MEpedia - User contributions [en]

Courtney Craig

2023-12-21T07:56:01Z

Drcraig:/* Online presence */ Updates about practice

[[File:Courtney Craig.png|200px|thumb|right|Courtney_Craig.png]]
Doctor '''Courtney Craig''' is a Nutritionist and Chiropractor who has a special interest in treating patients with [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]] (ME/CFS) and [[fibromyalgia]] (FM). She became ill with [[ME/CFS]] in 1998, at the age of 16, but greatly improved in 2010 utilizing both conventional and integrative medicine.<ref>http://www.healthrising.org/blog/2014/05/10/closer-look-natural-killer-cells-chronic-fatigue-syndrome-three-natural-ways-boost/</ref><ref>{{Cite web | url = https://www.drcourtneycraig.com/nutritionist-for-mecfs | title = About Dr. Craig | last = | first = | authorlink = | date = | website = | archive-url = | archive-date = |url-status = | access-date=}}</ref> She is featured in the 2016 documentary film, [[Unrest]], which is about [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]].

Dr. Craig hosted a podcast called [[Spoonie Radio]] for two years in which she interviewed doctors, researchers, and patients within the ME/CFS community.

==Education==
*Undergraduate study in exercise science at the College of William and Mary, Virginia
*Graduated with honors from the University of Bridgeport’s Human Nutrition Institute Master's program.
*Clinical training at Palmer College of Chiropractic, Florida
*Visiting Scientist at Cornell’s Center for Enervating Neuroimmune Disease
*Master Student in Nutrition and Biomedicine at Technical University Munich in Germany.

==Notable studies==
* 2015, Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets<ref name="craig2015" /> - a paper hypothesising that [[ME/CFS]] could be treated by improving mitochondrial function using [[fasting]], caloric restriction and a [[ketogenic diet]]. - [https://www.sciencedirect.com/science/article/abs/pii/S0306987715003187?via%3Dihub (Abstract)]

==Clinic location==
She is located in Germany and offers online courses in nutrition, therapeutic diets, supplements, and similar topics.

==Talks and interviews==
* 2015, Personal interview on the Intelligent Medicine Podcast: [https://drhoffman.com/podcast/chronic-fatigue-syndrome-part-1/ Part I] and [https://drhoffman.com/podcast/chronic-fatigue-syndrome-part-2/ Part II]

* 2019, Second personal interview on the Intelligent Medicine Podcast: [https://drhoffman.com/podcast/natural-treatment-for-chronic-fatigue-syndrome-part-1/ Part I] and [https://drhoffman.com/podcast/natural-treatment-for-chronic-fatigue-syndrome-part-2/ Part II]

==Books==
*Oct 23, 2014, ebook/digital: ''[[All My Test Results are Normal: A Smart Guide to Testing for Chronic Fatigue Syndrome]]''

==Online presence==
*[https://www.ncbi.nlm.nih.gov/pubmed/?term=Craig+Courtney%5BAuthor%5D PubMed - Courtney Craig]
*[https://www.threads.net/@craignutrition Threads]
*[https://www.facebook.com/drcourtneycraig Facebook]
*[https://www.instagram.com/craignutrition/ Instagram]
*[http://www.drcourtneycraig.com/ Website]
*[https://www.youtube.com/channel/UCWmVAjHnwL9Lu8tSJHV2NcA YouTube]
*[http://spoonieradio.libsyn.com/webpage Spoonie Radio website]

==See also==
*[[Ketogenic diet]]
*[[Mitochondrion]]

== Learn more ==

==References==
<references>
<ref name="craig2015">{{Citation | last = Craig | first1 = Courtney| author-link1 = Courtney Craig | title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets | journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693 | date =November 2015 | pmid = 26315446 | doi = 10.1016/j.mehy.2015.08.013 }}</ref>
</references>

[[Category:Researchers]]
[[Category:US researchers]]
[[Category:Clinicians]]
[[Category:American clinicians]]
[[Category:German clinicians]]
[[Category:Blogs]]
[[Category:People with ME, CFS, and/or FMS]]
[[Category:Authors]]

Courtney Craig

2019-11-13T12:40:06Z

Drcraig:/* References */

[[File:Courtney Craig.png|200px|thumb|right|Courtney_Craig.png]]
Doctor '''Courtney Craig''' is a Nutritionist and Chiropractor who has a special interest in treating patients with [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]] (ME/CFS) and [[fibromyalgia]] (FM). She became ill with [[ME/CFS]] in 1998, at the age of 16, but greatly improved in 2010 utilizing both conventional and integrative medicine.<ref>http://www.healthrising.org/blog/2014/05/10/closer-look-natural-killer-cells-chronic-fatigue-syndrome-three-natural-ways-boost/</ref><ref>{{Cite web|url=https://www.drcourtneycraig.com/nutritionist-for-mecfs|title=About Dr. Craig|last=|first=|authorlink=|last2=|first2=|authorlink2=|date=|website=|archive-url=|archive-date=|dead-url=|access-date=}}</ref> She is featured in the 2016 documentary film, [[Unrest]], which is about [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]].

Dr. Craig hosted a podcast called [[Spoonie Radio]] for two years in which she interviewed doctors, researchers, and patients within the ME/CFS community.

==Education==
*Undergraduate study in exercise science at the College of William and Mary, Virginia
*Graduated with honors from the University of Bridgeport’s Human Nutrition Institute Master's program.
*Clinical training at Palmer College of Chiropractic, Florida
*Visiting Scientist at Cornell’s Center for Enervating Neuroimmune Disease
*Master Student in Nutrition and Biomedicine at Technical University Munich in Germany.
*Member of the American Nutrition Association, the American College of Nutrition, and the Institute for Functional Medicine.

==Notable studies==
* 2015, Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets<ref name="craig2015" /> - a paper hypothesising that [[ME/CFS]] could be treated by improving mitochondrial function using [[fasting]], caloric restriction and a [[ketogenic diet]]. - [https://www.sciencedirect.com/science/article/abs/pii/S0306987715003187?via%3Dihub (Abstract)]

==Clinic location==
She has relocated to Germany and consults with patients via phone or Skype.

==Talks and interviews==
* 2015, Personal interview on the Intelligent Medicine Podcast: [https://drhoffman.com/podcast/chronic-fatigue-syndrome-part-1/ Part I] and [https://drhoffman.com/podcast/chronic-fatigue-syndrome-part-2/ Part II]

* 2019, Second personal interview on the Intelligent Medicine Podcast: [https://drhoffman.com/podcast/natural-treatment-for-chronic-fatigue-syndrome-part-1/ Part I] and [https://drhoffman.com/podcast/natural-treatment-for-chronic-fatigue-syndrome-part-2/ Part II]

==Books==
*Oct 23, 2014, ebook/digital: ''[[All My Test Results are Normal: A Smart Guide to Testing for Chronic Fatigue Syndrome]]''

==Online presence==
*[https://www.ncbi.nlm.nih.gov/pubmed/?term=Craig+Courtney%5BAuthor%5D PubMed - Courtney Craig]
*[https://twitter.com/courtney_37?lang=en-gb Twitter]
*[https://www.facebook.com/drcourtneycraig Facebook]
*[http://www.drcourtneycraig.com/ Website]
*[https://www.youtube.com/channel/UCWmVAjHnwL9Lu8tSJHV2NcA YouTube]
*[http://spoonieradio.libsyn.com/webpage Spoonie Radio website]

==See also==
*[[Ketogenic diet]]
*[[Mitochondria]]

== Learn more ==

==References==
<references>
<ref name="craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}
</ref>
</references>

[[Category:Researchers]]
[[Category:US researchers]]
[[Category:Clinicians]]
[[Category:American clinicians]]
[[Category:German clinicians]]
[[Category:Blogs]]
[[Category:People with ME, CFS, and/or FMS]]
[[Category:Authors]]

Spoonie Radio

2019-11-13T12:37:08Z

Drcraig:

'''Spoonie Radio''' is a podcast hosted by Dr. [[Courtney Craig]]. Guests included doctors, researchers, and patients within the [[ME/CFS]] community.<ref>http://spoonieradio.libsyn.com/webpage</ref> One can listen to archived episodes of the podcast and read the interview transcripts at [http://www.drcourtneycraig.com/ Dr. Craig's blog]. The podcast is also available on [https://podcasts.apple.com/us/podcast/spoonie-radio/id889652902 iTunes] and the [http://spoonieradio.libsyn.com/ Spoonie Radio Website] and [https://www.youtube.com/channel/UCWmVAjHnwL9Lu8tSJHV2NcA Dr Courtney Craig YouTube channel].

==Episodes==
*11/13/2019, Episode 17 Guest - Evan Golub & Nicole Krinick, founders of WANA - [http://spoonieradio.libsyn.com/ep-17-evan-nicole-from-wana Podcast] and No Full Transcript
*09/19/2019, Episode 16 Guest - [[Ken Lassesen]] - [https://www.drcourtneycraig.com/blog/2019/9/19/spoonie-radio-ep-16-ken-lassesen Podcast and Full Text Transcript]
*11/01/2015, Episode 15 Guest - Dr. [[Jarred Younger]] - [https://www.drcourtneycraig.com/blog/2015/11/1/spoonie-radio-ep-15-jarred-younger-phd Podcast and Full Text transcript)]
*10/01/2015, Episode 14 Guest - Dr. [[Jonathan Kerr]] - [http://www.drcourtneycraig.com/blog/2015/10/15/spoonie-radio-ep-14-dr-jonathan-kerr Podcast and Full Text Transcript]
*09/01/2015, Episode 13 Guest - Josh Grant of MENDUS - [http://www.drcourtneycraig.com/blog/2015/9/2/spoonie-radio-ep-13-joshua-grant-of-mendus Podcast and Full Text Transcript]
*07/01/2015, Episode 12 Guest - Dan Neuffer - [http://www.drcourtneycraig.com/blog/2015/7/2/spoonie-radio-ep-12-dan-neuffer Podcast and Full Text Transcript]
*06/01/2015, Episode 11 Guest - [[Toni Bernhard]] - [http://www.drcourtneycraig.com/blog/2015/5/31/spoonie-radio-ep-11-toni-bernhard Podcast and Full Text Transcript]
*05/01/2015, 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]
*04/01/2015, Episode 09 Guest - Dr. [[Suzanne Vernon]] - [http://www.drcourtneycraig.com/blog/2015/4/4/spoonie-radio-ep-09-suzanne-vernon Podcast and Full Text Transcript]
*03/01/2015, Episode 08 Guest - Dr. [[Judy Mikovits]] Part II - [http://www.drcourtneycraig.com/blog/2015/2/21/spoonie-radio-ep-08-judy-mikovits-part-ii Podcast and Full Text Transcript]
*02/04/2015, Episode 07 Guest - Dr. [[Judy Mikovits]] Part I - [http://www.drcourtneycraig.com/blog/2015/2/11/spoonie-radio-ep-07-judy-mikovits-part-i Podcast and Full Text Transcript]
*12/17/2014, Episode 06 Guest - Dr. Neil Nathan - [http://www.drcourtneycraig.com/blog/2014/12/19/spoonie-radio-ep-06-dr-neil-nathan Podcast and Full Text Transcript]
*11/06/2014, Episode 05 Guest - Dr. David Brady - [http://www.drcourtneycraig.com/blog/2014/11/12/spoonie-radio-ep-05-dr-david-brady Podcast and Full Text Transcript]
*10/13/2014, Episode 04 Guest - Sue Ingebretson - [http://www.drcourtneycraig.com/blog/2014/10/25/spoonie-radio-ep-04-sue-ingebretson Podcast and Full Text Transcript]
*09/08/2014, Episode 03 Guest - Dr. Terry Wahls - [http://www.drcourtneycraig.com/blog/2014/9/20/spoonie-radio-ep-03-terry-wahls Podcast and Full Text Transcript]
*07/14/2014, Episode 02 Guest - Damien Blenkinsopp - [http://www.drcourtneycraig.com/blog/spoonie-radio-ep-02-damien-blenkinsopp Podcast and Full Text Transcript]
*06/14/2014, Episode 01 Guest - Dr. [[Jacob Teitelbaum]] - [http://www.drcourtneycraig.com/blog/episode1-teitelbaum Podcast and Full Text Transcript]

==See also==
*[[Courtney Craig]]

==References==

[[Category:Podcasts]]
[[Category:Blogs]]
<references />

Spoonie Radio

2019-11-13T12:36:49Z

Drcraig:

'''Spoonie Radio''' is a podcast hosted by Dr. [[Courtney Craig]] during 2014 and 2015. Guests included doctors, researchers, and patients within the [[ME/CFS]] community.<ref>http://spoonieradio.libsyn.com/webpage</ref> One can listen to archived episodes of the podcast and read the interview transcripts at [http://www.drcourtneycraig.com/ Dr. Craig's blog]. The podcast is also available on [https://podcasts.apple.com/us/podcast/spoonie-radio/id889652902 iTunes] and the [http://spoonieradio.libsyn.com/ Spoonie Radio Website] and [https://www.youtube.com/channel/UCWmVAjHnwL9Lu8tSJHV2NcA Dr Courtney Craig YouTube channel].

==Episodes==
*11/13/2019, Episode 17 Guest - Evan Golub & Nicole Krinick, founders of WANA - [http://spoonieradio.libsyn.com/ep-17-evan-nicole-from-wana Podcast] and No Full Transcript
*09/19/2019, Episode 16 Guest - [[Ken Lassesen]] - [https://www.drcourtneycraig.com/blog/2019/9/19/spoonie-radio-ep-16-ken-lassesen Podcast and Full Text Transcript]
*11/01/2015, Episode 15 Guest - Dr. [[Jarred Younger]] - [https://www.drcourtneycraig.com/blog/2015/11/1/spoonie-radio-ep-15-jarred-younger-phd Podcast and Full Text transcript)]
*10/01/2015, Episode 14 Guest - Dr. [[Jonathan Kerr]] - [http://www.drcourtneycraig.com/blog/2015/10/15/spoonie-radio-ep-14-dr-jonathan-kerr Podcast and Full Text Transcript]
*09/01/2015, Episode 13 Guest - Josh Grant of MENDUS - [http://www.drcourtneycraig.com/blog/2015/9/2/spoonie-radio-ep-13-joshua-grant-of-mendus Podcast and Full Text Transcript]
*07/01/2015, Episode 12 Guest - Dan Neuffer - [http://www.drcourtneycraig.com/blog/2015/7/2/spoonie-radio-ep-12-dan-neuffer Podcast and Full Text Transcript]
*06/01/2015, Episode 11 Guest - [[Toni Bernhard]] - [http://www.drcourtneycraig.com/blog/2015/5/31/spoonie-radio-ep-11-toni-bernhard Podcast and Full Text Transcript]
*05/01/2015, 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]
*04/01/2015, Episode 09 Guest - Dr. [[Suzanne Vernon]] - [http://www.drcourtneycraig.com/blog/2015/4/4/spoonie-radio-ep-09-suzanne-vernon Podcast and Full Text Transcript]
*03/01/2015, Episode 08 Guest - Dr. [[Judy Mikovits]] Part II - [http://www.drcourtneycraig.com/blog/2015/2/21/spoonie-radio-ep-08-judy-mikovits-part-ii Podcast and Full Text Transcript]
*02/04/2015, Episode 07 Guest - Dr. [[Judy Mikovits]] Part I - [http://www.drcourtneycraig.com/blog/2015/2/11/spoonie-radio-ep-07-judy-mikovits-part-i Podcast and Full Text Transcript]
*12/17/2014, Episode 06 Guest - Dr. Neil Nathan - [http://www.drcourtneycraig.com/blog/2014/12/19/spoonie-radio-ep-06-dr-neil-nathan Podcast and Full Text Transcript]
*11/06/2014, Episode 05 Guest - Dr. David Brady - [http://www.drcourtneycraig.com/blog/2014/11/12/spoonie-radio-ep-05-dr-david-brady Podcast and Full Text Transcript]
*10/13/2014, Episode 04 Guest - Sue Ingebretson - [http://www.drcourtneycraig.com/blog/2014/10/25/spoonie-radio-ep-04-sue-ingebretson Podcast and Full Text Transcript]
*09/08/2014, Episode 03 Guest - Dr. Terry Wahls - [http://www.drcourtneycraig.com/blog/2014/9/20/spoonie-radio-ep-03-terry-wahls Podcast and Full Text Transcript]
*07/14/2014, Episode 02 Guest - Damien Blenkinsopp - [http://www.drcourtneycraig.com/blog/spoonie-radio-ep-02-damien-blenkinsopp Podcast and Full Text Transcript]
*06/14/2014, Episode 01 Guest - Dr. [[Jacob Teitelbaum]] - [http://www.drcourtneycraig.com/blog/episode1-teitelbaum Podcast and Full Text Transcript]

==See also==
*[[Courtney Craig]]

==References==

[[Category:Podcasts]]
[[Category:Blogs]]
<references />

Alpha-lipoic acid

2019-10-30T14:15:16Z

Drcraig:topic expansion with reference addition

{{Cleanup | reason=Needs citations adding, rewording in encyclopedic style, and categorising | date=2018}}

Alpha lipoic acid (ALA) is an antioxidant for liver and nerve health. It is synthesized by mitochondria. Food sources are protein bound and have no effect on increasing free form ALA plasma levels.<ref name=":0">{{Cite journal|last=Park|first=Sungmi|last2=Karunakaran|first2=Udayakumar|last3=Jeoung|first3=Nam Ho|last4=Jeon|first4=Jae-Han|last5=Lee|first5=In-Kyu|date=2014|title=Physiological effect and therapeutic application of alpha lipoic acid|url=https://www.ncbi.nlm.nih.gov/pubmed/25005184|journal=Current Medicinal Chemistry|volume=21|issue=32|pages=3636–3645|doi=10.2174/0929867321666140706141806|issn=1875-533X|pmid=25005184}}</ref>

Alpha lipoic acid is a cofactor for some of the key enzymes (alpha keto acid dehydrogenase, [[pyruvate dehydrogenase]], etc) involved in generating energy from food and oxygen in mitochondria and thus plays a critical role in energy production within the cell’s mitochondria.<ref name=":0" /> Since one theory of CFS/ME is mitochondria dysfunction, supplementation may aid in energy production and reduce fatigue. Co-administration of ALA with other mitochondrial nutrients, such as [[acetyl-L-carnitine]] and [[coenzyme Q10]], appears more effective in improving cognitive dysfunction and reducing oxidative mitochondrial dysfunction.<ref>{{Cite journal|last=Liu|first=Jiankang|date=2008-1|title=The effects and mechanisms of mitochondrial nutrient alpha-lipoic acid on improving age-associated mitochondrial and cognitive dysfunction: an overview|url=https://www.ncbi.nlm.nih.gov/pubmed/17605107|journal=Neurochemical Research|volume=33|issue=1|pages=194–203|doi=10.1007/s11064-007-9403-0|issn=0364-3190|pmid=17605107}}</ref>

=== Uses ===
In Germany lipoic acid has long been prescribed for diabetic neuropathy, cirrhosis, and mushroom and heavy metal poisonings.<ref name=":1">{{Cite journal|last=Waslo|first=Carin|last2=Bourdette|first2=Dennis|last3=Gray|first3=Nora|last4=Wright|first4=Kirsten|last5=Spain|first5=Rebecca|date=2019-05-06|title=Lipoic Acid and Other Antioxidants as Therapies for Multiple Sclerosis|url=https://www.ncbi.nlm.nih.gov/pubmed/31056714|journal=Current Treatment Options in Neurology|volume=21|issue=6|pages=26|doi=10.1007/s11940-019-0566-1|issn=1092-8480|pmid=31056714}}</ref>

Lipoic acid can be administered intravenously. Supplemental oral ALA is 30-40% absorbed from the gastrointestinal tract. Supplemental forms often comprise a 50-50 mixture of R- and S-lipoic acid enantiomers. The R-form is better absorbed. Liquid formulas are also better absorbed.<ref>{{Cite journal|last=Uchida|first=Ryota|last2=Okamoto|first2=Hinako|last3=Ikuta|first3=Naoko|last4=Terao|first4=Keiji|last5=Hirota|first5=Takashi|date=2015-09-21|title=Enantioselective Pharmacokinetics of α-Lipoic Acid in Rats|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4613335/|journal=International Journal of Molecular Sciences|volume=16|issue=9|pages=22781–22794|doi=10.3390/ijms160922781|issn=1422-0067|pmc=4613335|pmid=26402669}}</ref>

=== Side Effects ===
Supplementing ALA can result in nausea,malodorous urine, headache, weakness, pain, spams, and rash. Side effects are more commonly seen it higher doses.<ref name=":1" /> It may interact with diabetic medications to cause hypoglycemia.

=== Clinical Trials ===

==== Diabetic Neuropathy ====
Meta-analyses of randomized controlled trials suggest that infusion of 300 to 600 mg/day of lipoic acid for 2 to 4 weeks significantly reduced symptoms of diabetic neuropathy,<ref>{{Cite journal|last=Han|first=Tingting|last2=Bai|first2=Jiefei|last3=Liu|first3=Wei|last4=Hu|first4=Yaomin|date=2012-10|title=A systematic review and meta-analysis of α-lipoic acid in the treatment of diabetic peripheral neuropathy|url=https://www.ncbi.nlm.nih.gov/pubmed/22837391|journal=European Journal of Endocrinology|volume=167|issue=4|pages=465–471|doi=10.1530/EJE-12-0555|issn=1479-683X|pmid=22837391}}</ref> A randomized, double-blind, placebo-controlled trial in 181 patients with diabetic neuropathy found that oral supplementation with either 600 mg/day, 1,200 mg/day, or 1,800 mg/day of lipoic acid for 5 weeks significantly improved neuropathic symptoms. There was no difference between the low, moderate or high dose groups.<ref>{{Cite journal|last=Ziegler|first=Dan|last2=Ametov|first2=Alexander|last3=Barinov|first3=Alexey|last4=Dyck|first4=Peter J.|last5=Gurieva|first5=Irina|last6=Low|first6=Phillip A.|last7=Munzel|first7=Ullrich|last8=Yakhno|first8=Nikolai|last9=Raz|first9=Itamar|date=2006-11|title=Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy: the SYDNEY 2 trial|url=https://www.ncbi.nlm.nih.gov/pubmed/17065669|journal=Diabetes Care|volume=29|issue=11|pages=2365–2370|doi=10.2337/dc06-1216|issn=0149-5992|pmid=17065669}}</ref> Improvements in neuropathy from these trials are not always corroborated with electrodiagnostic testing. It is thought, that the beneficial effects of ALA on neuropathy may be due to effects on the small nerve fibers, making it a candidate treatment for [[Small fiber peripheral neuropathy|small fiber neuropathy]].<ref>{{Cite journal|last=Swiecka|first=Marta|author-link=|last2=Maslinska|first2=Maria|author-link2=|last3=Kwiatkowska|first3=Brygida|author-link3=|last4=|first4=|author-link4=|last5=|first5=|author-link5=|last6=|first6=|author-link6=|last7=|first7=|last8=|first8=|date=2018|title=Small fiber neuropathy as a part of fibromyalgia or a separate diagnosis?|url=https://www.openaccessjournals.com/articles/small-fiber-neuropathy-as-a-part-of-fibromyalgia-or-a-separate-diagnosis.pdf|journal=International Journal of Clinical Rheumatology|volume=13|issue=6|pages=353-359|doi=|pmc=|pmid=|access-date=10/30/2019|quote=|via=}}</ref>

==== Multiple Sclerosis ====
A small pilot study designed to evaluate the safety of lipoic acid in 30 people with relapsing or progressive multiple sclerosis found that treatment with 1,200 to 2,400 mg/day of oral lipoic acid for 2 weeks was safe. Those with the higher serum concentrations of lipoic acid had the lowest serum concentrations of MMP-9 — a marker of inflammation.<ref>{{Cite journal|last=Yadav|first=V.|last2=Marracci|first2=G.|last3=Lovera|first3=J.|last4=Woodward|first4=W.|last5=Bogardus|first5=K.|last6=Marquardt|first6=W.|last7=Shinto|first7=L.|last8=Morris|first8=C.|last9=Bourdette|first9=D.|date=2005-4|title=Lipoic acid in multiple sclerosis: a pilot study|url=https://www.ncbi.nlm.nih.gov/pubmed/15794388|journal=Multiple Sclerosis (Houndmills, Basingstoke, England)|volume=11|issue=2|pages=159–165|doi=10.1191/1352458505ms1143oa|issn=1352-4585|pmid=15794388}}</ref> A 2-year trial of 1,200 mg/day LA in secondary progressive MS demonstrated a significant reduction of whole-brain atrophy and trend toward improvement in walking speed.<ref name=":1" />

<references />

Magnesium

2019-10-24T15:22:13Z

Drcraig:/* Role in the body */

'''Magnesium''' (chemical or element symbol '''Mg''') is an essential [[mineral]] in the human body. It plays a key role in [[DNA]] and [[RNA]] synthesis and in the production of [[ATP]]. It is a cofactor in more than 300 [[enzyme]] systems.<ref name="NihMagnesium" /> Muscle and bone comprise 90% of the body's magnesium content. A serum value of 75–95 mmol/L is considered normal but some research would indicate that serum levels less than 85 mmol/l should be considered deficient. An individual may be profoundly deficient in total body or intracellular Mg, yet have a serum value within normal range.<ref name=":1">{{Cite journal|last=Schwalfenberg|first=Gerry K.|last2=Genuis|first2=Stephen J.|date=2017|title=The Importance of Magnesium in Clinical Healthcare|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5637834/|journal=Scientifica|volume=2017|doi=10.1155/2017/4179326|issn=2090-908X|pmc=5637834|pmid=29093983}}</ref>

==Role in the body==

==Deficiency==

Symptoms of magnesium deficiency include loss of appetite, [[nausea]], vomiting, [[fatigue]], and weakness. As magnesium deficiency worsens, numbness, tingling, muscle contractions and cramps, [[seizures]], personality changes, abnormal heart rhythms, and coronary spasms can occur. Severe magnesium deficiency can result in [[hypocalcemia]] or [[hypokalemia]] (low serum calcium or potassium levels, respectively) because mineral homeostasis is disrupted.<ref name="NihMagnesium" />

Magnesium deficiency disrupts the [[Hypothalamic-pituitary-adrenal axis|HPA axis]] and increases susceptibility to physiological damage produced by stress. Deficiency can promote activation of the N-methyl-D-aspartic acid (NMDA) receptor which triggers inflammatory pathways and [[cortisol]] release.<ref>{{Cite journal|last=Rayssiguier|first=Yves|last2=Libako|first2=Patrycja|last3=Nowacki|first3=Wojciech|last4=Rock|first4=Edmond|date=2010-6|title=Magnesium deficiency and metabolic syndrome: stress and inflammation may reflect calcium activation|url=https://www.ncbi.nlm.nih.gov/pubmed/20513641|journal=Magnesium Research|volume=23|issue=2|pages=73–80|doi=10.1684/mrh.2010.0208|issn=1952-4021|pmid=20513641}}</ref>

People with [[gastrointestinal]]<ref name="NihMagnesium" /> disorders and [[chronic fatigue syndrome]] are at higher risk of magnesium deficiency.

