Ukudla kwe-Ketogenic kulamula ithonya lofuzo

Ukudla kwe-ketogenic kulamula ithonya lofuzo

Ingabe kukhona isakhi sofuzo ku-bipolar disorder?

Kukhona ngempela isakhi sofuzo ku-bipolar disorder. I-Hereditability ilinganiselwa phakathi kuka-60-85%. Ezinye zezakhi zofuzo zikhonjwe njengezinhloso ezibalulekile zokungenelela kwezemithi. Ama-ketones angabalamuli abasebenzayo kwezinye zalezi zindlela zofuzo, kungaba ngokuvezwa noma ekukhulumeni ngokuya phansi komfula. Izidlo ze-Ketogenic okwamanje ziyaphenywa njengokwelashwa kwe-bipolar disorder.

Isingeniso

Ngokuvamile, lapho ngibhala ngokugula kwengqondo kanye nokusetshenziswa kokudla kwe-ketogenic njengokwelashwa, ngigxila ezicini ze-glucose hypometabolism, ukungalingani kwe-neurotransmitter, ukuvuvukala, nokucindezeleka okwenziwe nge-oxidative. Kodwa ngokwenza ucwaningo lwami lokuthunyelwe kwebhulogi nge-bipolar disorder, ngajabula ukubona ucwaningo olungaka lwenziwa ngezindlela zofuzo. Njengoba ngifunda ezinye zezakhi zofuzo ezikhonjiwe, ngabona eziningi zazo noma izindlela ezithonyayo njengokuthonywa ama-ketone.

My ngokushintsha izakhi zofuzo I-biochemistry akuyona into engingayibiza ngokuthi iqinile. Kodwa nganquma ukuthi ngenxa yokuthi ukuphazamiseka kwengqondo okuguquguqukayo kanye nokuphazamiseka kwemizwelo okwalandela kutholakala kunokuzalaniswa okuphezulu, kungase kusize ukukhuluma ngakho.

Ngokwesisekelo sezifundo zamawele nezomndeni, ifa le-BD lilinganiselwa ku-60-85%.

Mullins, N. et al., (2021). Ucwaningo lwe-Genome-wide association lwamacala angaphezu kuka-40,000 e-bipolar disorder lunikeza imininingwane emisha ngebhayoloji eyisisekelo.
https://doi.org/10.1038/s41588-021-00857-4

Kungani ngingafuna ukukhuluma ngamathonya ofuzo ku-bipolar disorder?

Ngoba ngezinye izikhathi lapho sitshelwa ukuthi ukugula kwethu kwengqondo kuwufuzo, sizizwa singenamandla okushintsha izimpawu. Futhi uma ngikwazi ukukukholisa ukuthi kunokuthile ongakwazi ukukwenza ukuze ulinganisele esinye isici sofuzo esitholakala sihlotshaniswa kakhulu nesifo sokuphazamiseka kwengqondo okuguquguqukayo, kungase kukunike ithemba lokuthi ungazizwa ungcono.

Ngiyazi ukuthi uma une-bipolar disorder futhi ufunda lokhu okuthunyelwe kwebhulogi, ungase ube ngomunye wezingxenye ezimbili kwezintathu zabantu abaphethwe yi-BPD, okuthi ngenkathi belashwa, basahlushwa izimpawu ze-prodromal ngisho nokudangala kwe-episodic. Ngakho-ke, ngenxa yokuthi ngifuna wazi zonke izindlela ongazizwa ungcono ngazo, ngizokwabelana nawe lokho engikufundile.

Njengoba ufunda ngezansi, khumbula ukuthi ubuchopho be-bipolar bulwa namazinga aphezulu okuvuvukala nokucindezeleka okwenziwe nge-oxidative, amandla obuchopho (i-glucose hypometabolism), nokungalingani kwe-neurotransmitter. Lokhu kuzokusiza ukuthi uqonde ukuthi ukudla kwe-ketogenic kanye nemiphumela yako ekuboniseni izakhi zofuzo kanye nemiphumela ezuzisayo eya phansi kunganikeza inketho yokwelapha ephumelelayo.

