For example- eating blueberries post workout to manage oxidative stress.
I recall in one of his videos he said it increased the oxidative stress. All of the research I have done says oxidative stress is bad. I am confused
I have been diagnosed with psychosis and anxiety. Recently found I might have undermethylation and possibly oxidative stress. What do you suggest?
https://doi.org/10.1016/j.lfs.2021.120227
https://pubmed.ncbi.nlm.nih.gov/34921866
Abstract
BACKGROUND
Ischemic kidney injury is a common clinical condition resulting from transient interruption of the kidney's normal blood flow, leading to oxidative stress, inflammation, and kidney dysfunction. The ketogenic diet (KD), a low-carbohydrate, high-fat diet that stimulates endogenous ketone body production, has potent antioxidant and anti-inflammatory effects in distinct tissues and might thus protect the kidney against ischemia and reperfusion (IR) injury.
MAIN METHODS
Male Wistar rats were fed a KD or a control diet (CD) for three days before analyzing metabolic parameters or testing nephroprotection. We used two different models of kidney IR injury and conducted biochemical, histological, and Western blot analyses at 24Β h and two weeks after surgery.
KEY FINDINGS
Acute KD feeding caused protein acetylation, liver AMPK activation, and increased resistance to IR-induced kidney injury. At 24Β h after IR, rats on KD presented reduced tubular damage and improved kidney functioning compared to rats fed with a CD. KD attenuated oxidative damage (protein nitration, 4-HNE adducts, and 8-OHdG), increased antioxidant defenses (GPx and SOD activity), and reduced inflammatory intermediates (IL6, TNFΞ±, MCP1), p50 NF-ΞΊB expression, and cellular infiltration. Also, KD prevented interstitial fibrosis development at two weeks, up-regulation of HSP70, and chronic Klotho deficiency.
SIGNIFICANCE
Our findings demonstrate for the first time that short-term KD increases tolerance to experimental kidney ischemia, opening the opportunity for future therapeutic exploration of a dietary preconditioning strategy to convey kidney protection in the clinic.
------------------------------------------ Info ------------------------------------------
Open Access: False
Authors: Pedro Rojas-Morales - Juan Carlos LeΓ³n-Contreras - MΓ³nica SΓ‘nchez-Tapia - Alejandro Silva-Palacios - Agustina Cano-MartΓnez - Susana GonzΓ‘lez-Reyes - AngΓ©lica SaraΓ JimΓ©nez-Osorio - Rogelio HernΓ‘ndez-Pando - Horacio Osorio-Alonso - Laura Gabriela SΓ‘nchez-Lozada - Armando R. Tovar - JosΓ© Pedraza-Chaverri - Edilia Tapia -
Additional links: None found
Ageing is defined as the progressive accumulation of changes, characterised by changes over time in physiological function and increased probability of pathological diseases and death.
https://doi.org/10.12182/20211160202
https://pubmed.ncbi.nlm.nih.gov/34841761
Abstract
Objective
To investigate the regulatory function and mechanism of Ξ²-hydroxybutyrate (Ξ²-OHB), a ketone body, on the mitochondrial oxidative stress of inflammatory human umbilical vein endothelial cells (HUVECs).
Methods
Lipopolysaccharide (LPS) and adenosine triphosphate (ATP) were used to induce macrophages to release proinflammatory factors, and the culture supernatant was collected as a macrophage-conditioned medium (MCM) to culture HUVECs. A total of 7 groups of cells were used in the study: β control group, or normal cultured HUVECs, β‘MCM group, or the MCM-cultured HUVECs, groups β’ to β¦ were all HUVECs co-cultured with different reagents, including β’MCM Ξ²-OHB group, β£MCM N-acetylcysteine (NAC) group, β€MCM Ξ²-OHB NAC group, β₯MCM Ξ²-OHB histone deacetylase agonist ITSA1 group, and β¦MCM Ξ²-OHB histone deacetylase inhibitor Entinostat group. MitoSOX immunofluorescence staining was conducted to analyzes the mitochondrial superoxide levels, real-time fluorescent quantitative polymerase chain reaction (RT-qPCR) was performed to examine the mRNA expression of antioxidant genes, and Seahorse mitochondrial energy analyzer was used to measure mitochondrial aerobic respiration capacity.
Results
Compared with the control group, mitochondrial superoxide production was significantly increased in the MCM cultured HUVECs cells, while Ξ²-OHB treatment significantly inhibited mitochondrial superoxide production, which was accompanied by an increase in the mRNA expression of antioxidant genes, and significant increase in the basal mitochondrial oxygen consumption rate and respiratory reserve capacity. NAC treatment did not further enhance the protective effect of Ξ²-OHB on mitochondrial functions. In addition, ITSA1 treatment could completely offset the antioxidant and mitochondrial protective effects of Ξ²-OHB, and these stated effects were still maintained after Entinostat treatment.
Conclusion
The ketone body Ξ²-OHB attenuates the mitochondrial oxidative stress of vascular endothelial cells through activating the antioxidant pathway and inhibiting histone deacetylase activity.
I recall him saying in a video that it increases oxidative stress, but all the research I have done says oxidative stress is harmful??? Help me understand.
Life Sciences Volume 289, 15 January 2022, 120227
A ketogenic diet attenuates acute and chronic ischemic kidney injury and reduces markers of oxidative stress and inflammation
Author links open overlay panelPedroRojas-MoralesabEdiliaTapiaa Show more Outline Share Cite https://doi.org/10.1016/j.lfs.2021.120227 Get rights and content Abstract Background Ischemic kidney injury is a common clinical condition resulting from transient interruption of the kidney's normal blood flow, leading to oxidative stress, inflammation, and kidney dysfunction. The ketogenic diet (KD), a low-carbohydrate, high-fat diet that stimulates endogenous ketone body production, has potent antioxidant and anti-inflammatory effects in distinct tissues and might thus protect the kidney against ischemia and reperfusion (IR) injury.
Main methods Male Wistar rats were fed a KD or a control diet (CD) for three days before analyzing metabolic parameters or testing nephroprotection. We used two different models of kidney IR injury and conducted biochemical, histological, and Western blot analyses at 24 h and two weeks after surgery.
Key findings Acute KD feeding caused protein acetylation, liver AMPK activation, and increased resistance to IR-induced kidney injury. At 24 h after IR, rats on KD presented reduced tubular damage and improved kidney functioning compared to rats fed with a CD. KD attenuated oxidative damage (protein nitration, 4-HNE adducts, and 8-OHdG), increased antioxidant defenses (GPx and SOD activity), and reduced inflammatory intermediates (IL6, TNFΞ±, MCP1), p50 NF-ΞΊB expression, and cellular infiltration. Also, KD prevented interstitial fibrosis development at two weeks, up-regulation of HSP70, and chronic Klotho deficiency.
Significance
Our findings demonstrate for the first time that short-term KD increases tolerance to experimental kidney ischemia, opening the opportunity for future therapeutic exploration of a dietary preconditioning strategy to convey kidney protection in the clinic
https://www.sciencedirect.com/science/article/abs/pii/S0024320521012145