Deficiency increases the risk of [[osteoporosis]]. Magnesium supplementation may help prevent [[migraine]].<ref name="NihMagnesium" />

== Forms of administration==

Magnesium may be taken as an oral supplement but may not be well absorbed. Magnesium oxide and citrate are poorly absorbed forms compared to glycinate and orotate.<ref name=":1" /> Other forms of magnesium administration include transdermal magnesium and intramuscular magnesium sulphate injections.

Magnesium is [[hypotonic]]. Administration can cause water to flow into cells in the local area where it is applied, which can cause a temporary stinging sensation.

==In human disease==
=== Chronic fatigue syndrome ===
In 1991, Cox et al., performed a randomized, double-blind, placebo-controlled trial of 20 United Kingdom [[CFS|chronic fatigue syndrome]] (CFS) patients finding that the subjects with CFS had lower [[red blood cell magnesium]] than healthy controls. Patients treated with intramuscular magnesium sulphate for six weeks had higher self-reported energy levels, better emotional state and less pain on the Nottingham health profile when compared to placebo.<ref name=":0">{{Cite journal|title=Red blood cell magnesium and chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/1672392|journal=Lancet (London, England)|date=1991-03-30|issn=0140-6736|pmid=1672392|pages=757–760|volume=337|issue=8744|first=I. M.|last=Cox|first2=M. J.|last2=Campbell|first3=D.|last3=Dowson}}</ref>

In contrast, three subsequent case‐report studies, two in the UK (Clague et al., 1992<ref>Clague JE, Edwards RH, Jackson MJ (1992). Intravenous magnesium loading in chronic fatigue syndrome. Lancet 340: 124–125. PMID:1352002</ref> and Hinds et al., 1994<ref>Hinds G, Bell NP, McMaster D, McCluskey DR (1994). Normal red cell magnesium concentrations and magnesium loading tests in patients with chronic fatigue syndrome. Ann Clin Biochem 31 (Pt 5): 459–461. DOI:10.1177/000456329403100506</ref>), and one in the Netherlands (Swanink et al., 1995<ref>{{Cite journal|last=Swanink|first=C. M.|author-link=|last2=Vercoulen|first2=J. H.|author-link2=|last3=Bleijenberg|first3=G.|author-link3=Gijs Bleijenberg|last4=Fennis|first4=J. F.|author-link4=|last5=Galama|first5=J. M.|author-link5=|last6=van der Meer|first6=J. W.|author-link6=Jos van der Meer|date=May 1995|title=Chronic fatigue syndrome: a clinical and laboratory study with a well matched control group|url=https://www.ncbi.nlm.nih.gov/pubmed/7738491|journal=Journal of Internal Medicine|volume=237|issue=5|pages=499–506|issn=0954-6820|pmid=7738491|quote=|via=}}</ref>), did not find magnesium deficiency in CFS trial subjects.

=== X-MEN ===
A 2014 study found magnesium transporter issues were linked to chronic [[Epstein-Barr virus]] infection, decreased [[Natural killer cell]] function, and neoplasia (sometimes-cancerous growths).<ref name="X-men_disease_1" /> This disorder, termed 'X-MEN' (for X-linked, EBV, and neoplasia) was identified as a [https://en.wikipedia.org/wiki/X-linked_recessive_inheritance recessive, X-linked disorder] that would therefore be many times more common in men. Due to magnesium's role as a 'second messenger', this magnesium transporter disorder also would result in a primary [[immunodeficiency]] that would worsen with age.<ref name="X-men_disease_1" /> Patients also have impaired T-cell activation and decreased natural killer (NK) cell function due to a decreased expression of "the NK stimulatory receptor 'natural-killer group 2, member D' (NKG2D)."<ref name="X-men_disease_2" /> Although T-cells are affected, there is no direct evidence of B-cell effects in X-MEN disease.<ref name="X-men_disease_2" />

Since chronic Epstein-Barr virus infection has been associated with chronic fatigue syndrome, this error in magnesium transport may be worth considering in male patients, especially with slow onset and history of childhood infection.<ref name="X-men_disease_1" />

===Mast cell activation disorder===
Magnesium is a cofactor in the production of [[diamine oxidase]]. It is an enzyme that breaks down [[histamine]], which is released by [[mast cell]]s.

== Studies ==
* 1991, Red blood cell magnesium and chronic fatigue syndrome.<ref name=":0" /> ([[pubmed:1672392|Abstract]])
* 1994, Normal red cell magnesium concentrations and magnesium loading tests in patients with chronic fatigue syndrome.<ref>{{Cite journal|title=Normal red cell magnesium concentrations and magnesium loading tests in patients with chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/7832571|journal=Annals of Clinical Biochemistry|date=Sep 1994|issn=0004-5632|pmid=7832571|pages=459–461|volume=31 ( Pt 5)|doi=10.1177/000456329403100506|first=G.|last=Hinds|first2=N. P.|last2=Bell|first3=D.|last3=McMaster|first4=D. R.|last4=McCluskey}}</ref> ([[pubmed:7832571|Abstract]])
* 1997, Magnesium deficit in a sample of the Belgian population presenting with chronic fatigue.<ref>{{Cite journal|last=Moorkens|first=G.|last2=Manuel y Keenoy|first2=B.|last3=Vertommen|first3=J.|last4=Meludu|first4=S.|last5=Noe|first5=M.|last6=De Leeuw|first6=I.|date=Dec 1997|title=Magnesium deficit in a sample of the Belgian population presenting with chronic fatigue|url=https://www.ncbi.nlm.nih.gov/pubmed/9513929|journal=Magnesium Research|volume=10|issue=4|pages=329–337|issn=0953-1424|pmid=9513929}}</ref> ([[pubmed:9513929|Abstract]])
* 2006, Increase of free Mg2+ in the skeletal muscle of chronic fatigue syndrome patients.<ref>{{Cite journal|last=McCully|first=Kevin K|author-link=|last2=Malucelli|first2=Emil|author-link2=|last3=Iotti|first3=Stefano|author-link3=|author-link4=|author-link5=|date=2006-01-11|title=Increase of free Mg2+ in the skeletal muscle of chronic fatigue syndrome patients|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360067/|journal=Dynamic Medicine|volume=5|issue=|pages=1|doi=10.1186/1476-5918-5-1|issn=1476-5918|pmc=1360067|pmid=16405724|quote=|via=}}</ref> ([https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360067/ Full text])

== See also ==
* [[:Category:Minerals|Minerals]]
* [[Electrolyte]]
* [[Ion transportation]]

==Learn more==

*[https://www.ncbi.nlm.nih.gov/pubmed/?term=magnesium+chronic+fatigue+syndrome PubMed - magnesium and CFS]
*2012, [https://cfsremission.wordpress.com/treatment/symptom-mitigation/magnesium-malic-acid-magnesium-malate/ Core: Magnesium / Malic Acid / Magnesium Malate]
*[http://lpi.oregonstate.edu/mic/minerals/magnesium Magnesium-Linus Pauling Institute Micronutrient Information Center]

==References==
<references>
<ref name="X-men_disease_1">{{Citation
| last1 = Li
| first1 = F.-Y.
| authorlink1 =
| last2 = Chaigne-Delalande
| first2 = B
| authorlink2 =
| last3 = Su
| first3 = H
| last4 = Matthews
| first4 = H
| last5 = Lenardo
| first5 = M.J.
| authorlink3 =
| display-authors =
| title = XMEN disease: a new primary immunodeficiency affecting Mg2+ regulation of immunity against Epstein-Barr virus.
| journal = Blood
| year = 2014
| doi = 10.1182/blood-2013-11-538686
}}
</ref>
<ref name="X-men_disease_2">{{Citation
| last1 = Ravell
| first1 = J
| authorlink1 =
| last2 = Chaigne-Delalande
| first2 = B
| authorlink2 =
| last3 = Lenardo
| first3 = M
| display-authors =
| title = XMEN disease: a combined immune deficiency with magnesium defect.
| journal = Current Opinion in Pediatrics
| year = 2014
| doi = 10.1097/MOP.0000000000000156
}}
</ref>
<ref name="NihMagnesium">{{Citation
| publisher = National Institutes of Health: Office of Dietary Supplements
| title = Magnesium: Fact sheet for health professionals
| access-date = 22 May 2018
| date = 2 March 2018
| url = https://ods.od.nih.gov/factsheets/Magnesium-HealthProfessional/
}}
</ref>
</references>

[[Category:Potential treatments]]
[[Category:Supplements]]
[[Category:Minerals]]
[[Category:Nutrients]]
[[Category:Chemical elements]]
[[Category:Electrolytes]]

Pyruvate dehydrogenase

2019-10-01T11:23:53Z

Drcraig:

'''Pyruvate dehydrogenase''' (PDH) is an [[enzyme]] that is part of the [[citric acid cycle]]. It catalyzes the reaction that transforms [[pyruvate]] into [[acetyl-CoA]], a process called [[pyruvate decarboxylation]]. PDH activity is inhibited by [[pyruvate dehydrogenase kinase]] (PDK).

PDH activity is controlled by multiple different factors, including but not limited to:

*PDH kinases (PDKs), that inhibit activity of PDH enzymes
*PDH phosphatases that yank away PDH’s phosphate group so it does not function properly
*Sirtuin 4 (SIRT4), which is also an inhibitor for PDH
*PDK1, 2, 3, and 4
*A shift in these or their expression means a shift towards higher glucose, lower pyruvate, lower Acetyl Co-A, and fewer energy-rich molecules produced in the cell to do work.
PDH activity can be increased by supplementing with [[L-carnitine]].<ref>{{Cite journal|last=Arenas|first=J.|last2=Huertas|first2=R.|last3=Campos|first3=Y.|last4=Díaz|first4=A. E.|last5=Villalón|first5=J. M.|last6=Vilas|first6=E.|date=1994-03-14|title=Effects of L-carnitine on the pyruvate dehydrogenase complex and carnitine palmitoyl transferase activities in muscle of endurance athletes|url=https://www.ncbi.nlm.nih.gov/pubmed/8137928|journal=FEBS letters|volume=341|issue=1|pages=91–93|doi=10.1016/0014-5793(94)80246-7|issn=0014-5793|pmid=8137928}}</ref>

==In ME/CFS==
A large study by [[Fluge]] and [[Mella]] of 200 patients meeting the [[Canadian Consensus Criteria]] and 102 controls found a pattern of amino acids that suggested functional impairment of pyruvate dehydrogenase (PDH), supported by increased mRNA expression of the inhibitory PDH kinases 1, 2, and 4; sirtuin 4; and PPARδ in peripheral blood mononuclear cells from both sexes.<ref>{{Cite journal|last=Tronstad|first=Karl J.|last2=Dahl|first2=Olav|last3=Ueland|first3=Per M.|last4=Helgeland|first4=Lars|last5=Sommerfelt|first5=Kristian|last6=McCann|first6=Adrian|last7=Schäfer|first7=Christoph|last8=Bohnen|first8=Louis M. L. J.|last9=Baranowska|first9=Katarzyna A.|date=2017-01-03|title=Metabolic profiling indicates impaired pyruvate dehydrogenase function in myalgic encephalopathy/chronic fatigue syndrome|url=https://insight.jci.org/articles/view/89376|journal=JCI Insight|language=en|volume=1|issue=21|doi=10.1172/jci.insight.89376|issn=0021-9738}}</ref>

==Learn more==

*[http://www.meaction.net/2016/12/23/fluge-mella-and-armstrong-more-support-for-disordered-metabolism-in-me-patients Fluge, Mella, and Armstrong: More Support for Disordered Metabolism in ME Patients], #MEAction, December 23, 2016

==References==
<references />
[[Category:Enzymes]]

Pyruvate dehydrogenase

2019-10-01T10:00:06Z

Drcraig:

'''Pyruvate dehydrogenase''' (PDH) is an [[enzyme]] that is part of the [[citric acid cycle]]. It catalyzes the reaction that transforms [[pyruvate]] into [[acetyl-CoA]], a process called [[pyruvate decarboxylation]]. PDH activity is inhibited by [[pyruvate dehydrogenase kinase]] (PDK).

PDH activity is controlled by multiple different factors, including but not limited to:

*PDH kinases (PDKs), that inhibit activity of PDH enzymes
*PDH phosphatases that yank away PDH’s phosphate group so it does not function properly
*Sirtuin 4 (SIRT4), which is also an inhibitor for PDH
*PDK1, 2, 3, and 4
*A shift in these or their expression means a shift towards higher glucose, lower pyruvate, lower Acetyl Co-A, and fewer energy-rich molecules produced in the cell to do work.
PDH activity can be increased by supplementing with L-carnitine.<ref>{{Cite journal|last=Arenas|first=J.|last2=Huertas|first2=R.|last3=Campos|first3=Y.|last4=Díaz|first4=A. E.|last5=Villalón|first5=J. M.|last6=Vilas|first6=E.|date=1994-03-14|title=Effects of L-carnitine on the pyruvate dehydrogenase complex and carnitine palmitoyl transferase activities in muscle of endurance athletes|url=https://www.ncbi.nlm.nih.gov/pubmed/8137928|journal=FEBS letters|volume=341|issue=1|pages=91–93|doi=10.1016/0014-5793(94)80246-7|issn=0014-5793|pmid=8137928}}</ref>

==In ME/CFS==
A large study by [[Fluge]] and [[Mella]] of 200 patients meeting the [[Canadian Consensus Criteria]] and 102 controls found a pattern of amino acids that suggested functional impairment of pyruvate dehydrogenase (PDH), supported by increased mRNA expression of the inhibitory PDH kinases 1, 2, and 4; sirtuin 4; and PPARδ in peripheral blood mononuclear cells from both sexes.<ref>{{Cite journal|last=Tronstad|first=Karl J.|last2=Dahl|first2=Olav|last3=Ueland|first3=Per M.|last4=Helgeland|first4=Lars|last5=Sommerfelt|first5=Kristian|last6=McCann|first6=Adrian|last7=Schäfer|first7=Christoph|last8=Bohnen|first8=Louis M. L. J.|last9=Baranowska|first9=Katarzyna A.|date=2017-01-03|title=Metabolic profiling indicates impaired pyruvate dehydrogenase function in myalgic encephalopathy/chronic fatigue syndrome|url=https://insight.jci.org/articles/view/89376|journal=JCI Insight|language=en|volume=1|issue=21|doi=10.1172/jci.insight.89376|issn=0021-9738}}</ref>

==Learn more==

*[http://www.meaction.net/2016/12/23/fluge-mella-and-armstrong-more-support-for-disordered-metabolism-in-me-patients Fluge, Mella, and Armstrong: More Support for Disordered Metabolism in ME Patients], #MEAction, December 23, 2016

==References==
<references />
[[Category:Enzymes]]

Courtney Craig

2019-09-11T12:06:42Z

Drcraig:/* Talks and interviews */

[[File:Courtney Craig.png|200px|thumb|right|Courtney_Craig.png]]
Doctor '''Courtney Craig''' is a Nutritionist and Chiropractor who has a special interest in treating patients with [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]] (ME/CFS) and [[fibromyalgia]] (FM). She became ill with [[ME/CFS]] in 1998, at the age of 16, but greatly improved in 2010 utilizing both conventional and integrative medicine.<ref>http://www.healthrising.org/blog/2014/05/10/closer-look-natural-killer-cells-chronic-fatigue-syndrome-three-natural-ways-boost/</ref> She is featured in the 2016 documentary film, [[Unrest]], which is about [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]].<ref>http://www.drcourtneycraig.com/about/</ref>

Dr. Craig hosted a podcast called [[Spoonie Radio]] for two years in which she interviewed doctors, researchers, and patients within the ME/CFS community.

==Education==
*Undergraduate study in exercise science at the College of William and Mary, Virginia
*Graduated with honors from the University of Bridgeport’s Human Nutrition Institute Master's program.
*Clinical training at Palmer College of Chiropractic, Florida
*Visiting Scientist at Cornell’s Center for Enervating Neuroimmune Disease
*Master Student in Nutrition and Biomedicine at Technical University Munich in Germany.
*Member of the American Nutrition Association, the American College of Nutrition, and the Institute for Functional Medicine.

==Notable studies==
She published a paper hypothesising that [[ME/CFS]] could be treated by improving mitochondrial function using [[fasting]], caloric restriction and a [[ketogenic diet]].<ref name="craig2015" />

==Clinic location==
She has relocated to Germany and consults with patients via phone or Skype.

==Talks and interviews==
Personal interview on the Intelligent Medicine Podcast: [https://drhoffman.com/podcast/chronic-fatigue-syndrome-part-1/ Part I] and [https://drhoffman.com/podcast/chronic-fatigue-syndrome-part-2/ Part II] (2015)

Second personal interview on the Intelligent Medicine Podcast: [https://drhoffman.com/podcast/natural-treatment-for-chronic-fatigue-syndrome-part-1/ Part I] and [https://drhoffman.com/podcast/natural-treatment-for-chronic-fatigue-syndrome-part-2/ Part II] (2019)

==Books==
*Oct 23, 2014, ebook/digital: ''[[All My Test Results are Normal: A Smart Guide to Testing for Chronic Fatigue Syndrome]]''

==Online presence==
*[https://www.ncbi.nlm.nih.gov/pubmed/?term=Craig+Courtney%5BAuthor%5D PubMed - Courtney Craig]
*[https://twitter.com/courtney_37?lang=en-gb Twitter]
*[https://www.facebook.com/drcourtneycraig Facebook]
*[http://www.drcourtneycraig.com/ Website]
*[https://www.youtube.com/channel/UCWmVAjHnwL9Lu8tSJHV2NcA YouTube]
*[http://spoonieradio.libsyn.com/webpage Spoonie Radio website]

==Learn more==
*Wikipedia
*Institution

==See also==
*[[Ketogenic diet]]
*[[Mitochondria]]

==References==
<references>
<ref name="craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}
</ref>
</references>

[[Category:Researchers]]
[[Category:US researchers]]
[[Category:Clinicians]]
[[Category:American clinicians]]
[[Category:German clinicians]]
[[Category:Blogs]]
[[Category:People with ME, CFS, and/or FMS]]
[[Category:Authors]]

Fasting

2019-09-03T11:06:23Z

Drcraig:/* Immune system */

== Types of fasting ==

=== Water only fasting ===
As the name implies, this is a type of fasting where only water may be consumed – no other food or beverage is permitted.

=== Liquid fasting ===

Some fasts include abstaining from solid foods but consuming calorie-containing liquids, such as vegetables juices or broth.

=== Intermittent fasting ===
In this form of fasting, a person alternates between periods of fasting and non-fasting, with a defined schedule. Intermittent fasting is of interest to researchers for its potential effects on insulin sensitivity and other aspects of health. Popular types of intermittent fasting include: 16:8, 16-hr fast with a 8-hr eating window, 18:6, 18-hr fast with a 6-hr eating window, 20:4, 20-hr fast with a 4-hr eating window. The alternate day fast is a 36 hour fast followed by a 12-hr eating window.

=== Caloric restriction ===
A calorie restricted (CR) diet reduces calorie intake without malnutrition. It is chronic and does not include a refeeding phase. Most clinical trials of CR aim for 25-30% total calorie reduction. The 5:2 diet is a calorically restricted diet in which 2 days per week one consumes 500-600 calories, and eats normally the remaining 5 week days.

== Physiological effects ==

A fast with duration sufficient to deplete the body's glycogen stores, at least 18 hours, increases the blood ketone β-hydroxybutyrate allowing for nutritional [[ketosis]].

Fasting increases [[autophagy]] in mice.