Izakhi zofuzo, ama-ketones kanye ne-bipolar disorder

Kuyathakazelisa kakhulu ukuqaphela ukuthi izakhi zofuzo ezihlobene ne-BPD zitholakala futhi zikhonjwa ngaso sonke isikhathi. Okune kwezinhloso ezithembisayo zokuthuthukiswa kwezidakamizwa ezintsha ze-BPD kuthonywa i-β-Hydroxybutyrate noma ezinye imizimba ye-ketone. Futhi kwenzeka nje ukuthi ama-ketone akhiqizwa njengengxenye yokudla kwe-ketogenic. Ukusesha kwezincwadi kubonise ukuthi imiphumela yayiqondile noma yehla nomfula ithinta indlela ehlobene ebonwa ku-pathology ye-bipolar disorder. Lokhu kufaka i-GRIN2A, CACNA1C, SCN2A, kanye ne-HDAC5.

I-HDAC5

I-β-Hydroxybutyrate, umzimba we-ketone, wehlisa umphumela we-cytotoxic we-cisplatin ngokwenza kusebenze i-HDAC5. Ukuvinjelwa kwe-HDAC5 kuboniswa njenge-neuroprotective ngokuvimbela izindlela ze-apoptosis. Kungani ama-ketone engeke akusize ekwelapheni ukuhlukahluka kofuzo kwe-HDAC5 ngokufaka imiphumela ye-neuroprotective? Ingabe siyayidinga ngempela imithi emisha ukuze sithonye uguquko lwe-HDAC5 ukuze selaphe ukuphazamiseka kwengqondo okuguquguqukayo?

Ingabe ukuguqulwa kwe-HDAC5 kanye nemiphumela ye-neuroprotective yama-ketones kule ndlela kungaba enye yezindlela ezenza ukwelashwa kwe-ketogenic yokudla kwe-bipolar disorder? Ngicabanga ukuthi kungaba njalo. Futhi lena yonke imibuzo engithemba ukuyibona iphikiswana ngayo futhi iphendulwe ezincwadini zocwaningo kule minyaka eyishumi ezayo.

I-GRIN2A

Ake sixoxe ngokulandelayo ngofuzo lwe-GRIN2A. Lesi sakhi sofuzo senza iphrotheni ye-GRIN2A. Le phrotheni iyingxenye ye-N-methyl-D-aspartate (NMDA) receptors (iziteshi ze-ion). Ama-NMDA receptors alawulwa, ngokwengxenye, nge-glutamate futhi athumele amasignali ajabulisayo ebuchosheni. Ama-NMDA receptors abandakanyeka ku-synaptic plasticity (ukufunda nenkumbulo) futhi adlala indima ebuthongweni obujulile. Ngifaka imiphumela yama-ketones endleleni ye-NMDA lapha, ikakhulukazi ngoba ama-receptors alawulwa yi-glutamate.

Kodwa ngingakubeka kalula nje esigabeni sokuvuvukala noma se-oxidative salokhu okuthunyelwe. Ngoba lapho i-glutamate iphezulu, ngokuvamile ibangelwa ukuvuvukala kwe-neurotransmitter okuthinta ukukhiqizwa nokulinganisela kwe-neurotransmitter. Yazi nje ukuthi ukungalingani ezinhlelweni ze-neurotransmitter (isb, ukukhuphuka kwamazinga e-glutamate kanye nomsebenzi we-NMDA receptor; ukwanda kwe-NMDA-excitotoxicity) kuhlotshaniswa ne-bipolar disorder. Ama-Ketones alamula ukuvuvukala ngokuqondile futhi athonye ukukhiqizwa kwe-glutamate ukuze ukuvuvukala kwehliselwe phansi futhi i-glutamate yenziwe ngamanani afanele kanye nezilinganiso.

