Mitochondrion: Difference between revisions

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==Biogenesis==
==Biogenesis==


Mitochondria biogenesis (the creation of new mitochondria) can be increased via [[hormesis]], the exposure of the body to short-term stressors. Healthy stressor include [[exercise]], [[fasting]], [[cryotherapy|cold]], and [[thermotherapy|heat]]. [[Resveratrol]] can also increase mitochondrial biogenesis.
Mitochondria biogenesis (the creation of new mitochondria) can be increased via [[hormesis]], the exposure of the body to short-term stressors. Healthy stressors include [[exercise]], [[fasting]], [[cryotherapy|cold]], [[thermotherapy|heat]] and light. [[Resveratrol]] can also increase mitochondrial biogenesis.


==Immunity==
==Immunity==
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Infection with pathogens, including viruses, bacteria, and parasites, can all induce changes in mitochondrial function and energy metabolism.
Infection with pathogens, including viruses, bacteria, and parasites, can all induce changes in mitochondrial function and energy metabolism.


Viruses can induce or inhibit mitochondrial processes in order to replicate. "Viruses like [[Herpes simplex virus]] 1 deplete the host mitochondrial DNA and some, like human immunodeficiency virus and Hepatitis C Virus, hijack the host mitochondrial proteins to function fully inside the host cell."<ref name="Anand2013"/><ref name="Siu2016"/>  [[Hepatitis C]] has also been shown to "fragment host mitochondria".<ref name="Siu2016"/>
Viruses can induce or inhibit mitochondrial processes in order to replicate. "Viruses like [[Herpes simplex virus]] 1 deplete the host mitochondrial DNA and some, like human immunodeficiency virus and Hepatitis C Virus, hijack the host mitochondrial proteins to function fully inside the host cell."<ref name="Anand2013" /><ref name="Siu2016" />  [[Hepatitis C]] has also been shown to "fragment host mitochondria".<ref name="Siu2016" />


Parasites such as ''[[Toxoplasma gondii]]'' have also been shown to modulate host energy metabolism and dysregulate mitochondrial function,<ref name="Saric2009"/>, as have bacteria <ref name="Rudel2010"/> such as ''[[E. coli]]'', which has been shown to modulate mitochondrial receptor function.<ref name="Nagai2005"/>
Parasites such as ''[[Toxoplasma gondii]]'' have also been shown to modulate host energy metabolism and dysregulate mitochondrial function,<ref name="Saric2009" />, as have bacteria <ref name="Rudel2010" /> such as ''[[E. coli]]'', which has been shown to modulate mitochondrial receptor function.<ref name="Nagai2005" />


Mitochondrial disease has a high prevalence of fatigue and debilitation.<ref name="Gorman2015"/>
Mitochondrial disease has a high prevalence of fatigue and debilitation.<ref name="Gorman2015" />


=== Chronic fatigue syndrome ===
=== Chronic fatigue syndrome ===


There is evidence of mitochondrial dysfunction in [[Chronic Fatigue Syndrome]] patients. Muscle biopsies have shown evidence of mitochondrial degeneration <ref name="Behan1991"/>, deletions of mitochondrial DNA <ref name="Vecchiet1996"/><ref name="ZhangC1995"/>, the reduction of mitochondrial activity <ref name="Vecchiet1996"/>, and [[Sarah Myhill]] found measurable mitochondrial dysfunction correlating with severity of illness.<ref name="Booth2012"/><ref name="Myhill2009"/> Myhill also produced improvement by targeting those dysfunctions.<ref name="Myhill2013"/>  Mitochondrial DNA variants correlate with symptoms, symptom clusters & symptom severity.<ref name="BillingRoss2016"/>
There is evidence of mitochondrial dysfunction in [[Chronic Fatigue Syndrome]] patients. Muscle biopsies have shown evidence of mitochondrial degeneration <ref name="Behan1991" />, deletions of mitochondrial DNA <ref name="Vecchiet1996" /><ref name="ZhangC1995" />, the reduction of mitochondrial activity <ref name="Vecchiet1996" />, and [[Sarah Myhill]] found measurable mitochondrial dysfunction correlating with severity of illness.<ref name="Booth2012" /><ref name="Myhill2009" /> Myhill also produced improvement by targeting those dysfunctions.<ref name="Myhill2013" />  Mitochondrial DNA variants correlate with symptoms, symptom clusters & symptom severity.<ref name="BillingRoss2016" />


