I was so excited about making this bread. I recently cut all grains out of my life and I’m also in the process of going gluten free because i have a lot of digestive issues. I followed the recipe precisely. Checked the temp before taking it out of oven. It looked amazing nice and golden brown. I cut into it and i couldn’t wait for that first bite. I was so disappointed it has an odd flavor I just couldnt stomach and it was very salty to me. I tried a few tiny bites with different condiments and couldn’t eat it. After reading some comments, I see it is supposed to be unsalted butter. I used salted, but why did it seem to have a bitter sour taste to it?
293. Geng T., Li P., Okutsu M., et al. PGC-1α plays a functional role in exercise-induced mitochondrial biogenesis and angiogenesis but not fiber-type transformation in mouse skeletal muscle. American Journal of Physiology-Cell Physiology. 2010;298(3):C572–C579. doi: 10.1152/ajpcell.00481.2009. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
That said, the nutrition facts that I get after entering the recipe into my app came up with almost twice the calories. My Tillamook Mild Cheddar cheese is 110 calories per ounce—so that alone gets me to 385 calories. Overall I end up with 51.5 grams of fat, 34.5 grams protein, 4.5 grams of carbs, and 632 calories. I am hoping to try it again with half the cheese to see if I can still get the great flavor and wonderful crispy taco shell.

The FOXO family of transcription factors is highly conserved and promotes longevity and resistance to cellular stress. Although there are a variety of FOXO isoforms with varying tissue distribution [318–320], FOXO3a has been the most thoroughly studied in relation to energy sensing, mitochondrial function, and antioxidant defense. Similar to PGC-1α, FOXO3a is activated through phosphorylation by AMPK [321–323] and deacetylation by SIRT1 [324, 325] and SIRT3 [326–329], and its transcriptional activity is at least partly dependent on AMPK [322] and SIRT1 [325]. In a variety of organisms, tissues, and cell types, FOXO3a increases mitochondrial biogenesis and expression of TFAM [329], but is more known for increasing expression of antioxidant and repair proteins, including SOD2 [287, 330, 331], catalase [287, 330, 332, 333], glutathione S-transferase (GST) [322], thioredoxins [287, 323], Prx3 [287, 334], Prx5 [287], and metallothioneins I and II [322], as well as UCP2 [287, 322] and the DNA repair enzyme growth arrest and DNA damage-inducible 45 (GADD45) [322, 324, 335, 336]. FOXO3a is also activated by oxidative stress [324, 331, 333], possibly in a SIRT1-dependent manner [324], and likely mediated through c-Jun N-terminal protein kinase (JNK), which allows FOXOs to translocate to the nucleus by promoting dissociation of 14-3-3 [337, 338]. Furthermore, FOXO3a and SIRT3 interact in mitochondria to induce mitochondrial gene expression in an AMPK-dependent manner [339]. FOXO3a also induces expression of LKB1 [340] and NAMPT [341], indicating a feed-forward cycle of activation with AMPK and sirtuins. Like PGC-1α, FOXO3a transcriptional activity is inhibited by insulin through PKB [331].
There are two main types of diabetes. In Type I diabetes, the insulin producing cells in the pancreas are destroyed by an immune response resulting in insulin deficiency. In Type II diabetes insulin is still secreted, but the cells in the body no longer respond adequately and so glucose uptake is not triggered. Sometimes pregnancy can trigger a period of diabetes (gestational diabetes), which resolves after giving birth. 
Acetone is a molecule that results from the breakdown of acetoacetate. Acetone is commonly referred to as a ‘waste product’ as it is less readily used as energy compared to BHB (although some studies have shown that acetone can be oxidised as a fuel4. That said, some evidence suggests that it is responsible for the antiseizure effects of ketogenic diets so in may not be completely inert. At low levels acetone in the breath corresponds well to levels of ketones in the blood 12,13, however this is not the case as blood BHB levels increase 13 and if the increase is rapid, such as with exogenous ketone consumption11. 
Cinnabon's got nothing on these keto-friendly treats from Gnom-Gnom. With only two grams of net carbs and 102 calories each, they taste more indulgent than they really are. Crafting the dough (made with almond flour and coconut flour) is a relatively involved process, but you can whip it up and keep it in the fridge for up to five days before you're ready to make (and eat) the cinnamon roll knots.
