Hypoxia

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

Hypoxia can be caused by insufficient blood supply or by inflammation[1].

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

In ME/CFS[edit | edit source]

Several findings in Myalgic encephalomyelitis suggest that patients might be experiencing local or global hypoxia. For example, many studies have found reduced blood flow to the heart[2][3], Cerebral hypoperfusion (reduced blood flow to the brain) in ME/CFS,[4][5][6][7][8][9][10][11], even in the absence of postural orthostatic tachycardia or neurally-mediated hypotension; cerebral hypo-metabolism (reduced metabolic activity in the brain)[12][13]; as well as elevated Lactic acid in the brain[14] and blood[15]. Peripheral endothelial dysfunction has also been found.[16]

Elevated WASF3 was found in one case study. WASF3 can be elevated in other conditions where hypoxia is a mechanism, such as cancer[17][18], and in animal models[19][20]. Natural killer cell function[21][22][23][24][25], lower in ME/CFS patients, is also reduced in conditions of hypoxia.[26] Mast cells, increased in ME/CFS patients, can create conditions similar to hypoxia while conversely, systemic hypoxia causes mast cell deganulation.[27]

Preliminary data from the UK ME/CFS biobank show an association between increased risk of ME/CFS and a gene variant that encodes for a subunit of prolyl 4-hydroxylase subunit alpha 1 (P4HA1), which encodes for procollagen-proline dioxygenase, an enzyme involved in the production of collagen. P4HA1 also plays a role in the regulation of energy metabolism via downregulation of pyruvate dehydrogenase during hypoxia.[28]

Creatine, elevated in #MECFS patients[29], is protective against hypoxia[30].

Hypoxia can induce mitochondrial damage and dysfunction[31], which has been found in ME/CFS patients[32][33].

In Long COVID[edit | edit source]

In mast cell activation syndrome[edit | edit source]

Learn more[edit | edit source]

See also[edit | edit source]

References[edit | edit source]