[[Mitochondrial disorders]] can be mistaken for [[Chronic Fatigue Syndrome]].<ref name="Galán2015"/>
[[Mitochondrial disorders]] can be mistaken for [[Chronic Fatigue Syndrome]].<ref name="Galán2015" />


There is evidence of genetic risk factors for mitochondrial dysfunction in related diseases such as complex regional pain syndrome, postural orthostatic tachycardia syndrome ([[POTS]]), and [[dysautonomia]].<ref name="Boles2015"/>
There is evidence of genetic risk factors for mitochondrial dysfunction in related diseases such as complex regional pain syndrome, postural orthostatic tachycardia syndrome ([[POTS]]), and [[dysautonomia]].<ref name="Boles2015" />


==Potential treatment==
==Potential treatment==
[[Garth Nicolson]] has proposed that mitochondrial [[lipid replacement therapy]] can ameliorate mitochondrial related fatigue using a proprietary blend of phospholipids called [[NT Factor]].
[[Garth Nicolson]] has proposed that mitochondrial [[lipid replacement therapy]] can ameliorate mitochondrial related fatigue using a proprietary blend of phospholipids called [[NT Factor]].


[[Courtney Craig]] has proposed treatment of mitochondrial damage in [[ME/CFS]] patients using [[fasting]], [[caloric restriction]] and a [[ketogenic diet]].<ref name="Craig2015"/>
[[Courtney Craig]] has proposed treatment of mitochondrial damage in [[ME/CFS]] patients using [[fasting]], [[caloric restriction]] and a [[ketogenic diet]].<ref name="Craig2015" />


==Notable studies==
==Notable studies==
*2016, [https://www.ncbi.nlm.nih.gov/pubmed/27389587 Exercise-induced mitochondrial dysfunction: a myth or reality?]
*2016, [https://www.ncbi.nlm.nih.gov/pubmed/27389587 Exercise-induced mitochondrial dysfunction: a myth or reality?]
*2016, [https://www.ncbi.nlm.nih.gov/pubmed/25788480 Pharmacological NAD-Boosting Strategies Improve Mitochondrial Homeostasis in Human Complex I-Mutant Fibroblasts]
*2016, [https://www.ncbi.nlm.nih.gov/pubmed/25788480 Pharmacological NAD-Boosting Strategies Improve Mitochondrial Homeostasis in Human Complex I-Mutant Fibroblasts]
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==Videos==
==Videos==
*[https://www.youtube.com/watch?v=uSlEmBeHlgg "Mitochondria: The Powerhouse of the Cell" by Bozeman Science]
*[https://www.youtube.com/watch?v=uSlEmBeHlgg "Mitochondria: The Powerhouse of the Cell" by Bozeman Science]


==Learn more==
==Learn more==
*[https://en.wikipedia.org/wiki/Mitochondrion Wikipedia - Mitochondrion]
*[https://en.wikipedia.org/wiki/Mitochondrion Wikipedia - Mitochondrion]
*2016, [http://www.labroots.com/trending/immunology/3536/immune-system-conserves-energy-altering-metabolism Immune System Conserves Energy By Altering Metabolism]
*2016, [http://www.labroots.com/trending/immunology/3536/immune-system-conserves-energy-altering-metabolism Immune System Conserves Energy By Altering Metabolism]
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==See also==
==See also==
*[[Cellular respiration]]
*[[Cellular respiration]]
*[[Sarah Myhill]]
*[[Sarah Myhill]]
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== Unused Citations ==
== Unused Citations ==