The US National Institute on Aging and the National Institute of Diabetes and Digestive and Kidney Diseases conducted the CALERIE (Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy) study using a 2-year CR diet (25% reduction) in non-obese adults (n = 143) compared to an ad libitum group (n =75). The CR group reported improvements in mood and improved sleep quality without adverse effects or immune compromise. There was also improvement in cardiovascular risk factors including C-reactive protein.<ref>{{Cite journal|last=Kraus|first=William E.|last2=Bhapkar|first2=Manjushri|last3=Huffman|first3=Kim M.|last4=Pieper|first4=Carl F.|last5=Krupa Das|first5=Sai|last6=Redman|first6=Leanne M.|last7=Villareal|first7=Dennis T.|last8=Rochon|first8=James|last9=Roberts|first9=Susan B.|date=2019-9|title=2 years of calorie restriction and cardiometabolic risk (CALERIE): exploratory outcomes of a multicentre, phase 2, randomised controlled trial|url=https://www.ncbi.nlm.nih.gov/pubmed/31303390|journal=The Lancet. Diabetes & Endocrinology|volume=7|issue=9|pages=673–683|doi=10.1016/S2213-8587(19)30151-2|issn=2213-8595|pmc=6707879|pmid=31303390}}</ref>

== Health effects ==

There is no evidence on the benefits or harms of fasting for ME and CFS patients. However, there is a growing body of evidence suggesting possible health benefits of water-only fasting to the microbiome,<ref name="remely2015" /> mitochondria<ref name="fernanda2011" /> and the immune system,<ref name="cheng2014" /> and as a cancer adjuvant.<ref name="changhan2012" /><ref name="lee2011" /><ref name="fernando2009" />

==Immune system==
[[Caloric restriction]] significantly reduced the amount of circulating [[lipopolysaccharide]]-binding protein.<ref name="zhang2013" /> In vitro, short-term (19 hour) fasting reduced monocyte metabolic and inflammatory activity and drastically reduced the number of circulating monocytes. This effect is thought to be due to redistribution of these cells to the bone marrow.<ref name=":0" /> Caloric restriction and intermittent fasting strongly reduced the accumulation of pathogenic monocytes in the central nervous system, reduced monocyte pro-inflammatory activity, and improved disease outcome in a mouse model of multiple sclerosis and in a preclinical model in multiple sclerosis patients.<ref name=":0">{{Cite journal|last=Cignarella|first=Francesca|last2=Cantoni|first2=Claudia|last3=Ghezzi|first3=Laura|last4=Salter|first4=Amber|last5=Dorsett|first5=Yair|last6=Chen|first6=Lei|last7=Phillips|first7=Daniel|last8=Weinstock|first8=George M.|last9=Fontana|first9=Luigi|date=2018-06-05|title=Intermittent Fasting Confers Protection in CNS Autoimmunity by Altering the Gut Microbiota|url=https://www.ncbi.nlm.nih.gov/pubmed/29874567|journal=Cell Metabolism|volume=27|issue=6|pages=1222–1235.e6|doi=10.1016/j.cmet.2018.05.006|issn=1932-7420|pmc=6460288|pmid=29874567}}</ref>

==Chronic fatigue syndrome==
Dr. [[Courtney Craig]] has proposed the use of fasting, [[caloric restriction]] and a [[ketogenic diet]] in the treatment of [[mitochondria]]l damage in [[ME/CFS]].<ref name="craig2015" />

== See also ==
* [[Caloric restriction]]
* [[ketogenic diet]]
* [[Intermittent fasting]]

==Learn more==
*2016, [http://well.blogs.nytimes.com/2016/03/07/intermittent-fasting-diets-are-gaining-acceptance/ Fasting Diets Are Gaining Acceptance]

==References==
<references>
<ref name="remely2015">{{Citation| doi = 10.1007/s00508-015-0755-1| issn = 1613-7671| volume = 127| issue = 9-10| pages = 394–398| last1 = Remely| first1 = Marlene| last2 = Hippe| first2 = Berit| last3 = Geretschlaeger| first3 = Isabella| last4 = Stegmayer| first4 = Sonja| last5 = Hoefinger| first5 = Ingrid| last6 = Haslberger| first6 = Alexander| title = Increased gut microbiota diversity and abundance of Faecalibacterium prausnitzii and Akkermansia after fasting: a pilot study| journal = Wiener Klinische Wochenschrift| date = May 2015| pmid = 25763563| pmc = }}</ref>
<ref name="fernanda2011">{{Citation| doi = 10.1371/journal.pone.0018433| issn = 1932-6203| volume = 6| issue = 3| pages = –18433| last1 = Cerqueira| first1 = Fernanda M.| last2 = Laurindo| first2 = Francisco R. M.| last3 = Kowaltowski| first3 = Alicia J.| title = Mild Mitochondrial Uncoupling and Calorie Restriction Increase Fasting eNOS, Akt and Mitochondrial Biogenesis| journal = PLOS ONE| accessdate = 2016-11-09| date = 2011-03-31| url = http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018433}}</ref>
<ref name="cheng2014">{{Citation| doi = 10.1016/j.stem.2014.04.014| issn = 1934-5909| volume = 14| issue = 6| pages = 810–823| last1 = Cheng| first1 = Chia-Wei| last2 = Adams| first2 = Gregor B.| last3 = Perin| first3 = Laura| last4 = Wei| first4 = Min| last5 = Zhou| first5 = Xiaoying| last6 = Lam| first6 = Ben S.| last7 = Da Sacco| first7 = Stefano| last8 = Mirisola| first8 = Mario| last9 = Quinn| first9 = David I.| last10 = Dorff| first10 = Tanya B.| last11 = Kopchick| first11 = John J.| last12 = Longo| first12 = Valter D.| title = Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression| journal = Cell Stem Cell| accessdate = 2016-11-09| date = 2014-06-05| url = http://www.sciencedirect.com/science/article/pii/S1934590914001519}}</ref>
<ref name="changhan2012">{{Citation| doi = 10.1126/scitranslmed.3003293| issn = 1946-6234| volume = 4| issue = 124| pages = 124–27-124ra27| last1 = Lee| first1 = Changhan| last2 = Raffaghello| first2 = Lizzia| last3 = Brandhorst| first3 = Sebastian| last4 = Safdie| first4 = Fernando M.| last5 = Bianchi| first5 = Giovanna| last6 = Martin-Montalvo| first6 = Alejandro| last7 = Pistoia| first7 = Vito| last8 = Wei| first8 = Min| last9 = Hwang| first9 = Saewon| last10 = Merlino| first10 = Annalisa| last11 = Emionite| first11 = Laura| last12 = Cabo| first12 = Rafael de| last13 = Longo| first13 = Valter D.| title = Fasting Cycles Retard Growth of Tumors and Sensitize a Range of Cancer Cell Types to Chemotherapy| journal = Science Translational Medicine| accessdate = 2016-11-09| date = 2012-03-07| url = http://stm.sciencemag.org/content/4/124/124ra27| pmid = 22323820}}</ref>
<ref name="lee2011">{{Citation| doi = 10.1038/onc.2011.91| issn = 0950-9232| volume = 30| issue = 30| pages = 3305–3316| last1 = Lee| first1 = C.| last2 = Longo| first2 = V. D.| title = Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients| journal = Oncogene| accessdate = 2016-11-09| date = 2011-07-28| url = http://www.nature.com/onc/journal/v30/n30/abs/onc201191a.html}}</ref>
<ref name="fernando2009">{{Citation| issn = 1945-4589| volume = 1| issue = 12| pages = 988–1007| last1 = Safdie| first1 = Fernando M.| last2 = Dorff| first2 = Tanya| last3 = Quinn| first3 = David| last4 = Fontana| first4 = Luigi| last5 = Wei| first5 = Min| last6 = Lee| first6 = Changhan| last7 = Cohen| first7 = Pinchas| last8 = Longo| first8 = Valter D.| title = Fasting and cancer treatment in humans: A case series report| journal = Aging (Albany NY)| accessdate = 2016-11-09| date = 2009-12-31| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815756/| pmid = 20157582| pmc = }}</ref>
<ref name="zhang2013">{{Citation| doi = 10.1038/ncomms3163| issn = 2041-1723| volume = 4| pages = 2163| last1 = Zhang| first1 = Chenhong| last2 = Li| first2 = Shoufeng| last3 = Yang| first3 = Liu| last4 = Huang| first4 = Ping| last5 = Li| first5 = Wenjun| last6 = Wang| first6 = Shengyue| last7 = Zhao| first7 = Guoping| last8 = Zhang| first8 = Menghui| last9 = Pang| first9 = Xiaoyan| last10 = Yan| first10 = Zhen| last11 = Liu| first11 = Yong| last12 = Zhao| first12 = Liping| title = Structural modulation of gut microbiota in life-long calorie-restricted mice| journal = Nature Communications| accessdate = 2016-11-09| date = 2013-07-16| url = http://www.nature.com/ncomms/2013/130716/ncomms3163/full/ncomms3163.html}}</ref>
<ref name="craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}
</ref>
</references>

[[Category:Potential treatments]]
[[Category:Diets]]
[[Category:Detoxification]]

Fasting

2019-09-02T13:16:50Z

Drcraig:/* Chronic fatigue syndrome */

== Types of fasting ==

=== Water only fasting ===
As the name implies, this is a type of fasting where only water may be consumed – no other food or beverage is permitted.

=== Liquid fasting ===

Some fasts include abstaining from solid foods but consuming calorie-containing liquids, such as vegetables juices or broth.

=== Intermittent fasting ===
In this form of fasting, a person alternates between periods of fasting and non-fasting, with a defined schedule. Intermittent fasting is of interest to researchers for its potential effects on insulin sensitivity and other aspects of health. Popular types of intermittent fasting include: 16:8, 16-hr fast with a 8-hr eating window, 18:6, 18-hr fast with a 6-hr eating window, 20:4, 20-hr fast with a 4-hr eating window. The alternate day fast is a 36 hour fast followed by a 12-hr eating window.

=== Caloric restriction ===
A calorie restricted (CR) diet reduces calorie intake without malnutrition. Most clinical trials of CR aim for 25-30% total calorie reduction. The 5:2 diet is a calorically restricted diet in which 2 days per week one consumes 500-600 calories, and eats normally the remaining 5 week days.

== Physiological effects ==

A fast with duration sufficient to deplete the body's glycogen stores, at least 18 hours, increases the blood ketone β-hydroxybutyrate allowing for nutritional [[ketosis]].

Fasting increases [[autophagy]] in mice.

The US National Institute on Aging and the National Institute of Diabetes and Digestive and Kidney Diseases conducted the CALERIE (Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy) study using a 2-year CR diet (25% reduction) in non-obese adults (n = 143) compared to an ad libitum group (n =75). The CR group reported improvements in mood and improved sleep quality without adverse effects or immune compromise. There was also improvement in cardiovascular risk factors including C-reactive protein.<ref>{{Cite journal|last=Kraus|first=William E.|last2=Bhapkar|first2=Manjushri|last3=Huffman|first3=Kim M.|last4=Pieper|first4=Carl F.|last5=Krupa Das|first5=Sai|last6=Redman|first6=Leanne M.|last7=Villareal|first7=Dennis T.|last8=Rochon|first8=James|last9=Roberts|first9=Susan B.|date=2019-9|title=2 years of calorie restriction and cardiometabolic risk (CALERIE): exploratory outcomes of a multicentre, phase 2, randomised controlled trial|url=https://www.ncbi.nlm.nih.gov/pubmed/31303390|journal=The Lancet. Diabetes & Endocrinology|volume=7|issue=9|pages=673–683|doi=10.1016/S2213-8587(19)30151-2|issn=2213-8595|pmc=6707879|pmid=31303390}}</ref>

== Health effects ==

There is no evidence on the benefits or harms of fasting for ME and CFS patients. However, there is a growing body of evidence suggesting possible health benefits of water-only fasting to the microbiome,<ref name="remely2015" /> mitochondria<ref name="fernanda2011" /> and the immune system,<ref name="cheng2014" /> and as a cancer adjuvant.<ref name="changhan2012" /><ref name="lee2011" /><ref name="fernando2009" />

==Immune system==
[[Caloric restriction]] significantly reduced the amount of circulating [[lipopolysaccharide]]-binding protein.<ref name="zhang2013" /> In vitro, short-term (19 hour) fasting reduced monocyte metabolic and inflammatory activity and drastically reduced the number of circulating monocytes.<ref>{{Cite journal|last=Jordan|first=Stefan|last2=Tung|first2=Navpreet|last3=Casanova-Acebes|first3=Maria|last4=Chang|first4=Christie|last5=Cantoni|first5=Claudia|last6=Zhang|first6=Dachuan|last7=Wirtz|first7=Theresa H.|last8=Naik|first8=Shruti|last9=Rose|first9=Samuel A.|date=2019-08-22|title=Dietary Intake Regulates the Circulating Inflammatory Monocyte Pool|url=https://www.ncbi.nlm.nih.gov/pubmed/31442403|journal=Cell|volume=178|issue=5|pages=1102–1114.e17|doi=10.1016/j.cell.2019.07.050|issn=1097-4172|pmid=31442403}}</ref> Caloric restriction and intermittent fasting strongly reduced the accumulation of pathogenic monocytes in the central nervous system, reduced monocyte pro-inflammatory activity, and improved disease outcome in a mouse model of multiple sclerosis and in a preclinical model in multiple sclerosis patients.<ref>{{Cite journal|last=Cignarella|first=Francesca|last2=Cantoni|first2=Claudia|last3=Ghezzi|first3=Laura|last4=Salter|first4=Amber|last5=Dorsett|first5=Yair|last6=Chen|first6=Lei|last7=Phillips|first7=Daniel|last8=Weinstock|first8=George M.|last9=Fontana|first9=Luigi|date=2018-06-05|title=Intermittent Fasting Confers Protection in CNS Autoimmunity by Altering the Gut Microbiota|url=https://www.ncbi.nlm.nih.gov/pubmed/29874567|journal=Cell Metabolism|volume=27|issue=6|pages=1222–1235.e6|doi=10.1016/j.cmet.2018.05.006|issn=1932-7420|pmc=6460288|pmid=29874567}}</ref>

==Chronic fatigue syndrome==
Dr. [[Courtney Craig]] has proposed the use of fasting, [[caloric restriction]] and a [[ketogenic diet]] in the treatment of [[mitochondria]]l damage in [[ME/CFS]].<ref name="craig2015" />

== See also ==
* [[Caloric restriction]]
* [[ketogenic diet]]
* [[Intermittent fasting]]

==Learn more==
*2016, [http://well.blogs.nytimes.com/2016/03/07/intermittent-fasting-diets-are-gaining-acceptance/ Fasting Diets Are Gaining Acceptance]

==References==
<references>
<ref name="remely2015">{{Citation| doi = 10.1007/s00508-015-0755-1| issn = 1613-7671| volume = 127| issue = 9-10| pages = 394–398| last1 = Remely| first1 = Marlene| last2 = Hippe| first2 = Berit| last3 = Geretschlaeger| first3 = Isabella| last4 = Stegmayer| first4 = Sonja| last5 = Hoefinger| first5 = Ingrid| last6 = Haslberger| first6 = Alexander| title = Increased gut microbiota diversity and abundance of Faecalibacterium prausnitzii and Akkermansia after fasting: a pilot study| journal = Wiener Klinische Wochenschrift| date = May 2015| pmid = 25763563| pmc = }}</ref>
<ref name="fernanda2011">{{Citation| doi = 10.1371/journal.pone.0018433| issn = 1932-6203| volume = 6| issue = 3| pages = –18433| last1 = Cerqueira| first1 = Fernanda M.| last2 = Laurindo| first2 = Francisco R. M.| last3 = Kowaltowski| first3 = Alicia J.| title = Mild Mitochondrial Uncoupling and Calorie Restriction Increase Fasting eNOS, Akt and Mitochondrial Biogenesis| journal = PLOS ONE| accessdate = 2016-11-09| date = 2011-03-31| url = http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018433}}</ref>
<ref name="cheng2014">{{Citation| doi = 10.1016/j.stem.2014.04.014| issn = 1934-5909| volume = 14| issue = 6| pages = 810–823| last1 = Cheng| first1 = Chia-Wei| last2 = Adams| first2 = Gregor B.| last3 = Perin| first3 = Laura| last4 = Wei| first4 = Min| last5 = Zhou| first5 = Xiaoying| last6 = Lam| first6 = Ben S.| last7 = Da Sacco| first7 = Stefano| last8 = Mirisola| first8 = Mario| last9 = Quinn| first9 = David I.| last10 = Dorff| first10 = Tanya B.| last11 = Kopchick| first11 = John J.| last12 = Longo| first12 = Valter D.| title = Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression| journal = Cell Stem Cell| accessdate = 2016-11-09| date = 2014-06-05| url = http://www.sciencedirect.com/science/article/pii/S1934590914001519}}</ref>
<ref name="changhan2012">{{Citation| doi = 10.1126/scitranslmed.3003293| issn = 1946-6234| volume = 4| issue = 124| pages = 124–27-124ra27| last1 = Lee| first1 = Changhan| last2 = Raffaghello| first2 = Lizzia| last3 = Brandhorst| first3 = Sebastian| last4 = Safdie| first4 = Fernando M.| last5 = Bianchi| first5 = Giovanna| last6 = Martin-Montalvo| first6 = Alejandro| last7 = Pistoia| first7 = Vito| last8 = Wei| first8 = Min| last9 = Hwang| first9 = Saewon| last10 = Merlino| first10 = Annalisa| last11 = Emionite| first11 = Laura| last12 = Cabo| first12 = Rafael de| last13 = Longo| first13 = Valter D.| title = Fasting Cycles Retard Growth of Tumors and Sensitize a Range of Cancer Cell Types to Chemotherapy| journal = Science Translational Medicine| accessdate = 2016-11-09| date = 2012-03-07| url = http://stm.sciencemag.org/content/4/124/124ra27| pmid = 22323820}}</ref>
<ref name="lee2011">{{Citation| doi = 10.1038/onc.2011.91| issn = 0950-9232| volume = 30| issue = 30| pages = 3305–3316| last1 = Lee| first1 = C.| last2 = Longo| first2 = V. D.| title = Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients| journal = Oncogene| accessdate = 2016-11-09| date = 2011-07-28| url = http://www.nature.com/onc/journal/v30/n30/abs/onc201191a.html}}</ref>
<ref name="fernando2009">{{Citation| issn = 1945-4589| volume = 1| issue = 12| pages = 988–1007| last1 = Safdie| first1 = Fernando M.| last2 = Dorff| first2 = Tanya| last3 = Quinn| first3 = David| last4 = Fontana| first4 = Luigi| last5 = Wei| first5 = Min| last6 = Lee| first6 = Changhan| last7 = Cohen| first7 = Pinchas| last8 = Longo| first8 = Valter D.| title = Fasting and cancer treatment in humans: A case series report| journal = Aging (Albany NY)| accessdate = 2016-11-09| date = 2009-12-31| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815756/| pmid = 20157582| pmc = }}</ref>
<ref name="zhang2013">{{Citation| doi = 10.1038/ncomms3163| issn = 2041-1723| volume = 4| pages = 2163| last1 = Zhang| first1 = Chenhong| last2 = Li| first2 = Shoufeng| last3 = Yang| first3 = Liu| last4 = Huang| first4 = Ping| last5 = Li| first5 = Wenjun| last6 = Wang| first6 = Shengyue| last7 = Zhao| first7 = Guoping| last8 = Zhang| first8 = Menghui| last9 = Pang| first9 = Xiaoyan| last10 = Yan| first10 = Zhen| last11 = Liu| first11 = Yong| last12 = Zhao| first12 = Liping| title = Structural modulation of gut microbiota in life-long calorie-restricted mice| journal = Nature Communications| accessdate = 2016-11-09| date = 2013-07-16| url = http://www.nature.com/ncomms/2013/130716/ncomms3163/full/ncomms3163.html}}</ref>
<ref name="craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}
</ref>
</references>

[[Category:Potential treatments]]
[[Category:Diets]]
[[Category:Detoxification]]

Fasting

2019-09-02T13:00:16Z

Drcraig:/* Intermittent fasting */

== Types of fasting ==

=== Water only fasting ===
As the name implies, this is a type of fasting where only water may be consumed – no other food or beverage is permitted.

=== Liquid fasting ===

Some fasts include abstaining from solid foods but consuming calorie-containing liquids, such as vegetables juices or broth.

=== Intermittent fasting ===
In this form of fasting, a person alternates between periods of fasting and non-fasting, with a defined schedule. Intermittent fasting is of interest to researchers for its potential effects on insulin sensitivity and other aspects of health. Popular types of intermittent fasting include: 16:8, 16-hr fast with a 8-hr eating window, 18:6, 18-hr fast with a 6-hr eating window, 20:4, 20-hr fast with a 4-hr eating window. The alternate day fast is a 36 hour fast followed by a 12-hr eating window.

=== Caloric restriction ===
A calorie restricted (CR) diet reduces calorie intake without malnutrition. Most clinical trials of CR aim for 25-30% total calorie reduction. The 5:2 diet is a calorically restricted diet in which 2 days per week one consumes 500-600 calories, and eats normally the remaining 5 week days.

== Physiological effects ==

A fast with duration sufficient to deplete the body's glycogen stores, at least 18 hours, increases the blood ketone β-hydroxybutyrate allowing for nutritional [[ketosis]].

Fasting increases [[autophagy]] in mice.

The US National Institute on Aging and the National Institute of Diabetes and Digestive and Kidney Diseases conducted the CALERIE (Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy) study using a 2-year CR diet (25% reduction) in non-obese adults (n = 143) compared to an ad libitum group (n =75). The CR group reported improvements in mood and improved sleep quality without adverse effects or immune compromise. There was also improvement in cardiovascular risk factors including C-reactive protein.<ref>{{Cite journal|last=Kraus|first=William E.|last2=Bhapkar|first2=Manjushri|last3=Huffman|first3=Kim M.|last4=Pieper|first4=Carl F.|last5=Krupa Das|first5=Sai|last6=Redman|first6=Leanne M.|last7=Villareal|first7=Dennis T.|last8=Rochon|first8=James|last9=Roberts|first9=Susan B.|date=2019-9|title=2 years of calorie restriction and cardiometabolic risk (CALERIE): exploratory outcomes of a multicentre, phase 2, randomised controlled trial|url=https://www.ncbi.nlm.nih.gov/pubmed/31303390|journal=The Lancet. Diabetes & Endocrinology|volume=7|issue=9|pages=673–683|doi=10.1016/S2213-8587(19)30151-2|issn=2213-8595|pmc=6707879|pmid=31303390}}</ref>

== Health effects ==

There is no evidence on the benefits or harms of fasting for ME and CFS patients. However, there is a growing body of evidence suggesting possible health benefits of water-only fasting to the microbiome,<ref name="remely2015" /> mitochondria<ref name="fernanda2011" /> and the immune system,<ref name="cheng2014" /> and as a cancer adjuvant.<ref name="changhan2012" /><ref name="lee2011" /><ref name="fernando2009" />

==Immune system==
[[Caloric restriction]] significantly reduced the amount of circulating [[lipopolysaccharide]]-binding protein.<ref name="zhang2013" /> In vitro, short-term (19 hour) fasting reduced monocyte metabolic and inflammatory activity and drastically reduced the number of circulating monocytes.<ref>{{Cite journal|last=Jordan|first=Stefan|last2=Tung|first2=Navpreet|last3=Casanova-Acebes|first3=Maria|last4=Chang|first4=Christie|last5=Cantoni|first5=Claudia|last6=Zhang|first6=Dachuan|last7=Wirtz|first7=Theresa H.|last8=Naik|first8=Shruti|last9=Rose|first9=Samuel A.|date=2019-08-22|title=Dietary Intake Regulates the Circulating Inflammatory Monocyte Pool|url=https://www.ncbi.nlm.nih.gov/pubmed/31442403|journal=Cell|volume=178|issue=5|pages=1102–1114.e17|doi=10.1016/j.cell.2019.07.050|issn=1097-4172|pmid=31442403}}</ref> Caloric restriction and intermittent fasting strongly reduced the accumulation of pathogenic monocytes in the central nervous system, reduced monocyte pro-inflammatory activity, and improved disease outcome in a mouse model of multiple sclerosis and in a preclinical model in multiple sclerosis patients.<ref>{{Cite journal|last=Cignarella|first=Francesca|last2=Cantoni|first2=Claudia|last3=Ghezzi|first3=Laura|last4=Salter|first4=Amber|last5=Dorsett|first5=Yair|last6=Chen|first6=Lei|last7=Phillips|first7=Daniel|last8=Weinstock|first8=George M.|last9=Fontana|first9=Luigi|date=2018-06-05|title=Intermittent Fasting Confers Protection in CNS Autoimmunity by Altering the Gut Microbiota|url=https://www.ncbi.nlm.nih.gov/pubmed/29874567|journal=Cell Metabolism|volume=27|issue=6|pages=1222–1235.e6|doi=10.1016/j.cmet.2018.05.006|issn=1932-7420|pmc=6460288|pmid=29874567}}</ref>

==Chronic fatigue syndrome==
[[Courtney Craig]] has proposed the use of fasting, [[caloric restriction]] and a [[ketogenic diet]] in the treatment of [[mitochondria]]l damage in [[ME/CFS]].<ref name="craig2015" />

== See also ==
* [[Caloric restriction]]
* [[ketogenic diet]]
* [[Intermittent fasting]]

==Learn more==
*2016, [http://well.blogs.nytimes.com/2016/03/07/intermittent-fasting-diets-are-gaining-acceptance/ Fasting Diets Are Gaining Acceptance]

