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Induced ketosis as a treatment for neuroprogressive disorders: food for thought?

Morris, Gerwyn, Puri, Basant K., Carvalho, Andre, Maes, Michael, Berk, Michael, Ruusunen, Anu and Olive, Lisa 2020, Induced ketosis as a treatment for neuroprogressive disorders: food for thought?, The international journal of neuropsychopharmacology, vol. 23, no. 6, pp. 366-384, doi: 10.1093/ijnp/pyaa008.

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Title Induced ketosis as a treatment for neuroprogressive disorders: food for thought?
Author(s) Morris, Gerwyn
Puri, Basant K.
Carvalho, Andre
Maes, Michael
Berk, MichaelORCID iD for Berk, Michael orcid.org/0000-0002-5554-6946
Ruusunen, AnuORCID iD for Ruusunen, Anu orcid.org/0000-0002-1169-7478
Olive, LisaORCID iD for Olive, Lisa orcid.org/0000-0003-4643-8561
Journal name The international journal of neuropsychopharmacology
Volume number 23
Issue number 6
Start page 366
End page 384
Total pages 19
Publisher Oxford University Press
Place of publication Oxford, Eng.
Publication date 2020-06
ISSN 1469-5111
Summary Induced ketosis (or ketone body ingestion) can ameliorate several changes associated with neuroprogressive disorders, including schizophrenia, bipolar disorder, and major depressive disorder. Thus, the effects of glucose hypometabolism can be bypassed through the entry of beta-hydroxybutyrate, providing an alternative source of energy to glucose. The weight of evidence suggests that induced ketosis reduces levels of oxidative stress, mitochondrial dysfunction, and inflammation-core features of the above disorders. There are also data to suggest that induced ketosis may be able to target other molecules and signaling pathways whose levels and/or activity are also known to be abnormal in at least some patients suffering from these illnesses such as peroxisome proliferator-activated receptors, increased activity of the Kelch-like ECH-associated protein/nuclear factor erythroid 2-related factor 2, Sirtuin-1 nuclear factor-κB p65, and nicotinamide adenine dinucleotide (NAD). This review explains the mechanisms by which induced ketosis might reduce mitochondrial dysfunction, inflammation, and oxidative stress in neuropsychiatric disorders and ameliorate abnormal levels of molecules and signaling pathways that also appear to contribute to the pathophysiology of these illnesses. This review also examines safety data relating to induced ketosis over the long term and discusses the design of future studies.
Language eng
DOI 10.1093/ijnp/pyaa008
Indigenous content off
Field of Research 110999 Neurosciences not elsewhere classified
11 Medical and Health Sciences
17 Psychology and Cognitive Sciences
Socio Economic Objective 920410 Mental Health
HERDC Research category C1 Refereed article in a scholarly journal
Free to Read? Yes
Persistent URL http://hdl.handle.net/10536/DRO/DU:30135588

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
Open Access Collection
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.