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😚
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!
I NEVER comment on posts or leave reviews (because I’m lazy lol) but I had to stop in and thank you for this recipe. I have been doing bad on keto because I just cannot stop having some kind of bread in the morning with my coffee. What can I say, I’m weak. I’ve tried the other bread recipes out there and they are disgusting. This was DELICIOUS!! OMG! I think I can get back into ketosis (and stop farting on everyone) thanks to you 😀
Jennifer, The yeast has no carbs. The coconut sugar does have carbs, but the yeast feeds on it and through the process of fermentation uses the sugar for energy and releases carbon dioxide gas as a result. The yeast is for flavor, aroma, and in our opinion does help with a little bit of rise. Additionally, we don’t like to consider any foods “bad”, “off-limits”, or not keto. Instead, we opt to mainly eat nourishing real foods that fit into our daily macro intake. We hope this helps! Best of luck on your keto journey.
Although mitohormesis has not been studied comprehensively in higher-level organisms, its occurrence is supported by compelling evidence in lower-level organisms. For example, inhibition of glycolysis in C. elegans increased fat oxidation (based on nematode triglyceride content) and mitochondrial O2 consumption, which was followed by increases in ROS production at day 2 and catalase activity at day 6 [72]. The increase in catalase activity occurred in conjunction with increases in lifespan and resistance to the mitochondrial stressors sodium azide and paraquat. However, antioxidant treatment (N-acetylcysteine) decreased the elevation of ROS at day 2 and eliminated the resistance to sodium azide and paraquat treatments, indicating a requirement of ROS as a stimulus [72].
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^ Bechtel PJ (2 December 2012). Muscle as Food. Elsevier Science. pp. 171–. ISBN 978-0-323-13953-3. Retrieved 19 May 2014. Freezing does stop the postmortem metabolism but only at about −18ºC and lower temperatures. Above −18ºC increasing temperatures of storage cause an increasing rate of ATP breakdown and glycolysis that is higher in the comminuted meat than in the intact tissue (Fisher et al., 1980b). If the ATP concentration in the frozen tissue falls below ~ 1 µmol/g no contraction or rigor can occur because they are prevented by the rigid matrix of ice.
Even though intracellular metabolism and activation of the ATP-sensitive K+ channels appear to be necessary for some signaling effects of FAs, a great amount of the FA responses in the ventromedial hypothalamic neurons are mediated by interactions with fatty acid translocase (FAT)/CD36. Translocase is a FA transporter/receptor that activates downstream signaling even in the absence of intracellular metabolism (Moulle et al., 2014).
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Moreover, recent studies show that the Inuit have evolved a number of rare genetic adaptations that make them especially well suited to eat large amounts of omega-3 fat.[57][58][59] And earlier studies showed that the Inuit have a very high frequency—68% to 81% in certain arctic coastal populations—of an extremely rare autosomal recessive mutation of the CPT1A gene—a key regulator of mitochondrial long-chain fatty-acid oxidation[60][61]—which results in a rare metabolic disorder known as carnitine palmitoyltransferase 1A (CPT1A) deficiency and promotes hypoketotic hypoglycemia—low levels of ketones and low blood sugar.[62] The condition presents symptoms of a fatty acid and ketogenesis disorder.[62] However, it appears highly beneficial to the Inuit[60] as it shunts free fatty acids away from liver cells to brown fat, for thermogenesis.[63][64] Thus the mutation may help the Inuit stay warm by preferentially burning fatty acids for heat in brown fat cells.[64] In addition to promoting low ketone levels, this disorder also typically results in hepatic encephalopathy (altered mental state due to improper liver function), enlarged liver and high infant mortality.[65] Inuit have been observed to have enlarged livers with an increased capacity for gluconeogenesis, and have greater capacity for excreting urea to remove ammonia, a toxic byproduct of protein breakdown.[57][66][67][68] Ethnographic texts have documented the Inuit's customary habit of snacking frequently [69] and this may well be a direct consequence of their high prevalence of the CPT1A mutation[70] as fasting, even for several hours, can be deleterious for individuals with that allele, particularly during strenuous exercise.[57][70] The high frequency of the CPT1A mutation in the Inuit therefore suggests that it is an important adaptation to their low carbohydrate diet and their extreme environment.[57][60][70]
NOTE: This article is based on research that utilizes the sources cited here as well as the collective experience of the Lab Tests Online Editorial Review Board. This article is periodically reviewed by the Editorial Board and may be updated as a result of the review. Any new sources cited will be added to the list and distinguished from the original sources used. To access online sources, copy and paste the URL into your browser.