==References==
<references>
<ref name="remely2015">{{Citation| doi = 10.1007/s00508-015-0755-1| issn = 1613-7671| volume = 127| issue = 9-10| pages = 394–398| last1 = Remely| first1 = Marlene| last2 = Hippe| first2 = Berit| last3 = Geretschlaeger| first3 = Isabella| last4 = Stegmayer| first4 = Sonja| last5 = Hoefinger| first5 = Ingrid| last6 = Haslberger| first6 = Alexander| title = Increased gut microbiota diversity and abundance of Faecalibacterium prausnitzii and Akkermansia after fasting: a pilot study| journal = Wiener Klinische Wochenschrift| date = May 2015| pmid = 25763563| pmc = }}</ref>
<ref name="fernanda2011">{{Citation| doi = 10.1371/journal.pone.0018433| issn = 1932-6203| volume = 6| issue = 3| pages = –18433| last1 = Cerqueira| first1 = Fernanda M.| last2 = Laurindo| first2 = Francisco R. M.| last3 = Kowaltowski| first3 = Alicia J.| title = Mild Mitochondrial Uncoupling and Calorie Restriction Increase Fasting eNOS, Akt and Mitochondrial Biogenesis| journal = PLOS ONE| accessdate = 2016-11-09| date = 2011-03-31| url = http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018433}}</ref>
<ref name="cheng2014">{{Citation| doi = 10.1016/j.stem.2014.04.014| issn = 1934-5909| volume = 14| issue = 6| pages = 810–823| last1 = Cheng| first1 = Chia-Wei| last2 = Adams| first2 = Gregor B.| last3 = Perin| first3 = Laura| last4 = Wei| first4 = Min| last5 = Zhou| first5 = Xiaoying| last6 = Lam| first6 = Ben S.| last7 = Da Sacco| first7 = Stefano| last8 = Mirisola| first8 = Mario| last9 = Quinn| first9 = David I.| last10 = Dorff| first10 = Tanya B.| last11 = Kopchick| first11 = John J.| last12 = Longo| first12 = Valter D.| title = Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression| journal = Cell Stem Cell| accessdate = 2016-11-09| date = 2014-06-05| url = http://www.sciencedirect.com/science/article/pii/S1934590914001519}}</ref>
<ref name="changhan2012">{{Citation| doi = 10.1126/scitranslmed.3003293| issn = 1946-6234| volume = 4| issue = 124| pages = 124–27-124ra27| last1 = Lee| first1 = Changhan| last2 = Raffaghello| first2 = Lizzia| last3 = Brandhorst| first3 = Sebastian| last4 = Safdie| first4 = Fernando M.| last5 = Bianchi| first5 = Giovanna| last6 = Martin-Montalvo| first6 = Alejandro| last7 = Pistoia| first7 = Vito| last8 = Wei| first8 = Min| last9 = Hwang| first9 = Saewon| last10 = Merlino| first10 = Annalisa| last11 = Emionite| first11 = Laura| last12 = Cabo| first12 = Rafael de| last13 = Longo| first13 = Valter D.| title = Fasting Cycles Retard Growth of Tumors and Sensitize a Range of Cancer Cell Types to Chemotherapy| journal = Science Translational Medicine| accessdate = 2016-11-09| date = 2012-03-07| url = http://stm.sciencemag.org/content/4/124/124ra27| pmid = 22323820}}</ref>
<ref name="lee2011">{{Citation| doi = 10.1038/onc.2011.91| issn = 0950-9232| volume = 30| issue = 30| pages = 3305–3316| last1 = Lee| first1 = C.| last2 = Longo| first2 = V. D.| title = Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients| journal = Oncogene| accessdate = 2016-11-09| date = 2011-07-28| url = http://www.nature.com/onc/journal/v30/n30/abs/onc201191a.html}}</ref>
<ref name="fernando2009">{{Citation| issn = 1945-4589| volume = 1| issue = 12| pages = 988–1007| last1 = Safdie| first1 = Fernando M.| last2 = Dorff| first2 = Tanya| last3 = Quinn| first3 = David| last4 = Fontana| first4 = Luigi| last5 = Wei| first5 = Min| last6 = Lee| first6 = Changhan| last7 = Cohen| first7 = Pinchas| last8 = Longo| first8 = Valter D.| title = Fasting and cancer treatment in humans: A case series report| journal = Aging (Albany NY)| accessdate = 2016-11-09| date = 2009-12-31| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815756/| pmid = 20157582| pmc = }}</ref>
<ref name="zhang2013">{{Citation| doi = 10.1038/ncomms3163| issn = 2041-1723| volume = 4| pages = 2163| last1 = Zhang| first1 = Chenhong| last2 = Li| first2 = Shoufeng| last3 = Yang| first3 = Liu| last4 = Huang| first4 = Ping| last5 = Li| first5 = Wenjun| last6 = Wang| first6 = Shengyue| last7 = Zhao| first7 = Guoping| last8 = Zhang| first8 = Menghui| last9 = Pang| first9 = Xiaoyan| last10 = Yan| first10 = Zhen| last11 = Liu| first11 = Yong| last12 = Zhao| first12 = Liping| title = Structural modulation of gut microbiota in life-long calorie-restricted mice| journal = Nature Communications| accessdate = 2016-11-09| date = 2013-07-16| url = http://www.nature.com/ncomms/2013/130716/ncomms3163/full/ncomms3163.html}}</ref>
<ref name="craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}
</ref>
</references>

[[Category:Potential treatments]]
[[Category:Diets]]
[[Category:Detoxification]]

Fasting

2019-08-28T14:34:16Z

Drcraig:/* Immune system */

== Types of fasting ==

=== Water only fasting ===
As the name implies, this is a type of fasting where only water may be consumed – no other food or beverage is permitted.

=== Liquid fasting ===

Some fasts include abstaining from solid foods but consuming calorie-containing liquids, such as vegetables juices or broth.

=== Intermittent fasting ===
In this form of fasting, a person alternates between periods of fasting and non-fasting, with a defined schedule. Intermittent fasting is of interest to researchers for its potential effects on insulin sensitivity and other aspects of health.

=== Caloric restriction ===

== Physiological effects ==

A fast with duration sufficient to deplete the body's glycogen stores may puts the body into a fat-burning mode called [[ketosis]].

Fasting also increases [[autophagy]].

== Health effects ==

There is no evidence on the benefits or harms of fasting for ME and CFS patients. However, there is a growing body of evidence suggesting possible health benefits of water-only fasting to the microbiome,<ref name="remely2015" /> mitochondria<ref name="fernanda2011" /> and the immune system,<ref name="cheng2014" /> and as a cancer adjuvant.<ref name="changhan2012" /><ref name="lee2011" /><ref name="fernando2009" />

==Immune system==
[[Caloric restriction]] significantly reduced the amount of circulating [[lipopolysaccharide]]-binding protein.<ref name="zhang2013" /> In vitro, short-term (19 hour) fasting reduced monocyte metabolic and inflammatory activity and drastically reduced the number of circulating monocytes.<ref>{{Cite journal|last=Jordan|first=Stefan|last2=Tung|first2=Navpreet|last3=Casanova-Acebes|first3=Maria|last4=Chang|first4=Christie|last5=Cantoni|first5=Claudia|last6=Zhang|first6=Dachuan|last7=Wirtz|first7=Theresa H.|last8=Naik|first8=Shruti|last9=Rose|first9=Samuel A.|date=2019-08-22|title=Dietary Intake Regulates the Circulating Inflammatory Monocyte Pool|url=https://www.ncbi.nlm.nih.gov/pubmed/31442403|journal=Cell|volume=178|issue=5|pages=1102–1114.e17|doi=10.1016/j.cell.2019.07.050|issn=1097-4172|pmid=31442403}}</ref> Caloric restriction and intermittent fasting strongly reduced the accumulation of pathogenic monocytes in the central nervous system, reduced monocyte pro-inflammatory activity, and improved disease outcome in a mouse model of multiple sclerosis and in a preclinical model in multiple sclerosis patients.<ref>{{Cite journal|last=Cignarella|first=Francesca|last2=Cantoni|first2=Claudia|last3=Ghezzi|first3=Laura|last4=Salter|first4=Amber|last5=Dorsett|first5=Yair|last6=Chen|first6=Lei|last7=Phillips|first7=Daniel|last8=Weinstock|first8=George M.|last9=Fontana|first9=Luigi|date=2018-06-05|title=Intermittent Fasting Confers Protection in CNS Autoimmunity by Altering the Gut Microbiota|url=https://www.ncbi.nlm.nih.gov/pubmed/29874567|journal=Cell Metabolism|volume=27|issue=6|pages=1222–1235.e6|doi=10.1016/j.cmet.2018.05.006|issn=1932-7420|pmc=6460288|pmid=29874567}}</ref>

==Chronic fatigue syndrome==
[[Courtney Craig]] has proposed the use of fasting, [[caloric restriction]] and a [[ketogenic diet]] in the treatment of [[mitochondria]]l damage in [[ME/CFS]].<ref name="craig2015" />

== See also ==
* [[Caloric restriction]]
* [[ketogenic diet]]
* [[Intermittent fasting]]

==Learn more==
*2016, [http://well.blogs.nytimes.com/2016/03/07/intermittent-fasting-diets-are-gaining-acceptance/ Fasting Diets Are Gaining Acceptance]

==References==
<references>
<ref name="remely2015">{{Citation| doi = 10.1007/s00508-015-0755-1| issn = 1613-7671| volume = 127| issue = 9-10| pages = 394–398| last1 = Remely| first1 = Marlene| last2 = Hippe| first2 = Berit| last3 = Geretschlaeger| first3 = Isabella| last4 = Stegmayer| first4 = Sonja| last5 = Hoefinger| first5 = Ingrid| last6 = Haslberger| first6 = Alexander| title = Increased gut microbiota diversity and abundance of Faecalibacterium prausnitzii and Akkermansia after fasting: a pilot study| journal = Wiener Klinische Wochenschrift| date = May 2015| pmid = 25763563| pmc = }}</ref>
<ref name="fernanda2011">{{Citation| doi = 10.1371/journal.pone.0018433| issn = 1932-6203| volume = 6| issue = 3| pages = –18433| last1 = Cerqueira| first1 = Fernanda M.| last2 = Laurindo| first2 = Francisco R. M.| last3 = Kowaltowski| first3 = Alicia J.| title = Mild Mitochondrial Uncoupling and Calorie Restriction Increase Fasting eNOS, Akt and Mitochondrial Biogenesis| journal = PLOS ONE| accessdate = 2016-11-09| date = 2011-03-31| url = http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018433}}</ref>
<ref name="cheng2014">{{Citation| doi = 10.1016/j.stem.2014.04.014| issn = 1934-5909| volume = 14| issue = 6| pages = 810–823| last1 = Cheng| first1 = Chia-Wei| last2 = Adams| first2 = Gregor B.| last3 = Perin| first3 = Laura| last4 = Wei| first4 = Min| last5 = Zhou| first5 = Xiaoying| last6 = Lam| first6 = Ben S.| last7 = Da Sacco| first7 = Stefano| last8 = Mirisola| first8 = Mario| last9 = Quinn| first9 = David I.| last10 = Dorff| first10 = Tanya B.| last11 = Kopchick| first11 = John J.| last12 = Longo| first12 = Valter D.| title = Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression| journal = Cell Stem Cell| accessdate = 2016-11-09| date = 2014-06-05| url = http://www.sciencedirect.com/science/article/pii/S1934590914001519}}</ref>
<ref name="changhan2012">{{Citation| doi = 10.1126/scitranslmed.3003293| issn = 1946-6234| volume = 4| issue = 124| pages = 124–27-124ra27| last1 = Lee| first1 = Changhan| last2 = Raffaghello| first2 = Lizzia| last3 = Brandhorst| first3 = Sebastian| last4 = Safdie| first4 = Fernando M.| last5 = Bianchi| first5 = Giovanna| last6 = Martin-Montalvo| first6 = Alejandro| last7 = Pistoia| first7 = Vito| last8 = Wei| first8 = Min| last9 = Hwang| first9 = Saewon| last10 = Merlino| first10 = Annalisa| last11 = Emionite| first11 = Laura| last12 = Cabo| first12 = Rafael de| last13 = Longo| first13 = Valter D.| title = Fasting Cycles Retard Growth of Tumors and Sensitize a Range of Cancer Cell Types to Chemotherapy| journal = Science Translational Medicine| accessdate = 2016-11-09| date = 2012-03-07| url = http://stm.sciencemag.org/content/4/124/124ra27| pmid = 22323820}}</ref>
<ref name="lee2011">{{Citation| doi = 10.1038/onc.2011.91| issn = 0950-9232| volume = 30| issue = 30| pages = 3305–3316| last1 = Lee| first1 = C.| last2 = Longo| first2 = V. D.| title = Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients| journal = Oncogene| accessdate = 2016-11-09| date = 2011-07-28| url = http://www.nature.com/onc/journal/v30/n30/abs/onc201191a.html}}</ref>
<ref name="fernando2009">{{Citation| issn = 1945-4589| volume = 1| issue = 12| pages = 988–1007| last1 = Safdie| first1 = Fernando M.| last2 = Dorff| first2 = Tanya| last3 = Quinn| first3 = David| last4 = Fontana| first4 = Luigi| last5 = Wei| first5 = Min| last6 = Lee| first6 = Changhan| last7 = Cohen| first7 = Pinchas| last8 = Longo| first8 = Valter D.| title = Fasting and cancer treatment in humans: A case series report| journal = Aging (Albany NY)| accessdate = 2016-11-09| date = 2009-12-31| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815756/| pmid = 20157582| pmc = }}</ref>
<ref name="zhang2013">{{Citation| doi = 10.1038/ncomms3163| issn = 2041-1723| volume = 4| pages = 2163| last1 = Zhang| first1 = Chenhong| last2 = Li| first2 = Shoufeng| last3 = Yang| first3 = Liu| last4 = Huang| first4 = Ping| last5 = Li| first5 = Wenjun| last6 = Wang| first6 = Shengyue| last7 = Zhao| first7 = Guoping| last8 = Zhang| first8 = Menghui| last9 = Pang| first9 = Xiaoyan| last10 = Yan| first10 = Zhen| last11 = Liu| first11 = Yong| last12 = Zhao| first12 = Liping| title = Structural modulation of gut microbiota in life-long calorie-restricted mice| journal = Nature Communications| accessdate = 2016-11-09| date = 2013-07-16| url = http://www.nature.com/ncomms/2013/130716/ncomms3163/full/ncomms3163.html}}</ref>
<ref name="craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}
</ref>
</references>

[[Category:Potential treatments]]
[[Category:Diets]]
[[Category:Detoxification]]

Ketogenic diet

2019-08-14T12:08:51Z

Drcraig:/* Evidence for a ketogenic diet */

The ketogenic diet is a high-[[fat]], medium [[protein]], low [[carbohydrate]] diet primarily used for children with treatment-resistant [[epilepsy]]. It induces [[ketosis]], a metabolic state in which the body derives most of its energy from [[ketones]] rather than [[glucose]]. A ketogenic diet increases blood ketone bodies: β-hydroxybutyrate, acetoacetate, and acetone. β-hydroxybutyrate comprises 70% of the ketone bodies produced from a ketogenic diet<ref>{{Cite journal|last=Dedkova|first=Elena N.|last2=Blatter|first2=Lothar A.|date=2014|title=Role of β-hydroxybutyrate, its polymer poly-β-hydroxybutyrate and inorganic polyphosphate in mammalian health and disease|url=https://www.ncbi.nlm.nih.gov/pubmed/25101001|journal=Frontiers in Physiology|volume=5|pages=260|doi=10.3389/fphys.2014.00260|issn=1664-042X|pmc=4102118|pmid=25101001}}</ref>. The therapeutic benefits of a ketogenic diet are believed to be due to β-hydroxybutyrate which acts as a signalling molecule.<ref name=":2">{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=Jan 2017|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>

Ketone bodies are a more efficient fuel than glucose. The brain can derive up to 60% of energy from ketones. The metabolic breakdown of ketone bodies produces more ATP per oxygen molecule consumed than other metabolic substrates. The ketone body β-hydroxybutyrate is converted to acetyl-CoA and distributed to metabolically active tissues as a fuel source (e.g. brain, skeletal muscle, heart). This acetyl-CoA is cycled directly into the Kreb’s cycle for energy production thereby bypassing glycolysis and [[Pyruvate dehydrogenase|pyruvate dehydrogenase (PDH)]].<ref>{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=Jan 2017|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>

Ketones may enhance antioxidant defenses by multiple mechanisms. β-hydroxybutyrate promotes transcription of genes associated with protective mechanisms including mitochondrial superoxide dismutase (MnSOD), catalase, and metallothionein. The effect is therefore reduced oxidative stress and lipid peroxidation. β-hydroxybutyrate upregulates production of the antioxidant [[glutathione]] likely through activation of the nrf2 pathway.<ref>{{Cite journal|last=Gross|first=Elena C.|last2=Klement|first2=Rainer J.|last3=Schoenen|first3=Jean|last4=D’Agostino|first4=Dominic P.|last5=Fischer|first5=Dirk|date=2019-04-10|title=Potential Protective Mechanisms of Ketone Bodies in Migraine Prevention|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520671/|journal=Nutrients|volume=11|issue=4|doi=10.3390/nu11040811|issn=2072-6643|pmc=6520671|pmid=30974836}}</ref>

== Types of Ketogenic Diets ==

A ketogenic diet is comprised of a dietary fat to carbohydrate ratio of 3:1 or 4:1. The diet should include <20 grams of carbohydrate per day, or 15-10% of total caloric intake. Ketogenic diets can be less strict if using exogenous ketones.<ref>{{Cite journal|last=Hashim|first=Sami A.|last2=VanItallie|first2=Theodore B.|date=Sep 2014|title=Ketone body therapy: from the ketogenic diet to the oral administration of ketone ester|url=https://www.ncbi.nlm.nih.gov/pubmed/24598140|journal=Journal of Lipid Research|volume=55|issue=9|pages=1818–1826|doi=10.1194/jlr.R046599|issn=1539-7262|pmc=4617348|pmid=24598140}}</ref>

== Evidence for a ketogenic diet ==

=== General Effects ===

In an animal model, a ketogenic diet was shown to increase [[mitochondria]]l biogenesis.<ref name="RhoJM2007" /> A similar result was found in a study of fasting mice.<ref name="Cerqueira2011" /> Ketone bodies scavenge free radicals ''in vivo''. <ref>{{Cite journal|last=Haces|first=María L.|last2=Hernández-Fonseca|first2=Karla|last3=Medina-Campos|first3=Omar N.|last4=Montiel|first4=Teresa|last5=Pedraza-Chaverri|first5=José|last6=Massieu|first6=Lourdes|date=May 2008|title=Antioxidant capacity contributes to protection of ketone bodies against oxidative damage induced during hypoglycemic conditions|url=https://www.ncbi.nlm.nih.gov/pubmed/18339375|journal=Experimental Neurology|volume=211|issue=1|pages=85–96|doi=10.1016/j.expneurol.2007.12.029|issn=0014-4886|pmid=18339375}}</ref> Ketogenic diets reduce circulating levels of insulin and insulin-like growth factors.<ref name=":0" /> Acute nutritional ketosis is shown to reduce lactate production and improve performance potential in cycling activity. It is shown to prevent muscle wasting.<ref>{{Cite journal|last=Cavaleri|first=Franco|last2=Bashar|first2=Emran|date=2018-04-01|title=Potential Synergies of β-Hydroxybutyrate and Butyrate on the Modulation of Metabolism, Inflammation, Cognition, and General Health|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5902005/|journal=Journal of Nutrition and Metabolism|volume=2018|doi=10.1155/2018/7195760|issn=2090-0724|pmc=5902005|pmid=29805804}}</ref>

=== Epilepsy ===

[[Neurotransmitter]]s regulate nerve impulses is the brain by either inhibiting impulse firing or exciting the [[neuron]] to fire. A primary inhibitory neurotransmitters is [[GABA]] and a primary excitatory neurotransmitters is [[glutamate]]. In patients with epilepsy, if the normal balance of inhibition and excitation is disrupted, a seizure can occur.

It is unknown why ketogenic diets are protective against epilepsy. In animal models, the ketone bodies [[acetoacetate]] and [[acetone]] have anticonvulsant properties through a novel pathway.<ref name="Hartman2007" />

The Charlie Foundation supports the use of ketogenic diets with children with severe epilepsy.<ref name="CharlieFoundation" />

=== Neurodegenerative Disease ===

There is evidence from uncontrolled clinical trials and animal models that ketogenic diets may be protective in neurodegenerative disorders including [[Alzheimer's]] and [[Parkinson's]].<ref name="Gasior2006" />

Mice fed a ketogenic diet had increased activity of [[dopamine]]rgic neurons.<ref name="ChurchWH2014" /> In a rat model of Parkinson's, a ketogenic diet was protective against neurotoxicity by up-regulating glutathione.<ref name="ChengB2009" /> A clinical trial of Parkinson’s disease compared a ketogenic diet to a low-fat diet with improvement in motor symptoms in both groups after 8 weeks but greater improvement in non-motor symptoms (fatigue, pain, and cognitive impairment) in the ketogenic group. <ref>{{Cite journal|last=Phillips|first=Matthew C. L.|last2=Murtagh|first2=Deborah K. J.|last3=Gilbertson|first3=Linda J.|last4=Asztely|first4=Fredrik J. S.|last5=Lynch|first5=Christopher D. P.|date=08 2018|title=Low-fat versus ketogenic diet in Parkinson's disease: A pilot randomized controlled trial|url=https://www.ncbi.nlm.nih.gov/pubmed/30098269/|journal=Movement Disorders: Official Journal of the Movement Disorder Society|volume=33|issue=8|pages=1306–1314|doi=10.1002/mds.27390|issn=1531-8257|pmc=6175383|pmid=30098269}}</ref> Another study found dietary ketosis enhanced memory in patients with mild cognitive impairment.<ref name="Krikorian2012" />

===Traumatic Brain Injury (TBI) ===
The ketogenic diet is an effective treatment for TBI recovery in rats and shows potential in humans.<ref>{{Cite journal|last=McDougall|first=Alexandre|last2=Bayley|first2=Mark|last3=Munce|first3=Sarah Ep|date=2018|title=The ketogenic diet as a treatment for traumatic brain injury: a scoping review|url=https://www.ncbi.nlm.nih.gov/pubmed/29359959|journal=Brain Injury|volume=32|issue=4|pages=416–422|doi=10.1080/02699052.2018.1429025|issn=1362-301X|pmid=29359959}}</ref>

=== Migraine ===
A study of 96 migraine patients on a 1-month ketogenic diet experienced up to 80% fewer migraines, less severity, and less reliance on medications.<ref>{{Cite journal|last=Di Lorenzo|first=C.|last2=Coppola|first2=G.|last3=Sirianni|first3=G.|last4=Di Lorenzo|first4=G.|last5=Bracaglia|first5=M.|last6=Di Lenola|first6=D.|last7=Siracusano|first7=A.|last8=Rossi|first8=P.|last9=Pierelli|first9=F.|date=2015-1|title=Migraine improvement during short lasting ketogenesis: a proof-of-concept study|url=https://www.ncbi.nlm.nih.gov/pubmed/25156013|journal=European Journal of Neurology|volume=22|issue=1|pages=170–177|doi=10.1111/ene.12550|issn=1468-1331|pmid=25156013}}</ref>

=== Multiple Sclerosis ===
A ketogenic diet reduced the expression of enzymes involved in the biosynthesis of pro-inflammatory eicosanoids and improved quality of life as measured by the Multiple Sclerosis Quality of Life-54 index.<ref>{{Cite journal|last=Bock|first=Markus|last2=Karber|first2=Mirjam|last3=Kuhn|first3=Hartmut|date=2018-10-03|title=Ketogenic diets attenuate cyclooxygenase and lipoxygenase gene expression in multiple sclerosis|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197715/|journal=EBioMedicine|volume=36|pages=293–303|doi=10.1016/j.ebiom.2018.08.057|issn=2352-3964|pmc=6197715|pmid=30292675}}</ref>

=== Chronic Fatigue Syndrome ===

No studies have been done on the effects of ketogenic diets in [[Chronic fatigue syndrome]]. Some CFS clinicians recommend ketogenic diets as a management strategy<ref name="Myhillketo1" /><ref name="Craig20150325" /> citing [[mitochondria]]l dysfunction<ref name="Myhill2009" />, [[immune system|immune]] dysfunction, and [[neuroinflammation]] as pathways through which ketogenic diets could confer some benefit.

