As described throughout the previous sections, there are many instances of codependencies and feed-forward loops in bioenergetic and antioxidant signal transduction, which supports the well-known potential for metabolic stimuli, such as diet or exercise, to have a profound physiological influence. Given the central role of mitochondria in oxidative phosphorylation and ROS production, the overlap between bioenergetic and antioxidant signaling is not surprising and is possibly an outcome of evolution favoring efficiency. PGC-1α is at the center of this overlapping and complex network of codependencies. The likely role of PGC-1α as a coactivator of FOXO3a indicates a possible dependence of FOXO3a transcriptional activity on PGC-1α , indicating FOXO3a as a central mediator as well. Furthermore, FOXO3a induces transcription of PGC-1α [287, 322, 367], and formation and antioxidant transcriptional activity of the PGC-1α-FOXO3a complex are partly dependent on interaction with SIRT1 . In muscle, expression of many of the bioenergetic and antioxidant proteins previously discussed is dependent on PGC-1α . Upstream, activation of PGC-1α is dependent on AMPK  and SIRT1 [242, 269] and partly dependent on SIRT3 . Furthermore, activation of SIRT1 is dependent on AMPK , which may also be the case for SIRT3. AMPK and PGC-1α are therefore two key factors, with critical supporting roles of the sirtuins, in the signal transduction linking bioenergetics to antioxidant defense. Further supporting the relevance of this linkage to nutritional ketosis, expression of AMPK, SIRT1, FOXO3a, and NFE2L2 is required for extension of lifespan in C. elegans by exogenous BHB , and expression of AMPK, p38 MAPK, and NFE2L2 is required for the extension of lifespan, also in C. elegans, by mitohormesis induced through inhibition of glucose metabolism . The induction of AMPK [259, 260], SIRT3 [263, 329], p38 MAPK [310–313], PGC-1α [76, 77, 260, 282, 283], FOXO3a [324, 331, 333], and NFE2L2 [358–360] activity by oxidative stress also makes this signaling highly relevant to mitohormesis [263, 282, 360], especially given that activation of these proteins has been shown to decrease mitochondrial or cellular ROS [76, 263, 282, 289, 323, 332, 334, 356, 359, 367]. Furthermore, mitochondrial biogenesis  and the activities of AMPK [259, 260], SIRT3 , p38 MAPK [311, 312], PGC-1α [76, 77, 260, 283], FOXO3a , and NFE2L2  are increased by H2O2, more specifically associating this signaling with mitohormesis. Given that AMPK and sirtuins are upstream of the majority of this signaling and that AMPK and sirtuin activities are stimulated by both bioenergetic and oxidative stressors, these stressors are likely the primary signals through which nutritional ketosis may induce the mitochondrial and antioxidant adaptations characteristic of mitohormesis (Figure 2).
Physical inactivity is a predictor of CVD events and related mortality. Many components of metabolic syndrome are associated with a sedentary lifestyle, including increased adipose tissue (predominantly central); reduced HDL cholesterol; and a trend toward increased triglycerides, blood pressure, and glucose in the genetically susceptible. Compared with individuals who watched television or videos or used their computers for less than one hour daily, those who carried out these behaviors for greater than four hours daily have a twofold increased risk of metabolic syndrome.
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β-hydroxybutyrate and, in some cases, acetoacetate contribute to protection against oxidative stress by decreasing production of mitochondrial reactive oxygen species (mtROS), by increasing expression or protein content of antioxidant enzymes through histone deacetylase (HDAC) inhibition, and by directly scavenging the hydroxyl radical (•OH). Upregulation of antioxidant enzymes through HDAC inhibition includes manganese superoxide dismutase (SOD2), catalase, and metallothionein II and is likely mediated by the transcription factor forkhead box O 3a (FOXO3a).
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I finally made this recipe. (I have made many of your others and use them often.) It did fall slighty but I was still able to slice it after it cooled. It was also purple, which is just fine with me. I toasted in the oven this morning and it was nice and crisp. I can’t tell you have happy I was to dip it in my fried egg this morning. Thanks, Maria, for all you do!
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Hi Maria! I just tried this recipe and it is ABSOLUTELY A.M.A.Z.I.N.G.!! Thank you SOOO much for sharing the recipe! One question- In the recipe you have 2 links to order the Psyllium. I just realized it after I placed my order through the first link, which is from your amazon store- The Frontiers Psyllium. I’m hoping that one works for the bread as good as the Jay Robb Brand!
