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Therefore the combustion enthalpy (∆H) of each fuel is an important factor in the energy it can provide to the cell. When expressed as the energy per 2 carbons in the molecule, ketones (BHB) have a higher combustion enthalpy (∆H) than pyruvate, lactate and glucose (see table). This means that the amount of energy that could possibly be transferred to ATP is higher than for those other substrates:
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.
Hi Danielle, The bread will not rise without the baking powder, but you could try it if you don’t mind that. Some people make homemade baking powder with baking soda, cream of tartar, and arrowroot powder. But, arrowroot is still a very small amount of starch. Divided among the slices, it’s actually fewer carbs than some of the other ingredients (e.g. almond flour has a small amount of carbs also).
In ketogenesis, two acetyl-CoA molecules instead condense to form acetoacetyl-CoA via thiolase. Acetoacetyl-CoA momentarily combines with another acetyl-CoA via HMG-CoA synthase to form hydroxy-β-methylglutaryl-CoA. Hydroxy-β-methylglutaryl-CoA form the ketone body acetoacetate via HMG-CoA lyase. Acetoacetate can then reversibly convert to another ketone body—D-β-hydroxybutyrate—via D-β-hydroxybutyrate dehydrogenase. Alternatively, acetoacetate can spontaneously degrade to a third ketone body (acetone) and carbon dioxide, although the process generates much greater concentrations of acetoacetate and D-β-hydroxybutyrate. When blood glucose levels are low, ketone bodies can be exported from the liver to supply crucial energy to the brain.[28]

Brittany, Thank you so much for leaving a comment! Without being there in the kitchen with you, it’s difficult to say what the issue was; however, I can definitely help you troubleshoot…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!
Glucose-sensitive neurons have been identified in a number of CNS regions including the metabolic control centers of the hypothalamus. Medeiros et. al. have used patch-clamp electrophysiology to examine whether neurons in a specific specialized region known as the subfornical organ (SFO), an area where the blood-brain barrier is not present, are also glucose sensitive or not. These experiments demonstrated that SFO neurons are glucose-responsive and that SFO is an important sensor and integrative center of circulating signals of energy status (Medeiros et al., 2012).
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 [130]. Knockout of UCP2 [131] or UCP3 [94, 132] increases mtROS production, and both proteins are inactivated through glutathionylation by GSH [133], further establishing their involvement in antioxidant defense. UCP2 and UCP3 may also be activated by products of lipid peroxidation induced by mtROS [122]. However, the potential for UCP2 and UCP3 to reduce mtROS through uncoupling is not fully agreed upon; [128] UCPs may alternatively protect against oxidative damage merely by exporting lipid hydroperoxides [128]. Furthermore, UCP3 is less abundant in type I and type IIa muscle fibers [134], 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.
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?
Hi Maria! I just want to say thank you for this bread recipe! It is awesome! It took me 4 times to get the technique down, but it works with both the Jay Rob psyllium and the bulk I get at my local store (which turns it purple). I watched your video and realized I was doing two things wrong… I was over-mixing and then I was squishing or handling the dough too much. With a little shorter mixing time, like you show on your video, and with light hands “shaping” the dough to fit in the pan, I have met with success! I also picked up the same size pan you use at the grocery store for about $5. This is the only low-carb gluten-free bread my daughter will eat. She loves it! Thanks again!

Longer-term ketosis may result from fasting or staying on a low-carbohydrate diet (ketogenic diet), and deliberately induced ketosis serves as a medical intervention for various conditions, such as intractable epilepsy, and the various types of diabetes.[6] In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed.[5][7] For this reason, ketosis is sometimes referred to as the body's "fat burning" mode.[8]

In order to obtain the most comparable measures, it is useful to measure blood ketones at the same time each day. Measuring immediately on waking means that there are fewer potential variables that could alter the measurement, such as exercise, or different food intake. However, it can also be useful to check ketone levels around 60-90 minutes after an intervention such after eating a fat rich meal or consuming exogenous ketones.      


As previously mentioned, numerous studies have demonstrated a profound increase in fat oxidation in response to ketogenic and low-carbohydrate diets. Some studies have even shown an increase in O2 consumption [148, 155–158]. However, fats contain fewer oxygen atoms per carbon than carbohydrates, thereby necessitating greater O2 intake to produce the same amount of energy [159]. Furthermore, since β-oxidation and ketolysis produce a greater proportion of FADH2 to NADH, the resulting decrease in passage of electrons through complex I decreases potential for ATP production per unit of O2 consumption [160]. Increased O2 consumption in response to a ketogenic diet may therefore merely be an effect of the differences in the metabolism and molecular structures of fat and carbohydrate rather than a true indication of increased capacity for oxidative phosphorylation. However, in rat hearts perfused with glucose, the addition of ketones has decreased O2 consumption [161]. This discrepancy may be related to variations in mitochondrial uncoupling. Either way, several studies have shown ketogenic diets to increase mitochondrial content, and numerous studies have shown these diets to increase expression, content, or activity of mitochondrial proteins involved in oxidative phosphorylation and fat oxidation. Compared to O2 consumption alone, these findings provide more conclusive support for an increase in oxidative capacity in response to nutritional ketosis.
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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!
Metabolic syndrome is thought to be caused by adipose tissue dysfunction and insulin resistance. Dysfunctional adipose tissue also plays an important role in the pathogenesis of obesity-related insulin resistance. [18] Both adipose cell enlargement and infiltration of macrophages into adipose tissue result in the release of proinflammatory cytokines and promote insulin resistance. [19]

