As with other sources of oxidative stress, mtROS can damage enzymes and cell membranes and subsequently facilitate the pathogenesis of chronic disease . Oxidative damage to mitochondrial DNA (mtDNA) is of particular concern because of its proximity to the electron transport chain (mtETC). Furthermore, compared to nuclear DNA, mtDNA is more prone to oxidative damage and is not repaired as effectively [42–45], although this has been debated based on more recent evidence [46–50]. Unrepaired mtDNA damage leads to mitochondrial dysfunction, which is implicated in the pathogenesis of a variety of chronic diseases  and associated with shorter lifespan . Therefore, while moderate levels of mtROS have important roles in signaling and health, protection against excessive levels is also important.
Nutritional ketosis may initiate bioenergetic and mitohormetic signaling through an increase in catecholamines or adiponectin, a decrease in insulin or glycogen, or an increase in β-oxidation that leads to an increase in mitochondrial reactive oxygen species (mtROS) or NAD+. This leads to further signaling involving AMP-activated protein kinase (AMPK), silent mating type information regulation 2 homologue 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), forkhead box O 3a (FOXO3a), and nuclear factor erythroid-derived 2-like 2 (NFE2L2), ultimately leading to transcription of genes related to oxidative capacity, mitochondrial uncoupling, and antioxidant defense. These adaptations collectively contribute to resistance against oxidative stress. Other proteins involved include liver kinase B1 (LKB1), which activates AMPK; nicotinamide phosphoribosyltransferase (NAMPT), which facilitates SIRT1 activation through NAD+ synthesis; and nuclear respiratory factors 1 and 2 (NRF-1 and NRF-2) and mitochondrial transcription factor A (TFAM), which promote mitochondrial biogenesis.
Ketoacidosis occurs mainly in people with type 1 diabetes if they do not take insulin. In diabetic ketoacidosis (DKA), blood sugar and ketones rise to dangerous levels, which disrupts the blood’s delicate acid-base balance. People in ketoacidosis feel extremely ill and experience profound dehydration, vomiting, abdominal pain, and weakness. DKA requires hospitalization so that IV fluids and insulin can be given to gradually and safely lower blood sugar.
LOVE this bread. As a pregnant type 1 diabetic, I was looking for something to toast. I’ve tried multiple different recipes from other sites, and the bread is always so crumbly that you can never spread anything on it. This one is AMAZING! I may have to experiment with more water so that it comes out less dense, but soooo happy to prevent blood sugar spikes with future sandwiches. I can even foresee being able to have traditional burgers again (not just wrapped in lettuce). My husband bakes his own “normal” bread, and now I get bread too and its even easier to make than his 🙂
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A study on hippocampal mitochondrial function in rats more directly supports the induction of mitohormesis by a ketogenic diet. After the first day of the diet (Bio-Serv F3666), H2O2 production by isolated mitochondria was increased . After the third day, mitochondrial levels of oxidized glutathione (GSSG) and hippocampal levels of 4-hydroxy-2-nonenal (4-HNE) were also increased, further indicating an increase in oxidative stress. However, at completion of the first week, upregulation of antioxidant signaling occurred, indicated by increased nuclear content and transcriptional activity of nuclear factor erythroid-derived 2-like 2 (NFE2L2), which persisted through the remainder of the study. By the third week, mitochondrial H2O2 production decreased to below baseline . In the liver, content of reduced acetyl CoA, which is indicative of mitochondrial redox status, decreased after three days of the ketogenic diet, but increased relative to the control diet after three weeks, indicating an initial increase in oxidative stress followed by a decrease . This was in conjunction with changes in NFE2L2 nuclear content and transcriptional activity similar to those observed in the hippocampus. As with the previously described C. elegans experiments, the time course of these observations is a strong indication of mitohormesis, and the similarity in results between the liver and hippocampus suggests that a ketogenic diet can induce mitohormesis in a variety of tissues.
Russel Wilder first used the ketogenic diet to treat epilepsy in 1921. He also coined the term "ketogenic diet." For almost a decade, the ketogenic diet enjoyed a place in the medical world as a therapeutic diet for pediatric epilepsy and was widely used until its popularity ceased with the introduction of antiepileptic agents. The resurgence of the ketogenic diet as a rapid weight loss formula is a relatively new concept the has shown to be quite effective, at least in the short run.
This is brilliant. I made it today not in a mug but a cereal bowl. So it was bigger. I could only eat half. Rather filling. I layered it with cream cheese and a thin slice of smoked ham for mid afternoon snack. Slight bitter after taste which i think is from the baking powder. I am going to make it again with herbs like some others have suggested. Thanks HBK😚
One of the foods that people tell us they miss most after going keto is bread. (And cookies or cakes, but you get the idea.) We get it, bread is undeniably comfort food. Growing up, it wasn’t unheard of to eat toast for breakfast, a sandwich for lunch, and maybe even a slice of buttered bread along with dinner. Not only is that ton of carbs, but it’s also a lot of empty calories when we could have been eating real-food alternatives, like this bread made from nutrient-dense ingredients!