==Risks & Side Effects==
*The ketogenic diet was found to regulate [[blood sugar]] but over the long term cause fat to accumulate in the [[liver]] in an animal model of Type II [[Diabetes]].<ref name="ZhangX2016" /> An open label, non-randomized, controlled study of the ketogenic diet in Type II Diabetes patients showed sustained long-term beneficial effects on multiple clinical markers of diabetes and cardiometabolic health at 2 years while utilizing less medication.<ref name=":0">{{Cite journal|last=Athinarayanan|first=Shaminie J.|last2=Adams|first2=Rebecca N.|last3=Hallberg|first3=Sarah J.|last4=McKenzie|first4=Amy L.|last5=Bhanpuri|first5=Nasir H.|last6=Campbell|first6=Wayne W.|last7=Volek|first7=Jeff S.|last8=Phinney|first8=Stephen D.|last9=McCarter|first9=James P.|date=2019|title=Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial|url=https://www.ncbi.nlm.nih.gov/pubmed/31231311|journal=Frontiers in Endocrinology|volume=10|pages=348|doi=10.3389/fendo.2019.00348|issn=1664-2392|pmc=6561315|pmid=31231311}}</ref>
*Two children on the diet for [[refractory epilepsy]] had [[selenium]] deficiency which resulted in sudden cardiac death.<ref>[http://www.pedneur.com/article/S0887-8994(08)00399-8/abstract?cc=y= Sudden Cardiac Death in Association With the Ketogenic Diet - Pediatric Neurology - December 2008]</ref>
*Up to 6% of those on a ketogenic diet may experience kidney stones.<ref name=":1">{{Cite journal|last=Hartman|first=Adam L.|last2=Vining|first2=Eileen P. G.|date=Jan 2007|title=Clinical aspects of the ketogenic diet|url=https://www.ncbi.nlm.nih.gov/pubmed/17241206|journal=Epilepsia|volume=48|issue=1|pages=31–42|doi=10.1111/j.1528-1167.2007.00914.x|issn=0013-9580|pmid=17241206}}</ref>
*Ketogenic diets may require additional supplemental nutrition to prevent deficiencies. Common deficiencies include calcium, zinc, selenium, and copper.<ref name=":1" />
*Ketogenic diets are not recommended for those with genetic primary carnitine deficiencies [including mutations in carnitine palmitoyl transferase (CPT) I or II and mitochondrial translocase] and fatty acid β-oxidation abnormalities (e.g., medium-chain acyl dehydrogenase deficiency). <ref>{{Cite journal|last=Stafstrom|first=Carl E.|last2=Rho|first2=Jong M.|date=2012-04-09|title=The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321471/|journal=Frontiers in Pharmacology|volume=3|doi=10.3389/fphar.2012.00059|issn=1663-9812|pmc=3321471|pmid=22509165}}</ref> It is safe for those with mitochondrial defects in complexes I, II, and IV<ref>{{Cite journal|last=Kang|first=Hoon-Chul|last2=Lee|first2=Young-Mock|last3=Kim|first3=Heung Dong|last4=Lee|first4=Joon Soo|last5=Slama|first5=Abdelhamid|date=Jan 2007|title=Safe and effective use of the ketogenic diet in children with epilepsy and mitochondrial respiratory chain complex defects|url=https://www.ncbi.nlm.nih.gov/pubmed/17241212|journal=Epilepsia|volume=48|issue=1|pages=82–88|doi=10.1111/j.1528-1167.2006.00906.x|issn=0013-9580|pmid=17241212}}</ref> and pyruvate dehydrogenase complex deficiency.<ref>{{Cite journal|last=Sofou|first=Kalliopi|last2=Dahlin|first2=Maria|last3=Hallböök|first3=Tove|last4=Lindefeldt|first4=Marie|last5=Viggedal|first5=Gerd|last6=Darin|first6=Niklas|date=2017|title=Ketogenic diet in pyruvate dehydrogenase complex deficiency: short- and long-term outcomes|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5306430/|journal=Journal of Inherited Metabolic Disease|volume=40|issue=2|pages=237–245|doi=10.1007/s10545-016-0011-5|issn=0141-8955|pmc=5306430|pmid=28101805}}</ref>

== Notable Studies ==
*[https://clinicaltrials.gov/ct2/show/NCT01906398 Efficacy and Safety of Ketogenic Diet as Adjunctive Treatment in Adults With Refractory Epilepsy (KD)] (This study is ongoing, but not recruiting participants.)
*[https://www.frontiersin.org/articles/10.3389/fendo.2019.00348/full Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial.]

==Medium chain triglycerides (MCT)==
Supplementation with [[medium-chain triglycerides]] (MCTs) increases blood levels of ketones.<ref name="WikiMCT" /> They are often used in ketogenic diets to help maintain ketosis at a lower proportion of fat intake. Regular intake of MCTs can increase expression of ketone transporter MCT1 at the brain, increasing uptake of ketones<ref>{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=Jan 2017|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>. A study showed improved cognition in [[Alzheimer's disease]] patients taking MCTs.<ref name="RegerMA2004" />

==Exogenous ketones==
A challenge of exogenous ketones is in the ability to deliver sufficient β-hydroxybutyrate to the brain and to sustain high levels of β-hydroxybutyrate. Uptake can be increased with a ketogenic diet or regular ingestion of MCT and/or supplemental ketones.<ref name=":2" /> Exogenous ketones have been found to increase blood ketone bodies without requiring such strict dietary measures. Exogenous ketones come in esters and salts, both have been found to raise β-hydroxybutyrate to therapeutic levels that can last for hours. <ref>{{Cite journal|last=Hashim|first=Sami A.|last2=VanItallie|first2=Theodore B.|date=Sep 2014|title=Ketone body therapy: from the ketogenic diet to the oral administration of ketone ester|url=https://www.ncbi.nlm.nih.gov/pubmed/24598140|journal=Journal of Lipid Research|volume=55|issue=9|pages=1818–1826|doi=10.1194/jlr.R046599|issn=1539-7262|pmc=4617348|pmid=24598140}}</ref>

==Clinical use==
Doctor [[Sarah Myhill]] has a page on her web site describing the ketogenic diet.<ref name="Myhillketo2" />
Dr. [[Courtney Craig]] has published a hypothesis on the use of ketogenic diets in [[ME/CFS]] and offers dietary consulting to patients.<ref name="Craig2015" />

==Learn more==
*2017, [https://www.healthrising.org/blog/2017/06/16/ketogenic-diets-fibromyalgia-mecfs-review/ Getting Clear on Ketogenic Diets (for Fibromyalgia and ME/CFS): A Review]
*[https://en.wikipedia.org/wiki/Ketogenic_diet Wikipedia - Ketogenic diet]
*[http://www.ketogenic-diet-resource.com/ Ketogenic Diet Resource]
*[https://en.wikipedia.org/wiki/Fatty_acid_metabolism Wikipedia - Fatty acid metabolism]

== See also ==
*[[Fasting]]
*[[Ketosis]]

==References==
<references>
<ref name="Cerqueira2011">{{Citation
| last1 = Cerqueira | first1 = Fernanda M
| last2 = Laurindo | first2 = Francisco R M
| last3 = Kowaltowski | first3 = Alicia J
| title = Mild Mitochondrial Uncoupling and Calorie Restriction Increase Fasting eNOS, Akt and Mitochondrial Biogenesis
| journal = PLOS ONE | volume = 6| issue = 3| pages = –18433
| date = 31 Mar 2011
| doi = 10.1371/journal.pone.0018433
| url = http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018433
}}</ref>
<ref name="CharlieFoundation">| title = The Charlie Foundation for Ketogenic Therapies
| url = http://www.charliefoundation.org/
</ref>
<ref name="ChengB2009">{{Citation
| last1 = Cheng | first1 = Baohua
| last2 = Yang | first2 = Xinxin
| last3 = An | first3 = Liangxiang
| last4 = Gao | first4 = Bo
| last5 = Liu | first5 = Xia
| last6 = Liu | first6 = Shuwei
| display-authors = 3
| title = Ketogenic diet protects dopaminergic neurons against 6-OHDA neurotoxicity via up-regulating glutathione in a rat model of Parkinson's disease
| journal = Brain Research | volume = 1286| pages = 25–31
| date = 2009-08-25
| doi = 10.1016/j.brainres.2009.06.060
| url = http://www.sciencedirect.com/science/article/pii/S0006899309012797
}}</ref>
<ref name="ChurchWH2014">{{Citation
| last1 = Church | first1 = William H
| last2 = Adams | first2 = Ryan E
| last3 = Wyss | first3 = Livia S
| title = Ketogenic diet alters dopaminergic activity in the mouse cortex
| journal = Neuroscience Letters | volume = 571| pages = 1–4
| date = 2014-06-13
| doi = 10.1016/j.neulet.2014.04.016
| pmid = 24769322
| URL = http://www.ncbi.nlm.nih.gov/pubmed/24769322
}}</ref>
<ref name="Craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}</ref>
<ref name="Craig20150325">{{citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = A Ketogenic Diet for ME/CFS & Fibro
| date = 30 Mar 2015
| url = http://www.drcourtneycraig.com/blog/2015/3/25/a-ketogenic-diet-for-mecfs-fibro
}}</ref>
<ref name="Gasior2006">{{Citation
| last1 = Gasior | first1 = Maciej
| last2 = Rogawski | first2 = Michael A
| last3 = Hartman | first3 = Adam L
| title = Neuroprotective and disease-modifying effects of the ketogenic diet
| journal = Behavioural Pharmacology | volume = 17| issue = 5-6| pages = 431–439
| date = Sep 2006
| pmid = 16940764
| url = http://www.ncbi.nlm.nih.gov/pubmed/16940764/
}}</ref>
<ref name="Hartman2007">{{Citation
| last1 = Hartman | first1 = Adam L
| last2 = Gasior | first2 = Maciej
| last3 = Vining | first3 = Eileen P G
| last4 = Rogawski | first4 = Michael A
| title = The Neuropharmacology of the Ketogenic Diet
| journal = Pediatric neurology | volume = 36| issue = 5| pages = 281–292
| date = May 2007
| pmid = 17509459
| doi = 10.1016/j.pediatrneurol.2007.02.008
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940242/
}}</ref>
<ref name="Krikorian2012">{{Citation
| last1 = Krikorian | first1 = Robert
| last2 = Shidler | first2 = Marcelle D
| last3 = Dangelo | first3 = Krista
| last4 = Couch | first4 = Sarah C
| last5 = Benoit | first5 = Stephen C
| last6 = Clegg | first6 = Deborah J
| title = Dietary ketosis enhances memory in mild cognitive impairment
| journal = Neurobiology of Aging | volume = 33| issue = 2| pages = 425–19-27
| date = Feb 2012
| pmid = 21130529
| doi = 10.1016/j.neurobiolaging.2010.10.006
| url = https://www.ncbi.nlm.nih.gov/pubmed/21130529/
}}</ref>
<ref name="Myhill2009">{{citation
| last1 = Myhill | first1 = S | authorlink1 = Sarah Myhill
| last2 = Booth | first2 = NE | authorlink2 = Norman Booth
| last3 = McLaren-Howard | first3 = J | authorlink3 = John McLaren-Howard
| title = Chronic fatigue syndrome and mitochondrial dysfunction
| journal = Int J Clin Exp Med | volume = 2| issue = 1| pages = 1–16
| date = 15 Jan 2009
| pmid = 19436827
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/
}}</ref>
<ref name="Myhillketo1">{{citation
| last1 = Segura | first1 = Gabriela
| title = Ketogenic diet - a connection between mitochondria and diet
| date = 9 Aug 2013
| url = http://www.drmyhill.co.uk/wiki/Ketogenic_diet_-_a_connection_between_mitochondria_and_diet
}}</ref>
<ref name="Myhillketo2">{{citation
| last1 = Myhill | first1 = Sarah | authorlink1 = Sarah Myhill
| title = Ketogenic diet - the practical details
| url = http://www.doctormyhill.co.uk/wiki/Ketogenic_diet_-_the_practical_details
}}</ref>
<ref name="RegerMA2004">{{citation
| last1 = Reger | first1 = Mark A
| last2 = Henderson | first2 = Samuel T
| last3 = Hale | first3 = Cathy
| last4 = Cholerton | first4 = Brenna
| last5 = Baker | first5 = Laura D
| last6 = Watson | first6 = G S
| last7 = Hyde | first7 = Karen
| last8 = Chapman | first8 = Darla
| last9 = Craft | first9 = Suzanne
| display-authors = 3
| title = Effects of beta-hydroxybutyrate on cognition in memory-impaired adults
| journal = Neurobiology of Aging | volume = 25| issue = 3| pages = 311–314
| date = Mar 2004
| doi = 10.1016/S0197-4580(03)00087-3
| pmid = 15123336
}}</ref>
<ref name="RhoJM2007">{{Citation
| last1 = Rho | first1 = Jong M
| last2 = Rogawski | first2 = Michael A
| title = The Ketogenic Diet: Stoking the Powerhouse of the Cell
| journal = Epilepsy Currents | volume = 7| issue = 2| pages = 58–60
| date = Mar 2007
| doi = 10.1111/j.1535-7511.2007.00170.x
| pmid = 17505556
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867088/
}}</ref>
<ref name="WikiMCT">{{citation
| title = Wikipedia - Ketogenic diet, MCT oil
| url = https://en.wikipedia.org/wiki/Ketogenic_diet#MCT_oil
}}</ref>
<ref name="ZhangX2016">{{citation
| last1 = Zhang | first1 = Xiaoyu
| last2 = Qin | first2 = Juliang
| last3 = Zhao | first3 = Yihan
| last4 = Shi | first4 = Jueping
| last5 = Lan | first5 = Rong
| last6 = Gan | first6 = Yunqiu
| last7 = Ren | first7 = Hua
| last8 = Zhu | first8 = Bing
| last9 = Qian | first9 = Min
| last10 = Du | first10 = Bing
| title = Long-term ketogenic diet contributes to glycemic control but promotes lipid accumulation and hepatic steatosis in type 2 diabetic mice
| journal = Nutrition Research | volume = 36| issue = 4| pages = 349–358
| date = 1 Apr 2016
| doi = 10.1016/j.nutres.2015.12.002
| url = http://www.nrjournal.com/article/S0271531715003012/abstract
}}</ref>
</references>

[[Category:Potential treatments]]
[[Category:Diets]]

Ketogenic diet

2019-08-14T11:49:19Z

Drcraig:/* Exogenous ketones */

The ketogenic diet is a high-[[fat]], medium [[protein]], low [[carbohydrate]] diet primarily used for children with treatment-resistant [[epilepsy]]. It induces [[ketosis]], a metabolic state in which the body derives most of its energy from [[ketones]] rather than [[glucose]]. A ketogenic diet increases blood ketone bodies: β-hydroxybutyrate, acetoacetate, and acetone. β-hydroxybutyrate comprises 70% of the ketone bodies produced from a ketogenic diet<ref>{{Cite journal|last=Dedkova|first=Elena N.|last2=Blatter|first2=Lothar A.|date=2014|title=Role of β-hydroxybutyrate, its polymer poly-β-hydroxybutyrate and inorganic polyphosphate in mammalian health and disease|url=https://www.ncbi.nlm.nih.gov/pubmed/25101001|journal=Frontiers in Physiology|volume=5|pages=260|doi=10.3389/fphys.2014.00260|issn=1664-042X|pmc=4102118|pmid=25101001}}</ref>. The therapeutic benefits of a ketogenic diet are believed to be due to β-hydroxybutyrate which acts as a signalling molecule.<ref name=":2">{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=Jan 2017|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>

Ketone bodies are a more efficient fuel than glucose. The brain can derive up to 60% of energy from ketones. The metabolic breakdown of ketone bodies produces more ATP per oxygen molecule consumed than other metabolic substrates. The ketone body β-hydroxybutyrate is converted to acetyl-CoA and distributed to metabolically active tissues as a fuel source (e.g. brain, skeletal muscle, heart). This acetyl-CoA is cycled directly into the Kreb’s cycle for energy production thereby bypassing glycolysis and [[Pyruvate dehydrogenase|pyruvate dehydrogenase (PDH)]].<ref>{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=Jan 2017|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>

Ketones may enhance antioxidant defenses by multiple mechanisms. β-hydroxybutyrate promotes transcription of genes associated with protective mechanisms including mitochondrial superoxide dismutase (MnSOD), catalase, and metallothionein. The effect is therefore reduced oxidative stress and lipid peroxidation. β-hydroxybutyrate upregulates production of the antioxidant [[glutathione]] likely through activation of the nrf2 pathway.<ref>{{Cite journal|last=Gross|first=Elena C.|last2=Klement|first2=Rainer J.|last3=Schoenen|first3=Jean|last4=D’Agostino|first4=Dominic P.|last5=Fischer|first5=Dirk|date=2019-04-10|title=Potential Protective Mechanisms of Ketone Bodies in Migraine Prevention|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520671/|journal=Nutrients|volume=11|issue=4|doi=10.3390/nu11040811|issn=2072-6643|pmc=6520671|pmid=30974836}}</ref>

== Types of Ketogenic Diets ==

A ketogenic diet is comprised of a dietary fat to carbohydrate ratio of 3:1 or 4:1. The diet should include <20 grams of carbohydrate per day, or 15-10% of total caloric intake. Ketogenic diets can be less strict if using exogenous ketones.<ref>{{Cite journal|last=Hashim|first=Sami A.|last2=VanItallie|first2=Theodore B.|date=Sep 2014|title=Ketone body therapy: from the ketogenic diet to the oral administration of ketone ester|url=https://www.ncbi.nlm.nih.gov/pubmed/24598140|journal=Journal of Lipid Research|volume=55|issue=9|pages=1818–1826|doi=10.1194/jlr.R046599|issn=1539-7262|pmc=4617348|pmid=24598140}}</ref>

== Evidence for a ketogenic diet ==

=== General Effects ===

In an animal model, a ketogenic diet was shown to increase [[mitochondria]]l biogenesis.<ref name="RhoJM2007" /> A similar result was found in a study of fasting mice.<ref name="Cerqueira2011" /> Ketone bodies scavenge free radicals ''in vivo''. <ref>{{Cite journal|last=Haces|first=María L.|last2=Hernández-Fonseca|first2=Karla|last3=Medina-Campos|first3=Omar N.|last4=Montiel|first4=Teresa|last5=Pedraza-Chaverri|first5=José|last6=Massieu|first6=Lourdes|date=May 2008|title=Antioxidant capacity contributes to protection of ketone bodies against oxidative damage induced during hypoglycemic conditions|url=https://www.ncbi.nlm.nih.gov/pubmed/18339375|journal=Experimental Neurology|volume=211|issue=1|pages=85–96|doi=10.1016/j.expneurol.2007.12.029|issn=0014-4886|pmid=18339375}}</ref> Ketogenic diets reduce circulating levels of insulin and insulin-like growth factors.<ref name=":0" />

=== Epilepsy ===

[[Neurotransmitter]]s regulate nerve impulses is the brain by either inhibiting impulse firing or exciting the [[neuron]] to fire. A primary inhibitory neurotransmitters is [[GABA]] and a primary excitatory neurotransmitters is [[glutamate]]. In patients with epilepsy, if the normal balance of inhibition and excitation is disrupted, a seizure can occur.

It us unknown why ketogenic diets are protective against epilepsy. In animal models, the ketone bodies [[acetoacetate]] and [[acetone]] have anticonvulsant properties through a novel pathway.<ref name="Hartman2007" />

The Charlie Foundation supports the use of ketogenic diets with children with severe epilepsy.<ref name="CharlieFoundation" />

=== Neurodegenerative Disease ===

There is evidence from uncontrolled clinical trials and animal models that ketogenic diets may be protective in neurodegenerative disorders including [[Alzheimer's]] and [[Parkinson's]].<ref name="Gasior2006" />

Mice fed a ketogenic diet had increased activity of [[dopamine]]rgic neurons.<ref name="ChurchWH2014" /> In a rat model of Parkinson's, a ketogenic diet was protective against neurotoxicity by up-regulating glutathione.<ref name="ChengB2009" /> A clinical trial of Parkinson’s disease compared a ketogenic diet to a low-fat diet with improvement in motor symptoms in both groups after 8 weeks but greater improvement in non-motor symptoms (fatigue, pain, and cognitive impairment) in the ketogenic group. <ref>{{Cite journal|last=Phillips|first=Matthew C. L.|last2=Murtagh|first2=Deborah K. J.|last3=Gilbertson|first3=Linda J.|last4=Asztely|first4=Fredrik J. S.|last5=Lynch|first5=Christopher D. P.|date=08 2018|title=Low-fat versus ketogenic diet in Parkinson's disease: A pilot randomized controlled trial|url=https://www.ncbi.nlm.nih.gov/pubmed/30098269/|journal=Movement Disorders: Official Journal of the Movement Disorder Society|volume=33|issue=8|pages=1306–1314|doi=10.1002/mds.27390|issn=1531-8257|pmc=6175383|pmid=30098269}}</ref> Another study found dietary ketosis enhanced memory in patients with mild cognitive impairment.<ref name="Krikorian2012" />

=== Traumatic Brain Injury (TBI) ===
The ketogenic diet is an effective treatment for TBI recovery in rats and shows potential in humans.<ref>{{Cite journal|last=McDougall|first=Alexandre|last2=Bayley|first2=Mark|last3=Munce|first3=Sarah Ep|date=2018|title=The ketogenic diet as a treatment for traumatic brain injury: a scoping review|url=https://www.ncbi.nlm.nih.gov/pubmed/29359959|journal=Brain Injury|volume=32|issue=4|pages=416–422|doi=10.1080/02699052.2018.1429025|issn=1362-301X|pmid=29359959}}</ref>

=== Multiple Sclerosis ===
A ketogenic diet reduced the expression of enzymes involved in the biosynthesis of pro-inflammatory eicosanoids and improved quality of life as measured by the Multiple Sclerosis Quality of Life-54 index.<ref>{{Cite journal|last=Bock|first=Markus|last2=Karber|first2=Mirjam|last3=Kuhn|first3=Hartmut|date=2018-10-03|title=Ketogenic diets attenuate cyclooxygenase and lipoxygenase gene expression in multiple sclerosis|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197715/|journal=EBioMedicine|volume=36|pages=293–303|doi=10.1016/j.ebiom.2018.08.057|issn=2352-3964|pmc=6197715|pmid=30292675}}</ref>

=== Chronic Fatigue Syndrome ===

No studies have been done on the effects of ketogenic diets in [[Chronic fatigue syndrome]]. Some CFS clinicians recommend ketogenic diets as a management strategy<ref name="Myhillketo1" /><ref name="Craig20150325" /> citing [[mitochondria]]l dysfunction<ref name="Myhill2009" />, [[immune system|immune]] dysfunction, and [[neuroinflammation]] as pathways through which ketogenic diets could confer some benefit.

==Risks & Side Effects==
*The ketogenic diet was found to regulate [[blood sugar]] but over the long term cause fat to accumulate in the [[liver]] in an animal model of Type II [[Diabetes]].<ref name="ZhangX2016" /> An open label, non-randomized, controlled study of the ketogenic diet in Type II Diabetes patients showed sustained long-term beneficial effects on multiple clinical markers of diabetes and cardiometabolic health at 2 years while utilizing less medication.<ref name=":0">{{Cite journal|last=Athinarayanan|first=Shaminie J.|last2=Adams|first2=Rebecca N.|last3=Hallberg|first3=Sarah J.|last4=McKenzie|first4=Amy L.|last5=Bhanpuri|first5=Nasir H.|last6=Campbell|first6=Wayne W.|last7=Volek|first7=Jeff S.|last8=Phinney|first8=Stephen D.|last9=McCarter|first9=James P.|date=2019|title=Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial|url=https://www.ncbi.nlm.nih.gov/pubmed/31231311|journal=Frontiers in Endocrinology|volume=10|pages=348|doi=10.3389/fendo.2019.00348|issn=1664-2392|pmc=6561315|pmid=31231311}}</ref>
*Two children on the diet for [[refractory epilepsy]] had [[selenium]] deficiency which resulted in sudden cardiac death.<ref>[http://www.pedneur.com/article/S0887-8994(08)00399-8/abstract?cc=y= Sudden Cardiac Death in Association With the Ketogenic Diet - Pediatric Neurology - December 2008]</ref>
*Up to 6% of those on a ketogenic diet may experience kidney stones. <ref name=":1">{{Cite journal|last=Hartman|first=Adam L.|last2=Vining|first2=Eileen P. G.|date=Jan 2007|title=Clinical aspects of the ketogenic diet|url=https://www.ncbi.nlm.nih.gov/pubmed/17241206|journal=Epilepsia|volume=48|issue=1|pages=31–42|doi=10.1111/j.1528-1167.2007.00914.x|issn=0013-9580|pmid=17241206}}</ref>
*Ketogenic diets may require additional supplemental nutrition to prevent deficiencies. Common deficiencies include calcium, zinc, selenium, and copper.<ref name=":1" />
*Ketogenic diets are not recommended for those with genetic primary carnitine deficiencies [including mutations in carnitine palmitoyl transferase (CPT) I or II and mitochondrial translocase] and fatty acid β-oxidation abnormalities (e.g., medium-chain acyl dehydrogenase deficiency). <ref>{{Cite journal|last=Stafstrom|first=Carl E.|last2=Rho|first2=Jong M.|date=2012-04-09|title=The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321471/|journal=Frontiers in Pharmacology|volume=3|doi=10.3389/fphar.2012.00059|issn=1663-9812|pmc=3321471|pmid=22509165}}</ref> It is safe for those with mitochondrial defects in complexes I, II, and IV<ref>{{Cite journal|last=Kang|first=Hoon-Chul|last2=Lee|first2=Young-Mock|last3=Kim|first3=Heung Dong|last4=Lee|first4=Joon Soo|last5=Slama|first5=Abdelhamid|date=Jan 2007|title=Safe and effective use of the ketogenic diet in children with epilepsy and mitochondrial respiratory chain complex defects|url=https://www.ncbi.nlm.nih.gov/pubmed/17241212|journal=Epilepsia|volume=48|issue=1|pages=82–88|doi=10.1111/j.1528-1167.2006.00906.x|issn=0013-9580|pmid=17241212}}</ref> and pyruvate dehydrogenase complex deficiency<ref>{{Cite journal|last=Sofou|first=Kalliopi|last2=Dahlin|first2=Maria|last3=Hallböök|first3=Tove|last4=Lindefeldt|first4=Marie|last5=Viggedal|first5=Gerd|last6=Darin|first6=Niklas|date=2017|title=Ketogenic diet in pyruvate dehydrogenase complex deficiency: short- and long-term outcomes|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5306430/|journal=Journal of Inherited Metabolic Disease|volume=40|issue=2|pages=237–245|doi=10.1007/s10545-016-0011-5|issn=0141-8955|pmc=5306430|pmid=28101805}}</ref>.