  1. ↑ Karhausen, Jörn; Haase, Volker H.; Colgan, Sean P. (February 19, 2005). "Inflammatory Hypoxia: Role of Hypoxia-Inducible Factor". Cell Cycle. 4 (2): 255–257. doi:10.4161/cc.4.2.1407. ISSN 1538-4101.
  2. ↑ Patrick Neary, J.; Roberts, Andy D.W.; Leavins, Nina; Harrison, Michael F.; Croll, James C.; Sexsmith, James R. (November 2008). "Prefrontal cortex oxygenation during incremental exercise in chronic fatigue syndrome". Clinical Physiology and Functional Imaging. 28 (6): 364–372. doi:10.1111/j.1475-097x.2008.00822.x. ISSN 1475-0961.
  3. ↑ Peterson, PK; Sirr, SA; Grammith, FC; Schenck, CH; Pheley, AM; Hu, S; Chao, C C (March 1994). "Effects of mild exercise on cytokines and cerebral blood flow in chronic fatigue syndrome patients". Clinical and Diagnostic Laboratory Immunology. 1 (2): 222–226. ISSN 1071-412X. PMID 7496949.
  4. ↑ Natelson, Benjamin; Mao, Xiangling; Stegner, Aaron J; Lange, Gudrun; Vu, Diana; Blate, Michelle; Kang, Guoxin; Soto, Eli; Kapusuz, Tolga; Shungu, Dikoma C (2017). "Multimodal and simultaneous assessments of brain and spinal fluid abnormalities in chronic fatigue syndrome and the effects of psychiatric comorbidity". Journal of the Neurological Sciences. 375: 411-416. doi:10.1016/j.jns.2017.02.046. PMC 5393352.
  5. ↑ Costa, D.C.; Tannock, C.; Brostoff, J. (November 1995). "Brainstem perfusion is impaired in chronic fatigue syndrome". QJM: monthly journal of the Association of Physicians. 88 (11): 767–773. ISSN 1460-2725. PMID 8542261.
  6. ↑ Barnden, Leighton R.; Crouch, Benjamin; Kwiatek, Richard; Burnet, Richard; Mernone, Anacleto; Chryssidis, Steve; Scroop, Garry; Fante, Peter Del (2011). "A brain MRI study of chronic fatigue syndrome: evidence of brainstem dysfunction and altered homeostasis". NMR in Biomedicine. 24 (10): 1302–1312. doi:10.1002/nbm.1692. ISSN 1099-1492. PMC 4369126. PMID 21560176.
  7. ↑ Biswal, Bharat; Kunwar, Pratap; Natelson, Benjamin H. (February 15, 2011). "Cerebral blood flow is reduced in chronic fatigue syndrome as assessed by arterial spin labeling". Journal of the Neurological Sciences. 301 (1): 9–11. doi:10.1016/j.jns.2010.11.018. ISSN 0022-510X.
  8. ↑ Yoshiuchi, Kazuhiro; Farkas, Jeffrey; Natelson, Benjamin H. (2006). "Patients with chronic fatigue syndrome have reduced absolute cortical blood flow". Clinical Physiology and Functional Imaging. 26 (2): 83–86. doi:10.1111/j.1475-097X.2006.00649.x. ISSN 1475-097X.
  9. ↑ Freedman, M.; Kirsh, J.C.; Gray, B.; Chung, D.G.; Abbey, S.E.; Salit, I.E.; Ichise, M. (October 1992). "Assessment of regional cerebral perfusion by 99Tcm-HMPAO SPECT in chronic fatigue syndrome". Nuclear medicine communications. 13 (10): 767–772. ISSN 0143-3636. PMID 1491843.
  10. ↑ Chao, C.C.; Hu, S.; Pheley, A.M.; Schenck, C.H.; Grammith, F.C.; Sirr, S.A.; Peterson, P.K. (March 1, 1994). "Effects of mild exercise on cytokines and cerebral blood flow in chronic fatigue syndrome patients". Clinical and Diagnostic Laboratory Immunology. 1 (2): 222–226. ISSN 1071-412X. PMID 7496949.
  11. ↑ Lange, Gudrun; Wang, Samuel; DeLuca, John; Natelson, Benjamin H. (September 28, 1998). "Neuroimaging in chronic fatigue syndrome". The American Journal of Medicine. 105 (3, Supplement 1): 50S–53S. doi:10.1016/S0002-9343(98)00175-2. ISSN 0002-9343.
  12. ↑ Bartenstein, P.; Egle, U.T.; Schreckenberger, M.; Hardt, J.; Nix, W.A.; Siessmeier, T. (July 1, 2003). "Observer independent analysis of cerebral glucose metabolism in patients with chronic fatigue syndrome". Journal of Neurology, Neurosurgery & Psychiatry. 74 (7): 922–928. doi:10.1136/jnnp.74.7.922. ISSN 0022-3050. PMID 12810781.
  13. ↑ Tirelli, Umberto; Chierichetti, Franca; Tavio, Marcello; Simonelli, Cecilia; Bianchin, Gianluigi; Zanco, Pierluigi; Ferlin, Giorgio (September 28, 1998). "Brain positron emission tomography (PET) in chronic fatigue syndrome: preliminary data". The American Journal of Medicine. 105 (3, Supplement 1): 54S–58S. doi:10.1016/S0002-9343(98)00179-X. ISSN 0002-9343.
  14. ↑ Natelson, Benjamin; Mao, Xiangling; Stegner, Aaron J; Lange, Gudrun; Vu, Diana; Blate, Michelle; Kang, Guoxin; Soto, Eli; Kapusuz, Tolga; Shungu, Dikoma C (2017). "Multimodal and simultaneous assessments of brain and spinal fluid abnormalities in chronic fatigue syndrome and the effects of psychiatric comorbidity". Journal of the Neurological Sciences. 375: 411-416. doi:10.1016/j.jns.2017.02.046. PMC 5393352.
  15. ↑ Ghali, Alaa; Lacout, Carole; Ghali, Maria; Gury, Aline; Beucher, Anne-Berengere; Lozac’h, Pierre; Lavigne, Christian; Urbanski, Geoffrey (December 11, 2019). "Elevated blood lactate in resting conditions correlate with post-exertional malaise severity in patients with Myalgic encephalomyelitis/Chronic fatigue syndrome". Scientific Reports. 9 (1): 1–9. doi:10.1038/s41598-019-55473-4. ISSN 2045-2322.
