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This bread looks amazingly awesome and I will be trying it soon, but with a gluten free psyllium husk brand. I just wanted to point out that J Robb’s Psyllium Husk package declares the presence of WHEAT. Read the label listed on his website. Using his Psyllium Husk would make the bread NOT gluten free. It also states that it has a multitude of other allergens and possibly all of them are in a package at the same time. Just a heads up.

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I have never commented on a recipe post ever. But i’ve tried so many mug breads and honestly Paola, this is the best hands down. It tasted lovely with a pleasing texture, more biscuit/scone like, which i am not complaining about. I used vanilla whey protein (which was sweetened) omitted the sweetener and used heavy cream in place of sour cream. Such a treat. Will be making again and again for sure.
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.
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The coordinated effects of AMPK, SIRT1, and SIRT3 are primarily mediated through PGC-1α, which is activated through phosphorylation by AMPK [242, 265] and deacetylation by SIRT1 [77, 242, 266–269]. SIRT3 also increases PGC-1α activity [270], possibly through cAMP response element binding protein (CREB) [271, 272], but the exact mechanism has not been elucidated. In addition to phosphorylating PGC-1α, activated AMPK also increases PGC-1α expression [260, 273–276]. Activation of β2-adrenergic receptors [277–280] and the adiponectin AdipoR1 receptor [281] also increase PGC-1α expression, independently of AMPK activation [278, 281]. PGC-1α activity is increased by oxidative stress [76, 77, 282–284], possibly through activation of AMPK [259, 260] or p38 mitogen-activated protein kinase (MAPK) [283, 284], or inhibition of glycogen synthase kinase 3β, which inhibits PGC-1α through phosphorylation [77, 283]. In contrast, insulin decreases PGC-1α activity through phosphorylation by PKB [285]. Once activated, PGC-1α interacts with the PPAR family of nuclear receptors [286] and the FOXO family of transcription factors [287] to influence expression of a variety of bioenergetic and antioxidant proteins. PGC-1α most notably increases transcription of proteins involved in mitochondrial biogenesis and respiration [76, 242, 265, 267, 269, 274, 279, 282, 285, 288–293] but also increases transcription of antioxidant proteins including SOD1 [76], SOD2 [76, 282, 289, 292–294], catalase [282], GPx [76, 294], thioredoxins [282, 283, 292], TRXR [282, 292], Prx3 [282, 292], and Prx5 [282, 292], as well as the mitochondrial uncoupling proteins UCP2 [76, 265, 282, 288, 294], UCP3 [76, 265, 294], and ANT [76, 295].
So when i made this bread it didnt really stay the way i wanted it to be because when i took it out it looked like regular bread but after like 5-10 minutes it sunk down and mine turned blueish-purpleish….is that good?? I dont think i will be making this again….and i measured out all the ingredients too so i dont know what i did wrong…. PLEASE HELP!!!!!!!!!!!!!
This savory frittata recipe by Ketogasm is loaded with nutrients to power your day.It’s hearty and filling, without taking you past your carb limit. Each serving has 333 calories, 26 grams of fat, 20 grams of protein, and only 1 net gram of carbs. This bloggers uses spinach, mushroom and uncured sausage, but feel free to play around with your veggies or swap sausage for chicken or steak.
Hi Melissa, Are you beating the whole eggs? It needs to be egg whites only. Whole eggs will never form peaks. Adding a little cream of tartar helps, as well as making sure you start with a very clean bowl (preferably not plastic if you’re having issues). Having the egg whites at room temperature can be a little easier, too, though I usually don’t need to. Hope this answers your question!
thank to doctor obor ,I was diagnosed of (HIV) in 2012 and I have tried all possible means to get cured, i even visited phonologist but all to no avail, until i saw a post in a health forum about a herbal doctor from Africa who prepare herbal medicine to cure all kind of diseases including HIV/AIDS, at first i doubted if it was real but decided to give it a try, when i contacted this herbal doctor via his email he sent me the Hiv/ Aids herbal medicine through courier service, when i received this herbal medicine, he gave me step by instructions on how to apply it, when i applied it as instructed i was totally cured of this deadly disease within 12-14 days of usage, if you are suffering of this diseases you can as well Contact this great herbal doctor via his email-.( or whatsapp now +2348105813057

Ketogenic and low-carbohydrate diets greatly increase reliance on fat oxidation [78–89], which would logically be expected to increase mitochondrial respiration and mtROS production and, in turn, induce mitohormesis. Furthermore, mtROS produced through RET appears to have particular relevance to hormetic adaptation, including increased lifespan [90]. Nutritional ketosis is likely to increase RET by altering the FADH2 to NADH ratio. As the primary source of acetyl CoA shifts from glycolysis to β-oxidation and ketolysis, this ratio increases, more than doubling for β-oxidation of longer-chain fatty acids. Electrons from FADH2 reduce the CoQ pool through complex II and ETF-QO, thereby increasing RET [91, 92]. This induction of RET by alteration of substrate availability can also be influenced by configuration of mtETC complexes into supercomplexes [90]. The greater potential for mtROS production through RET is consistent with evidence of mitochondria producing more H2O2 during oxidation of palmitoyl carnitine versus pyruvate [93, 94]. Furthermore, succinate is generated during ketolysis by succinyl-CoA:3-oxoacid CoA-transferase (SCOT), which also promotes RET by reducing the CoQ pool through complex II. Demonstrating the likely role of RET in mitohormesis, particularly within the context of nutritional ketosis, extension of lifespan in C. elegans through BHB treatment is dependent on both complex I function and expression of bioenergetic and antioxidant proteins [95].