== Notable Studies ==
*[https://clinicaltrials.gov/ct2/show/NCT01906398 Efficacy and Safety of Ketogenic Diet as Adjunctive Treatment in Adults With Refractory Epilepsy (KD)] (This study is ongoing, but not recruiting participants.)
*[https://www.frontiersin.org/articles/10.3389/fendo.2019.00348/full Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial.]

==Medium chain triglycerides (MCT)==
Supplementation with [[medium-chain triglycerides]] (MCTs) increases blood levels of ketones.<ref name="WikiMCT" /> They are often used in ketogenic diets to help maintain ketosis at a lower proportion of fat intake. Regular intake of MCTs can increase expression of ketone transporter MCT1 at the brain, increasing uptake of ketones<ref>{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=Jan 2017|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>. A study showed improved cognition in [[Alzheimer's disease]] patients.<ref name="RegerMA2004" />

==Exogenous ketones==
A challenge of exogenous ketones is in the ability to deliver sufficient β-hydroxybutyrate to the brain and to sustain high levels of β-hydroxybutyrate. Uptake can be increased with a ketogenic diet or regular ingestion of MCT and/or supplemental ketones.<ref name=":2" /> Exogenous ketones have been found to increase blood ketone bodies without requiring such strict dietary measures. Exogenous ketones come in esters and salts, both have been found to raise β-hydroxybutyrate to therapeutic levels that can last for hours. <ref>{{Cite journal|last=Hashim|first=Sami A.|last2=VanItallie|first2=Theodore B.|date=Sep 2014|title=Ketone body therapy: from the ketogenic diet to the oral administration of ketone ester|url=https://www.ncbi.nlm.nih.gov/pubmed/24598140|journal=Journal of Lipid Research|volume=55|issue=9|pages=1818–1826|doi=10.1194/jlr.R046599|issn=1539-7262|pmc=4617348|pmid=24598140}}</ref>

==Clinical use==
Doctor [[Sarah Myhill]] has a page on her web site describing the ketogenic diet.<ref name="Myhillketo2" />
Dr. [[Courtney Craig]] has published a hypothesis on the use of ketogenic diets in [[ME/CFS]] and offers dietary consulting to patients.<ref name="Craig2015" />

==Learn more==
*2017, [https://www.healthrising.org/blog/2017/06/16/ketogenic-diets-fibromyalgia-mecfs-review/ Getting Clear on Ketogenic Diets (for Fibromyalgia and ME/CFS): A Review]
*[https://en.wikipedia.org/wiki/Ketogenic_diet Wikipedia - Ketogenic diet]
*[http://www.ketogenic-diet-resource.com/ Ketogenic Diet Resource]
*[https://en.wikipedia.org/wiki/Fatty_acid_metabolism Wikipedia - Fatty acid metabolism]

== See also ==
*[[Fasting]]
*[[Ketosis]]

==References==
<references>
<ref name="Cerqueira2011">{{Citation
| last1 = Cerqueira | first1 = Fernanda M
| last2 = Laurindo | first2 = Francisco R M
| last3 = Kowaltowski | first3 = Alicia J
| title = Mild Mitochondrial Uncoupling and Calorie Restriction Increase Fasting eNOS, Akt and Mitochondrial Biogenesis
| journal = PLOS ONE | volume = 6| issue = 3| pages = –18433
| date = 31 Mar 2011
| doi = 10.1371/journal.pone.0018433
| url = http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018433
}}</ref>
<ref name="CharlieFoundation">| title = The Charlie Foundation for Ketogenic Therapies
| url = http://www.charliefoundation.org/
</ref>
<ref name="ChengB2009">{{Citation
| last1 = Cheng | first1 = Baohua
| last2 = Yang | first2 = Xinxin
| last3 = An | first3 = Liangxiang
| last4 = Gao | first4 = Bo
| last5 = Liu | first5 = Xia
| last6 = Liu | first6 = Shuwei
| display-authors = 3
| title = Ketogenic diet protects dopaminergic neurons against 6-OHDA neurotoxicity via up-regulating glutathione in a rat model of Parkinson's disease
| journal = Brain Research | volume = 1286| pages = 25–31
| date = 2009-08-25
| doi = 10.1016/j.brainres.2009.06.060
| url = http://www.sciencedirect.com/science/article/pii/S0006899309012797
}}</ref>
<ref name="ChurchWH2014">{{Citation
| last1 = Church | first1 = William H
| last2 = Adams | first2 = Ryan E
| last3 = Wyss | first3 = Livia S
| title = Ketogenic diet alters dopaminergic activity in the mouse cortex
| journal = Neuroscience Letters | volume = 571| pages = 1–4
| date = 2014-06-13
| doi = 10.1016/j.neulet.2014.04.016
| pmid = 24769322
| URL = http://www.ncbi.nlm.nih.gov/pubmed/24769322
}}</ref>
<ref name="Craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}</ref>
<ref name="Craig20150325">{{citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = A Ketogenic Diet for ME/CFS & Fibro
| date = 30 Mar 2015
| url = http://www.drcourtneycraig.com/blog/2015/3/25/a-ketogenic-diet-for-mecfs-fibro
}}</ref>
<ref name="Gasior2006">{{Citation
| last1 = Gasior | first1 = Maciej
| last2 = Rogawski | first2 = Michael A
| last3 = Hartman | first3 = Adam L
| title = Neuroprotective and disease-modifying effects of the ketogenic diet
| journal = Behavioural Pharmacology | volume = 17| issue = 5-6| pages = 431–439
| date = Sep 2006
| pmid = 16940764
| url = http://www.ncbi.nlm.nih.gov/pubmed/16940764/
}}</ref>
<ref name="Hartman2007">{{Citation
| last1 = Hartman | first1 = Adam L
| last2 = Gasior | first2 = Maciej
| last3 = Vining | first3 = Eileen P G
| last4 = Rogawski | first4 = Michael A
| title = The Neuropharmacology of the Ketogenic Diet
| journal = Pediatric neurology | volume = 36| issue = 5| pages = 281–292
| date = May 2007
| pmid = 17509459
| doi = 10.1016/j.pediatrneurol.2007.02.008
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940242/
}}</ref>
<ref name="Krikorian2012">{{Citation
| last1 = Krikorian | first1 = Robert
| last2 = Shidler | first2 = Marcelle D
| last3 = Dangelo | first3 = Krista
| last4 = Couch | first4 = Sarah C
| last5 = Benoit | first5 = Stephen C
| last6 = Clegg | first6 = Deborah J
| title = Dietary ketosis enhances memory in mild cognitive impairment
| journal = Neurobiology of Aging | volume = 33| issue = 2| pages = 425–19-27
| date = Feb 2012
| pmid = 21130529
| doi = 10.1016/j.neurobiolaging.2010.10.006
| url = https://www.ncbi.nlm.nih.gov/pubmed/21130529/
}}</ref>
<ref name="Myhill2009">{{citation
| last1 = Myhill | first1 = S | authorlink1 = Sarah Myhill
| last2 = Booth | first2 = NE | authorlink2 = Norman Booth
| last3 = McLaren-Howard | first3 = J | authorlink3 = John McLaren-Howard
| title = Chronic fatigue syndrome and mitochondrial dysfunction
| journal = Int J Clin Exp Med | volume = 2| issue = 1| pages = 1–16
| date = 15 Jan 2009
| pmid = 19436827
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/
}}</ref>
<ref name="Myhillketo1">{{citation
| last1 = Segura | first1 = Gabriela
| title = Ketogenic diet - a connection between mitochondria and diet
| date = 9 Aug 2013
| url = http://www.drmyhill.co.uk/wiki/Ketogenic_diet_-_a_connection_between_mitochondria_and_diet
}}</ref>
<ref name="Myhillketo2">{{citation
| last1 = Myhill | first1 = Sarah | authorlink1 = Sarah Myhill
| title = Ketogenic diet - the practical details
| url = http://www.doctormyhill.co.uk/wiki/Ketogenic_diet_-_the_practical_details
}}</ref>
<ref name="RegerMA2004">{{citation
| last1 = Reger | first1 = Mark A
| last2 = Henderson | first2 = Samuel T
| last3 = Hale | first3 = Cathy
| last4 = Cholerton | first4 = Brenna
| last5 = Baker | first5 = Laura D
| last6 = Watson | first6 = G S
| last7 = Hyde | first7 = Karen
| last8 = Chapman | first8 = Darla
| last9 = Craft | first9 = Suzanne
| display-authors = 3
| title = Effects of beta-hydroxybutyrate on cognition in memory-impaired adults
| journal = Neurobiology of Aging | volume = 25| issue = 3| pages = 311–314
| date = Mar 2004
| doi = 10.1016/S0197-4580(03)00087-3
| pmid = 15123336
}}</ref>
<ref name="RhoJM2007">{{Citation
| last1 = Rho | first1 = Jong M
| last2 = Rogawski | first2 = Michael A
| title = The Ketogenic Diet: Stoking the Powerhouse of the Cell
| journal = Epilepsy Currents | volume = 7| issue = 2| pages = 58–60
| date = Mar 2007
| doi = 10.1111/j.1535-7511.2007.00170.x
| pmid = 17505556
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867088/
}}</ref>
<ref name="WikiMCT">{{citation
| title = Wikipedia - Ketogenic diet, MCT oil
| url = https://en.wikipedia.org/wiki/Ketogenic_diet#MCT_oil
}}</ref>
<ref name="ZhangX2016">{{citation
| last1 = Zhang | first1 = Xiaoyu
| last2 = Qin | first2 = Juliang
| last3 = Zhao | first3 = Yihan
| last4 = Shi | first4 = Jueping
| last5 = Lan | first5 = Rong
| last6 = Gan | first6 = Yunqiu
| last7 = Ren | first7 = Hua
| last8 = Zhu | first8 = Bing
| last9 = Qian | first9 = Min
| last10 = Du | first10 = Bing
| title = Long-term ketogenic diet contributes to glycemic control but promotes lipid accumulation and hepatic steatosis in type 2 diabetic mice
| journal = Nutrition Research | volume = 36| issue = 4| pages = 349–358
| date = 1 Apr 2016
| doi = 10.1016/j.nutres.2015.12.002
| url = http://www.nrjournal.com/article/S0271531715003012/abstract
}}</ref>
</references>

[[Category:Potential treatments]]
[[Category:Diets]]

Ketogenic diet

2019-08-14T11:28:24Z

Drcraig:/* Evidence for a ketogenic diet */

The ketogenic diet is a high-[[fat]], medium [[protein]], low [[carbohydrate]] diet primarily used for children with treatment-resistant [[epilepsy]]. It induces [[ketosis]], a metabolic state in which the body derives most of its energy from [[ketones]] rather than [[glucose]]. A ketogenic diet increases blood ketone bodies: β-hydroxybutyrate, acetoacetate, and acetone. β-hydroxybutyrate comprises 70% of the ketone bodies produced from a ketogenic diet<ref>{{Cite journal|last=Dedkova|first=Elena N.|last2=Blatter|first2=Lothar A.|date=2014|title=Role of β-hydroxybutyrate, its polymer poly-β-hydroxybutyrate and inorganic polyphosphate in mammalian health and disease|url=https://www.ncbi.nlm.nih.gov/pubmed/25101001|journal=Frontiers in Physiology|volume=5|pages=260|doi=10.3389/fphys.2014.00260|issn=1664-042X|pmc=4102118|pmid=25101001}}</ref>. The therapeutic benefits of a ketogenic diet are believed to be due to β-hydroxybutyrate which acts as a signalling molecule.<ref>{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=Jan 2017|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>

Ketone bodies are a more efficient fuel than glucose. The brain can derive up to 60% of energy from ketones. The metabolic breakdown of ketone bodies produces more ATP per oxygen molecule consumed than other metabolic substrates. The ketone body β-hydroxybutyrate is converted to acetyl-CoA and distributed to metabolically active tissues as a fuel source (e.g. brain, skeletal muscle, heart). This acetyl-CoA is cycled directly into the Kreb’s cycle for energy production thereby bypassing glycolysis and [[Pyruvate dehydrogenase|pyruvate dehydrogenase (PDH)]].<ref>{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=Jan 2017|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>

Ketones may enhance antioxidant defenses by multiple mechanisms. β-hydroxybutyrate promotes transcription of genes associated with protective mechanisms including mitochondrial superoxide dismutase (MnSOD), catalase, and metallothionein. The effect is therefore reduced oxidative stress and lipid peroxidation. β-hydroxybutyrate upregulates production of the antioxidant [[glutathione]] likely through activation of the nrf2 pathway.<ref>{{Cite journal|last=Gross|first=Elena C.|last2=Klement|first2=Rainer J.|last3=Schoenen|first3=Jean|last4=D’Agostino|first4=Dominic P.|last5=Fischer|first5=Dirk|date=2019-04-10|title=Potential Protective Mechanisms of Ketone Bodies in Migraine Prevention|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520671/|journal=Nutrients|volume=11|issue=4|doi=10.3390/nu11040811|issn=2072-6643|pmc=6520671|pmid=30974836}}</ref>

== Types of Ketogenic Diets ==

A ketogenic diet is comprised of a dietary fat to carbohydrate ratio of 3:1 or 4:1. The diet should include <20 grams of carbohydrate per day, or 15-10% of total caloric intake. Ketogenic diets can be less strict if using exogenous ketones.<ref>{{Cite journal|last=Hashim|first=Sami A.|last2=VanItallie|first2=Theodore B.|date=Sep 2014|title=Ketone body therapy: from the ketogenic diet to the oral administration of ketone ester|url=https://www.ncbi.nlm.nih.gov/pubmed/24598140|journal=Journal of Lipid Research|volume=55|issue=9|pages=1818–1826|doi=10.1194/jlr.R046599|issn=1539-7262|pmc=4617348|pmid=24598140}}</ref>

== Evidence for a ketogenic diet ==

=== General Effects ===

In an animal model, a ketogenic diet was shown to increase [[mitochondria]]l biogenesis.<ref name="RhoJM2007" /> A similar result was found in a study of fasting mice.<ref name="Cerqueira2011" /> Ketone bodies scavenge free radicals ''in vivo''. <ref>{{Cite journal|last=Haces|first=María L.|last2=Hernández-Fonseca|first2=Karla|last3=Medina-Campos|first3=Omar N.|last4=Montiel|first4=Teresa|last5=Pedraza-Chaverri|first5=José|last6=Massieu|first6=Lourdes|date=May 2008|title=Antioxidant capacity contributes to protection of ketone bodies against oxidative damage induced during hypoglycemic conditions|url=https://www.ncbi.nlm.nih.gov/pubmed/18339375|journal=Experimental Neurology|volume=211|issue=1|pages=85–96|doi=10.1016/j.expneurol.2007.12.029|issn=0014-4886|pmid=18339375}}</ref> Ketogenic diets reduce circulating levels of insulin and insulin-like growth factors.<ref name=":0" />

=== Epilepsy ===

[[Neurotransmitter]]s regulate nerve impulses is the brain by either inhibiting impulse firing or exciting the [[neuron]] to fire. A primary inhibitory neurotransmitters is [[GABA]] and a primary excitatory neurotransmitters is [[glutamate]]. In patients with epilepsy, if the normal balance of inhibition and excitation is disrupted, a seizure can occur.

It us unknown why ketogenic diets are protective against epilepsy. In animal models, the ketone bodies [[acetoacetate]] and [[acetone]] have anticonvulsant properties through a novel pathway.<ref name="Hartman2007" />

The Charlie Foundation supports the use of ketogenic diets with children with severe epilepsy.<ref name="CharlieFoundation" />

=== Neurodegenerative Disease ===

There is evidence from uncontrolled clinical trials and animal models that ketogenic diets may be protective in neurodegenerative disorders including [[Alzheimer's]] and [[Parkinson's]].<ref name="Gasior2006" />

Mice fed a ketogenic diet had increased activity of [[dopamine]]rgic neurons.<ref name="ChurchWH2014" /> In a rat model of Parkinson's, a ketogenic diet was protective against neurotoxicity by up-regulating glutathione.<ref name="ChengB2009" /> A clinical trial of Parkinson’s disease compared a ketogenic diet to a low-fat diet with improvement in motor symptoms in both groups after 8 weeks but greater improvement in non-motor symptoms (fatigue, pain, and cognitive impairment) in the ketogenic group. <ref>{{Cite journal|last=Phillips|first=Matthew C. L.|last2=Murtagh|first2=Deborah K. J.|last3=Gilbertson|first3=Linda J.|last4=Asztely|first4=Fredrik J. S.|last5=Lynch|first5=Christopher D. P.|date=08 2018|title=Low-fat versus ketogenic diet in Parkinson's disease: A pilot randomized controlled trial|url=https://www.ncbi.nlm.nih.gov/pubmed/30098269/|journal=Movement Disorders: Official Journal of the Movement Disorder Society|volume=33|issue=8|pages=1306–1314|doi=10.1002/mds.27390|issn=1531-8257|pmc=6175383|pmid=30098269}}</ref> Another study found dietary ketosis enhanced memory in patients with mild cognitive impairment.<ref name="Krikorian2012" />

=== Traumatic Brain Injury (TBI) ===
The ketogenic diet is an effective treatment for TBI recovery in rats and shows potential in humans.<ref>{{Cite journal|last=McDougall|first=Alexandre|last2=Bayley|first2=Mark|last3=Munce|first3=Sarah Ep|date=2018|title=The ketogenic diet as a treatment for traumatic brain injury: a scoping review|url=https://www.ncbi.nlm.nih.gov/pubmed/29359959|journal=Brain Injury|volume=32|issue=4|pages=416–422|doi=10.1080/02699052.2018.1429025|issn=1362-301X|pmid=29359959}}</ref>

=== Multiple Sclerosis ===
A ketogenic diet reduced the expression of enzymes involved in the biosynthesis of pro-inflammatory eicosanoids and improved quality of life as measured by the Multiple Sclerosis Quality of Life-54 index.<ref>{{Cite journal|last=Bock|first=Markus|last2=Karber|first2=Mirjam|last3=Kuhn|first3=Hartmut|date=2018-10-03|title=Ketogenic diets attenuate cyclooxygenase and lipoxygenase gene expression in multiple sclerosis|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197715/|journal=EBioMedicine|volume=36|pages=293–303|doi=10.1016/j.ebiom.2018.08.057|issn=2352-3964|pmc=6197715|pmid=30292675}}</ref>

=== Chronic Fatigue Syndrome ===

No studies have been done on the effects of ketogenic diets in [[Chronic fatigue syndrome]]. Some CFS clinicians recommend ketogenic diets as a management strategy<ref name="Myhillketo1" /><ref name="Craig20150325" /> citing [[mitochondria]]l dysfunction<ref name="Myhill2009" />, [[immune system|immune]] dysfunction, and [[neuroinflammation]] as pathways through which ketogenic diets could confer some benefit.

==Risks & Side Effects==
*The ketogenic diet was found to regulate [[blood sugar]] but over the long term cause fat to accumulate in the [[liver]] in an animal model of Type II [[Diabetes]].<ref name="ZhangX2016" /> An open label, non-randomized, controlled study of the ketogenic diet in Type II Diabetes patients showed sustained long-term beneficial effects on multiple clinical markers of diabetes and cardiometabolic health at 2 years while utilizing less medication.<ref name=":0">{{Cite journal|last=Athinarayanan|first=Shaminie J.|last2=Adams|first2=Rebecca N.|last3=Hallberg|first3=Sarah J.|last4=McKenzie|first4=Amy L.|last5=Bhanpuri|first5=Nasir H.|last6=Campbell|first6=Wayne W.|last7=Volek|first7=Jeff S.|last8=Phinney|first8=Stephen D.|last9=McCarter|first9=James P.|date=2019|title=Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial|url=https://www.ncbi.nlm.nih.gov/pubmed/31231311|journal=Frontiers in Endocrinology|volume=10|pages=348|doi=10.3389/fendo.2019.00348|issn=1664-2392|pmc=6561315|pmid=31231311}}</ref>
*Two children on the diet for [[refractory epilepsy]] had [[selenium]] deficiency which resulted in sudden cardiac death.<ref>[http://www.pedneur.com/article/S0887-8994(08)00399-8/abstract?cc=y= Sudden Cardiac Death in Association With the Ketogenic Diet - Pediatric Neurology - December 2008]</ref>
*Up to 6% of those on a ketogenic diet may experience kidney stones. <ref name=":1">{{Cite journal|last=Hartman|first=Adam L.|last2=Vining|first2=Eileen P. G.|date=Jan 2007|title=Clinical aspects of the ketogenic diet|url=https://www.ncbi.nlm.nih.gov/pubmed/17241206|journal=Epilepsia|volume=48|issue=1|pages=31–42|doi=10.1111/j.1528-1167.2007.00914.x|issn=0013-9580|pmid=17241206}}</ref>
*Ketogenic diets may require additional supplemental nutrition to prevent deficiencies. Common deficiencies include calcium, zinc, selenium, and copper.<ref name=":1" />
*Ketogenic diets are not recommended for those with genetic primary carnitine deficiencies [including mutations in carnitine palmitoyl transferase (CPT) I or II and mitochondrial translocase] and fatty acid β-oxidation abnormalities (e.g., medium-chain acyl dehydrogenase deficiency). <ref>{{Cite journal|last=Stafstrom|first=Carl E.|last2=Rho|first2=Jong M.|date=2012-04-09|title=The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321471/|journal=Frontiers in Pharmacology|volume=3|doi=10.3389/fphar.2012.00059|issn=1663-9812|pmc=3321471|pmid=22509165}}</ref> It is safe for those with mitochondrial defects in complexes I, II, and IV<ref>{{Cite journal|last=Kang|first=Hoon-Chul|last2=Lee|first2=Young-Mock|last3=Kim|first3=Heung Dong|last4=Lee|first4=Joon Soo|last5=Slama|first5=Abdelhamid|date=Jan 2007|title=Safe and effective use of the ketogenic diet in children with epilepsy and mitochondrial respiratory chain complex defects|url=https://www.ncbi.nlm.nih.gov/pubmed/17241212|journal=Epilepsia|volume=48|issue=1|pages=82–88|doi=10.1111/j.1528-1167.2006.00906.x|issn=0013-9580|pmid=17241212}}</ref> and pyruvate dehydrogenase complex deficiency<ref>{{Cite journal|last=Sofou|first=Kalliopi|last2=Dahlin|first2=Maria|last3=Hallböök|first3=Tove|last4=Lindefeldt|first4=Marie|last5=Viggedal|first5=Gerd|last6=Darin|first6=Niklas|date=2017|title=Ketogenic diet in pyruvate dehydrogenase complex deficiency: short- and long-term outcomes|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5306430/|journal=Journal of Inherited Metabolic Disease|volume=40|issue=2|pages=237–245|doi=10.1007/s10545-016-0011-5|issn=0141-8955|pmc=5306430|pmid=28101805}}</ref>.