Armstrong2014 <ref name="Armstrong2014"/>
Armstrong2014 <ref name="Armstrong2014" />
Vermeulen2010 <ref name="Vermeulen2010"/>
Vermeulen2010 <ref name="Vermeulen2010" />
Maes2009 <ref name="Maes2009"/>
Maes2009 <ref name="Maes2009" />
Morris2013 <ref name="Morris2013"/>.
Morris2013 <ref name="Morris2013" />.
Morris2014 <ref name="Morris2014"/>
Morris2014 <ref name="Morris2014" />
Meeus2013 <ref name="Meeus2013"/>
Meeus2013 <ref name="Meeus2013" />


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| url    = http://www.hindawi.com/journals/av/2013/738794/abs/
| url    = http://www.hindawi.com/journals/av/2013/738794/abs/
}}</ref>
}}</ref>
<ref name="Behan1991">{{citation
<ref name="Behan1991">{{citation
| last1  = Behan            | first1 = WMH                | authorlink1 = Wilhelmina Behan
| last1  = Behan            | first1 = WMH                | authorlink1 = Wilhelmina Behan
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| url    = http://www.ncbi.nlm.nih.gov/pubmed/1792865/  
| url    = http://www.ncbi.nlm.nih.gov/pubmed/1792865/  
}}</ref>
}}</ref>
<ref name="BillingRoss2016">{{citation
<ref name="BillingRoss2016">{{citation
| last1  = Billing-Ross    | first1 = Paul              | authorlink1 = Paul Billing-Ross
| last1  = Billing-Ross    | first1 = Paul              | authorlink1 = Paul Billing-Ross
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| lay-url = http://hansonlab.org/research/cfs_me/mitochondria/
| lay-url = http://hansonlab.org/research/cfs_me/mitochondria/
}}</ref>
}}</ref>
<ref name="Boles2015">{{citation
<ref name="Boles2015">{{citation
| last1  = Boles            | first1 = RG                | authorlink1 = Richard Boles
| last1  = Boles            | first1 = RG                | authorlink1 = Richard Boles
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| url    = http://www.sciencedirect.com/science/article/pii/S1567724915000483
| url    = http://www.sciencedirect.com/science/article/pii/S1567724915000483
}}</ref>
}}</ref>
<ref name="Booth2012">{{citation
<ref name="Booth2012">{{citation
| last1  = Booth            | first1 = NE                | authorlink1 = Norman Booth
| last1  = Booth            | first1 = NE                | authorlink1 = Norman Booth
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| url    = http://www.ncbi.nlm.nih.gov/pubmed/22837795
| url    = http://www.ncbi.nlm.nih.gov/pubmed/22837795
}}</ref>
}}</ref>
<ref name="Craig2015">{{citation
<ref name="Craig2015">{{citation
| last1  = Craig            | first1 = Courtney          | authorlink1 = Courtney Craig
| last1  = Craig            | first1 = Courtney          | authorlink1 = Courtney Craig
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| url    = http://www.medical-hypotheses.com/article/S0306-9877(15)00318-7/abstract
| url    = http://www.medical-hypotheses.com/article/S0306-9877(15)00318-7/abstract
}}</ref>
}}</ref>
<ref name="Galán2015">{{citation
<ref name="Galán2015">{{citation
| last1  = Galán            | first1 = Fernando          | authorlink1 =  
| last1  = Galán            | first1 = Fernando          | authorlink1 =  
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| url    = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4748504/
| url    = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4748504/
}}</ref>
}}</ref>
<ref name="Gorman2015">{{citation
<ref name="Gorman2015">{{citation
| last1  = Gorman          | first1 = Gráinne S          | authorlink1 = Gráinne Gorman
| last1  = Gorman          | first1 = Gráinne S          | authorlink1 = Gráinne Gorman
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| url    = http://www.nmd-journal.com/article/S0960-8966(15)00087-5/abstract
| url    = http://www.nmd-journal.com/article/S0960-8966(15)00087-5/abstract
}}</ref>
}}</ref>
<ref name="Myhill2009">{{citation
<ref name="Myhill2009">{{citation
| last1  = Myhill          | first1 = S                  | authorlink1 = Sarah Myhill
| last1  = Myhill          | first1 = S                  | authorlink1 = Sarah Myhill
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| url    = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/
| url    = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/
}}</ref>
}}</ref>
<ref name="Vecchiet1996">{{citation
<ref name="Vecchiet1996">{{citation
| last1  = Vecchiet              | first1 = L
| last1  = Vecchiet              | first1 = L
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| url    = http://www.ncbi.nlm.nih.gov/pubmed/8859904
| url    = http://www.ncbi.nlm.nih.gov/pubmed/8859904
}}</ref>
}}</ref>
<ref name="ZhangC1995">{{citation
<ref name="ZhangC1995">{{citation
| last1  = Zhang                  | first1 = C
| last1  = Zhang                  | first1 = C
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| url    = http://www.ncbi.nlm.nih.gov/pubmed/7633428
| url    = http://www.ncbi.nlm.nih.gov/pubmed/7633428
}}</ref>
}}</ref>
<ref name="Saric2009">{{citation
<ref name="Saric2009">{{citation
| last1  = Saric            | first1 = J
| last1  = Saric            | first1 = J
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| url    = http://http://doi.org/10.1021/pr901019z
| url    = http://http://doi.org/10.1021/pr901019z
}}</ref>
}}</ref>
 