All information contained on dLife.com is intended for informational and educational purposes only. The information is not intended to be a replacement or substitute for consultation with a qualified medical professional or for professional medical advice related to diabetes or another medical condition. Please contact your physician or medical professional with any questions and concerns about your medical condition. All content on dLife.com is created and reviewed in compliance with our Editorial Policy.

There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if they are consequences of a more far-reaching metabolic derangement. A number of markers of systemic inflammation, including C-reactive protein, are often increased, as are fibrinogen, interleukin 6, tumor necrosis factor-alpha (TNF-α), and others. Some have pointed to a variety of causes, including increased uric acid levels caused by dietary fructose.[18][19][20]
Nutrient-sensitive neurons reacting to glucose but also to fatty acids (FAs) concentrations are present at many sites throughout the brain and may play a key role in the neural control of energy and glucose homoeostasis. Central administration of oleate, for example, inhibits food intake and glucose production in rats. This suggests that daily variations in plasma FA concentrations could be detected by the CNS as a signal that contributes to the regulation of energy balance (Moulle et al., 2014).

You should always be in touch with your doctor about your disease and any changes you make or problems that you notice. Having that line of open communication is key to gaining knowledge and insight into what can make your life and your health better. Try the things mentioned in this article, but if they don’t help, then talk to your physician about what else is available for you.


Given the prevalence of this category of illness, and the insidious nature of the conditions, an intervention with minimal side effects (vs. drugs) such as ketosis could be used as a first line intervention before attempting treatment with medication in some cases. However, there is still some way to go before research can conclusively address this possibility, individuals considering the diet should do so with full medical supervision.
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Although there are numerous sites of mtROS formation, the most prominent are those in the mtETC, where the superoxide radical (O2•−) is formed through reduction of O2 by leaked electrons, particularly at complexes I and III [41, 53–55]. Production of O2•− at complex I is particularly high during reverse electron transport (RET), which occurs when a high proton-motive force (Δp) develops across the inner mitochondrial membrane in conjunction with the pool of coenzyme Q (CoQ) being in a highly reduced state (i.e., mostly present as ubiquinol) as a result of electron transfer through complex II and electron transfer flavoprotein:ubiquinone oxidoreductase (ETF-QO) [56–62]. This dependence of mtROS production on Δp during RET is mainly influenced by proton gradient (ΔpH) [59].
Optimally, the management approach results in weight loss based on a healthy diet and regular physical activity, which includes a combination of aerobic activity and resistance training, reinforced with behavioral therapy. Metformin, an insulin sensitizer, or a thiazolidinedione (eg, rosiglitazone, pioglitazone) may be useful. Weight loss of ≈ 7% may be sufficient to reverse the syndrome, but if not, each feature of the syndrome should be managed to achieve recommended targets; available drug treatment is very effective.
I used the coconut flour, Now whole psyllium husks (ground by me), and whole eggs…this bread is exactly what I have been looking for, for such a long time. Yes a bit dense with the whole eggs but super-tasty nonetheless. I know if doing egg whites would make a bit lighter. Mine did not turn purple either, and I didn’t order a special pan, just used a regular loaf pan. Also, used coconut vinegar instead as all I had on hand and subbed perfectly. Thank you Thank you for a terrific recipe!
