|pmid=28303641|issn=1096-9071}}</ref><ref>{{Citation|title=The Role of EBV-dUTPase in Modulating Neuro-Immune Dysfunction Associated with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome|date=2020|url=https://kb.osu.edu/handle/1811/91637|last=Hasik|first=Julia|access-date=2023-08-30|language=en-US}}</ref> Ohio State believe dUTPase may be a biomarker in a subset of ME/CFS patients.

== Treatment of Abortive Infections in Non-Permissive Cells ==
In terms of antiviral treatment for abortive infections in ME/CFS, Dr Lerner points out that:<blockquote>No antiviral drug is active in vitro vs. any latent, nonpermissive persistent herpesvirus infection.

However, implicit in this unified hypothesis is the assumption that low-level, continuing, infectious herpesvirus multiplication is occurring in susceptible B cells (EBV) and epithelial cells (EBV), and/or in tissue macrophages (HCMV) and cardiac myocytes (EBV and HCMV).

Infectious EBV or HCMV might, we presume, intermittently be carried to the heart by the blood within productively infected B cells (EBV) or monocytes macrophages (HCMV). Eradication of productive virus infection by an effective antiviral drug might inhibit the slowly active, persisting pathologic process we hypothesize.<ref>{{Cite journal|title=A UNIFIED THEORY OF THE CAUSE OF CHRONIC FATIGUE SYNDROME|date=1997|url=https://journals.lww.com/infectdis/citation/1997/05000/a_unified_theory_of_the_cause_of_chronic_fatigue.5.aspx|journal=Infectious Diseases in Clinical Practice|volume=6|issue=4|pages=239|last=Lerner|first=A. Martin|last2=Zervos|first2=Marcus|last3=Dworkin|first3=Howard J.|last4=Chang|first4=Chung Ho|last5=O'Neill|first5=William|language=en-US|issn=1536-9943}}</ref></blockquote>In other words, Dr Lerner says existing commercial anti-herpesvirus antiviral drugs are not effective against abortive infections in non-permissive cells. But he suggests that low-level productive herpesvirus infections elsewhere in the body may be supplying more herpesvirus virions that re-seed the abortive infections, to keep the abortive infection going. Therefore, antivirals that target the productive infections may eventually indirectly reduce abortive infection levels as well.

== Learn more ==

* [https://www.healthrising.org/blog/2018/11/17/could-crippled-herpesviruses-be-contributing-to-chronic-fatigue-syndrome-me-cfs-and-other-diseases/ A team at Ohio State University, led by Dr Maria Ariza and Dr Marshall Williams, are currently researching the hypothesis that chronic abortive herpesvirus infections may be causing ME/CFS and other diseases].
* [https://medicine.osu.edu/news/biomarker-for-chronic-fatigue-syndrome Ohio State researchers isolate biomarker to test for chronic fatigue syndrome]
* [http://web.archive.org/web/20191101170704/http://www.treatmentcenterforcfs.com/cfs_publications/index.html List of Dr A Martin Lerner's published ME/CFS studies]

== See also ==

* [[Herpesviruses|Herpesvirus]]<nowiki/>es
* [[List of herpesvirus infection studies]]
* [[Epstein-Barr virus]]
* [[Cytomegalovirus]]
* [[A Martin Lerner|Dr A Martin Lerner]]
* [[Non-cytolytic enterovirus]]
== References ==

Sphingolipid

2025-05-09T21:06:34Z

Notjusttired:/* Learn more */ add

'''Sphingolipids''' are any of a class of compounds that are [[:Category:Fatty acids |fatty acid]] conjugates of sphingosine and occur chiefly in the [[cell membrane]]s of the [[brain]] and nervous tissue. They not only help make up the structure of membranes but also have important [[cell signaling]] roles.<ref name="Heung2006">Heung, LJ (2006). Luberto, C & Del Poeta, M. [http://iai.asm.org/content/74/1/28.full Role of sphingolipids in microbial pathogenesis]. Infect Immun. 74(1):28-39. DOI: 10.1128/IAI.74.1.28-39.</ref>

==Notable studies==
* 2025, A research perspective on sphingolipid metabolism and myalgic encephalomyelitis/chronic fatigue syndrome<ref name="Xiao2025">{{Cite journal|title=A research perspective on sphingolipid metabolism and myalgic encephalomyelitis/chronic fatigue syndrome|date=2025|url=https://journals.lww.com/nrronline/citation/9900/a_research_perspective_on_sphingolipid_metabolism.770.aspx|journal=Neural Regeneration Research|pages=10.4103/NRR.NRR|last=Xiao|first=Junhua|author-link=Junhua Xiao|language=en-US|doi=10.4103/NRR.NRR-D-24-01506|issn=1673-5374}}</ref> [https://doi.org/10.4103/NRR.NRR-D-24-01506 (Full text)]