<ref name="Armstrong2014">{{Citation
<ref name="Armstrong2014">
{{Citation
| last1  =  Armstrong            | first1 = CW            | authorlink1 = Christopher Armstrong
| last1  =  Armstrong            | first1 = CW            | authorlink1 = Christopher Armstrong
| last2  =  McGregor            | first2 = NR            | authorlink2 = Neil McGregor
| last2  =  McGregor            | first2 = NR            | authorlink2 = Neil McGregor
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}}
}}
</ref>
</ref>
 
<ref name="Myhill2013">{{Citation
<ref name="Myhill2013">
{{Citation
| last1  = Myhill                | first1 = Sarah            | authorlink1 = Sarah Myhill
| last1  = Myhill                | first1 = Sarah            | authorlink1 = Sarah Myhill
| last2  = Booth                  | first2 = NE              | authorlink2 = NE Booth
| last2  = Booth                  | first2 = NE              | authorlink2 = NE Booth
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}}
}}
</ref>
</ref>
 
<ref name="Vermeulen2010">{{Citation
<ref name="Vermeulen2010">
{{Citation
| last1  = Vermeulen            | first1 = RC                | authorlink1 = RC Vermeulen
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| last2  = Kirk                  | first2 = RM                | authorlink2 = RM Kirk
| last2  = Kirk                  | first2 = RM                | authorlink2 = RM Kirk
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}}
}}
</ref>
</ref>
 
<ref name="Maes2009">{{Citation
<ref name="Maes2009">
{{Citation
| last1  = Maes                  | first1 = M                | authorlink1 = Michael Maes
| last1  = Maes                  | first1 = M                | authorlink1 = Michael Maes
| last2  = Mihaylova            | first2 = I                | authorlink2 = I Mihaylova
| last2  = Mihaylova            | first2 = I                | authorlink2 = I Mihaylova
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}}
}}
</ref>
</ref>
 
<ref name="Morris2013">{{Citation
<ref name="Morris2013">
{{Citation
| last1  = Morris                | first1 = G                  | authorlink1 = Gerwyn Morris
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| last2  = Maes                  | first2 = M                  | authorlink2 = Michael Maes
| last2  = Maes                  | first2 = M                  | authorlink2 = Michael Maes
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<ref name="Morris2014">{{Citation
<ref name="Morris2014">
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| last2  = Maes                  | first2 = Michael                | authorlink2 = Michael Maes
| last2  = Maes                  | first2 = Michael                | authorlink2 = Michael Maes
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<ref name="Rudel2010">{{Citation
<ref name="Rudel2010">
{{Citation
| last1  = Rudel T                | first1 = T                  | authorlink1 = Rudel
| last1  = Rudel T                | first1 = T                  | authorlink1 = Rudel
| last2  = Kepp O                  | first2 = O                  | authorlink2 = Kepp
| last2  = Kepp O                  | first2 = O                  | authorlink2 = Kepp
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}}
</ref>
</ref>
 