Garlic: Potent, but effective. Garlic is known as one of the oldest medicines in the world…and with good reason. An animal study that administered high doses of raw garlic to rats for 4 weeks found that it had a profound effect of reducing blood glucose levels, as well as cholesterol and triglycerides compared to rats who did not receive raw garlic (2). They also tested rats with boiled garlic, and saw no changes in blood glucose, so the benefit comes from raw garlic.
I am so impressed by your bread recipes. Have spent the last two days just baking away and they taste absolutely great! What a joy to finally find something this tasty and healthy. I noticed in your previous post that we could expect to read about “What I eat” from you next. We’re staying tuned and waiting with great curiosity. Will pass on to our libraries about your books, for sure.
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.
Exogenous ketones: Very little is known about the effects of exogenous ketones on cancer. However, as exogenous ketones can also lower blood sugar and elevate BHB they could be helpful by a similar mechanism to the ketogenic diet. Exogenous ketones may even be preferable to the ketogenic diet, as patients can eat a wider range of palatable and calorically dense food to maintain their strength during treatment. One animal study showed that ketone ester supplementation (acetoacetate diester) decreased tumour size and prolonged the survival of mice with metastatic cancer100.
My point here is that the warnings about the ketogenic principles are well taken and well documented. My concern is implications that this is a fad. I don’t use the word diet with my patients and I’m concerned that the principles behind the label and the real results that these readers have commented on might get minimized. I have found it best to encourage patients to read authors like: Stephen Phinney, Jeff Volek, Patricia Daly, and Charles Gant and the be partners with their doctors and check blood work as they move along. I am not for or against the article. If ketogenic principles offer people enduring, satisfying, and cohesive change then why not read about its potential and flexilbity?
I made it tonight and use a mini loaf pan. It came out delicious. I used the http://www.tasteofhome.com/article/how-to-cut-down-recipes/ link to adjust the recipe measurements using the one third column. I used 2 egg whites. The slices will be small but it was delicious with melted butter. Keto bread recipes and I have tried quite a few have not turned out well for me. I do not like to waste expensive ingredients that is why I will usually do a small amount first. This recipe has been the exception. It is good simple and delicious. I will make it again using the recipe as written. Note: I whipped the egg whites for 10 minutes to get the right consistency. I hope this helps and thank You Maya for finally for me making a bread that tastes great and is easy to make.
As previously discussed, RET is a prominent source of mtROS and is dependent on a high Δp across the inner mitochondrial membrane. During ATP production, Δp is dissipated as H+ enters the mitochondrial matrix through ATP synthase. Mitochondrial uncoupling also dissipates Δp, but by allowing translocation of H+ into the matrix independent of ATP synthase. Uncoupling is therefore regarded as an antioxidant defense in that it can mitigate mtROS production [122–126]. In fact, only a small dissipation of ΔΨ or ΔpH (components of Δp) is needed for a large decrease in mtROS production [57–60, 127].
Several other rodent studies provide additional evidence of ketogenic diets upregulating antioxidant defense, but without enough data to convincingly attribute the results to mitohormesis. Content of SOD2 has increased in the livers of mice fed a ketogenic diet (% energy: 89 fat, <1 carbohydrate, and 10 protein), which occurred in conjunction with increased median lifespan and decreases in tumors and age-associated losses of physical and cognitive performance . In addition, activity of GCL and the protein content of its two subunits increased in the hippocampal homogenate of rats fed a ketogenic diet (Bio-Serv F3666) for 3 weeks . This was in conjunction with higher levels of reduced glutathione (GSH) and lower ROS production in hippocampal mitochondria. The ketogenic diet also increased resistance to mtDNA damage in hippocampal mitochondria exposed to H2O2 . Consistent with these results, total antioxidant capacity and activities of GPx and catalase were increased in hippocampal homogenate of rats fed a ketogenic diet (% energy: 86 fat, <1 carbohydrate, and 13 protein) for 8 weeks . Furthermore, in cortical homogenate of rats induced with traumatic brain injury, a ketogenic diet increased cytosolic and mitochondrial protein contents of NAD(P)H:quinone oxidoreductase 1 (NQO1) and SOD1, as well as mitochondrial protein content of SOD2, and also prevented mitochondrial oxidative damage (indicated by 4-HNE) .