*2016, Metabolic features of chronic fatigue syndrome<ref name="Naviaux2016">{{Cite journal | last1 = Naviaux | first1 = Robert K | authorlink1 = Robert Naviaux | last2 = Naviaux | first2 = Jane C. | authorlink2 = | last3 = Li | first3 = Kefeng | author-link3 = | last4 = Bright | first4 = A. Taylor | authorlink4 = | last5 = Alaynick | first5 = William A. | authorlink5 = | last6 = Wang | first6 = Lin | authorlink6 = | last7 = Baxter | first7 = Asha | authorlink7 = | last8 = Nathan | first8 = Neil | authorlink8 = | last9 =Anderson | first9 = Wayne | authorlink9 = | last10 = Gordon | first10 = Eric | authorlink10 = Eric Gordon | title = Metabolic features of chronic fatigue syndrome |journal = PNAS | volume = 113 | issue = 37 | page = | date = Sep 13, 2016 | doi = 10.1073/pnas.1607571113}}</ref> [http://www.pnas.org/content/early/2016/08/24/1607571113.long (Full Text)]

==Learn more==
*2025, [https://www.meresearch.org.uk/reduced-sphingolipid-metabolism-in-me-cfs/ Reduced sphingolipid metabolism in ME/CFS] - ME Research UK
*[http://www.meaction.net/2016/08/30/naviauxs-metabolism-paper-is-about-as-big-as-you-think/ Naviaux's metabolism paper is about as big as you think], #MEAction, August 30th 2016

==See also==
* [[Metabolic features of chronic fatigue syndrome]]
* [[Robert Naviaux]]

==References==
{{Reflist}}

[[Category:Lipids]]

Sphingolipid

2025-05-09T21:03:00Z

Notjusttired:/* Notable studies */ add link

'''Sphingolipids''' are any of a class of compounds that are [[:Category:Fatty acids |fatty acid]] conjugates of sphingosine and occur chiefly in the [[cell membrane]]s of the [[brain]] and nervous tissue. They not only help make up the structure of membranes but also have important [[cell signaling]] roles.<ref name="Heung2006">Heung, LJ (2006). Luberto, C & Del Poeta, M. [http://iai.asm.org/content/74/1/28.full Role of sphingolipids in microbial pathogenesis]. Infect Immun. 74(1):28-39. DOI: 10.1128/IAI.74.1.28-39.</ref>

==Notable studies==
* 2025, A research perspective on sphingolipid metabolism and myalgic encephalomyelitis/chronic fatigue syndrome<ref name="Xiao2025">{{Cite journal|title=A research perspective on sphingolipid metabolism and myalgic encephalomyelitis/chronic fatigue syndrome|date=2025|url=https://journals.lww.com/nrronline/citation/9900/a_research_perspective_on_sphingolipid_metabolism.770.aspx|journal=Neural Regeneration Research|pages=10.4103/NRR.NRR|last=Xiao|first=Junhua|author-link=Junhua Xiao|language=en-US|doi=10.4103/NRR.NRR-D-24-01506|issn=1673-5374}}</ref> [https://doi.org/10.4103/NRR.NRR-D-24-01506 (Full text)]

*2016, Metabolic features of chronic fatigue syndrome<ref name="Naviaux2016">{{Cite journal | last1 = Naviaux | first1 = Robert K | authorlink1 = Robert Naviaux | last2 = Naviaux | first2 = Jane C. | authorlink2 = | last3 = Li | first3 = Kefeng | author-link3 = | last4 = Bright | first4 = A. Taylor | authorlink4 = | last5 = Alaynick | first5 = William A. | authorlink5 = | last6 = Wang | first6 = Lin | authorlink6 = | last7 = Baxter | first7 = Asha | authorlink7 = | last8 = Nathan | first8 = Neil | authorlink8 = | last9 =Anderson | first9 = Wayne | authorlink9 = | last10 = Gordon | first10 = Eric | authorlink10 = Eric Gordon | title = Metabolic features of chronic fatigue syndrome |journal = PNAS | volume = 113 | issue = 37 | page = | date = Sep 13, 2016 | doi = 10.1073/pnas.1607571113}}</ref> [http://www.pnas.org/content/early/2016/08/24/1607571113.long (Full Text)]