<ref name="Siu2016">{{Citation
<ref name="Siu2016">
{{Citation
| last1  = Siu                | first1 = GK                | authorlink1 = GK Siu
| last1  = Siu                | first1 = GK                | authorlink1 = GK Siu
| last2  = Zhou              | first2 = F                | authorlink2 = F Zhou
| last2  = Zhou              | first2 = F                | authorlink2 = F Zhou
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}}
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</ref>
 
<ref name="Nagai2005">{{Citation
<ref name="Nagai2005">
{{Citation
| last1  =  Nagai              | first1 = T                  | authorlink1 = T Nagai
| last1  =  Nagai              | first1 = T                  | authorlink1 = T Nagai
| last2  =  Abe                | first2 = A                  | authorlink2 = A Abe
| last2  =  Abe                | first2 = A                  | authorlink2 = A Abe
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}}
}}
</ref>
</ref>
 
<ref name="Meeus2013">{{Citation
<ref name="Meeus2013">
{{Citation
| last1  = Meeus                | first1 = M                  | authorlink1 =  
| last1  = Meeus                | first1 = M                  | authorlink1 =  
| last2  = Nijs                  | first2 = J                  | authorlink2 = Jo Nijs
| last2  = Nijs                  | first2 = J                  | authorlink2 = Jo Nijs
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</references>
</references>


[[Category:Biochemistry and cell biology]][[Category:Organelles]][[Category:Energy System]]
[[Category:Biochemistry and cell biology]]
[[Category:Organelles]]
[[Category:Energy System]]

Revision as of 04:37, April 20, 2018

A single cellular mitochondrion

Mitochondria are organelles found in all cells that have a nucleus. In the human body, that would be all cells except red blood cells. They generate most of a cell's energy by manufacturing adenosine triphosphate, ATP. Mitochondria have their own independent genome called mitochondrial DNA.

Biogenesis[edit | edit source]

Mitochondria biogenesis (the creation of new mitochondria) can be increased via hormesis, the exposure of the body to short-term stressors. Healthy stressors include exercise, fasting, cold, heat and light. Resveratrol can also increase mitochondrial biogenesis.

Immunity[edit | edit source]

Mitochondria play crucial role in innate immunity, namely through their induction of interferon production and apoptosis through mitochondrial antiviral signaling protein (MAVS). Many viruses evade host immunity by cleaving or downregulating MAVS.

In human disease[edit | edit source]

Infection with pathogens, including viruses, bacteria, and parasites, can all induce changes in mitochondrial function and energy metabolism.

Viruses can induce or inhibit mitochondrial processes in order to replicate. "Viruses like Herpes simplex virus 1 deplete the host mitochondrial DNA and some, like human immunodeficiency virus and Hepatitis C Virus, hijack the host mitochondrial proteins to function fully inside the host cell."[1][2] Hepatitis C has also been shown to "fragment host mitochondria".[2]

Parasites such as Toxoplasma gondii have also been shown to modulate host energy metabolism and dysregulate mitochondrial function,[3], as have bacteria [4] such as E. coli, which has been shown to modulate mitochondrial receptor function.[5]

Mitochondrial disease has a high prevalence of fatigue and debilitation.[6]

Chronic fatigue syndrome[edit | edit source]

There is evidence of mitochondrial dysfunction in Chronic Fatigue Syndrome patients. Muscle biopsies have shown evidence of mitochondrial degeneration [7], deletions of mitochondrial DNA [8][9], the reduction of mitochondrial activity [8], and Sarah Myhill found measurable mitochondrial dysfunction correlating with severity of illness.[10][11] Myhill also produced improvement by targeting those dysfunctions.[12] Mitochondrial DNA variants correlate with symptoms, symptom clusters & symptom severity.[13]