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 🙂
I think next time I will either use less psyllium or less egg. I had to halve the recipe and I used a bit more egg and water by accident. Next time I’ll try it with coconut flour since I think as a very “dry” flour it works best with flours/meals that are very “wet” like flax meal and psyllium. They cancel each other out in the end it seems. I’ll also bake it a bit longer because the crust is yummy!
In regard to the practicality of BHB signaling, many of the outcomes described above, including HDAC inhibition, were achieved with BHB concentrations within the range of 0.6–2 mM [37, 103, 105, 108, 109, 111, 112, 116], which is well within the physiological range of nutritional ketosis for humans and even suggests potential benefit at low to moderate levels.
Normally, the body breaks down carbohydrates, fat, and (sometimes) proteins to provide energy. When carbohydrate is consumed in the diet, some is used immediately to maintain blood glucose levels, and the rest is stored. The hormone that signals to cells to store carbohydrate is insulin. The liver stores carbohydrate as glycogen, this is broken down and released between meals to keep blood glucose levels constant. Muscles also store glycogen, when broken down this provides fuel for exercise. Most cells in the body can switch readily between using carbohydrates and fat as fuel. Fuel used depends on substrate availability, on the energy demands of the cell and other neural and hormonal signals.
Ketone bodies are acidic, but acid-base homeostasis in the blood is normally maintained through bicarbonate buffering, respiratory compensation to vary the amount of CO2 in the bloodstream, hydrogen ion absorption by tissue proteins and bone, and renal compensation through increased excretion of dihydrogen phosphate and ammonium ions. Prolonged excess of ketone bodies can overwhelm normal compensatory mechanisms, defined as acidosis if blood pH falls below 7.35.
How, exactly, does our body take pyruvate (from glucose) or acetyl CoA (from fat) and generate so much ATP? The answer lies in the beauty of the Krebs Cycle, which feeds into a process called the electron transport chain (or ETC), I alluded to above. Since the adage ‘you can’t get something for nothing’ is as true in biochemistry as it appears to be in life, to get all that ATP (i.e., stored energy in the form of the phosphate bond), we need to give up something. What the ETC does give up, as its name suggests, is electrons. Through a series of redox reactions the ETC trades the stored energy held by electrons going from higher to lower energy states in exchange for the chemical energy stored in the bonds of the third phosphate group on an ATP molecule.
Keto Bread Recipe - Four Ways - quick and simple way to make low carb, individual keto bread rolls, in ramekins and just a few healthy ingredients. You can either bake it in the microwave for 90 seconds or in the oven for 10-15 minutes. The the-easiest, the-best kept bread recipe I've ever tried. There are four different options available - you can make cheese keto bread, broccoli ketogenic bread, bacon and spinach and feta. And of course you can leave it as it is, if you prefer plain kept bread rolls.
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The reason a starving person can live for 40-60 days is precisely because we can turn fat into ketones and convert ketones into substrate for the Krebs Cycle in the mitochondria of our neurons. In fact, the more fat you have on your body, the longer you can survive. As an example of this, you may want to read this remarkable case report of a 382 day medically supervised fast (with only water and electrolytes)! If we had to rely on glucose, we’d die in a few days. If we could only rely on protein, we’d live a few more days but become completely debilitated with muscle wasting.
Maria – Love this recipe – took me 4 times before I got it how I wanted it and I add sesame seeds. Then I slice really really thin – about 1/2 cm then dry all the slices in the oven ready for toasting. However, right now I can only find baking powder with vanilla. Can I sub baking soda which together with the vinegar should work but how much? Can you help please?
For those whose bread keeps sinking or falling, make sure your baking powder is fresh. It does expire and usually a sunken baked good is evidence of it. I think it only lasts about half a year to a year. I made some strawberry muffins with almond flour last year and they were such a pretty pink but all of them caved in in the middle. 🙁 Bad baking powder.
It’s well known that adherence to the prescribed diet is usually low and self-reported food intake is very unreliable. So there’s no way to guarantee that the participants strictly adhered to the diet. Because it requires a lot of discipline and planning to stay in ketosis for a long time without interruption, it won’t be possible to perform a long-term study that guarantees uninterrupted ketosis using old study methods. This may change soon with improved self-tracking devices.