I-SCN2A

I-SCN2A isakhi sofuzo esinikeza imiyalelo yokwenza iphrotheni yesiteshi se-sodium ebizwa ngokuthi i-NaV1.2. Le phrotheni ivumela ama-neurons ukuthi axhumane kusetshenziswa amasignali kagesi abizwa ngokuthi amandla esenzo. Izidlo ze-Ketogenic sekuyisikhathi eside zisetshenziselwa ukwelapha isithuthwane futhi zisetshenziselwa ngokukhethekile ukwelapha labo abanezinguquko ezithile zofuzo ku-SCN2A. Angikholwa ukuthi kuwukunwebeka okungenangqondo ukucabanga ukuthi ukudla okune-ketogenic kungasiza ekwelapheni ukuhlukahluka kofuzo esakhini sofuzo se-SCN2A esikubona kubantu be-bipolar.

I-CACNA1C

I-CACNA1C iphinde ikhonjwe njengokuhlangana okuqinile ne-bipolar disorder. Iphinde ithinte iziteshi ze-calcium ezincike ku-voltage, ezibalulekile ekusebenzeni kwe-membrane ku-neuron. Udinga ulwelwesi olunempilo lwe-neuronal cell ukuze ufeze imigomo ebalulekile njengokugcina izakhi, ukukhiqizwa kwe-neurotransmitter, nokuxhumana phakathi kwamaseli.

I-CACNA1C iwusizo ekusebenzeni kwesiteshi se-calcium subunit alpha1. Futhi nakuba izinga lami lamanje le-genetic biochemistry lingangivumeli ukuthi ngilandele kahle le ndlela, ngiyazi ukuthi into ebizwa ngokuthi ama-paroxysmal depolarization shifts (PDS) kucatshangwa ukuthi ihileleke ekubanjweni kwesithuthwane. Izidlo ze-Ketogenic zibonakala zizinzisa ukuguquguquka kwe-depolarization kubantu abanesithuthwane, futhi lokhu kucatshangwa ukuthi kungenye yezindlela lapho ukudla kwe-ketogenic kusebenza khona kulesi sibalo. Futhi ngomsebenzi, ngiqonde ukunciphisa ngokoqobo futhi ngezinye izikhathi ukumisa ukubanjwa.

Ukwenziwa kabusha kwe-repolarization okuthuthukisiwe kanye nokuzinzisa ulwelwesi kungase kwenzeke ngokungaqondile ngokukhuphula amandla eseli kanye nokudlula ukungasebenzi kahle kwemetabolism yobuchopho. Ama-ketone ahlinzeka ngalo mthombo wamandla othuthukisiwe, ngakho-ke nakuba ama-ketone angase angathinti ngokuqondile indlela yokukhuluma ye-CACNA1C, angase anikeze ikhambi lomthelela we-CACNA1C snip ethonya izimpawu ze-bipolar.

Ukuphazamiseka kokuthunjwa kuye kwaphathwa kusetshenziswa ukudla kwe-ketogenic kusukela ngawo-1920, futhi le miphumela ibhalwe kahle futhi ayinakuphikiswa kuleli phuzu. Ithonya lama-ketone eziteshini ze-calcium kanye nokuphindaphinda kwe-neuronal membranes kubhalwe kahle ezincwadini zesithuthwane.

Kodwa iphuzu lami ukuthi ukudla kwe-ketogenic kuphatha ukungasebenzi kwesiteshi se-calcium futhi kuthuthukise impilo ye-neuronal membrane yezempilo nokusebenza. Ngakho-ke kungani kungasebenzi ukusiza labo abane-bipolar disorder? Lokhu ngeke kube enye indlela lapho ukudla kwe-ketogenic kungasiza ekunciphiseni izimpawu ze-bipolar?

Isiphetho

Lezi izibonelo zezakhi zofuzo ezihlonzwe njengezinomthelela enqubweni yesifo se-bipolar disorder, okungenzeka ukuthi ilawulwa ngesenzo sama-ketone ngokuqondile noma ezansi nomfula emikhiqizweni ephilayo eyenziwa yibhayoloji nokuthi isetshenziswa kanjani. Ngakho-ke nakuba kunesici esibalulekile sofuzo ku-bipolar disorder, zikhona futhi izindlela zokuthonya lezo zakhi zofuzo nendlela ezivezwa ngayo, ukuguqula indlela ezivezwa ngayo ngokuqhubekayo ezindleleni ezibalulekile.

