The Therapeutic Role of Ketogenic Diet in Neurological Disorders

Pietrzak, Diana; Kasperek, Kamila; Rękawek, Paweł; Piątkowska‐Chmiel, Iwona

doi:10.3390/nu14091952

Cited by 43 publications

(41 citation statements)

References 240 publications

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“…Ketone bodies are thought to have direct effects on inflammatory molecules ( 74 , 75 ), mitochondria ( 76 ), histone deacetylases ( 77 ), and BDNF expression (see above). Therefore, there are a number of important pathways through which the KD could be specifically benefiting the BACHD model as well as generally neurodegeneration ( 24 , 25 , 78 ).…”

Section: Discussionmentioning

confidence: 99%

“…An important consequence of TRF is an increase in ketone bodies (23) and there has been speculation that at least some of the benefits of TRF are due to the switch from glucose to lipids as fuel source and the subsequent reduction in reactive oxygen species. This raises the question of whether a ketogenic diet (KD), similar to TRF, could also be beneficial for HD and other neurodegenerative disorders (24)(25)(26).…”

Section: Introductionmentioning

confidence: 99%

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Dietary ketosis improves circadian dysfunction as well as motor symptoms in the BACHD mouse model of Huntington’s disease

et al. 2022

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Disturbances in sleep/wake cycles are common among patients with neurodegenerative diseases including Huntington’s disease (HD) and represent an appealing target for chrono-nutrition-based interventions. In the present work, we sought to determine whether a low-carbohydrate, high-fat diet would ameliorate the symptoms and delay disease progression in the BACHD mouse model of HD. Adult WT and BACHD male mice were fed a normal or a ketogenic diet (KD) for 3 months. The KD evoked a robust rhythm in serum levels of β-hydroxybutyrate and dramatic changes in the microbiome of male WT and BACHD mice. NanoString analysis revealed transcriptional changes driven by the KD in the striatum of both WT and BACHD mice. Disturbances in sleep/wake cycles have been reported in mouse models of HD and are common among HD patients. Having established that the KD had effects on both the WT and mutant mice, we examined its impact on sleep/wake cycles. KD increased daytime sleep and improved the timing of sleep onset, while other sleep parameters were not altered. In addition, KD improved activity rhythms, including rhythmic power, and reduced inappropriate daytime activity and onset variability. Importantly, KD improved motor performance on the rotarod and challenging beam tests. It is worth emphasizing that HD is a genetically caused disease with no known cure. Life-style changes that not only improve the quality of life but also delay disease progression for HD patients are greatly needed. Our study demonstrates the therapeutic potential of diet-based treatment strategies in a pre-clinical model of HD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dietary ketosis improves circadian dysfunction as well as motor symptoms in the BACHD mouse model of Huntington’s disease

et al. 2022

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“…The ketogenic diet (KD) is defined as a high-fat (70–80% fat from total daily calories), adequate-protein (10–20%), low-carbohydrate (5–10%) intake [ 424 ]. As a result of such changes in macronutrient proportions, a process called ketosis results, which allows glucose to be replaced by ketone bodies in the form of acetoacetic acid, β-hydroxybutyrate (BHB), and acetone [ 425 , 426 ].…”

Section: Parkinson’s Disease and Gut Microbiota: Therapeutic Approachesmentioning

confidence: 99%

The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment

Varesi¹,

Campagnoli²,

Fahmideh³

et al. 2022

IJMS

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The bidirectional interaction between the gut microbiota (GM) and the Central Nervous System, the so-called gut microbiota brain axis (GMBA), deeply affects brain function and has an important impact on the development of neurodegenerative diseases. In Parkinson’s disease (PD), gastrointestinal symptoms often precede the onset of motor and non-motor manifestations, and alterations in the GM composition accompany disease pathogenesis. Several studies have been conducted to unravel the role of dysbiosis and intestinal permeability in PD onset and progression, but the therapeutic and diagnostic applications of GM modifying approaches remain to be fully elucidated. After a brief introduction on the involvement of GMBA in the disease, we present evidence for GM alterations and leaky gut in PD patients. According to these data, we then review the potential of GM-based signatures to serve as disease biomarkers and we highlight the emerging role of probiotics, prebiotics, antibiotics, dietary interventions, and fecal microbiota transplantation as supportive therapeutic approaches in PD. Finally, we analyze the mutual influence between commonly prescribed PD medications and gut-microbiota, and we offer insights on the involvement also of nasal and oral microbiota in PD pathology, thus providing a comprehensive and up-to-date overview on the role of microbial features in disease diagnosis and treatment.

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“…The safety and efficacy of KD in human subjects has been extensively studied and confirmed in chronic neurological disorders (Walczyk and Wick, 2017;Gough et al, 2021;Yurista et al, 2021;Pietrzak et al, 2022;Zhu et al, 2022). While safety in chronic use has been established and confirmed with some acute injury studies, there is a relative lack in understanding the therapeutic potential of KD in acute injury states such as ischemic stroke, cerebral hemorrhages, and TBI.…”

Section: Conclusion/future Directionsmentioning

confidence: 99%

Diet-microbiome-gut-brain nexus in acute and chronic brain injury

et al. 2022

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In recent years, appreciation for the gut microbiome and its relationship to human health has emerged as a facilitator of maintaining healthy physiology and a contributor to numerous human diseases. The contribution of the microbiome in modulating the gut-brain axis has gained significant attention in recent years, extensively studied in chronic brain injuries such as Epilepsy and Alzheimer’s Disease. Furthermore, there is growing evidence that gut microbiome also contributes to acute brain injuries like stroke(s) and traumatic brain injury. Microbiome-gut-brain communications are bidirectional and involve metabolite production and modulation of immune and neuronal functions. The microbiome plays two distinct roles: it beneficially modulates immune system and neuronal functions; however, abnormalities in the host’s microbiome also exacerbates neuronal damage or delays the recovery from acute injuries. After brain injury, several inflammatory changes, such as the necrosis and apoptosis of neuronal tissue, propagates downward inflammatory signals to disrupt the microbiome homeostasis; however, microbiome dysbiosis impacts the upward signaling to the brain and interferes with recovery in neuronal functions and brain health. Diet is a superlative modulator of microbiome and is known to impact the gut-brain axis, including its influence on acute and neuronal injuries. In this review, we discussed the differential microbiome changes in both acute and chronic brain injuries, as well as the therapeutic importance of modulation by diets and probiotics. We emphasize the mechanistic studies based on animal models and their translational or clinical relationship by reviewing human studies.

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The Therapeutic Role of Ketogenic Diet in Neurological Disorders

Cited by 43 publications

References 240 publications

Dietary ketosis improves circadian dysfunction as well as motor symptoms in the BACHD mouse model of Huntington’s disease

Dietary ketosis improves circadian dysfunction as well as motor symptoms in the BACHD mouse model of Huntington’s disease

The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment

Diet-microbiome-gut-brain nexus in acute and chronic brain injury

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