== Notable Studies ==
*[https://clinicaltrials.gov/ct2/show/NCT01906398 Efficacy and Safety of Ketogenic Diet as Adjunctive Treatment in Adults With Refractory Epilepsy (KD)] (This study is ongoing, but not recruiting participants.)
*[https://www.frontiersin.org/articles/10.3389/fendo.2019.00348/full Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial.]

==Medium chain triglycerides (MCT)==
Supplementation with [[medium-chain triglycerides]] (MCTs) increases blood levels of ketones.<ref name="WikiMCT" /> They are often used in ketogenic diets to help maintain ketosis at a lower proportion of fat intake. Regular intake of MCTs can increase expression of ketone transporter MCT1 at the brain, increasing uptake of ketones<ref>{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=Jan 2017|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>. A study showed improved cognition in [[Alzheimer's disease]] patients.<ref name="RegerMA2004" />

==Exogenous ketones==
Exogenous ketones may be used to increase blood ketone bodies without requiring such strict dietary measures. Exogenous ketones come in esters and salts, both have been found to raise β-hydroxybutyrate to therapeutic levels that can last for hours. <ref>{{Cite journal|last=Hashim|first=Sami A.|last2=VanItallie|first2=Theodore B.|date=Sep 2014|title=Ketone body therapy: from the ketogenic diet to the oral administration of ketone ester|url=https://www.ncbi.nlm.nih.gov/pubmed/24598140|journal=Journal of Lipid Research|volume=55|issue=9|pages=1818–1826|doi=10.1194/jlr.R046599|issn=1539-7262|pmc=4617348|pmid=24598140}}</ref>

==Clinical use==
Doctor [[Sarah Myhill]] has a page on her web site describing the ketogenic diet.<ref name="Myhillketo2" />
Dr. [[Courtney Craig]] has published a hypothesis on the use of ketogenic diets in [[ME/CFS]] and offers dietary consulting to patients.<ref name="Craig2015" />

==Learn more==
*2017, [https://www.healthrising.org/blog/2017/06/16/ketogenic-diets-fibromyalgia-mecfs-review/ Getting Clear on Ketogenic Diets (for Fibromyalgia and ME/CFS): A Review]
*[https://en.wikipedia.org/wiki/Ketogenic_diet Wikipedia - Ketogenic diet]
*[http://www.ketogenic-diet-resource.com/ Ketogenic Diet Resource]
*[https://en.wikipedia.org/wiki/Fatty_acid_metabolism Wikipedia - Fatty acid metabolism]

== See also ==
*[[Fasting]]
*[[Ketosis]]

==References==
<references>
<ref name="Cerqueira2011">{{Citation
| last1 = Cerqueira | first1 = Fernanda M
| last2 = Laurindo | first2 = Francisco R M
| last3 = Kowaltowski | first3 = Alicia J
| title = Mild Mitochondrial Uncoupling and Calorie Restriction Increase Fasting eNOS, Akt and Mitochondrial Biogenesis
| journal = PLOS ONE | volume = 6| issue = 3| pages = –18433
| date = 31 Mar 2011
| doi = 10.1371/journal.pone.0018433
| url = http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018433
}}</ref>
<ref name="CharlieFoundation">| title = The Charlie Foundation for Ketogenic Therapies
| url = http://www.charliefoundation.org/
</ref>
<ref name="ChengB2009">{{Citation
| last1 = Cheng | first1 = Baohua
| last2 = Yang | first2 = Xinxin
| last3 = An | first3 = Liangxiang
| last4 = Gao | first4 = Bo
| last5 = Liu | first5 = Xia
| last6 = Liu | first6 = Shuwei
| display-authors = 3
| title = Ketogenic diet protects dopaminergic neurons against 6-OHDA neurotoxicity via up-regulating glutathione in a rat model of Parkinson's disease
| journal = Brain Research | volume = 1286| pages = 25–31
| date = 2009-08-25
| doi = 10.1016/j.brainres.2009.06.060
| url = http://www.sciencedirect.com/science/article/pii/S0006899309012797
}}</ref>
<ref name="ChurchWH2014">{{Citation
| last1 = Church | first1 = William H
| last2 = Adams | first2 = Ryan E
| last3 = Wyss | first3 = Livia S
| title = Ketogenic diet alters dopaminergic activity in the mouse cortex
| journal = Neuroscience Letters | volume = 571| pages = 1–4
| date = 2014-06-13
| doi = 10.1016/j.neulet.2014.04.016
| pmid = 24769322
| URL = http://www.ncbi.nlm.nih.gov/pubmed/24769322
}}</ref>
<ref name="Craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}</ref>
<ref name="Craig20150325">{{citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = A Ketogenic Diet for ME/CFS & Fibro
| date = 30 Mar 2015
| url = http://www.drcourtneycraig.com/blog/2015/3/25/a-ketogenic-diet-for-mecfs-fibro
}}</ref>
<ref name="Gasior2006">{{Citation
| last1 = Gasior | first1 = Maciej
| last2 = Rogawski | first2 = Michael A
| last3 = Hartman | first3 = Adam L
| title = Neuroprotective and disease-modifying effects of the ketogenic diet
| journal = Behavioural Pharmacology | volume = 17| issue = 5-6| pages = 431–439
| date = Sep 2006
| pmid = 16940764
| url = http://www.ncbi.nlm.nih.gov/pubmed/16940764/
}}</ref>
<ref name="Hartman2007">{{Citation
| last1 = Hartman | first1 = Adam L
| last2 = Gasior | first2 = Maciej
| last3 = Vining | first3 = Eileen P G
| last4 = Rogawski | first4 = Michael A
| title = The Neuropharmacology of the Ketogenic Diet
| journal = Pediatric neurology | volume = 36| issue = 5| pages = 281–292
| date = May 2007
| pmid = 17509459
| doi = 10.1016/j.pediatrneurol.2007.02.008
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940242/
}}</ref>
<ref name="Krikorian2012">{{Citation
| last1 = Krikorian | first1 = Robert
| last2 = Shidler | first2 = Marcelle D
| last3 = Dangelo | first3 = Krista
| last4 = Couch | first4 = Sarah C
| last5 = Benoit | first5 = Stephen C
| last6 = Clegg | first6 = Deborah J
| title = Dietary ketosis enhances memory in mild cognitive impairment
| journal = Neurobiology of Aging | volume = 33| issue = 2| pages = 425–19-27
| date = Feb 2012
| pmid = 21130529
| doi = 10.1016/j.neurobiolaging.2010.10.006
| url = https://www.ncbi.nlm.nih.gov/pubmed/21130529/
}}</ref>
<ref name="Myhill2009">{{citation
| last1 = Myhill | first1 = S | authorlink1 = Sarah Myhill
| last2 = Booth | first2 = NE | authorlink2 = Norman Booth
| last3 = McLaren-Howard | first3 = J | authorlink3 = John McLaren-Howard
| title = Chronic fatigue syndrome and mitochondrial dysfunction
| journal = Int J Clin Exp Med | volume = 2| issue = 1| pages = 1–16
| date = 15 Jan 2009
| pmid = 19436827
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/
}}</ref>
<ref name="Myhillketo1">{{citation
| last1 = Segura | first1 = Gabriela
| title = Ketogenic diet - a connection between mitochondria and diet
| date = 9 Aug 2013
| url = http://www.drmyhill.co.uk/wiki/Ketogenic_diet_-_a_connection_between_mitochondria_and_diet
}}</ref>
<ref name="Myhillketo2">{{citation
| last1 = Myhill | first1 = Sarah | authorlink1 = Sarah Myhill
| title = Ketogenic diet - the practical details
| url = http://www.doctormyhill.co.uk/wiki/Ketogenic_diet_-_the_practical_details
}}</ref>
<ref name="RegerMA2004">{{citation
| last1 = Reger | first1 = Mark A
| last2 = Henderson | first2 = Samuel T
| last3 = Hale | first3 = Cathy
| last4 = Cholerton | first4 = Brenna
| last5 = Baker | first5 = Laura D
| last6 = Watson | first6 = G S
| last7 = Hyde | first7 = Karen
| last8 = Chapman | first8 = Darla
| last9 = Craft | first9 = Suzanne
| display-authors = 3
| title = Effects of beta-hydroxybutyrate on cognition in memory-impaired adults
| journal = Neurobiology of Aging | volume = 25| issue = 3| pages = 311–314
| date = Mar 2004
| doi = 10.1016/S0197-4580(03)00087-3
| pmid = 15123336
}}</ref>
<ref name="RhoJM2007">{{Citation
| last1 = Rho | first1 = Jong M
| last2 = Rogawski | first2 = Michael A
| title = The Ketogenic Diet: Stoking the Powerhouse of the Cell
| journal = Epilepsy Currents | volume = 7| issue = 2| pages = 58–60
| date = Mar 2007
| doi = 10.1111/j.1535-7511.2007.00170.x
| pmid = 17505556
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867088/
}}</ref>
<ref name="WikiMCT">{{citation
| title = Wikipedia - Ketogenic diet, MCT oil
| url = https://en.wikipedia.org/wiki/Ketogenic_diet#MCT_oil
}}</ref>
<ref name="ZhangX2016">{{citation
| last1 = Zhang | first1 = Xiaoyu
| last2 = Qin | first2 = Juliang
| last3 = Zhao | first3 = Yihan
| last4 = Shi | first4 = Jueping
| last5 = Lan | first5 = Rong
| last6 = Gan | first6 = Yunqiu
| last7 = Ren | first7 = Hua
| last8 = Zhu | first8 = Bing
| last9 = Qian | first9 = Min
| last10 = Du | first10 = Bing
| title = Long-term ketogenic diet contributes to glycemic control but promotes lipid accumulation and hepatic steatosis in type 2 diabetic mice
| journal = Nutrition Research | volume = 36| issue = 4| pages = 349–358
| date = 1 Apr 2016
| doi = 10.1016/j.nutres.2015.12.002
| url = http://www.nrjournal.com/article/S0271531715003012/abstract
}}</ref>
</references>

[[Category:Potential treatments]]
[[Category:Diets]]

Ketogenic diet

2019-08-12T15:38:36Z

Drcraig:/* Evidence for a ketogenic diet */

The ketogenic diet is a high-[[fat]], medium [[protein]], low [[carbohydrate]] diet primarily used for children with treatment-resistant [[epilepsy]]. It induces [[ketosis]], a metabolic state in which the body derives most of its energy from [[ketones]] rather than [[glucose]]. A ketogenic diet increases blood ketone bodies: β-hydroxybutyrate, acetoacetate, and acetone. β-hydroxybutyrate comprises 70% of the ketone bodies produced from a ketogenic diet<ref>{{Cite journal|last=Dedkova|first=Elena N.|last2=Blatter|first2=Lothar A.|date=2014|title=Role of β-hydroxybutyrate, its polymer poly-β-hydroxybutyrate and inorganic polyphosphate in mammalian health and disease|url=https://www.ncbi.nlm.nih.gov/pubmed/25101001|journal=Frontiers in Physiology|volume=5|pages=260|doi=10.3389/fphys.2014.00260|issn=1664-042X|pmc=4102118|pmid=25101001}}</ref>. The therapeutic benefits of a ketogenic diet are believed to be due to β-hydroxybutyrate which acts as a signalling molecule.<ref>{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=2017-1|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>

Ketone bodies are a more efficient fuel than glucose. The brain can derive up to 60% of energy from ketones. The metabolic breakdown of ketone bodies produces more ATP per oxygen molecule consumed than other metabolic substrates. The ketone body β-hydroxybutyrate is converted to acetyl-CoA and distributed to metabolically active tissues as a fuel source (e.g. brain, skeletal muscle, heart). This acetyl-CoA is cycled directly into the Kreb’s cycle for energy production thereby bypassing glycolysis and [[Pyruvate dehydrogenase|pyruvate dehydrogenase (PDH)]].<ref>{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=2017-1|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>

Ketones may enhance antioxidant defenses by multiple mechanisms. β-hydroxybutyrate promotes transcription of genes associated with protective mechanisms including mitochondrial superoxide dismutase (MnSOD), catalase, and metallothionein. The effect is therefore reduced oxidative stress and lipid peroxidation. β-hydroxybutyrate upregulates production of the antioxidant [[glutathione]] likely through activation of the nrf2 pathway.<ref>{{Cite journal|last=Gross|first=Elena C.|last2=Klement|first2=Rainer J.|last3=Schoenen|first3=Jean|last4=D’Agostino|first4=Dominic P.|last5=Fischer|first5=Dirk|date=2019-04-10|title=Potential Protective Mechanisms of Ketone Bodies in Migraine Prevention|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520671/|journal=Nutrients|volume=11|issue=4|doi=10.3390/nu11040811|issn=2072-6643|pmc=6520671|pmid=30974836}}</ref>

== Types of ketogenic diets ==

A ketogenic diet is comprised of a dietary fat to carbohydrate ratio of 3:1 or 4:1. The diet should include <20 grams of carbohydrate per day, or 15-10% of total caloric intake. Ketogenic diets can be less strict if using exogenous ketones.<ref>{{Cite journal|last=Hashim|first=Sami A.|last2=VanItallie|first2=Theodore B.|date=2014-9|title=Ketone body therapy: from the ketogenic diet to the oral administration of ketone ester|url=https://www.ncbi.nlm.nih.gov/pubmed/24598140|journal=Journal of Lipid Research|volume=55|issue=9|pages=1818–1826|doi=10.1194/jlr.R046599|issn=1539-7262|pmc=4617348|pmid=24598140}}</ref>

== Evidence for a ketogenic diet ==

=== General effects ===

In an animal model, a ketogenic diet was shown to increase [[mitochondria]]l biogenesis.<ref name="RhoJM2007" /> A similar result was found in a study of fasting mice.<ref name="Cerqueira2011" /> Ketone bodies scavenge free radicals ''in vivo''. <ref>{{Cite journal|last=Haces|first=María L.|last2=Hernández-Fonseca|first2=Karla|last3=Medina-Campos|first3=Omar N.|last4=Montiel|first4=Teresa|last5=Pedraza-Chaverri|first5=José|last6=Massieu|first6=Lourdes|date=2008-5|title=Antioxidant capacity contributes to protection of ketone bodies against oxidative damage induced during hypoglycemic conditions|url=https://www.ncbi.nlm.nih.gov/pubmed/18339375|journal=Experimental Neurology|volume=211|issue=1|pages=85–96|doi=10.1016/j.expneurol.2007.12.029|issn=0014-4886|pmid=18339375}}</ref>

=== Epilepsy ===

[[Neurotransmitter]]s regulate nerve impulses is the brain by either inhibiting impulse firing or exciting the [[neuron]] to fire. A primary inhibitory neurotransmitters is [[GABA]] and a primary excitatory neurotransmitters is [[glutamate]]. In patients with epilepsy, if the normal balance of inhibition and excitation is disrupted, a seizure can occur.

It us unknown why ketogenic diets are protective against epilepsy. In animal models, the ketone bodies [[acetoacetate]] and [[acetone]] have anticonvulsant properties through a novel pathway.<ref name="Hartman2007" />

The Charlie Foundation supports the use of ketogenic diets with children with severe epilepsy.<ref name="CharlieFoundation" />

=== Neurodegenerative diseases ===

There is evidence from uncontrolled clinical trials and animal models that ketogenic diets may be protective in neurodegenerative disorders including [[Alzheimer's]] and [[Parkinson's]].<ref name="Gasior2006" />

Mice fed a ketogenic diet had increased activity of [[dopamine]]rgic neurons.<ref name="ChurchWH2014" /> In a rat model of Parkinson's, a ketogenic diet was protective against neurotoxicity by up-regulating glutathione.<ref name="ChengB2009" />

A study found dietary ketosis enhanced memory in patients with mild cognitive impairment.<ref name="Krikorian2012" />

=== '''Multiple Sclerosis''' ===
A ketogenic diet reduced the expression of enzymes involved in the biosynthesis of pro-inflammatory eicosanoids and improved quality of life as measured by the Multiple Sclerosis Quality of Life-54 index.<ref>{{Cite journal|last=Bock|first=Markus|last2=Karber|first2=Mirjam|last3=Kuhn|first3=Hartmut|date=2018-10-03|title=Ketogenic diets attenuate cyclooxygenase and lipoxygenase gene expression in multiple sclerosis|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197715/|journal=EBioMedicine|volume=36|pages=293–303|doi=10.1016/j.ebiom.2018.08.057|issn=2352-3964|pmc=6197715|pmid=30292675}}</ref>

=== Chronic fatigue syndrome ===

No studies have been done on the effects of ketogenic diets in [[Chronic fatigue syndrome]]. Some CFS clinicians recommend ketogenic diets as a management strategy<ref name="Myhillketo1" /><ref name="Craig20150325" /> citing [[mitochondria]]l dysfunction<ref name="Myhill2009" />, [[immune system|immune]] dysfunction, and [[neuroinflammation]] as pathways through which ketogenic diets could confer some benefit.

==Risks & Side Effects==
*The ketogenic diet was found to regulate [[blood sugar]] but over the long term cause fat to accumulate in the [[liver]] in an animal model of Type II [[Diabetes]].<ref name="ZhangX2016" /> An open label, non-randomized, controlled study of the ketogenic diet in Type II Diabetes patients showed sustained long-term beneficial effects on multiple clinical markers of diabetes and cardiometabolic health at 2 years while utilizing less medication.<ref>{{Cite journal|last=Athinarayanan|first=Shaminie J.|last2=Adams|first2=Rebecca N.|last3=Hallberg|first3=Sarah J.|last4=McKenzie|first4=Amy L.|last5=Bhanpuri|first5=Nasir H.|last6=Campbell|first6=Wayne W.|last7=Volek|first7=Jeff S.|last8=Phinney|first8=Stephen D.|last9=McCarter|first9=James P.|date=2019|title=Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial|url=https://www.ncbi.nlm.nih.gov/pubmed/31231311|journal=Frontiers in Endocrinology|volume=10|pages=348|doi=10.3389/fendo.2019.00348|issn=1664-2392|pmc=6561315|pmid=31231311}}</ref>
*Two children on the diet for [[refractory epilepsy]] had [[selenium]] deficiency which resulted in sudden cardiac death.<ref>[http://www.pedneur.com/article/S0887-8994(08)00399-8/abstract?cc=y= Sudden Cardiac Death in Association With the Ketogenic Diet - Pediatric Neurology - December 2008]</ref>
*Up to 6% of those on a ketogenic diet may experience kidney stones. <ref>{{Cite journal|last=Hartman|first=Adam L.|last2=Vining|first2=Eileen P. G.|date=2007-1|title=Clinical aspects of the ketogenic diet|url=https://www.ncbi.nlm.nih.gov/pubmed/17241206|journal=Epilepsia|volume=48|issue=1|pages=31–42|doi=10.1111/j.1528-1167.2007.00914.x|issn=0013-9580|pmid=17241206}}</ref>
*Ketogenic diets may require additional supplemental nutrition to prevent deficiencies. Common deficiencies include calcium, zinc, selenium, and copper.<ref>{{Cite journal|last=Hartman|first=Adam L.|last2=Vining|first2=Eileen P. G.|date=2007-1|title=Clinical aspects of the ketogenic diet|url=https://www.ncbi.nlm.nih.gov/pubmed/17241206|journal=Epilepsia|volume=48|issue=1|pages=31–42|doi=10.1111/j.1528-1167.2007.00914.x|issn=0013-9580|pmid=17241206}}</ref>
*Ketogenic diets are not recommended for those with genetic primary carnitine deficiencies [including mutations in carnitine palmitoyl transferase (CPT) I or II and mitochondrial translocase] and fatty acid β-oxidation abnormalities (e.g., medium-chain acyl dehydrogenase deficiency). <ref>{{Cite journal|last=Stafstrom|first=Carl E.|last2=Rho|first2=Jong M.|date=2012-04-09|title=The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321471/|journal=Frontiers in Pharmacology|volume=3|doi=10.3389/fphar.2012.00059|issn=1663-9812|pmc=3321471|pmid=22509165}}</ref> It is safe for those with mitochondrial defects in complexes I, II, and IV<ref>{{Cite journal|last=Kang|first=Hoon-Chul|last2=Lee|first2=Young-Mock|last3=Kim|first3=Heung Dong|last4=Lee|first4=Joon Soo|last5=Slama|first5=Abdelhamid|date=2007-1|title=Safe and effective use of the ketogenic diet in children with epilepsy and mitochondrial respiratory chain complex defects|url=https://www.ncbi.nlm.nih.gov/pubmed/17241212|journal=Epilepsia|volume=48|issue=1|pages=82–88|doi=10.1111/j.1528-1167.2006.00906.x|issn=0013-9580|pmid=17241212}}</ref> and pyruvate dehydrogenase complex deficiency<ref>{{Cite journal|last=Sofou|first=Kalliopi|last2=Dahlin|first2=Maria|last3=Hallböök|first3=Tove|last4=Lindefeldt|first4=Marie|last5=Viggedal|first5=Gerd|last6=Darin|first6=Niklas|date=2017|title=Ketogenic diet in pyruvate dehydrogenase complex deficiency: short- and long-term outcomes|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5306430/|journal=Journal of Inherited Metabolic Disease|volume=40|issue=2|pages=237–245|doi=10.1007/s10545-016-0011-5|issn=0141-8955|pmc=5306430|pmid=28101805}}</ref>.

== Notable studies ==
*[https://clinicaltrials.gov/ct2/show/NCT01906398 Efficacy and Safety of Ketogenic Diet as Adjunctive Treatment in Adults With Refractory Epilepsy (KD)] (This study is ongoing, but not recruiting participants.)

