Some clinicians regard eliminating carbohydrates as unhealthy and dangerous. However, it is not necessary to eliminate carbohydrates from the diet completely to achieve ketosis. Other clinicians regard ketosis as a safe biochemical process that occurs during the fat-burning state. Ketosis, which is accompanied by gluconeogenesis (the creation of glucose de novo from pyruvate), is the specific state that concerns some clinicians. However, it is unlikely for a normally functioning person to reach life-threatening levels of ketosis, defined as serum beta-hydroxybutyrate (B-OHB) levels above 15 millimolar (mM) compared to ketogenic diets among non diabetics, which "rarely run serum B-OHB levels above 3 mM." This is avoided with proper basal secretion of pancreatic insulin. People who are unable to secrete basal insulin, such as type 1 diabetics and long-term type II diabetics, are liable to enter an unsafe level of ketosis, eventually resulting in a coma that requires emergency medical treatment. The anti-ketosis conclusions have been challenged by a number of doctors and advocates of low-carbohydrate diets, who dispute assertions that the body has a preference for glucose and that there are dangers associated with ketosis.
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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?
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It is important to note that these herbs and spices are intended to support blood sugar maintenance and are not meant to replace diabetes/hyperglycemic medications. Research does show benefits to incorporating these herbs and spices, so enjoy incorporating them daily into your favorite recipes for a boost of flavor and blood sugar-lowering benefit.
The situation for Type II diabetics is different because some insulin production remains and some cells of the body can still respond to insulin. It is worth noting that insulin sensitivity can be different between the different tissues of the body such as liver, adipose tissue and muscle. A small amount of insulin release can help to prevent development of DKA unless the body is totally insulin resistant. Insulin resistance is a term used to indicate that for a given amount of insulin, the cells of the body are less responsive and take up less glucose. This means that blood glucose levels remain higher for longer when insulin resistant Type II diabetics eat a carbohydrate rich meal. Over time, the pancreas secretes more insulin to compensate for reduced insulin sensitivity, which can damage the insulin producing (beta) cells. Furthermore, having high blood glucose can lead to a number of side effects:
I just made it using all the the optional ingredients but I didn’t have a food processor so I whipped/mixed everything by hand. One thing I noticed is that the top of the bread cracked unevenly. Could I have over fluffed the egg whites? Maybe creating an artificial cut in the middle could solve that next time? It rose very well and nearly doubled in size, though the size is still a bit small for my liking. I will most likely use 1.5x the amount next time. It smells great and I’m about to chow down on this!
A giant, late-night dinner is your blood sugar’s worst enemy. That’s because our bodies become more insulin resistant as the day goes on—so a meal that you eat in the evening will cause a greater spike in blood sugar than a meal you eat in the morning. Because of this, many nutrition experts advise front-loading your meals, or eating bigger meals earlier in the day and having a smaller dinner at least three hours before bed.
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 . 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  and cytosol , where copper/zinc superoxide dismutase (SOD1) can dismutate it into H2O2 . 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 . GPx also removes other peroxides, including lipid hydroperoxides . 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 , 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.) , and since NADH is required for recycling of NADPH , 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 , 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 . •OH is scavenged by metallothioneins I and II [69, 70] and glutatathione , 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 .
A reduced availability of dietary carbohydrates leads to an increased liver production of KBs. The liver cannot utilize KBs because it lacks the mitochondrial enzyme succinyl-CoA: 3-ketoacid (oxoacid) CoA transferase (SCOT) necessary for activation of acetoacetate to acetoacetyl CoA. KBs are utilized by tissues, in particularly by brain. KBs enter the citric acid cycle after being converted to acetyl CoA by hydroxybutyrate dehydrogenase (HBD), succinyl-CoA: 3–CoA transferase (SCOT), and methylacetoacetyl CoA thiolase (MAT). Modified from Owen (2005), Paoli et al. (2014).
Hi Kerstin, Sorry you had issues whipping the whites. It can sometimes be more difficult with the kind from a carton. The cream of tartar helps, but sometimes isn’t enough. Did you wait for the whites to be at room temp before beginning? This can help with whipping. Unfortunately the bread won’t turn out very well without getting the whites to stiff peaks. I hope it works for you next time, and if the cartons don’t work for you, you can try with the whites from whole eggs. You can use the yolks to make hollandaise sauce or creme brulee like this.
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].
Central obesity is a key feature of the syndrome, being both a sign and a cause, in that the increasing adiposity often reflected in high waist circumference may both result from and contribute to insulin resistance. However, despite the importance of obesity, patients who are of normal weight may also be insulin-resistant and have the syndrome.