Mitochondrial disorders can be mistaken for Chronic Fatigue Syndrome.[14]

There is evidence of genetic risk factors for mitochondrial dysfunction in related diseases such as complex regional pain syndrome, postural orthostatic tachycardia syndrome (POTS), and dysautonomia.[15]

Potential treatment[edit | edit source]

Garth Nicolson has proposed that mitochondrial lipid replacement therapy can ameliorate mitochondrial related fatigue using a proprietary blend of phospholipids called NT Factor.

Courtney Craig has proposed treatment of mitochondrial damage in ME/CFS patients using fasting, caloric restriction and a ketogenic diet.[16]

Notable studies[edit | edit source]

Videos[edit | edit source]

Learn more[edit | edit source]

See also[edit | edit source]

Unused Citations[edit | edit source]

Armstrong2014 [17] Vermeulen2010 [18] Maes2009 [19] Morris2013 [20]. Morris2014 [21] Meeus2013 [22]

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Citations[edit | edit source]

  1. ↑ Anand, Sanjeev K; Tikoo, Suresh K (October 24, 2013), "Viruses as Modulators of Mitochondrial Functions", Advances in Virology, Advances in Virology, 2013, 2013: –738794, doi:10.1155/2013/738794
  2. ↑ 2.0 2.1 Siu, GK; Zhou, F; Yu, MK; Zhang, L; Wang, T; Liang, Y; Chen, Y; Chan, HC; Yu, S (March 2016), "Hepatitis C virus NS5A protein cooperates with phosphatidylinositol 4-kinase IIIα to induce mitochondrial fragmentation", Sci. Rep., doi:10.1038/srep23464, PMID 27010100
  3. ↑ Saric, J; Li, JV; Swann, JR; et al. (November 8, 2010), "Integrated cytokine and metabolic analysis of pathological responses to parasite exposure in rodents" Check |url= value (help), Journal of proteome research, 9: 2255–2264
  4. ↑ Rudel T, T; Kepp O, O; Kozjak-Pavlovic V, V (October 2010), "Interactions between bacterial pathogens and mitochondrial cell death pathways", Nat Rev Microbiol., doi:10.1038/nrmicro2421, PMID 20818415
  5. ↑ Nagai, T; Abe, A; Sasakawa, C (January 2005), "Targeting of enteropathogenic Escherichia coli EspF to host mitochondria is essential for bacterial pathogenesis: critical role of the 16th leucine residue in EspF", J Bio. Chem., doi:10.1074/jbc.M411550200, PMID 15533930
  6. ↑ Gorman, Gráinne S; Elson, Joanna L; Newman, Jane; et al. (July 2015), "Perceived fatigue is highly prevalent and debilitating in patients with mitochondrial disease", Neuromuscular disorders: NMD, 25 (7): 563–566, doi:10.1016/j.nmd.2015.03.001, ISSN 1873-2364, PMID 26031904
  7. ↑ Behan, WMH; More, IAR; Behan, PO (1991), "Mitochondrial abnormalities in the postviral fatigue syndrome", Acta Neuropathologica, 83 (1): 61–65, PMID 1792865
  8. ↑ 8.0 8.1 Vecchiet, L; Montanari, G; Pizzigallo, E; et al. (April 19, 1996), "Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome", Neuroscience Letters, 208 (2): 117–120, PMID 8859904
  9. ↑ Zhang, C; Baumer, A; Mackay, IR; et al. (April 1995), "Unusual pattern of mitochondrial DNA deletions in skeletal muscle of an adult human with chronic fatigue syndrome", Human Molecular Genetics, 4 (4): 751–754, PMID 7633428
  10. ↑ Booth, NE; Myhill, S; McLaren-Howard, J (2012), "Mitochondrial dysfunction and the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)", Int J Clin Exp Med, 5 (3): 208–220, PMID 22837795
  11. ↑ Myhill, S; Booth, NE; McLaren-Howard, J (January 15, 2009), "Chronic fatigue syndrome and mitochondrial dysfunction", Int J Clin Exp Med, 2 (1): 1–16, PMID 19436827