==Learn more==
*[http://www.meaction.net/2016/08/30/naviauxs-metabolism-paper-is-about-as-big-as-you-think/ Naviaux's metabolism paper is about as big as you think], #MEAction, August 30th 2016

==See also==
* [[Metabolic features of chronic fatigue syndrome]]
* [[Robert Naviaux]]

==References==
{{Reflist}}

[[Category:Lipids]]

Sphingolipid

2025-05-09T20:57:08Z

Notjusttired:/* Notable studies */ add Naviaux study

'''Sphingolipids''' are any of a class of compounds that are [[:Category:Fatty acids |fatty acid]] conjugates of sphingosine and occur chiefly in the [[cell membrane]]s of the [[brain]] and nervous tissue. They not only help make up the structure of membranes but also have important [[cell signaling]] roles.<ref name="Heung2006">Heung, LJ (2006). Luberto, C & Del Poeta, M. [http://iai.asm.org/content/74/1/28.full Role of sphingolipids in microbial pathogenesis]. Infect Immun. 74(1):28-39. DOI: 10.1128/IAI.74.1.28-39.</ref>

==Notable studies==
* 2025, A research perspective on sphingolipid metabolism and myalgic encephalomyelitis/chronic fatigue syndrome<ref name="Xiao2025">https://doi.org/10.4103/NRR.NRR-D-24-01506</ref> [https://doi.org/10.4103/NRR.NRR-D-24-01506 (Full text)]

*2016, Metabolic features of chronic fatigue syndrome<ref name="Naviaux2016">{{Cite journal | last1 = Naviaux | first1 = Robert K | authorlink1 = Robert Naviaux | last2 = Naviaux | first2 = Jane C. | authorlink2 = | last3 = Li | first3 = Kefeng | author-link3 = | last4 = Bright | first4 = A. Taylor | authorlink4 = | last5 = Alaynick | first5 = William A. | authorlink5 = | last6 = Wang | first6 = Lin | authorlink6 = | last7 = Baxter | first7 = Asha | authorlink7 = | last8 = Nathan | first8 = Neil | authorlink8 = | last9 =Anderson | first9 = Wayne | authorlink9 = | last10 = Gordon | first10 = Eric | authorlink10 = Eric Gordon | title = Metabolic features of chronic fatigue syndrome | journal = PNAS | volume = 113 | issue = 37 | page = | date = Sep 13, 2016
| doi = 10.1073/pnas.1607571113}}</ref>[http://www.pnas.org/content/early/2016/08/24/1607571113.long (Full Text)]

==Learn more==
*[http://www.meaction.net/2016/08/30/naviauxs-metabolism-paper-is-about-as-big-as-you-think/ Naviaux's metabolism paper is about as big as you think], #MEAction, August 30th 2016

==See also==
*[[Robert Naviaux]]
*[[Xiao]]

==References==
{{Reflist}}
[[Category:Lipids]]

Robert Naviaux

2025-05-09T20:55:32Z

Notjusttired:/* Notable studies */ tidy

[[File:Robert Naviaux.png|thumb|Source: gordonmedical.com]]
'''Robert K. Naviaux,''' MD, PhD, is a Professor in Residence at the University of California, San Diego, California, US. His work "has focused on the role of mitochondrial DNA replication, copy number regulation, DNA damage, and nucleotide signaling in development, aging, healing and regeneration in mitochondrial mechanisms of disease and development."<ref>{{Cite web|url=http://profiles.ucsd.edu/robert.naviaux | title = Robert Naviaux {{!}} UCSD Profiles|website=profiles.ucsd.edu|language=en|access-date=2018-08-15}}</ref> He was invited to join the [[Open Medicine Foundation]]'s research team in 2016, following a announcement that the [[ME/CFS Severely Ill, Big Data Study]] had a significant result in the area of [[Mitochondrion|mitochondria]].<ref name=":0">{{Cite news | url=https://www.omf.ngo/2016/02/10/welcome-dr-naviaux-to-our-team/ | title = Welcome Dr. Naviaux to our Team {{!}} Open Medicine Foundation | date = 2016-02-10|work=Open Medicine Foundation|access-date=2018-08-15|language=en-US}}</ref>