Kubalulekile kimina ukuthi uzazi zonke izindlela ongazizwa ungcono ngazo, futhi uqonde ukuthi ngenxa yokuthi into ethile iwufuzo, akusho ukuthi awukwazi ukuvula noma ukuvala ezinye zalezo zakhi ngendlela yokuphila noma ezinye izici. Futhi akusho ukuthi izakhi zakho zofuzo ziyakwazi ukusho ikusasa lakho uma kuziwa ekuguleni okungamahlalakhona - ngisho nesifo sengqondo esingamahlalakhona, njenge-bipolar disorder.

I-Bipolar Disorder (BD) yisifo sengqondo esibi kakhulu esibonakala ngezimo eziphikisanayo eziphindaphindayo ze-manic ne-depressive. Ngaphezu kwezakhi zofuzo, ukusebenzisana okuyinkimbinkimbi kwezakhi zofuzo, okushintsha isimo se-epigenetic ebuchosheni, kunomthelela ku-etiology kanye ne-pathophysiology ye-BD..

(kugcizelelwe) Sugawara, H., Bundo, M., Kasahara, T. et al., (I-2022). https://doi.org/10.1186/s13041-021-00894-4

Uma ukuthandile lokhu okuthunyelwe kwebhulogi mayelana nezakhi zofuzo ku-bipolar disorder, cishe uzothola okuthunyelwe kwami ​​​​kubhulogi mayelana nokudla kwe-ketogenic kwe-bipolar disorder kuwusizo.

Uyakuthanda lokho okufunda kubhulogi? Ingabe ufuna ukufunda mayelana nama-webinars azayo, izifundo, ngisho neminikelo ezungezayo yosekelo nokusebenzisana nami ekufezeni imigomo yakho yokuphila kahle? bhalisela!

Ungathola futhi okuthunyelwe kwebhulogi okulandelayo kuwusizo ohambweni lwakho lokuphulukisa:

Njengenjwayelo, lokhu okuthunyelwe kwebhulogi akusona iseluleko sezokwelapha.


Okubhekwayo

Beurel, E., Grieco, SF, & Jope, RS (2015). I-Glycogen synthase kinase-3 (GSK3): Umthetho, izenzo, nezifo. I-Pharmacology & Therapeutics, 0, 114. https://doi.org/10.1016/j.pharmthera.2014.11.016

I-Bhat, S., Dao, DT, Terrillion, CE, Arad, M., Smith, RJ, Soldatov, NM, & Gould, TD (2012). I-CACNA1C (Cav1.2) ku-pathophysiology yesifo sengqondo. Intuthuko e-Neurobiology, 99(1), i-1-14. https://doi.org/10.1016/j.pneurobio.2012.06.001

U-Chen, S., Xu, D., Fan, L., Fang, Z., Wang, X., & Li, M. (2022). Izindima ze-N-Methyl-D-Aspartate Receptors (NMDARs) ku-Epilepsy. Frontiers kwiMoleky Neuroscience, 14, 797253. https://doi.org/10.3389/fnmol.2021.797253

Cohen, P., & Goedert, M. (2004). I-GSK3 inhibitors: Ukuthuthukiswa kanye namandla okwelapha. Ukubuyekezwa Kwemvelo. Ukutholwa Kwezidakamizwa, 3, 479-487. https://doi.org/10.1038/nrd1415

U-Conde, S., Pérez, DI, Martínez, A., Perez, C., & Moreno, FJ (2003). I-Thienyl ne-phenyl alpha-halomethyl ketones: Ama-inhibitor amasha e-glycogen synthase kinase (GSK-3beta) asuka kumtapo wolwazi wokusesha okuyinhlanganisela. Ijenali ye-Medicinal Chemistry, 46(22), i-4631-4633. https://doi.org/10.1021/jm034108b

U-Erro, R., Bhatia, KP, Espay, AJ, & Striano, P. (2017). I-spectrum ye-epileptic ne-nonepileptic ye-paroxysmal dyskinesias: i-Channelopathies, i-synaptopathies, ne-transportopathies. Izinkinga zokuhamba, 32(3), i-310-318. https://doi.org/10.1002/mds.26901