The clinical relevance of nutritional ketosis to mitochondrial function is further indicated by promotion of ketogenic diets for treatment of mitochondrial disorders [19, 20, 26, 30, 247, 403]. The most prominent example is the study of mitochondrial adaptations as a mechanism for the well-known antiseizure effect of ketogenic diets [19, 29, 33, 162, 247, 403–405]. As previously discussed, the dramatic shift in energy metabolism and subsequent increase in circulating ketones induced by a ketogenic diet can enhance mitochondrial function and endogenous antioxidant defense. The primary mechanism behind these adaptations appears to be the increased demand for fat oxidation resulting from carbohydrate restriction. However, ketones themselves have important metabolic and signaling effects that enhance mitochondrial function and endogenous antioxidant defense, implying that a well-formulated ketogenic diet should have greater benefit than a nonketogenic low-carbohydrate diet. Regardless of the mechanism(s), the potential outcomes imply protection against chronic disease through improved mitochondrial function and, in turn, decreased potential for oxidative stress and subsequent pathology. However, further research is needed to better understand how nutritional ketosis influences mitochondrial function across different tissues and how these influences relate to human disease. Future research should also focus on further differentiation of the effects of carbohydrate restriction from the direct effects of ketones.
My loaves always had air pockets and a gummy texture. I made a loaf yesterday and when I was putting it in the oven, the power went out. The dough sat on the counter for 3 – 4 hours until the power came back on and I was able to bake it. The finished loaf cooled in the oven all night (I took it out of the loaf pan) and when I cut into it this morning, the texture was perfect – no gooey middle, no air pocket! Perhaps the secret is to let the dough rest before baking??
Lately anecdotal evidence has been building that a ketogenic diet can yield transformative results with respect to weight loss: with people taking to social media to share ‘before and after keto’ photos and to stories of ‘how keto changed my life.’ Despite this, concrete clinical evidence confirming that a ketogenic diet is superior to any other diet that creates a calorie deficit is lacking. At the moment the most accurate statement is that ‘the best diet for you is one you can stick to,” a pattern of eating that maintains a small calorie deficit should, over time, lead to weight loss.
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The brain is a particularly greedy organ when it comes to energy requirement. To put this comment in perspective consider the following: though our brain represents only about 2% of our body mass, it accounts for about 20% of our energy expenditure. (In children, by the way, this may be closer to 40-50% of basal metabolic demand.) So, beyond the ATP issue, above, there is a substrate issue with the brain as neurons derive most of their energy from glucose. While there is emerging evidence that neurons can also oxidize fatty acids directly in small amounts and may even prefer lactate (over glucose), these two substrates do not approach the levels of consumption by neurons that glucose does. So, for the purpose of this discussion, let’s just focus on the need of the body to provide glucose to the brain.
^ Jump up to: a b Cardona A, Pagani L, Antao T, Lawson DJ, Eichstaedt CA, Yngvadottir B, Shwe MT, Wee J, Romero IG, Raj S, Metspalu M, Villems R, Willerslev E, Tyler-Smith C, Malyarchuk BA, Derenko MV, Kivisild T (2014). "Genome-wide analysis of cold adaptation in indigenous Siberian populations". PLOS One. 9 (5): e98076. Bibcode:2014PLoSO...998076C. doi:10.1371/journal.pone.0098076. PMC 4029955. PMID 24847810.
Metabolic syndrome, also known as Insulin Resistance Syndrome (IRS) and Syndrome X, is a cluster of metabolic and anthropometric traits including glucose intolerance, upper body fat distribution (increased intra-abdominal fat mass), hypertension, dysfibrinolysis, and a dyslipidemia (characterized by high triglycerides, low high-density lipoprotein [HDL] cholesterol, and small dense low-density lipoprotein [LDL] particles).1 Metabolic syndrome constitutes a powerful risk factor complex to identify individuals at increased risk for future Type 2 diabetes and cardiovascular disease (CVD). Insulin resistance and abdominal obesity are two central components of the syndrome and are integrally involved in its pathogenesis. Insulin resistance is a metabolic abnormality in which peripheral tissues exhibit a subnormal biologic response to the glucose-lowering action of insulin. Insulin resistance not only antedates the development of diabetes but is also a major metabolic defect (together with impaired insulin secretion and elevated hepatic glucose production) that maintains hyperglycemia in patients with overt disease. The central role of abdominal adiposity underscores the importance of body fat distribution regarding the metabolic consequences of obesity. Individuals with metabolic syndrome are also more prone to develop other pathologic conditions including polycystic ovary syndrome, non-alcoholic steatohepatitis (NASH), cholesterol gallstones, sleep disorders, and some types of cancer. Thus, metabolic syndrome is responsible for a tremendous burden of human disease and social costs, and nutritional therapy is key to both its prevention and limiting its progression to Type 2 diabetes and CVD.
As with PGC-1α, nutritional ketosis may activate FOXO3a by increasing activity of AMPK and sirtuins or by decreasing insulin. Expression of FOXO3a is increased by fasting, caloric restriction, and BHB [103, 105], all of which are or can be components of a ketogenic diet. Furthermore, BHB treatment has extended lifespan in C. elegans in a manner dependent on FOXO3a , and a ketogenic diet (% energy: 89 fat, <1 carbohydrate, and 10 protein) has increased median lifespan and decreased tumors and age-associated losses of physical and cognitive performance, all in conjunction with increased hepatic content of FOXO3a .