Dr. Naviaux directs the Robert Naviaux Laboratory at University of California, San Diego (UCSD) whose work is "divided into two groups: 1) Mitochondrial Mechanisms of Disease and Development, and 2) Evolutionary Systems Biology and Marine Metagenomics."<ref>{{Cite web|url=http://med.ucsd.edu/divisions/med-genetics/research/Pages/Naviaux-Lab.aspx | title = Naviaux Laboratory Genetics Research at UC San Diego|website=UC San Diego School of Medicine|language=en-US|access-date=2018-08-15}}</ref> He is founder and co-director of the Mitochondrial and Metabolic Disease Center at UCSD, the co-founder and a former president of the Mitochondrial Medicine Society, as well as, a founding associate editor of the journal, ''Mitochondrion''.<ref name=":0" />

Dr. Naviaux "discovered the cause and created the diagnostic test for Alpers syndrome, a mitochondrial disease... [and] is the director of the first FDA-approved clinical trial to study [https://www.drugs.com/cons/suramin-injection.html suramin] [an antiparasitic drug] as a treatment for autism."<ref name=":0" /><ref>{{Cite web|url=https://health.ucsd.edu/news/releases/Pages/2015-06-10-clinical-trial-for-autism-treatment.aspx | title = Clinical Trial Launched to Assess Safety and Efficacy of Autism Drug Treatment | last = LaFee | first = Scott | date = Jun 10, 2015 | website = UC Health - UC San Diego|language=en-US|archive-url=|archive-date=|url-status=|access-date=2018-08-15}}</ref>

Currently, Dr. Naviaux is using his mitochondria expertise, especially in metabolomics, to look for a biomarker and potential treatment for [[ME/CFS]].<ref>{{Cite news | url=http://www.healthrising.org/forums/threads/the-mitochondria-man-gets-his-money-and-the-uk-goes-mega-me-cfs-research-moving-forward.4360/ | title = The Mitochondria Man Gets His Money and The UK Goes MEGA: ME/CFS Research Moving Forward | last = | first = | date = May 19, 2016|work=Health Rising's Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Forums|access-date=2018-08-15|archive-url=|archive-date=|url-status=|language=en-US|type=Forum Discussion}}</ref>

In May 2016, a study was launched, led by Dr. Naviaux and Dr. [[Ronald Davis]], in collaboration with Dr. [[Eric Gordon]], Dr. [[Paul Cheney]], and the Stanford Genome Technology Center in order "to validate earlier findings of a possible diagnostic signature for ME/CFS by measuring metabolites and to evaluate the contribution of genetics to the variation in observed metabolic signatures in this disease." The initial phase, with a total of 90 participants, has been completed and suggests "the mitochondria is in hypometabolism due to a chronic [[Cell danger response hypothesis|cell danger response]] state in ME/CFS patients."<ref>{{Cite news | url=https://www.omf.ngo/expanded-mecfs-metabolomics-study/ | title = Metabolomics and Genetics Study {{!}} Open Medicine Foundation|work=Open Medicine Foundation|access-date=2018-08-15|language=en-US}}</ref>

==Education==
*1977-1978 - Undergraduate (Biochemistry), Georg August Universität, Göttingen, Germany
*1979 - B.S. (Biological Sciences), University of California, Davis, California
*1981 - M.S. (Zoology), Indiana University, Bloomington, Indiana
*1986, 1989 - M.D., Ph.D. (Genetics, Virology), Indiana University School of Medicine, Indianapolis, Indiana
*1986-1990 - Internship and Residency, Internal Medicine, American Board of Internal Medicine (ABIM), Clinical Investigator Pathway, University of California, Davis
*1990-1994 - Postdoctorate (Retrovirology, Gene Therapy), The Salk Institute, La Jolla, California
*1994-1997 - Fellowship (Biochemical Genetics, mtDNA Replication), University of California, San Diego Medical Center, San Diego, California