Ghasemi, M., & Schachter, SC (2011). I-NMDA receptor complex njengenhloso yokwelapha esithuthwaneni: Ukubuyekezwa. Isifo sokuwa nokuziphatha, 22(4), i-617-640. https://doi.org/10.1016/j.yebeh.2011.07.024

I-GRIN2A gene: I-MedlinePlus Genetics. (nd). Ibuyiselwe ngoJanuwari 29, 2022, kusukela https://medlineplus.gov/genetics/gene/grin2a/

Haggarty, SJ, Karmacharya, R., & Perlis, RH (2021). Ukuthuthukela emuthini onembayo we-bipolar disorder: Izindlela nama-molecule. I-Psychiatry yamaphilisi, 26(1), i-168-185. https://doi.org/10.1038/s41380-020-0831-4

Hensley, K., & Kursula, P. (2016). I-Collapsin Response Mediator Protein-2 (CRMP2) iyi-Plausible Etiological Factor and Potential Therapeutic Target in Alzheimer's Disease: Qhathanisa futhi Qhathanisa ne-Microtubule-Associated Protein Tau. I-Journal yezifo ze-Alzheimer, 53(1), i-1-14. https://doi.org/10.3233/JAD-160076

Jope, RS, Yuskaitis, CJ, & Beurel, E. (2007). I-Glycogen Synthase Kinase-3 (GSK3): Ukuvuvukala, Izifo, kanye Nezokwelapha. Ucwaningo lwe-Neurochemical, 32(4–5), 577. https://doi.org/10.1007/s11064-006-9128-5

Knisatschek, H., & Bauer, K. (1986). Ukuvinjelwa okuqondile kwe-post proline cleaving enzyme nge-benzyloxycarbonyl-Gly-Pro-diazomethyl ketone. Ukuxhumana Kwama-Biochemical and Biophysical Research, 134(2), i-888-894. https://doi.org/10.1016/s0006-291x(86)80503-4

Ko, A., Jung, DE, Kim, SH, Kang, H.-C., Lee, JS, Lee, ST, Choi, JR, & Kim, HD (2018). Ukusebenza Kwe-Ketogenic Diet for Specific Genetic Mutation in Developmental and Epileptic Encephalopathy. Frontiers e-Neurology, 9. https://doi.org/10.3389/fneur.2018.00530

Kubista, H., Boehm, S., & Hotka, M. (2019). I-Paroxysmal Depolarization Shift: Ukucabangela Kabusha Indima Yayo Esithuthwaneni, I-Epileptogenesis Nangaphezulu. I-International Journal of Sciences Molecular, 20(3), i-577. https://doi.org/10.3390/ijms20030577

U-Lett, TAP, Zai, CC, Tiwari, AK, Shaikh, SA, Likhodi, O., Kennedy, JL, & Müller, DJ (2011). I-ANK3, CACNA1C kanye ne-ZNF804A okuhlukile kofuzo ekuphazamisekeni kwe-bipolar kanye ne-psychosis subphenotype. I-World Journal ye-Biological Psychiatry, 12(5), i-392-397. https://doi.org/10.3109/15622975.2011.564655

U-Lund, TM, Ploug, KB, Iversen, A., Jensen, AA, & Jansen-Olesen, I. (2015). Umthelela we-metabolic we-β-hydroxybutyrate ku-neurotransmission: I-glycolysis encishisiwe ilamula izinguquko ekuphenduleni kwe-calcium kanye nokuzwela kwe-KATP ye-receptor. I-Journal ye-Neurochemistry, 132(5), i-520-531. https://doi.org/10.1111/jnc.12975

Marx, W., McGuinness, AJ, Rocks, T., Ruusunen, A., Cleminson, J., Walker, AJ, Gomes-da-Costa, S., Lane, M., Sanches, M., Diaz, AP , Tseng, P.-T., Lin, P.-Y., Berk, M., Clarke, G., O'Neil, A., Jacka, F., Stubbs, B., Carvalho, AF, Quevedo, J., … Fernandes, BS (2021). Indlela ye-kynurenine ku-depressive disorder enkulu, i-bipolar disorder, ne-schizophrenia: Ukuhlaziywa kwe-meta kwezifundo ze-101. I-Psychiatry yamaphilisi, 26(8), i-4158-4178. https://doi.org/10.1038/s41380-020-00951-9