  12. ↑ Myhill, Sarah; Booth, NE; McLaren-Howard, John (2013), "Targeting mitochondrial dysfunction in the treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) - a clinical audit.", International Journal of Clinical and Experimental Medicine, PMID 23236553
  13. ↑ Billing-Ross, Paul; Germain, Arnaud; Ye, Kaixiong; et al. (2016), "Mitochondrial DNA variants correlate with symptoms in myalgic encephalomyelitis/chronic fatigue syndrome", Journal of Translational Medicine, 14: 19, doi:10.1186/s12967-016-0771-6, ISSN 1479-5876, PMID 26791940, lay summary
  14. ↑ Galán, Fernando; de Lavera, Isabel; Cotán, David; Sánchez-Alcázar, José A (September 24, 2015), "Mitochondrial Myopathy in Follow-up of a Patient With Chronic Fatigue Syndrome", J Investig Med High Impact Case Rep, 3 (3), doi:10.1177/2324709615607908, PMID 26904705
  15. ↑ Boles, RG; Zaki, EA; Kerr, JR; et al. (July 2015), "Increased prevalence of two mitochondrial DNA polymorphisms in functional disease: Are we describing different parts of an energy-depleted elephant?", Mitochondrion, 23: 1-6, doi:10.1016/j.mito.2015.04.005, PMID 25934187
  16. ↑ Craig, Courtney (November 2015), "Mitoprotective dietary approaches for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Caloric restriction, fasting, and ketogenic diets", Medical Hypotheses, 85 (5): 690-693, doi:10.1016/j.mehy.2015.08.013, PMID 26315446
  17. ↑ Armstrong, CW; McGregor, NR; Butt, HL; Gooley, PR (October 2014), "Metabolism in chronic fatigue syndrome", Adv Clin Chem, 66: 121-72, doi:10.1016/B978-0-12-801401-1.00005-0, PMID 25344988
  18. ↑ Vermeulen, RC; Kirk, RM; Visser, FC; Sluiter, W; Scholte, HR (October 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, doi:10.1186/1479-5876-8-93, PMID 20937116
  19. ↑ Maes, M; Mihaylova, I; Kubera, M; Uytterhoeven, M; Vrydags, N; Bosmans, E (2009), "Coenzyme Q10 deficiency in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardiovascular disorder", Neuro Endocrinol Lett., PMID 20010505
  20. ↑ Morris, G; Maes, M (September 2013), "Myalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristics.", BMC Med, doi:10.1186/1741-7015-11-205, PMID 24229326
  21. ↑ Morris, Gerwyn; Maes, Michael (March 2014), "Mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome explained by activated immuno-inflammatory, oxidative and nitrosative stress pathways", Metab Brain Dis., doi:10.1007/s11011-013-9435-x, PMID 24557875
  22. ↑ Meeus, M; Nijs, J; Hermans, L; Goubert, D; Calders, P (September 2013), "The role of mitochondrial dysfunctions due to oxidative and nitrosative stress in the chronic pain or chronic fatigue syndromes and fibromyalgia patients: peripheral and central mechanisms as therapeutic targets?", Expert Opin Ther Targets, doi:10.1517/14728222.2013.818657, PMID 23834645

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

genome an organism's complete set of DNA, including all of its genes

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

tachycardia An unusually rapid heart beat. Can be caused by exercise or illness. A symptom of postural orthostatic tachycardia syndrome (POTS). (Learn more: www.heart.org)

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

coenzyme Q10 (CoQ10) - Coenzyme Q10 (also known as ubiquinone) is found in the mitochondria and, as a component of the electron transport chain, plays an important role in aerobic respiration. The chemically-reduced form of CoQ10 is called ubiquinol.

myalgic encephalomyelitis (M.E.) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.

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