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schade en dysfunctie

als oorzaak van









Een recent gepubliceerde overzichtstudie van Filler en collega's legt een relatie tussen

mitochondriale afwijkingen (structurele afwijkingen en verminderde werking) en "vermoeidheid".


Misschien kunnen "vermoeidheidsdeskundigen" hun aandacht van "dysfunctionele gedachten"

en "ziektegedrag" eens verleggen naar de kern het probleem: de ontoereikende energieproductie.





Association of mitochondrial dysfunction and fatigue: A review of the literature.

Biochim Biophys Acta Clin. 2014. doi: 10.1016/j.bbacli.2014.04.001.

Filler K , Lyon D, Bennett J, McCain N, Elswick R, Lukkahatai N, Saligan LN.





  1. Etiologic mechanisms underlying the symptom of fatigue are not well understood.
  2. This review investigates the association of mitochondrial dysfunction with fatigue.
  3. Inconsistent associations observed between mitochondria dysfunction and fatigue.




Fatigue is often described by patients as

a lack of energy, mental or physical tiredness, diminished endurance,

and prolonged recovery after physical activity.


Etiologic mechanisms underlying fatigue are not well understood;

however, fatigue is a hallmark symptom of mitochondrial disease,

making mitochondrial dysfunction

a putative biological mechanism for fatigue.


Therefore, this review examined studies that investigated

the association of markers of mitochondrial dysfunction with fatigue and

proposes possible research directions

to enhance understanding of the role of mitochondrial dysfunction in fatigue.


A thorough search using PubMed, Scopus, Web of Science, and Embase databases

returned 1220 articles.


After the application of inclusion and exclusion criteria,

a total of 25 articles meeting eligibility criteria were selected for full review.


Dysfunctions in

the mitochondrial structure,

mitochondrial function

(mitochondrial enzymes and oxidative/nitrosative stress),

mitochondrial energy metabolism (ATP production and fatty acid metabolism),

immune response, and genetics

were investigated as potential contributors to fatigue.


Carnitine was the most investigated mitochondrial function marker.


Dysfunctional levels were reported in all the studies investigating carnitine;

however, the specific type of carnitine that was dysfunctional varied.


Genetic profiles were the second most studied mitochondrial parameter.


Six common pathways were proposed:

  • metabolism,
  • energy production,
  • protein transport,
  • mitochondrial morphology,
  • central nervous system dysfunction and
  • post-viral infection.

Coenzyme Q10 was the most commonly investigated mitochondrial enzyme.


Low levels of Coenzyme Q10 were consistently associated with fatigue.


Potential targets for further investigation were identified as well as gaps in the current literature.





Fatigue; Mitochondria; Review



Graphical abstract