Mikami, D., Kobayashi, M., Uwada, J., Yazawa, T., Kamiyama, K., Nishimori, K., Nishikawa, Y., Morikawa, Y., Yokoi, S., Takahashi, N., Kasuno, K., Taniguchi, T., & Iwano, M. (2019). I-β-Hydroxybutyrate, umzimba we-ketone, wehlisa umphumela we-cytotoxic we-cisplatin ngokwenza kusebenze i-HDAC5 kumaseli e-epithelial e-renal cortical. I-Life Sciences, 222, 125-132. https://doi.org/10.1016/j.lfs.2019.03.008

Mullins, N., Forstner, AJ, O'Connell, KS, Coombes, B., Coleman, JRI, Qiao, Z., Als, TD, Bigdeli, TB, Børte, S., Bryois, J., Charney, AW , Drange, OK, Gandal, MJ, Hagenaars, SP, Ikeda, M., Kamitaki, N., Kim, M., Krebs, K., Panagiotaropoulou, G., … Andreassen, OA (2021). Ucwaningo lwe-Genome-wide association lwamacala angaphezu kuka-40,000 e-bipolar disorder lunikeza imininingwane emisha ngebhayoloji eyisisekelo. Nature Ufuzo, 53(6), i-817-829. https://doi.org/10.1038/s41588-021-00857-4

Nyegaard, M., Demontis, D., Foldager, L., Hedemand, A., Flint, TJ, Sørensen, KM, Andersen, PS, Nordentoft, M., Werge, T., Pedersen, CB, Hougaard, DM, Mortensen, PB, Mors, O., & Børglum, AD (2010). I-CACNA1C (rs1006737) ihlotshaniswa ne-schizophrenia. I-Psychiatry yamaphilisi, 15(2), i-119-121. https://doi.org/10.1038/mp.2009.69

SCN2A.com. (nd). SCN2A.Com. Ibuyiselwe ngoJanuwari 29, 2022, kusukela https://scn2a.com/scn2a-overview/

Sugawara, H., Bundo, M., Kasahara, T. et al. Ukuhlaziywa kwe-DNA methylation ye-cell-type-specific ye-cortices yangaphambili ye-mutant Isilinganiso1 amagundane e-transgenic ane-neuronal accumulation ye-mitochondrial DNA esusiwe. Mol Brain 15, 9 (2022). https://doi.org/10.1186/s13041-021-00894-4

Thaler, S., Choragiewicz, TJ, Rejdak, R., Fiedorowicz, M., Turski, WA, Tulidowicz-Bielak, M., Zrenner, E., Schuettauf, F., & Zarnowski, T. (2010). I-Neuroprotection nge-acetoacetate kanye ne-β-hydroxybutyrate ngokumelene nomonakalo we-RGC owenziwe yi-NMDA kumagundane—Ukubandakanyeka okungenzeka kwe-kynurenic acid. Ingobo yomlando ka-Graefe ye-Clinical and Experimental Ophthalmology = I-Albrecht Von Graefes Archiv Fur Klinische Und Experimentelle Ophthalmologie, 248(12), i-1729-1735. https://doi.org/10.1007/s00417-010-1425-7

Ubuso obuningi be-Beta-hydroxybutyrate (BHB). (2021, Septhemba 27). I-KetoNutrition. https://ketonutrition.org/the-many-faces-of-beta-hydroxybutyrate-bhb/

Tian, ​​X., Zhang, Y., Zhang, J., Lu, Y., Men, X., & Wang, X. (2021). Ukudla Kwe-Ketogenic Ezinsaneni Ezine-Early-Onse Epileptic Encephalopathy kanye ne-SCN2A Mutation. Yonsei Medical Journal, 62(4), i-370-373. https://doi.org/10.3349/ymj.2021.62.4.370

I-β-Hydroxybutyrate Modulates N-Type Calcium Channels kumaRat Sympathetic Neurons Ngokusebenza njenge-Agonist ye-G-Protein-Coupled Receptor FFA3—PMC. (nd). Ibuyiselwe ngoJanuwari 29, 2022, kusukela https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3850046/

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