==Notable studies==
*2004, [http://www.ncbi.nlm.nih.gov/pubmed/16120397 Developing a systematic approach to the diagnosis and classification of mitochondrial disease]
*2008, [http://www.tandfonline.com/doi/pdf/10.4161/cbt.7.8.6741 Mitochondrial control of epigenetics]
*2014, Metabolic features of the cell danger response<ref name="Naviaux, 2014">{{Citation | last1 = Naviaux | first1 = Robert K. | authorlink1 = Robert Naviaux | title = Metabolic features of the cell danger response | journal = Mitochondrion | volume = 16 | issue = | page = 7–17 | date = May 2014 | pmid = 23981537
| doi = 10.1016/j.mito.2013.08.006 }}</ref> [http://www.sciencedirect.com/science/article/pii/S1567724913002390 (Full Text)]
*2016, Metabolic features of chronic fatigue syndrome<ref name="Naviaux, 2016">{{Cite journal | last1 = Naviaux | first1 = Robert K | authorlink1 = Robert Naviaux | last2 = Naviaux | first2 = Jane C. | authorlink2 = | last3 = Li | first3 = Kefeng | author-link3 = | last4 = Bright | first4 = A. Taylor | authorlink4 = | last5 = Alaynick | first5 = William A. | authorlink5 = | last6 = Wang | first6 = Lin | authorlink6 = | last7 = Baxter | first7 = Asha | authorlink7 = | last8 = Nathan | first8 = Neil | authorlink8 = | last9 =Anderson | first9 = Wayne | authorlink9 = | last10 = Gordon | first10 = Eric | authorlink10 = Eric Gordon | title = Metabolic features of chronic fatigue syndrome | journal = PNAS | volume = 113 | issue = 37 | page = | date = Sep 13, 2016
| doi = 10.1073/pnas.1607571113}}</ref>[http://www.pnas.org/content/early/2016/08/24/1607571113.long (Full Text)]
::* 2016, Reply to Vogt et al.: Metabolomics and chronic fatigue syndrome<ref name="Naviaux, Nov152016">{{Citation | last1 = Naviaux | first1 = Robert K | authorlink1 = Robert Naviaux | last2 = Naviaux | first2 = Jane C. | authorlink2 = | last3 = Li | first3 = Kefeng | author-link3 = | last4 = Bright | first4 = A. Taylor | authorlink4 = | last5 = Alaynick | first5 = William A. | authorlink5 = | last6 = Wang | first6 = Lin | authorlink6 = | last7 = Baxter | first7 = Asha | authorlink7 = | last8 = Nathan | first8 = Neil | authorlink8 = | last9 =Anderson | first9 = Wayne | authorlink9 = | last10 = Gordon | first10 = Eric | authorlink10 = Eric Gordon | title = Reply to Vogt et al.: Metabolomics and chronic fatigue syndrome | journal = Proc Natl Acad Sci USA | volume = 113 | issue = 46 | page = E7142–E7143 | date = Nov 15, 2016 | pmid = | doi = 10.1073/pnas.1616261113}}</ref>
::*Feb 7, 2017, Reply to Roerink et al.: Metabolomics of chronic fatigue syndrome<ref name="Naviaux, Feb72017">{{Citation | last1 = Naviaux | first1 = Robert K | authorlink1 = Robert Naviaux | last2 = Gordon | first2 = Eric | authorlink2 = Eric Gordon | title = Reply to Roerink et al.: Metabolomics of chronic fatigue syndrome. | journal = Proc Natl Acad Sci USA | volume = 114 | issue = 6 | page = E911-E912 | date = Feb 7, 2017 | pmid = | doi = 10.1073/pnas.1618984114}}</ref>
*2017, A robust, single-injection method for targeted, broad-spectrum plasma metabolomics<ref name="Li, 2017">{{Citation | last1 = Li | first1 = Kefeng | author-link1 = | last2 = Naviaux | first2 = Jane C. | authorlink2 = | last3 = Bright | first3 = A. Taylor | authorlink3 = | last4 = Wang | first4 = Lin | authorlink4 = | last5 = Naviaux | first5 = Robert K | authorlink5 = Robert Naviaux | title = A robust, single-injection method for targeted, broad-spectrum plasma metabolomics| journal = Metabolomics | volume = 13 | issue = 122 | page = | date = 2017
| doi = 10.1007/s11306-017-1264-1}}</ref>[https://link.springer.com/article/10.1007/s11306-017-1264-1 (Full Text)]
*2020, Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome<ref name="Schreiner2020">{{Cite journal | last = Schreiner | first=Philipp | author-link = | last2 = Harrer | first2 = Thomas | authorlink2 = Thomas Harrer | last3 = Scheibenbogen | first3 = Carmen | author-link3 = Carmen Scheibenbogen | last4 = Lamer | first4 = Stephanie | authorlink4 = | last5 = Schlosser | first5 = Andreas | authorlink5 = | last6 = Naviaux | first6 = Robert K. | authorlink6 = Robert Naviaux | last7 = Prusty | first7 = Bhupesh K. | authorlink7 = Bhupesh Prusty | date = 2020-04-01 | title = Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome|url=https://www.immunohorizons.org/content/4/4/201|journal=ImmunoHorizons|language=en|volume=4|issue=4|pages=201–215|doi=10.4049/immunohorizons.2000006|issn=2573-7732|pmc=|pmid=32327453|access-date=|quote=|via=}}</ref> [https://www.immunohorizons.org/content/4/4/201 (Full text)]