Ketosis is a sensitive state so as soon as you increase your carb intake above your carb tolerance, you’re out! You probably don’t want to continuously weigh and count your food for the rest of your life. So even if you stick to the approved list of ketogenic food, there is no guarantee that you will be in ketosis without interruption. That’s OK. Now if you’re in ketosis to manage cancer or epilepsy, that’s a different story obviously.
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Maria, can you clarify the recipe as far as fluid ounces versus weighted ounces? For example, for the boiling water, 1.5 cups of water is 12 fluid ounces, but 1.5 cups of water does not weigh 12 weighted ounces. As I watch your video, you weigh the boiling water in a measuring cup, but once again I’m not sure if it’s supposed to be 12 fluid or weighted ounces. And is that true for the vinegar and egg whites as well… fluid ounces versus weighted ounces?
The advice on carbohydrate-rich foods, for example, may make a person with type 2 diabetes require initiation of treatment with insulin injections. One single year’s insulin-consumption may easily cost $2000 or more. Multiply this number by the 422 million diagnosed people diabetes worldwide and you will see the enormous economical interests in this.
Thank you Mira for your quick reply. I didn’t make it that same day but I just made a batch now and they are excellent! I really enjoyed them. I made the recipe times 10 for 12 large muffin slots in the muffin tin. I’m thinking of shaping a larger round of batter on a parchment lined pan next time and after baking, carefully cutting in half to make 2 rounds to make a pizza crust. Thank you so much!!!
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!!!!!!!!!!!!!
I made this today. I did not have almond flour so I took some slivered almonds and made flour from them in my nutribullet. This turned out fabulous. Only a pinch of salt is necessary. The variations are endless! I don’t do Keto but I will definitely be making this often for everything!! This is a great save if you are out of bread! Thanks so much for this recipe! It is DELISH!
BHB, in addition to being an important energy substrate, is also a signaling molecule [100–102]. Although not induced through mtROS, BHB inhibits class I and II histone deacetylases (HDACs) in a dose-dependent manner, resulting in greater histone acetylation regardless of whether BHB is elevated through fasting, caloric restriction, or infusion . This inhibition is associated with increased expression of forkhead box O (FOXO) 3a and metallothionein II and increased protein content of FOXO3a, SOD2, and catalase . Consistent with these changes, the kidneys of mice with elevated blood BHB concentrations (∼1.2 mM) were protected from paraquat-induced (50 mg/kg) oxidative damage to proteins and lipids, which was indicated by lower levels of protein carbonyls, 4-HNE, and lipid peroxides . Upregulation of antioxidant defense by BHB-induced HDAC inhibition also appears to be the mechanism through which exogenous BHB extends lifespan in C. elegans . The dependence of this response on FOXO3a, NFE2L2, and several bioenergetic signaling proteins that influence the activities of these two transcription factors  is indicative of the overlap between bioenergetics and antioxidant defense that is characteristic of mitohormesis.
141. Khailova L. S., Prikhodko E. A., Dedukhova V. I., Mokhova E. N., Popov V. N., Skulachev V. P. Participation of ATP/ADP antiporter in oleate- and oleate hydroperoxide-induced uncoupling suppressed by GDP and carboxyatractylate. Biochimica et Biophysica Acta. 2006;1757(9-10):1324–1329. doi: 10.1016/j.bbabio.2006.04.024. [PubMed] [CrossRef] [Google Scholar]
High blood sugar levels coupled with high blood ketones, on the other hand, will mean that you have a pathologically low level of insulin – something non-diabetics do not suffer from. This can lead to ketoacidosis – a potentially life-threatening condition. If this happens, you’ll need to inject more insulin; if you’re at all unsure of what to do, contact a medical professional. Coveting really high blood ketones for weight control is not worth the risk for type 1 diabetics.
The distribution of adipose tissue appears to affect its role in metabolic syndrome. Fat that is visceral or intra-abdominal correlates with inflammation, whereas subcutaneous fat does not. There are a number of potential explanations for this, including experimental observations that omental fat is more resistant to insulin and may result in a higher concentration of toxic free fatty acids in the portal circulation. 
Hi Jen, It sounds like it needed to bake for longer – this is why it sunk and was still moist. The timing varies by ovens and even different pans. I hope you’ll try it again and just keep it in there for longer. You can cover the top if it starts to brown too much. For the one you made, depending on how moist it was in the middle, you may be able to salvage it somewhat by pan frying the slices.
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Carbohydrates ultimately break down into glucose. Many people believe that carbs are bad for people with diabetes. This is not true. Carbs are fuel for the body, so they have to be eaten. You just need to be smart about which ones you eat and how much you eat of them. Picking foods that are high in carbs but have no other nutrition is not smart. Examples of these foods are:
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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?
Hello Angie, the same happened here. The taste is great except the bread did not rise. It came out flat. Do I have to slice the load in the middle to get it to rise? I replaced the ghee with regular butter but everything else was the same. Also I read on a different site that if the eggs are not room temperature than that would definitely effect the rise of the bread. I took the cold eggs straight out of the fridge to get the egg whites. What do you think?