Carbohydrate-restricted Diet and Exercise Increase Brain-derived Neurotrophic Factor and Cognitive Function: A Randomized Crossover Trial

https://pubmed.ncbi.nlm.nih.gov/31700717/

Conclusion This study shows the short-term beneficial effects of carbohydrate-restricted diet on serum BDNF and executive function in those individuals characterized with MetS. We have shown that the addition of exercise can further improve neuroprotection and cognitive function beyond the results of diet alone.

Gyorkos A, Baker MH, Miutz LN, Lown DA, Jones MA, Houghton-Rahrig LD. Carbohydrate-restricted Diet and Exercise Increase Brain-derived Neurotrophic Factor and Cognitive Function: A Randomized Crossover Trial. Cureus. 2019 Sep 9;11(9):e5604. doi: 10.7759/cureus.5604. PMID: 31700717; PMCID: PMC6822553.

Induction of ketosis as a potential therapeutic option to limit hyperglycemia and prevent cytokine storm in COVID-19

Källa: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7416786

”Abstract

The severe form of coronavirus disease 19 (COVID-19) is characterized by cytokine storm syndrome (CSS) and disseminated intravascular coagulation (DIC). Diabetes, obesity, and hypertension have, as minor common denominators, chronic low-grade inflammation and high plasma myeloperoxidase levels, which could be linked to pulmonary phagocytic hyperactivation and CSS. The hyperactivation of M1 macrophages with a proinflammatory phenotype, which is linked to aerobic glycolysis, leads to the recruitment of monocytes, neutrophils, and platelets from circulating blood and plays a crucial role in thrombo-inflammation (as recently demonstrated in COVID-19) through the formation of neutrophil extracellular traps and monocyte-platelet aggregates, which could be responsible for DIC. The modulation of glucose availability for activated M1 macrophages by means of a eucaloric ketogenic diet (EKD) could represent a possible metabolic tool for reducing adenosine triphosphate production from aerobic glycolysis in the M1 macrophage phenotype during the exudative phase. This approach could reduce the overproduction of cytokines and, consequently, the accumulation of neutrophils, monocytes, and platelets from the blood. Second, an EKD could be advantageous for the metabolism of anti-inflammatory M2 macrophages because these cells predominantly express oxidative phosphorylation enzymes and are best fed by the oxidation of fatty acids in the mitochondria. An EKD could guarantee the availability of free fatty acids, which are an optimal fuel supply for these cells. Third, an EKD, which could reduce high lactate formation by macrophages due to glycolysis, could favor the production of interferon type I, which are inhibited by excessive lactate production. From a practical point of view, the hypothesis, in addition to being proven in clinical studies, must obviously take into account the contraindications of an EKD, particularly type 1 or 2 diabetes treated with drugs that can cause hypoglycemia, to avoid the risk for side effects of the diet.”

Sukkar SG, Bassetti M. Induction of ketosis as a potential therapeutic option to limit hyperglycemia and prevent cytokine storm in COVID-19. Nutrition. 2020;79-80:110967. doi:10.1016/j.nut.2020.110967

Anti-aging effect of DL-β-hydroxybutyrate against hepatic cellular senescence induced by D-galactose or γ-irradiation via autophagic flux stimulation in male rats – ScienceDirect

https://www.sciencedirect.com/science/article/pii/S0167494320302855

 

”Taken together, these findings suggest that βOHB may be useful in combating hepatic cellular senescence induced by d-galactose or γ-irradiation via autophagy dependent mechanisms.”

 Habieb, M. E., Mohamed, M. A., El Gamal, D. M., Hawas, A. M. & Mohamed, T. M. (2021). Anti-aging effect of DL-β-hydroxybutyrate against hepatic cellular senescence induced by D-galactose or γ-irradiation via autophagic flux stimulation in male rats. Archives of Gerontology and Geriatrics, 92, s. 104288. doi:https://ift.tt/3omSboU

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The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease – PubMed

https://pubmed.ncbi.nlm.nih.gov/25686106/

”Our findings suggest that the anti-inflammatory effects of caloric
restriction or ketogenic diets may be linked to BHB-mediated inhibition
of the NLRP3 inflammasome”

Youm YH, Nguyen KY, Grant RW, et al. The ketone metabolite
β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory
disease. Nat Med. 2015;21(3):263-269. doi:10.1038/nm.3804

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Is the restricted ketogenic diet a viable alternative to the standard of care for managing malignant brain cancer? – PubMed

https://pubmed.ncbi.nlm.nih.gov/21885251/

 