==Awards and Honors==
*2002, Honored in a non-fiction book entitled, ''Anna’s Friends — Lessons Learned from a Short and Beautiful Life''
*2007, Thomson ESI - Science Citation Index “Fast Moving Front Article”
*2007, United Mitochondrial Disease Foundation Mitochondrial Medicine - Best Abstract Award
*2008, Hailey’s Wish Foundation - Hailey’s Hero Award, For Outstanding Research and Clinical Care of children with mitochondrial disease

==Talks and interviews==
*2011, [https://www.youtube.com/watch?v=1Sq2Os0mtrQ Mitochondria and Autism (Spring 2011) - Robert K. Naviaux, M.D., Ph.D.]<ref>{{Cite web|url=https://www.youtube.com/watch?v=1Sq2Os0mtrQ | title = Mitochondria and Autism (Spring 2011) - Robert K. Naviaux, M.D., Ph.D. | last=Naviaux | first = Robert K. | date = Jan 27, 2013 | website = YouTube|publisher=Saul Colquhoun|archive-url=|archive-date=|url-status=|access-date=}}</ref>
*Aug 12, 2017, [[Community Symposium on the Molecular Basis of ME/CFS - 2017]]
*''Sep 28, 2017,'' [https://www.youtube.com/watch?v=u028TAyB9S4 Robert Naviaux, MD, PhD | ME/CFS Cell Danger Response, Metabolic Features, Low-energy in Nature]<ref>{{Cite web|url=https://www.youtube.com/watch?v=u028TAyB9S4 | title = Robert Naviaux, MD, PhD {{!}} ME/CFS Cell Danger Response, Metabolic Features, Low-energy in Nature | last = Naviaux | first = Robert | date = Sep 28, 2017 | website = YouTube|publisher=Open Medicine Foundation - OMF|archive-url=|archive-date=|url-status=|access-date=}}</ref>
:([https://www.youtube.com/watch?v=snQnfFTx1Do with Spanish subtitles])<ref>{{Cite web|url=https://www.youtube.com/watch?v=snQnfFTx1Do | title = PART 2 ME CFS Symposium at Stanford trimmed | last = Naviaux | first = Robert | date = Aug 13, 2017 | website = YouTube|publisher=Asociación Síndrome Fatiga Crónica-SQM|archive-url=|archive-date=|url-status=|access-date=}}</ref>

==Articles==
*2016, [http://www.healthrising.org/blog/2016/05/19/mitochondria-man-gets-money-uk-goes-mega-chronic-fatigue-syndrome-research-moves-forward/ "Mitochondria Man Gets His Money and the UK Goes Mega: Chronic Fatigue Syndrome Research Moving Forward"]<ref>{{Cite news | url=https://www.healthrising.org/blog/2016/05/19/mitochondria-man-gets-money-uk-goes-mega-chronic-fatigue-syndrome-research-moves-forward/ | title = The Mitochondria Man Gets His Money and The UK Goes MEGA: ME/CFS Research Moving Forward - Health Rising | last = Johnson | first =Cort | date = 2016-05-19|work=Health Rising|access-date=2018-08-15|archive-url=|archive-date=|url-status=|language=en-US}}</ref>

* 2018, [https://timesofsandiego.com/tech/2018/09/07/ucsd-researcher-possibly-makes-breakthrough-in-treatment-of-chronic-illness/ "UCSD Researcher Suggests Chronic Illness Could Be Breakdown in Normal Healing"]<ref>{{Cite news | url=https://timesofsandiego.com/tech/2018/09/07/ucsd-researcher-possibly-makes-breakthrough-in-treatment-of-chronic-illness/ | title = UCSD Researcher Suggests Chronic Illness Could Be Breakdown in Normal Healing - Times of San Diego | date = 2018-09-07|work=Times of San Diego|access-date=2018-09-13|language=en-US}}</ref>

== Online presence ==
*[http://www.healthrising.org/forums/threads/an-eye-on-the-mitochondria-man-robert-naviaux-and-chronic-fatigue-syndrome-me-cfs.4163/ Health Rising Forum for Robert Naviaux]
*[http://www.ncbi.nlm.nih.gov/pubmed/?term=Naviaux%20RK%5Bauth%5D PubMed]
*[http://profiles.ucsd.edu/robert.naviaux University of California, San Diego Faculty Website]
*[https://www.youtube.com/results?search_query=%22Robert+Naviaux%22 Youtube - Talks on Autism]