The easiest way to make sure that your carb intake is appropriate is to count carbohydrates. It is a simplified way to evaluate foods based on their nutritional value. The best place to start when counting is to aim for 45 to 60 grams of carbohydrates per meal and roughly 15 to 30 grams for each snack in between meals. You may have to adjust this based on your individual needs and your blood sugar readings. It is a lot easier to calculate the carbohydrates when you have a food with a label, but many foods do not. Check the serving size on the label to be sure that you are counting correctly. The US Department of Agriculture has a website that allows you to type in any food and it will give you the nutritional values. Check it out at https://ndb.nal.usda.gov/ndb/. A few examples of 15 grams of carbs include:
Formation of O2•− at complexes I and III primarily occurs in the mitochondrial matrix, but some of the O2•− produced at complex III is produced in the intermembrane space [63]. Within the matrix, O2•− is rapidly dismutated into hydrogen peroxide (H2O2) by manganese superoxide dismutase (SOD2) [41, 53]. Some O2•− may escape into the mitochondrial intermembrane space [64] and cytosol [65], where copper/zinc superoxide dismutase (SOD1) can dismutate it into H2O2 [41]. The large majority of mitochondrial H2O2 is removed by peroxiredoxin (Prx) 3, followed by much smaller contributions from Prx5 and glutathione peroxidases (GPx) 1 and 4 [66]. GPx also removes other peroxides, including lipid hydroperoxides [41]. Catalase is another antioxidant enzyme capable of removing H2O2 but is primarily located in peroxisomes and is therefore unlikely to directly remove mitochondrial H2O2 [41, 66]. However, H2O2 can be transported out of mitochondria [67], and it is possible that the majority of mitochondrial H2O2 is removed in the cytosol. Since Prxs and GPxs rely on NADPH for recycling of their cofactors (thioredoxins and glutathione, resp.) [41], and since NADH is required for recycling of NADPH [68], activity of these enzymes would decrease availability of NADH for oxidative phosphorylation. Therefore, transport of H2O2 out of mitochondria for removal in the cytosol may be a more likely defense mechanism [67], implying a more important role of catalase and other antioxidant enzymes outside of mitochondria. Despite the lower reactivity of H2O2, it is still reactive and can oxidize metal ions, particularly iron, to form the hydroxyl radical (•OH), which readily damages DNA, lipids, and proteins [41]. •OH is scavenged by metallothioneins I and II [69, 70] and glutatathione [71], indicating that these antioxidant proteins may be important defenses against byproducts of unaddressed mtROS. Other important antioxidant enzymes include glutamate-cysteine ligase (GCL), which is the rate-limiting step in glutathione synthesis, and glutathione reductase (GSR) and thioredoxin reductase (TRXR), which recycle glutathione and thioredoxin, respectively, to their reduced forms [41].
I have tried four times to make the bread recipe with no success, but on my next try I will make sure the egg whites are truly room temp. I have not seen that come up in any discussion but it’s the only thing I can think of at this point. I am an experienced baker, not a novice. I added 1/8 tsp each garlic powder and onion powder and added 1/2 tsp stevia powder. These make the flavor a little more complex and definitely solves the complaint of vinegar or fiber taste. The taste is very good. However unlike some other disappointed bakers on this site, I did not throw away the failed attempts. I took the wet heavy bread from one failed try and tore it into small bits to dry for bread pudding with whiskey sauce. That is DELICIOUS, the next failed batch was sliced very thin and cut in half vertically for “toast points.”. I dried the pieces on a cookie sheet in a 300 degree oven until dry and somewhat brown and crispy. They taste EXACTLY like bagel chips we used to buy. My next batch became seasoned bagel crisps. I still want bread, but these are GREAT! Please don’t throw away failed attempts! There are other uses! I also fried some of my dried cubes in garlic oil for croutons, which were also delicious. I’m still trying, because I think if you can do it, surely I can do it.
Bailey, We’re so happy to hear you enjoyed this recipe! Regarding having bread fall, did you cook it for the full amount of time the recipe calls for, and did you cover the top with foil for the last 15 minutes? If so, there might be an issue with your oven’s calibration (you can get an inexpensive oven thermometer to check this). Another tip is to let your eggs come to room temperature first. Another factor is the altitude at which you’re baking; if you’re at high altitude, you might need to slightly adjust the oven temperature and bake time. The other thing to remember is that there will usually be a little bit of fall to most keto breads (in fact, every keto bread we’ve ever made) because keto flours lack gluten and are naturally quite dense; however, you can see in the photos, we still got a good rise on this loaf. I hope these tips help!
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