Abstract

Malignant brain cancer persists as a major disease of morbidity
and mortality. The failure to recognize brain cancer as a disease of
energy metabolism has contributed in large part to the failure in
management. As long as brain tumor cells have access to glucose and
glutamine, the disease will progress. The current standard of care
provides brain tumors with access to glucose and glutamine. The high fat
low carbohydrate ketogenic diet (KD) will target glucose availability
and possibly that of glutamine when administered in carefully restricted
amounts to reduce total caloric intake and circulating levels of
glucose. The restricted KD (RKD) targets major signaling pathways
associated with glucose and glutamine metabolism including the
IGF-1/PI3K/Akt/Hif pathway. The RKD is anti-angiogenic, anti-invasive,
anti-inflammatory, and pro-apoptotic when evaluated in mice with
malignant brain cancer. The therapeutic efficacy of the restricted KD
can be enhanced when combined with drugs that also target glucose and
glutamine. Therapeutic efficacy of the RKD was also seen against
malignant gliomas in human case reports. Hence, the RKD can be an
effective non-toxic therapeutic option to the current standard of care
for inhibiting the growth and invasive properties of malignant brain
cancer.

 

Seyfried TN, Marsh
J, Shelton LM, Huysentruyt LC, Mukherjee P. Is the restricted ketogenic
diet a viable alternative to the standard of care for managing malignant
brain cancer? Epilepsy Res. 2012 Jul;100(3):310-26. doi:
10.1016/j.eplepsyres.2011.06.017. Epub 2011 Aug 31. PMID: 21885251.

 

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In Alzheimer Research, Glucose Metabolism Moves to Center Stage

https://jamanetwork.com/journals/jama/fullarticle/2758712

”Six weeks after completing the modified ketogenic diet, patients had improved Alzheimer disease biomarkers in their cerebrospinal fluid. “With the ketogenic diet, we are moving the β-amyloid in a healthier direction,” Craft said. Patients also had better blood flow to the hippocampus and improved body-wide insulin sensitivity. A larger trial of the modified ketogenic diet is now under way.”


Kuehn BM. In Alzheimer Research, Glucose Metabolism Moves to Center Stage. JAMA.2020;323(4):297–299. doi:10.1001/jama.2019.20939


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Effects of a low carbohydrate diet on energy expenditure during weight loss maintenance: randomized trial | The BMJ

https://www.bmj.com/content/363/bmj.k4583

Conclusions Consistent with the carbohydrate-insulin model, lowering dietary carbohydrate increased energy expenditure during weight loss maintenance. This metabolic effect may improve the success of obesity treatment, especially among those with high insulin secretion.


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To Keto or Not to Keto? A Systematic Review of Randomized Controlled Trials Assessing the Effects of Ketogenic Therapy on Alzheimer Disease | Advances in Nutrition | Oxford Academic

https://academic.oup.com/advances/article-abstract/doi/10.1093/advances/nmaa073/5864685

””… interventions, and outcome measures, ketogenic therapy appears promising
in improving both acute and long-term cognition among patients with
Alzheimer disease/mild cognitive impairment.”

Maria G Grammatikopoulou, Dimitrios G Goulis, Konstantinos Gkiouras,
Xenophon Theodoridis, Kalliopi K Gkouskou, Athanasios Evangeliou,
Efthimis Dardiotis, Dimitrios P Bogdanos, To Keto or Not to Keto? A
Systematic Review of Randomized Controlled Trials Assessing the Effects
of Ketogenic Therapy on Alzheimer Disease, Advances in Nutrition, , nmaa073, https://doi.org/10.1093/advances/nmaa073

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Intermittent fasting from dawn to sunset for 30 consecutive days is associated with anticancer proteomic signature and upregulates key regulatory proteins of glucose and lipid metabolism, circadian clock, DNA repair, cytoskeleton remodeling, immune system and cognitive function in healthy subjects – ScienceDirect

https://www.sciencedirect.com/science/article/pii/S1874391920300130

Highlights

  • First human serum proteomics study of 30-day intermittent fasting from dawn to sunset in healthy subjects 
  • The 30-day intermittent fasting from dawn to sunset is associated with a serum proteome protective against cancer 
  • Intermittent fasting from dawn to sunset for 30 days upregulates proteins protective against obesity, diabetes, and metabolic syndrome 
  • Intermittent fasting from dawn to sunset for 30 days induces key regulatory proteins of DNA repair and immune system 
  • Intermittent fasting from dawn to sunset for 30 days upregulates proteins protective against Alzheimer’s disease and neuropsychiatric disorders

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Ketogenic diet activates protective γδ T cell responses against influenza virus infection | The Journal of Immunology

https://www.jimmunol.org/content/202/1_Supplement/62.7.abstract

”Ketogenic diet (KD) feeding resulted in an expansion of γδ T cells in the lung that improved barrier functions, thereby enhancing anti-viral resistance.”

Therefore, KD mediated immune-metabolic integration represents a viable avenue towards preventing or alleviating influenza disease.”

Goldberg, E. L., Molony, R., Sidorov, S., Kudo, E., Dixit, V. D. & Iwasaki, A. (2019). Ketogenic diet activates protective γδ T cell responses against influenza virus infection. The Journal of Immunology, 202(1 Supplement), ss. 62.7-62.7. 

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