My first try at this recipe –lower half was gummy. Crust tasted amazing to I’m eating the ends as toast. I’m too frugal to throw away 3 cups of almond flour, so I cubed up the rest of the loaf, put it in to bake at 350 for 30 minutes or so. Cubes are great on salad -taste like toasted almond/sesame. Now I’m making savory bread pudding with about 2 cups of the cubes (6 eggs, 3/4c almond milk, 1/4c cream, cooked bacon bits, shallots, basil and chives). Baking in muffin tins. Will be taking them for lunches.
Ketone esters (BHB-BD) could help to accelerate glycogen resynthesis32. After exercise that depletes muscle glycogen, the muscle uses carbohydrate from the diet to replenish these stores. An experiment was carried out where athletes undertook depletive exercise and then were given a ketone drink (or carbohydrate placebo) as well as glucose intravenously to maintain a high blood level (10mM). In this experiment, when the recovery drink contained ketone ester, more glucose was infused in order to maintain blood glucose at 10 mM, and muscle glycogen levels were 50% higher. However, the evidence is not conclusive: another study. 31 found that adding ketone ester to a protein and carbohydrate recovery drink did not enhance the normal rate of glycogen re-synthesis.
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Whilst the diet is broadly acknowledged to be safe strategy where medications have failed, side effects such as kidney stones, hyperlipidemia and can occur47. Furthermore, maintaining dietary adherence in young school age children can be very challenging for caregivers. Exogenous ketones may be an alternative or a adjunct to the ketogenic diet in epilepsy. Early work suggests that exogenous ketones could have antiseizure effects. Injection of the ketones acetoacetate and acetone have been found to have anticonvulsant properties in animal models48, and an acetoacetate diester was found to protect against seizures in rats exposed to high levels of oxygen49. Further studies are required to understand specifically how ketone bodies affect seizure control, however for children who experience daily seizures a combination of the ketogenic diet and exogenous ketones could be helpful to manage their condition.
Mitochondrial uncoupling is primarily facilitated by uncoupling proteins (UCPs) and adenine nucleotide translocase (ANT) [124, 128, 129]. Although UCP1 is primarily expressed in brown adipose, UCP2 is expressed across a wide variety of tissues, and expression of UCP3 appears to be limited to skeletal muscle and the heart . Knockout of UCP2  or UCP3 [94, 132] increases mtROS production, and both proteins are inactivated through glutathionylation by GSH , further establishing their involvement in antioxidant defense. UCP2 and UCP3 may also be activated by products of lipid peroxidation induced by mtROS . However, the potential for UCP2 and UCP3 to reduce mtROS through uncoupling is not fully agreed upon;  UCPs may alternatively protect against oxidative damage merely by exporting lipid hydroperoxides . Furthermore, UCP3 is less abundant in type I and type IIa muscle fibers , which are more oxidative, and its expression and content are further decreased by endurance exercise training [135, 136], suggesting that UCP3 may not be a primary defense against mtROS.
I’m following the ketogenic diet and I find it very easy, pleasant and varied. I can even say that my diet today is more varied than the previous one. I do not intend to leave this diet and I cannot really see why. My initial focus was not to lose weight, I’ve always been lean, but to feel better, well disposed. And I got it! I am very pleased, I have read a lot about it (including scientific literature) and I have influenced other people who need to lose weight or improve some aspects of their health. But from the beginning I went on my own way, without the help of a nutritionist because I did not want to suffer the influence of others’ ideas.
Make nonstarchy vegetables the star of your plate, taking up half of it. “For anybody at risk of diabetes, it's important to take your vegetable intake to the next level,” Wright says. “Balancing your plate with half vegetables will fill you up without loading you down with tons of carbs.” Credit the fiber and water in the vegetables for helping keep you satisfied.
In type 2 diabetes the body has an increasingly harder time to handle all the sugar in the blood. Large amounts of the blood sugar-lowering hormone insulin are produced, but it’s still not enough, as insulin sensitivity decreases. At the time of being diagnosed with type 2 diabetes, people usually have ten times more insulin in their bodies than normal. As a side effect, this insulin stores fat and causes weight gain, something that has often been in progress for many years before the disease was diagnosed.
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This paleo keto bread recipe makes a delicious option for coconut lovers. For a low-fuss loaf, blend coconut flour with ingredients like eggs, coconut oil, and salt — then bake away for a sturdy bread with only 1.3 net carbs per serving. Make this recipe totally nut-free (and more Bulletproof) by swapping almond milk with full-fat canned coconut milk.