  16. ↑ Scherbakov, Nadja; Szklarski, Marvin; Hartwig, Jelka; Sotzny, Franziska; Lorenz, Sebastian; Meyer, Antje; Grabowski, Patricia; Doehner, Wolfram; Scheibenbogen, Carmen (2020). "Peripheral endothelial dysfunction in myalgic encephalomyelitis/chronic fatigue syndrome". ESC Heart Failure. 7 (3): 1064–1071. doi:10.1002/ehf2.12633. ISSN 2055-5822. PMC 7261521. PMID 32154656.
  17. ↑ Ghoshal, Pushpankur; Teng, Yong; Lesoon, Leslie Ann; Cowell, John K. (September 15, 2012). "HIF1A induces expression of the WASF3 metastasis-associated gene under hypoxic conditions". International Journal of Cancer. 131 (6): E905–E915. doi:10.1002/ijc.27631. PMC 3629704. PMID 22581642.
  18. ↑ Loveless, Reid; Teng, Yong (2021-01). "Targeting WASF3 Signaling in Metastatic Cancer". International Journal of Molecular Sciences. 22 (2): 836. doi:10.3390/ijms22020836. ISSN 1422-0067. PMC 7830529. PMID 33467681. Check date values in: |date= (help)
  19. ↑ Yang, Yujia; Fu, Qiang; Wang, Xiaozhu; Liu, Yang; Zeng, Qifan; Li, Yun; Gao, Sen; Bao, Lisui; Liu, Shikai; Gao, Dongya; Dunham, Rex (August 1, 2018). "Comparative transcriptome analysis of the swimbladder reveals expression signatures in response to low oxygen stress in channel catfish, Ictalurus punctatus". Physiological Genomics. 50 (8): 636–647. doi:10.1152/physiolgenomics.00125.2017. ISSN 1094-8341.
  20. ↑ Zhang, J; Chen, L; Long, K R; Mu, Z P (September 1, 2015). "Hypoxia-related gene expression in porcine skeletal muscle tissues at different altitude". Genetics and molecular research. 14 (3): 11587–11593. doi:10.4238/2015.september.28.10. ISSN 1676-5680. PMID 26436399.
  21. ↑ Barker, Edward; Fujimura, Sue F.; Fadem, Mitchell B.; Landay, Alan L.; Levy, Jay A. (1994). "Immunologic Abnormalities Associated with Chronic Fatigue Syndrome". Clin Infect Dis. 18 (Suppl 1): S136–S141. doi:10.1093/clinids/18.Supplement_1.S136.
  22. ↑ Whiteside, TL; Friberg, D (1998), "Natural killer cells and natural killer cell activity in chronic fatigue syndrome.", Am J Med, 105 (3A): 27S–34S, PMID 9790479
  23. ↑ Brenu, EW; Huth, TK; Hardcastle, SL; Fuller, K; Kaur, M; Johnston, S; Ramos, S; Staines, D; Marshall-Gradisnik, S (2014). "The Role of adaptive and innate immune cells in chronic fatigue syndrome/myalgic encephalomyelitis". International Immunology. 26 (4): 233–42. doi:10.1093/intimm/dxt068. PMID 24343819.
  24. ↑ Fletcher, Mary Ann; Maher, Kevin J; Klimas, Nancy (April 2002), "Natural killer cell function in chronic fatigue syndrome", Clinical and Applied Immunology Reviews, 2 (2): 129–139, doi:10.1016/S1529-1049(01)00047-2
  25. ↑ Brenu, Ekua W; van Driel, Mieke L; Staines, Donald R; Ashton, Kevin J; Hardcastle, Sharni L; Keane, James; Tajouri, Lotti; Peterson, Daniel; Ramos, Sandra B; Marshall-Gradisnik, Sonya M (2012), "Longitudinal investigation of natural killer cells and cytokines in chronic fatigue syndrome/myalgic encephalomyelitis", Journal of Translational Medicine, 10: 88, doi:10.1186/1479-5876-10-88
  26. ↑ Garcés-Lázaro, Irene; Kotzur, Rebecca; Cerwenka, Adelheid; Mandelboim, Ofer (2022). "NK Cells Under Hypoxia: The Two Faces of Vascularization in Tumor and Pregnancy". Frontiers in Immunology. 13. doi:10.3389/fimmu.2022.924775/full. ISSN 1664-3224.
  27. ↑ Steiner, Dawn R. S.; Gonzalez, Norberto C.; Wood, John G. (January 1, 2003). "Mast cells mediate the microvascular inflammatory response to systemic hypoxia". Journal of Applied Physiology. 94 (1): 325–334. doi:10.1152/japplphysiol.00637.2002. ISSN 8750-7587.
  28. ↑ Schneider, Martin; Harnoss, Jonathan Michael; Strowitzki, Moritz J.; Radhakrishnan, Praveen; Platzer, Lisa; Harnoss, Julian Camill; Hank, Thomas; Cai, Jun; Ulrich, Alexis (January 2015). "Therapeutic inhibition of prolyl hydroxylase domain-containing enzymes in surgery: putative applications and challenges". Hypoxia. 3: 1. doi:10.2147/HP.S60872. ISSN 2324-1128.
  29. ↑ Albrecht, Robert (March 21, 1964). "Epidemic Neuromyasthenia Outbreak in a Convent in New York State". Journal of the American Medical Association. 187: 904–907.
  30. ↑ Balestrino, Maurizio; Rebaudo, Renata; Lunardi, Gianluigi (January 16, 1999). "Exogenous creatine delays anoxic depolarization and protects from hypoxic damage: dose–effect relationship". Brain Research. 816 (1): 124–130. doi:10.1016/S0006-8993(98)01131-7. ISSN 0006-8993.
  31. ↑ Dhar-Mascareño, Manya; Cárcamo, Juan M.; Golde, David W. (May 15, 2005). "Hypoxia–reoxygenation-induced mitochondrial damage and apoptosis in human endothelial cells are inhibited by vitamin C". Free Radical Biology and Medicine. 38 (10): 1311–1322. doi:10.1016/j.freeradbiomed.2005.01.017. ISSN 0891-5849.
  32. ↑ Behan, W. M.H.; More, I.A.R.; Behan, P.O. (December 1991). "Mitochondrial abnormalities in the postviral fatigue syndrome". Acta Neuropathologica. 83 (1): 61–65. doi:10.1007/bf00294431. ISSN 0001-6322.
  33. ↑ "Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome". Neuroscience Letters. 208 (2): 117–120. April 19, 1996. doi:10.1016/0304-3940(96)12559-3. ISSN 0304-3940.
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