Many neurological conditions share a common feature of impaired brain energy metabolism. It isn’t always clear if this impairment is the cause or the effect of the disease, but nonetheless, interventions that even partially restore or improve brain energy metabolism could help to prevent, slow or even reverse some conditions of the brain. Because ketones can: 1) get into the brain; 2) undergo metabolism by a distinct pathway that bypasses glucose metabolism, providing ketones by either following a ketogenic diet or by taking exogenous ketones could impact the natural course of some neurological conditions. 
Cheryl, We use beef gelatin in this recipe to act as a binder and add a bit more chewiness to help simulate regular bread. (If you’re interested, we talk more about using beef gelatin in keto baking in this post: We haven’t experimented with this recipe to omit the beef gelatin, but you might be able to get a similar result using a bit more psyllium husk powder, flaxseed meal, ground chia seeds, xanthan gum, or guar gum. If you decide to play around with the recipe, please let us know how it goes!
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Dr. Campos, it is so discouraging to see that you disparage the ketogenic diet based on your assumption that it is very heavy in poor quality processed meats. No diet that relies on processed foods can be viewed as “healthy”. Become better informed by getting up to speed with what Jeff Volek, RD, PhD, calls a “well-formulated ketogenic diet.” Also, learn more about the potential of the diet to slow cancer progression (my specialty). You owe it to your patients who are depending on you for advice. Present them with facts, not opinions.
Some of the benefits of ketosis occur due to the restriction of dietary carbohydrate. Others occur due to the presence of ketones in the blood. Two of the most commonly sought after effects are weight-loss and improved insulin sensitivity. These are conferred by the low carbohydrate content of the diet allowing increased fat burning and the gradual restoration of insulin sensitivity. In this article we discuss the basics of ketone production and metabolism, and some of the many ways that KETONES themselves (endogenous AND exogenous) can benefit health and performance. 
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Acetoacetate diester did not improve performance37: a different ketone ester to that used by Cox et al (an acetoacetate diester) decreased cycling performance by 2% given before a 50’ cycling race. Reasons for the difference in findings could be: this ketone ester drink was given along with a can of diet cola 30 mins before exercise and caused GI upset in many athletes. Delivering acetoacetate causes the muscle cells to become more ‘oxidised,’ which is a less favourable state for ATP production. Risk of some gastrointestinal upset with all ketone supplements. The dose, tonicity, time taken before competition and overall volume of a ketone drink will affect how easy it is to tolerate. Many athletes take ketone supplements without side effects, however there are differences between individuals, so practice with ketone supplements in training is advisable to ensure they don’t experience any GI side effects in competition. Geoff Woo discussed this study in a blog post.
Hi Jodi, I haven’t tried that, but don’t think it would work well for this recipe. First, yeast needs sugar (for it to consume – it’s not typically in the end result), so you’d need to add that. But also, just with how we are making the bread fluffy with beaten egg whites, I don’t think yeast would work. If you want to try adding yeast to a low carb bread, I would do it with this low carb bread recipe instead.
Based on the reciprocal activation described above, nutritional ketosis is likely to activate SIRT1 and SIRT3 indirectly through activation of AMPK. However, more direct activation of sirtuins by nutritional ketosis is possible. Since reduction of NAD+ to NADH occurs outside of mitochondria only during glycolysis, which is less active during nutritional ketosis, more cytosolic NAD+ remains oxidized, further facilitating activation of SIRT1 [247]. In addition to the decrease in glucose availability during nutritional ketosis, glycolysis may be further inhibited through activation of pyruvate dehydrogenase kinase and subsequent inhibition of pyruvate dehydrogenase (PDH), which occurs in response to dietary carbohydrate restriction [248–251] or infusion of BHB, ACA, or fatty acids [252]. Consistent with the relevance of these factors to nutritional ketosis, a ketogenic diet (% energy: 89 fat, <1 carbohydrate, and 10 protein) has decreased expression of PDH in mouse liver [36]. More importantly, there is direct evidence of nutritional ketosis promoting an increase in NAD+ concentration. Treatment with BHB + ACA (1 mM each) has increased NADH oxidation in rat neocortical mitochondria [109], and a ketogenic diet (Bio-Serv F3666) has increased NAD+ concentration in rat hippocampus [253]. There is also evidence of nutritional ketosis regulating sirtuin expression. A low-carbohydrate (20% of energy) diet combined with ketone esters (6% w/v) has increased SIRT1 protein content in brown adipose of mice [149], and a ketogenic diet (% energy: 90 fat, 0 carbohydrate, and 10 protein) has increased SIRT3 expression in mouse liver [37].
In dairy cattle, ketosis is a common ailment that usually occurs during the first weeks after giving birth to a calf. Ketosis is in these cases sometimes referred to as acetonemia. A study from 2011 revealed that whether ketosis is developed or not depends on the lipids a cow uses to create butterfat. Animals prone to ketosis mobilize fatty acids from adipose tissue, while robust animals create fatty acids from blood phosphatidylcholine (lecithin). Healthy animals can be recognized by high levels of milk glycerophosphocholine and low levels of milk phosphocholine.[76] Point of care diagnostic tests are available and are reasonably useful.[77]
Hi Christy, It might be a little more difficult, but in theory possible. You’d need to stir the dry ingredients, then use a hand mixer instead of food processor to mix them with the butter. Then, after beating the egg whites separately, you’d need to mix in part of them, trying not to break them down, then fold in the rest once it’s easier to fold.
In order to simulate a bread-like texture without using gluten, grain free and gluten free bread recipes often use a variety of different flours and binders. We’ve tried so many keto bread recipes that taste way too eggy or too much like almonds or coconut. The trick is to find a combination of ingredients that yields good flavor, as well as bready texture and a loaf that rises nicely.