==Medium chain triglycerides (MCT)==
Supplementation with [[medium-chain triglycerides]] (MCTs) increases blood levels of ketones.<ref name="WikiMCT" /> They are often used in ketogenic diets to help maintain ketosis at a lower proportion of fat intake. Regular intake of MCTs can increase expression of ketone transporter MCT1 at the brain, increasing uptake of ketones<ref>{{Cite journal|last=Achanta|first=Lavanya B.|last2=Rae|first2=Caroline D.|date=2017-1|title=β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms|url=https://www.ncbi.nlm.nih.gov/pubmed/27826689/|journal=Neurochemical Research|volume=42|issue=1|pages=35–49|doi=10.1007/s11064-016-2099-2|issn=1573-6903|pmid=27826689}}</ref>. A study showed improved cognition in [[Alzheimer's disease]] patients.<ref name="RegerMA2004" />

==Exogenous ketones==
Exogenous ketones may be used to increase blood ketone bodies without requiring such strict dietary measures. Exogenous ketones come in esters and salts, both have been found to raise β-hydroxybutyrate to therapeutic levels that can last for hours. <ref>{{Cite journal|last=Hashim|first=Sami A.|last2=VanItallie|first2=Theodore B.|date=2014-9|title=Ketone body therapy: from the ketogenic diet to the oral administration of ketone ester|url=https://www.ncbi.nlm.nih.gov/pubmed/24598140|journal=Journal of Lipid Research|volume=55|issue=9|pages=1818–1826|doi=10.1194/jlr.R046599|issn=1539-7262|pmc=4617348|pmid=24598140}}</ref>

==Clinical use==
Doctor [[Sarah Myhill]] has a page on her web site describing the ketogenic diet.<ref name="Myhillketo2" />
Dr. [[Courtney Craig]] has published a hypothesis on the use of ketogenic diets in [[ME/CFS]] and offers dietary consulting to patients.<ref name="Craig2015" />

==Learn more==
*2017, [https://www.healthrising.org/blog/2017/06/16/ketogenic-diets-fibromyalgia-mecfs-review/ Getting Clear on Ketogenic Diets (for Fibromyalgia and ME/CFS): A Review]
*[https://en.wikipedia.org/wiki/Ketogenic_diet Wikipedia - Ketogenic diet]
*[http://www.ketogenic-diet-resource.com/ Ketogenic Diet Resource]
*[https://en.wikipedia.org/wiki/Fatty_acid_metabolism Wikipedia - Fatty acid metabolism]

== See also ==
*[[Fasting]]
*[[Ketosis]]

==References==
<references>
<ref name="Cerqueira2011">{{Citation
| last1 = Cerqueira | first1 = Fernanda M
| last2 = Laurindo | first2 = Francisco R M
| last3 = Kowaltowski | first3 = Alicia J
| title = Mild Mitochondrial Uncoupling and Calorie Restriction Increase Fasting eNOS, Akt and Mitochondrial Biogenesis
| journal = PLOS ONE | volume = 6| issue = 3| pages = –18433
| date = 31 Mar 2011
| doi = 10.1371/journal.pone.0018433
| url = http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018433
}}</ref>
<ref name="CharlieFoundation">| title = The Charlie Foundation for Ketogenic Therapies
| url = http://www.charliefoundation.org/
</ref>
<ref name="ChengB2009">{{Citation
| last1 = Cheng | first1 = Baohua
| last2 = Yang | first2 = Xinxin
| last3 = An | first3 = Liangxiang
| last4 = Gao | first4 = Bo
| last5 = Liu | first5 = Xia
| last6 = Liu | first6 = Shuwei
| display-authors = 3
| title = Ketogenic diet protects dopaminergic neurons against 6-OHDA neurotoxicity via up-regulating glutathione in a rat model of Parkinson's disease
| journal = Brain Research | volume = 1286| pages = 25–31
| date = 2009-08-25
| doi = 10.1016/j.brainres.2009.06.060
| url = http://www.sciencedirect.com/science/article/pii/S0006899309012797
}}</ref>
<ref name="ChurchWH2014">{{Citation
| last1 = Church | first1 = William H
| last2 = Adams | first2 = Ryan E
| last3 = Wyss | first3 = Livia S
| title = Ketogenic diet alters dopaminergic activity in the mouse cortex
| journal = Neuroscience Letters | volume = 571| pages = 1–4
| date = 2014-06-13
| doi = 10.1016/j.neulet.2014.04.016
| pmid = 24769322
| URL = http://www.ncbi.nlm.nih.gov/pubmed/24769322
}}</ref>
<ref name="Craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}</ref>
<ref name="Craig20150325">{{citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = A Ketogenic Diet for ME/CFS & Fibro
| date = 30 Mar 2015
| url = http://www.drcourtneycraig.com/blog/2015/3/25/a-ketogenic-diet-for-mecfs-fibro
}}</ref>
<ref name="Gasior2006">{{Citation
| last1 = Gasior | first1 = Maciej
| last2 = Rogawski | first2 = Michael A
| last3 = Hartman | first3 = Adam L
| title = Neuroprotective and disease-modifying effects of the ketogenic diet
| journal = Behavioural Pharmacology | volume = 17| issue = 5-6| pages = 431–439
| date = Sep 2006
| pmid = 16940764
| url = http://www.ncbi.nlm.nih.gov/pubmed/16940764/
}}</ref>
<ref name="Hartman2007">{{Citation
| last1 = Hartman | first1 = Adam L
| last2 = Gasior | first2 = Maciej
| last3 = Vining | first3 = Eileen P G
| last4 = Rogawski | first4 = Michael A
| title = The Neuropharmacology of the Ketogenic Diet
| journal = Pediatric neurology | volume = 36| issue = 5| pages = 281–292
| date = May 2007
| pmid = 17509459
| doi = 10.1016/j.pediatrneurol.2007.02.008
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940242/
}}</ref>
<ref name="keystoketosisbegin">{{citation
| last1 = Keys to Ketosis
| title = The Beginner's Guide to Exogenous Ketones
| date = 11 Jan 2016
| url = http://keystoketosis.com/the-beginners-guide-to-exogenous-ketones/
}}</ref>
<ref name="Krikorian2012">{{Citation
| last1 = Krikorian | first1 = Robert
| last2 = Shidler | first2 = Marcelle D
| last3 = Dangelo | first3 = Krista
| last4 = Couch | first4 = Sarah C
| last5 = Benoit | first5 = Stephen C
| last6 = Clegg | first6 = Deborah J
| title = Dietary ketosis enhances memory in mild cognitive impairment
| journal = Neurobiology of Aging | volume = 33| issue = 2| pages = 425–19-27
| date = Feb 2012
| pmid = 21130529
| doi = 10.1016/j.neurobiolaging.2010.10.006
| url = https://www.ncbi.nlm.nih.gov/pubmed/21130529/
}}</ref>
<ref name="Myhill2009">{{citation
| last1 = Myhill | first1 = S | authorlink1 = Sarah Myhill
| last2 = Booth | first2 = NE | authorlink2 = Norman Booth
| last3 = McLaren-Howard | first3 = J | authorlink3 = John McLaren-Howard
| title = Chronic fatigue syndrome and mitochondrial dysfunction
| journal = Int J Clin Exp Med | volume = 2| issue = 1| pages = 1–16
| date = 15 Jan 2009
| pmid = 19436827
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/
}}</ref>
<ref name="Myhillketo1">{{citation
| last1 = Segura | first1 = Gabriela
| title = Ketogenic diet - a connection between mitochondria and diet
| date = 9 Aug 2013
| url = http://www.drmyhill.co.uk/wiki/Ketogenic_diet_-_a_connection_between_mitochondria_and_diet
}}</ref>
<ref name="Myhillketo2">{{citation
| last1 = Myhill | first1 = Sarah | authorlink1 = Sarah Myhill
| title = Ketogenic diet - the practical details
| url = http://www.doctormyhill.co.uk/wiki/Ketogenic_diet_-_the_practical_details
}}</ref>
<ref name="RegerMA2004">{{citation
| last1 = Reger | first1 = Mark A
| last2 = Henderson | first2 = Samuel T
| last3 = Hale | first3 = Cathy
| last4 = Cholerton | first4 = Brenna
| last5 = Baker | first5 = Laura D
| last6 = Watson | first6 = G S
| last7 = Hyde | first7 = Karen
| last8 = Chapman | first8 = Darla
| last9 = Craft | first9 = Suzanne
| display-authors = 3
| title = Effects of beta-hydroxybutyrate on cognition in memory-impaired adults
| journal = Neurobiology of Aging | volume = 25| issue = 3| pages = 311–314
| date = Mar 2004
| doi = 10.1016/S0197-4580(03)00087-3
| pmid = 15123336
}}</ref>
<ref name="RhoJM2007">{{Citation
| last1 = Rho | first1 = Jong M
| last2 = Rogawski | first2 = Michael A
| title = The Ketogenic Diet: Stoking the Powerhouse of the Cell
| journal = Epilepsy Currents | volume = 7| issue = 2| pages = 58–60
| date = Mar 2007
| doi = 10.1111/j.1535-7511.2007.00170.x
| pmid = 17505556
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867088/
}}</ref>
<ref name="WikiMCT">{{citation
| title = Wikipedia - Ketogenic diet, MCT oil
| url = https://en.wikipedia.org/wiki/Ketogenic_diet#MCT_oil
}}</ref>
<ref name="ZhangX2016">{{citation
| last1 = Zhang | first1 = Xiaoyu
| last2 = Qin | first2 = Juliang
| last3 = Zhao | first3 = Yihan
| last4 = Shi | first4 = Jueping
| last5 = Lan | first5 = Rong
| last6 = Gan | first6 = Yunqiu
| last7 = Ren | first7 = Hua
| last8 = Zhu | first8 = Bing
| last9 = Qian | first9 = Min
| last10 = Du | first10 = Bing
| title = Long-term ketogenic diet contributes to glycemic control but promotes lipid accumulation and hepatic steatosis in type 2 diabetic mice
| journal = Nutrition Research | volume = 36| issue = 4| pages = 349–358
| date = 1 Apr 2016
| doi = 10.1016/j.nutres.2015.12.002
| url = http://www.nrjournal.com/article/S0271531715003012/abstract
}}</ref>
</references>

[[Category:Potential treatments]]
[[Category:Diets]]

Courtney Craig

2019-04-13T11:43:35Z

Drcraig:/* Talks and interviews */

[[File:Courtney Craig.png|200px|thumb|right|Courtney_Craig.png]]
Doctor '''Courtney Craig''' is a Nutritionist and Chiropractor who has a special interest in treating patients with [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]] (ME/CFS) and [[fibromyalgia]] (FM). She became ill with [[ME/CFS]] in 1998, at the age of 16, but greatly improved in 2010 utilizing both conventional and integrative medicine.<ref>http://www.healthrising.org/blog/2014/05/10/closer-look-natural-killer-cells-chronic-fatigue-syndrome-three-natural-ways-boost/</ref> She is featured in the 2016 documentary film, [[Unrest]], which is about [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]].<ref>http://www.drcourtneycraig.com/about/</ref>

Dr. Craig hosted a podcast called [[Spoonie Radio]] for two years in which she interviewed doctors, researchers, and patients within the ME/CFS community.

==Education==
*Undergraduate study in exercise science at the College of William and Mary, Virginia
*Graduated with honors from the University of Bridgeport’s Human Nutrition Institute Master's program.
*Clinical training at Palmer College of Chiropractic, Florida
*Visiting Scientist at Cornell’s Center for Enervating Neuroimmune Disease
*Master Student in Nutrition and Biomedicine at Technical University Munich in Germany.
*Member of the American Nutrition Association, the American College of Nutrition, and the Institute for Functional Medicine.

==Notable studies==
She published a paper hypothesising that [[ME/CFS]] could be treated by improving mitochondrial function using [[fasting]], caloric restriction and a [[ketogenic diet]].<ref name="craig2015" />

==Clinic location==
She has relocated to Germany and consults with patients via phone or Skype.

==Talks and interviews==
Personal interview on the Intelligent Medicine Podcast: [https://drhoffman.com/podcast/chronic-fatigue-syndrome-part-1/ Part I] and [https://drhoffman.com/podcast/chronic-fatigue-syndrome-part-2/ Part II]

==Books==
*Oct 23, 2014, ebook/digital: ''[[All My Test Results are Normal: A Smart Guide to Testing for Chronic Fatigue Syndrome]]''

==Online presence==
*[https://www.ncbi.nlm.nih.gov/pubmed/?term=Craig+Courtney%5BAuthor%5D PubMed - Courtney Craig]
*[https://twitter.com/courtney_37?lang=en-gb Twitter]
*[https://www.facebook.com/drcourtneycraig Facebook]
*[http://www.drcourtneycraig.com/ Website]
*[https://www.youtube.com/channel/UCWmVAjHnwL9Lu8tSJHV2NcA YouTube]
*[http://spoonieradio.libsyn.com/webpage Spoonie Radio website]

==Learn more==
*Wikipedia
*Institution

==See also==
*[[Ketogenic diet]]
*[[Mitochondria]]

==References==
<references>
<ref name="craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}
</ref>
</references>

[[Category:Researchers]]
[[Category:USA researchers]]
[[Category:Clinicians]]
[[Category:American clinicians]]
[[Category:German clinicians]]
[[Category:Blogs]]
[[Category:People with ME, CFS, and/or FMS]]
[[Category:Authors]]

Courtney Craig

2019-04-13T11:40:34Z

Drcraig:Updating my profile

[[File:Courtney Craig.png|200px|thumb|right|Courtney_Craig.png]]
Doctor '''Courtney Craig''' is a Nutritionist and Chiropractor who has a special interest in treating patients with [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]] (ME/CFS) and [[fibromyalgia]] (FM). She became ill with [[ME/CFS]] in 1998, at the age of 16, but greatly improved in 2010 utilizing both conventional and integrative medicine.<ref>http://www.healthrising.org/blog/2014/05/10/closer-look-natural-killer-cells-chronic-fatigue-syndrome-three-natural-ways-boost/</ref> She is featured in the 2016 documentary film, [[Unrest]], which is about [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]].<ref>http://www.drcourtneycraig.com/about/</ref>

Dr. Craig hosted a podcast called [[Spoonie Radio]] for two years in which she interviewed doctors, researchers, and patients within the ME/CFS community.

==Education==
*Undergraduate study in exercise science at the College of William and Mary, Virginia
*Graduated with honors from the University of Bridgeport’s Human Nutrition Institute Master's program.
*Clinical training at Palmer College of Chiropractic, Florida
*Visiting Scientist at Cornell’s Center for Enervating Neuroimmune Disease
*Master Student in Nutrition and Biomedicine at Technical University Munich in Germany.
*Member of the American Nutrition Association, the American College of Nutrition, and the Institute for Functional Medicine.

==Notable studies==
She published a paper hypothesising that [[ME/CFS]] could be treated by improving mitochondrial function using [[fasting]], caloric restriction and a [[ketogenic diet]].<ref name="craig2015" />

==Clinic location==
She has relocated to Germany and consults with patients via phone or Skype.

==Talks and interviews==

==Books==
*Oct 23, 2014, ebook/digital: ''[[All My Test Results are Normal: A Smart Guide to Testing for Chronic Fatigue Syndrome]]''

==Online presence==
*[https://www.ncbi.nlm.nih.gov/pubmed/?term=Craig+Courtney%5BAuthor%5D PubMed - Courtney Craig]
*[https://twitter.com/courtney_37?lang=en-gb Twitter]
*[https://www.facebook.com/drcourtneycraig Facebook]
*[http://www.drcourtneycraig.com/ Website]
*[https://www.youtube.com/channel/UCWmVAjHnwL9Lu8tSJHV2NcA YouTube]
*[http://spoonieradio.libsyn.com/webpage Spoonie Radio website]

==Learn more==
*Wikipedia
*Institution

==See also==
*[[Ketogenic diet]]
*[[Mitochondria]]

==References==
<references>
<ref name="craig2015">{{Citation
| last1 = Craig | first1 = Courtney | authorlink1 = Courtney Craig
| title = Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets
| journal = Medical Hypotheses | volume = 85 | issue = 5 | page = 690-693
| date = November 2015
| pmid = 26315446
| doi = 10.1016/j.mehy.2015.08.013
}}
</ref>
</references>

[[Category:Researchers]]
[[Category:USA researchers]]
[[Category:Clinicians]]
[[Category:American clinicians]]
[[Category:German clinicians]]
[[Category:Blogs]]
[[Category:People with ME, CFS, and/or FMS]]
[[Category:Authors]]

Creatine

2019-04-13T11:33:36Z

Drcraig:additional info about creatine as well as a study of supplementation for Fibromyalgia

{{stub}}
'''Creatine''' is a nitrogenous [[organic acid]] that helps supply [[energy]] to all [[cell]]s in the body, especially [[muscle]]. It increases the formation of [[ATP]]. It is produced from the [[amino acid]]s [[glycine]] and [[arginine]]. Creatine can also be synthesized in the brain and can cross the blood-brain barrier via specific creatine transporters. In the brain, it plays a major role in ATP/ADP balance by providing a steady phosphorous group to ADP to replenish ATP. In addition to an energy substrate, creatine can be released from neurons and function as a neurotransmitter.<ref>{{Cite journal|last=Riesberg|first=Lisa A.|last2=Weed|first2=Stephanie A.|last3=McDonald|first3=Thomas L.|last4=Eckerson|first4=Joan M.|last5=Drescher|first5=Kristen M.|date=2016-8|title=Beyond Muscles: The Untapped Potential of Creatine|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4915971/|journal=International immunopharmacology|volume=37|pages=31–42|doi=10.1016/j.intimp.2015.12.034|issn=1567-5769|pmc=PMCPMC4915971|pmid=26778152}}</ref>

Creatine is metabolized to creatinine and excreted in the urine. Raised urinary creatine excretion was found in two, separate [[outbreaks]] of [[myalgic encephalomyelitis]] in New York State in [[1950 New York State outbreak|1950]] and in [[1961 New York State outbreak|1961]].<ref name=":0">{{Cite journal|last=Parish|first=JG|date=1978|title=Early outbreaks of 'epidemic neuromyasthenia'|url=https://www.ncbi.nlm.nih.gov/pubmed/370810|journal=Postgraduate Medical Journal|volume=54|pages=711-7|via=}}</ref> Creatine was high during periods of relapse and normal during periods of recovery.<ref>{{Cite journal|url=https://www.ncbi.nlm.nih.gov/pubmed/14100144|title=Epidemic Neuromyasthenia Outbreak in a Convent in New York State|last=Albrecht|first=Robert|date=March 21, 1964|journal=Journal of the American Medical Association|volume=187|pages=904-907|via=}}</ref>

A 16-week double-blind, randomized control study in [[fibromyalgia]] patients showed creatine supplementation increased intramuscular phosphorylcreatine content by ~80% and improved lower- and upper-body muscle function, with some additional positive effects on general symptoms.<ref>{{Cite journal|last=Alves|first=Christiano R. R.|last2=Santiago|first2=Bianca M.|last3=Lima|first3=Fernanda R.|last4=Otaduy|first4=Maria C. G.|last5=Calich|first5=Ana Luisa|last6=Tritto|first6=Aline C. C.|last7=de Sá Pinto|first7=Ana Lúcia|last8=Roschel|first8=Hamilton|last9=Leite|first9=Cláudia C.|date=2013-9|title=Creatine supplementation in fibromyalgia: a randomized, double-blind, placebo-controlled trial|url=https://www.ncbi.nlm.nih.gov/pubmed/23554283|journal=Arthritis Care & Research|volume=65|issue=9|pages=1449–1459|doi=10.1002/acr.22020|issn=2151-4658|pmid=23554283}}</ref>

'''Supplement Safety'''

The International Society of Sport Nutrition has stated that creatine supplementation up to 30 g/day for 5 years is safe and well-tolerated in healthy individuals and in a number of patient populations ranging from infants to the elderly.<ref>{{Cite journal|last=Kreider|first=Richard B.|last2=Kalman|first2=Douglas S.|last3=Antonio|first3=Jose|last4=Ziegenfuss|first4=Tim N.|last5=Wildman|first5=Robert|last6=Collins|first6=Rick|last7=Candow|first7=Darren G.|last8=Kleiner|first8=Susan M.|last9=Almada|first9=Anthony L.|date=2017|title=International Society of Sports Nutrition position stand: safety and efficacy of creatine supplementation in exercise, sport, and medicine|url=https://www.ncbi.nlm.nih.gov/pubmed/28615996|journal=Journal of the International Society of Sports Nutrition|volume=14|pages=18|doi=10.1186/s12970-017-0173-z|issn=1550-2783|pmc=PMCPMC5469049|pmid=28615996}}</ref>

[[Category:Biochemistry and cell biology]]
[[Category:Amino acids]]
[[Category:Potential treatments]]
[[Category:Supplements]]

== References ==
<references />
[[Category:Nutrients]]

Creatine kinase

2019-04-13T11:18:44Z

Drcraig:added 2 studies regarding creatine kinase

Creatine kinase (CK) is an enzyme that uses [[ATP]] to convert [[creatine]] into [[phosphocreatine]] and [[adenosine diphosphate]]. It is an enzyme found in the inner mitochondrial membrane. Creatine kinase is a [[biomarker|marker]] of tissue damage. There are 3 isoenzymes of creatine kinase: skeletal muscle CK-MM, myocardium CK-MB, & brain and smooth muscle CK-BB. Elevated levels are found in patients suffering from [[heart attack]], severe muscle breakdown, and [[muscular dystrophy]].

A study found increased levels of creatine kinase in the [[Muscle biopsy|muscle biopses]] of patients with [[postviral fatigue syndrome]].<ref>{{Cite journal|last=Archard|first=L. C.|last2=Bowles|first2=N. E.|last3=Behan|first3=P. O.|last4=Bell|first4=E. J.|last5=Doyle|first5=D.|date=1988|title=Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase|url=http://www.ncbi.nlm.nih.gov/pubmed/3404526|journal=Journal of the Royal Society of Medicine|volume=81|issue=6|pages=326–329|doi=10.1177/014107688808100608|issn=0141-0768|pmc=|pmid=3404526|via=}}</ref> A study measured plasma creatine kinase as a surrogate measure of a lowered oxidative phosphorylation in skeletal muscle of ME/CFS patients (n=15) and healthy controls. They found low plasma creatine kinase levels before and 24 h after an exercise challenge in ME/CFS patients and healthy controls. This suggested muscle mitochondria were normal, since 24 h after strenuous exercise CK did not leak to the blood, as is the case in patients with defective oxidative phosphorylation.<ref>{{Cite journal|last=Vermeulen|first=Ruud CW|last2=Kurk|first2=Ruud M|last3=Visser|first3=Frans C|last4=Sluiter|first4=Wim|last5=Scholte|first5=Hans R|date=2010-12|title=Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity|url=https://translational-medicine.biomedcentral.com/articles/10.1186/1479-5876-8-93|journal=Journal of Translational Medicine|language=en|volume=8|issue=1|doi=10.1186/1479-5876-8-93|issn=1479-5876|pmc=PMC2964609|pmid=20937116}}</ref> A 2019 study found markedly reduced serum CK concentrations in severe ME/CFS (n=56) but not in less severe cases.<ref>{{Cite journal|last=Nacul|last2=de Barros|last3=Kingdon|last4=Cliff|last5=Clark|last6=Mudie|last7=Dockrell|last8=Lacerda|date=2019-04-10|title=Evidence of Clinical Pathology Abnormalities in People with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) from an Analytic Cross-Sectional Study|url=https://www.mdpi.com/2075-4418/9/2/41|journal=Diagnostics|language=en|volume=9|issue=2|pages=41|doi=10.3390/diagnostics9020041|issn=2075-4418}}</ref>

==References==
<references />
[[Category:Biochemistry and cell biology]]
[[Category:Enzymes]]

Creatine kinase

2019-04-13T10:55:21Z

Drcraig:/* References */

Creatine kinase is an enzyme that uses [[ATP]] to convert [[creatine]] into [[phosphocreatine]] and [[adenosine diphosphate]].

A study found increased levels of creatine kinase in the [[Muscle biopsy|muscle biopses]] of patients with [[postviral fatigue syndrome]].<ref>{{Cite journal|last=Archard|first=L. C.|last2=Bowles|first2=N. E.|last3=Behan|first3=P. O.|last4=Bell|first4=E. J.|last5=Doyle|first5=D.|date=1988|title=Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase|url=http://www.ncbi.nlm.nih.gov/pubmed/3404526|journal=Journal of the Royal Society of Medicine|volume=81|issue=6|pages=326–329|doi=10.1177/014107688808100608|issn=0141-0768|pmc=|pmid=3404526|via=}}</ref>

Creatine kinase is a [[biomarker|marker]] of tissue damage. Elevated levels are found in patients suffering from [[heart attack]], severe muscle breakdown, and [[muscular dystrophy]].

==References==
<references />2. Nacul, L. et al. (2019). "Evidence of Clinical Pathology Abnormalities in People with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) from an Analytic Cross-Sectional Study." Diagnostics. '''9''', 41; doi:10.3390/diagnostics9020041

3. Vermeulen, R. C., Kurk, R. M., Visser, F. C., Sluiter, W., & Scholte, H. R. (2010). Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity. ''Journal of translational medicine'', ''8'', 93. doi:10.1186/1479-5876-8-93
[[Category:Biochemistry and cell biology]]
[[Category:Enzymes]]

Creatine kinase

2019-04-13T10:54:44Z

Drcraig:Addition of 2 studies of creatine kinase levels in ME/CFS patients

Creatine kinase is an enzyme that uses [[ATP]] to convert [[creatine]] into [[phosphocreatine]] and [[adenosine diphosphate]].

A study found increased levels of creatine kinase in the [[Muscle biopsy|muscle biopses]] of patients with [[postviral fatigue syndrome]].<ref>{{Cite journal|last=Archard|first=L. C.|last2=Bowles|first2=N. E.|last3=Behan|first3=P. O.|last4=Bell|first4=E. J.|last5=Doyle|first5=D.|date=1988|title=Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase|url=http://www.ncbi.nlm.nih.gov/pubmed/3404526|journal=Journal of the Royal Society of Medicine|volume=81|issue=6|pages=326–329|doi=10.1177/014107688808100608|issn=0141-0768|pmc=|pmid=3404526|via=}}</ref>

Creatine kinase is a [[biomarker|marker]] of tissue damage. Elevated levels are found in patients suffering from [[heart attack]], severe muscle breakdown, and [[muscular dystrophy]].

==References==
<references />Nacul, L. et al. (2019). "Evidence of Clinical Pathology Abnormalities in People with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) from an Analytic Cross-Sectional Study." Diagnostics. '''9''', 41; doi:10.3390/diagnostics9020041

Vermeulen, R. C., Kurk, R. M., Visser, F. C., Sluiter, W., & Scholte, H. R. (2010). Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity. ''Journal of translational medicine'', ''8'', 93. doi:10.1186/1479-5876-8-93
[[Category:Biochemistry and cell biology]]
[[Category:Enzymes]]