==Learn more==
*[http://naviauxlab.ucsd.edu Robert Naviaux Laboratory at UC San Diego]<ref>{{Cite web|url=http://naviauxlab.ucsd.edu/ | title = Naviaux Lab|website=naviauxlab.ucsd.edu|language=en-US|access-date=2018-08-15}}</ref>
*[http://www.nofone.org/#!significance-of-naviaux-2015-fragile-x/ctef The Significance of Reversing Autism-Like Features in Two Distinct Mouse Models With a Single Drug, Suramin]<ref>{{Cite web|url=http://www.nofone.org/significance-of-naviaux-2015-fragile-x | title = N of One {{!}} Promising Research Update | last = Rodakis | first = John | date = Jan 15, 2015 | website = N of One: Autism Research Foundation|language=en|archive-url=|archive-date=|url-status=|access-date=2018-08-15}}</ref>

==See also==
*[[Metabolomics]]
*[[Mitochondrion]]
*[[Dauer]]
*[[Metabolic features of chronic fatigue syndrome]]

==References==
{{Reflist}}

[[Category:Researchers]]
[[Category:US researchers]]
[[Category:OMF Scientific Advisory Board members]]

Sphingolipid

2025-05-09T20:50:17Z

Notjusttired:add ref

Tetrahydrobiopterin

2024-10-29T22:26:43Z

Notjusttired:/* Notable studies */ correction

{{stub|date=October 2024}}
'''Tetrahydrobiopterin''' (BH4) is cofactor in the synthesis of the [[neurotransmitter]]s [[dopamine]], [[norepinephrine]], [[epinephrine]] and [[melatonin]]. It is also a cofactor in the synthesis of [[nitric oxide]].

== MTHFR mutations ==
[[MTHFR]] [[A1298C]] is involved in converting [[5-methylfolate]] (5MTHF) to [[tetrahydrofolate]] (THF), a reaction that produces one molecule of BH4. Mutations in this gene down regulate the methylation cycle and consequently, the production of BH4.{{Citation needed|date=29 October 2024}}

==Function==

==ME/CFS==
BH4 was found to be raised in a pilot study of ME/CFS patients with [[orthostatic intolerance]] by Gottschalk and colleagues in 2023.<ref name="Gottschalk2023" />

==Notable studies==
*2024, Dysregulation of tetrahydrobiopterin metabolism in myalgic encephalomyelitis/chronic fatigue syndrome by pentose phosphate pathway<ref name="Bulbule2024">https://journals.sagepub.com/doi/full/10.1177/11795735241271675</ref> - [https://journals.sagepub.com/doi/full/10.1177/11795735241271675 (Full text)]
*2023, Detection of Elevated Level of Tetrahydrobiopterin in Serum Samples of ME/CFS Patients with Orthostatic Intolerance: A Pilot Study<ref name="Gottschalk2023">{{Cite journal|title=Detection of Elevated Level of Tetrahydrobiopterin in Serum Samples of ME/CFS Patients with Orthostatic Intolerance: A Pilot Study|date=May 13, 2023|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC10218672/|journal=International Journal of Molecular Sciences|volume=24|issue=10|pages=8713|last=Gottschalk|first=Carl Gunnar|last2=Whelan|first2=Ryan|last3=Peterson|first3=Daniel|last4=Roy|first4=Avik|language=en|doi=10.3390/ijms24108713|pmc=10218672|pmid=37240059}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/37240059/ (Full text)]

==Learn more==
*
*

==References==
{{reflist}}

[[Category:Biochemistry and cell biology]] [[Category:Cofactors]] [[Category:Coenzymes]]

Tetrahydrobiopterin

2024-10-29T22:20:05Z

Notjusttired:ref

{{stub|date=October 2024}}
'''Tetrahydrobiopterin''' (BH4) is cofactor in the synthesis of the [[neurotransmitter]]s [[dopamine]], [[norepinephrine]], [[epinephrine]] and [[melatonin]]. It is also a cofactor in the synthesis of [[nitric oxide]].

== MTHFR mutations ==
[[MTHFR]] [[A1298C]] is involved in converting [[5-methylfolate]] (5MTHF) to [[tetrahydrofolate]] (THF), a reaction that produces one molecule of BH4. Mutations in this gene down regulate the methylation cycle and consequently, the production of BH4.{{Citation needed|date=29 October 2024}}

==Function==

==ME/CFS==
BH4 was found to be raised in a pilot study of ME/CFS patients with [[orthostatic intolerance]] by Gottschalk and colleagues in 2023.<ref name="Gottschalk2023" />

==Notable studies==
*2023, Detection of Elevated Level of Tetrahydrobiopterin in Serum Samples of ME/CFS Patients with Orthostatic Intolerance: A Pilot Study<ref name="Gottschalk2023">{{Cite journal|title=Detection of Elevated Level of Tetrahydrobiopterin in Serum Samples of ME/CFS Patients with Orthostatic Intolerance: A Pilot Study|date=May 13, 2023|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC10218672/|journal=International Journal of Molecular Sciences|volume=24|issue=10|pages=8713|last=Gottschalk|first=Carl Gunnar|last2=Whelan|first2=Ryan|last3=Peterson|first3=Daniel|last4=Roy|first4=Avik|language=en|doi=10.3390/ijms24108713|pmc=10218672|pmid=37240059}}</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/37240059/ (Full text)]
*2023, Detection of Elevated Level of Tetrahydrobiopterin in Serum Samples of ME/CFS Patients with Orthostatic Intolerance: A Pilot Study<ref name="Bulbule2023">https://www.mdpi.com/1422-0067/24/10/8713/htm</ref> - [https://www.mdpi.com/1422-0067/24/10/8713/htm (Full text)]

==Learn more==
*
*

==References==
{{reflist}}

[[Category:Biochemistry and cell biology]] [[Category:Cofactors]] [[Category:Coenzymes]]

Tetrahydrobiopterin

2024-10-29T22:17:21Z

Notjusttired:/* Notable studies */ fix

{{stub|date=October 2024}}
'''Tetrahydrobiopterin''' (BH4) is cofactor in the synthesis of the [[neurotransmitter]]s [[dopamine]], [[norepinephrine]], [[epinephrine]] and [[melatonin]]. It is also a cofactor in the synthesis of [[nitric oxide]].

== MTHFR mutations ==
[[MTHFR]] [[A1298C]] is involved in converting [[5-methylfolate]] (5MTHF) to [[tetrahydrofolate]] (THF), a reaction that produces one molecule of BH4. Mutations in this gene down regulate the methylation cycle and consequently, the production of BH4.

==Function==

==ME/CFS==
BH4 was found to be raised in ME/CFS patients with [[orthostatic intolerance]] by Gottschalk and colleagues in 2023.

==Notable studies==
*2023, Detection of Elevated Level of Tetrahydrobiopterin in Serum Samples of ME/CFS Patients with Orthostatic Intolerance: A Pilot Study<ref name="Gottschalk2023">https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/37240059/</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/37240059/ (Full text)]
*2023, Detection of Elevated Level of Tetrahydrobiopterin in Serum Samples of ME/CFS Patients with Orthostatic Intolerance: A Pilot Study<ref name="Bulbule2023">https://www.mdpi.com/1422-0067/24/10/8713/htm</ref> - [https://www.mdpi.com/1422-0067/24/10/8713/htm (Full text)]

==Learn more==
*
*

==References==
{{reflist}}

[[Category:Biochemistry and cell biology]] [[Category:Cofactors]] [[Category:Coenzymes]]

Tetrahydrobiopterin

2024-10-29T22:16:43Z

Notjusttired:add study

Tetrahydrobiopterin

2024-10-29T22:03:18Z

Notjusttired:study

'''Tetrahydrobiopterin''' (BH4) is cofactor in the synthesis of the [[neurotransmitter]]s [[dopamine]], [[norepinephrine]], [[epinephrine]] and [[melatonin]]. It is also a cofactor in the synthesis of [[nitric oxide]].
{{stub|date=October 2024}}

== MTHFR mutations ==

[[MTHFR]] [[A1298C]] is involved in converting [[5-methylfolate]] (5MTHF) to [[tetrahydrofolate]] (THF), a reaction that produces one molecule of BH4. Mutations in this gene down regulate the methylation cycle and consequently, the production of BH4.
==Function==

==ME/CFS==

==Notable studies==
*2023, Detection of Elevated Level of Tetrahydrobiopterin in Serum Samples of ME/CFS Patients with Orthostatic Intolerance: A Pilot Study<ref name="Gottschalk2023">https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/37240059/</ref> - [https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/37240059/ (Full text)]

==Learn more==
*
*

==References==
{{reflist}}

[[Category:Biochemistry and cell biology]] [[Category:Cofactors]] [[Category:Coenzymes]]

BH4

2024-10-29T22:00:17Z

Notjusttired:fix

#redirect [[Tetrahydrobiopterin]]

[[Category:Biochemistry and cell biology]] [[Category:Cofactors]] [[Category:Coenzymes]]