My first attempt of this bread leaves something to be desired. It looked great when it came out of the oven but as it cooled it caved a bit; and when I took it out of the pan when it had cooled, I realized that the bottom inch looked undercooked, very wet. After reading ALL of Maria’s remarks to other folks who have had problems (I am not alone), I will try again adding less water next time. For now I will use the loaf I just made and turn it into croutons or bagel chips as suggested by Ellen (thanks for sharing some positives from a negative). Maria, I applaud you for your endless patience with all of us all who keep asking the same questions over and over again.

Forget Atkins and Paleo — the new low-carb diet du jour is called keto, as in ketogenic. Although there are many similarities between these diets, a keto diet is all about restricting carbohydrates and increasing healthy fats. The goal is to force your body’s metabolism into ketosis, which means it burns fat instead of glucose — because without carbs, glucose isn’t readily available.
PGC-1α coactivates all three known PPAR isoforms (PPARα, PPARδ, and PPARγ) [286]. Although each isoform is expressed in a variety of tissues, PPARα is prominently expressed in the liver, PPARδ in skeletal muscle, the heart, and the pancreas, and PPARγ in adipose [286, 296]. PGC-1α was discovered and named based on its promotion of brown adipose differentiation through coactivation of PPARγ and subsequent induction of mitochondrial biogenesis and UCP1 expression [297]. However, it is the PGC-1α coactivation of PPARα that is responsible for the upregulated transcription of many of the enzymes responsible for increased ketogenesis and fatty acid metabolism in response to a ketogenic diet [120]. Consistent with the role of PGC-1α in inducing mitochondrial biogenesis, it also shifts skeletal muscle fiber composition towards type I [298, 299] and type IIa [299], which are more oxidative. AMPK also contributes to fiber type changes and is required for the transition of highly glycolytic, type IIb fibers to more oxidative, type IIa fibers [276]. Although PGC-1α is primarily known for inducing transcription of nuclear DNA, it may also, in conjunction with SIRT1, induce expression of mtDNA [300].

When the kidneys filter blood, metabolic substrates such as glucose and ketones are re-absorbed to prevent energy wastage. If blood levels of a metabolite exceed the capacity of the kidney to reabsorb them, then a ‘spillover’ effect occurs and the metabolite (i.e. glucose or ketones) appear in the urine. However, urine is not a very reliable measure. Firstly, whilst following a ketogenic diet, adaptation occurs over time that means more ketones are reabsorbed in comparison to the early phase of the diet9. Furthermore, at higher levels of ketones, the appearance in the urine does not correlate to levels in the blood10. Similarly, after consumption of exogenous ketones, urine ketone levels were not in proportion to the levels in the blood11 this may be because of the rapid onset of ketosis in comparison to when ketosis is achieved with fasting or diet. Therefore urine test strips are useful as a guide but have several disadvantages to their use to accurately quantify levels of ketosis. 
Keeping a log of your blood sugars is a great way to be knowledgeable about your body and how it is reacting to foods and events. To start, check before and after every meal, along with one in-between meal check. It is important that you keep a log of these blood sugars, along with all of the foods that you are eating, activities you are performing and any insulin or medications that you are taking. Do this for a week, and see if you can identify any patterns. Take this log to your doctor and talk to them about your findings.

Most of these benefits occur due to the decrease in dietary carbohydrate intake; it is largely unknown what role ketones themselves play in the efficacy of the diet. Because of this, it is unclear how exogenous ketones could be used to help treat diabetes. One effect that is consistently reported is that ketone ester and ketone salt drinks and infusions lower blood glucose and lipid levels 11,106 ,107. It is also possible that exogenous ketones have a positive effect on insulin sensitivity; ketone ester supplementation increased insulin sensitivity in rodents by 73%108. It is possible that exogenous ketones could be used alongside diet and lifestyle changes to help control blood in diabetes, but further research must be done before this can be realised. 
Losing weight is 80% diet. Volek and Phinney did a study where they put people on a High fat (65-80% of calories from fat, 50-75 grams protein and low carb) and had one group do no exercise, one do resistance training and one to resistance training and cardio. All 3 groups lost the same amount of weight on average. But the resistance training group lost almost entirely fat while preserving muscle mass, which is important. So I always advocate some resistance training. 🙂

As ketones are the only other metabolic substrate that can fuel the brain, there is a compelling mechanism whereby ketosis could improve brain energy metabolism and therefore improve symptoms of AD. Despite a declining ability of the brain to use glucose, cerebral ketone metabolism is preserved in AD (Castellano2015). This means that ketosis could be used to prevent an energy deficit in the brain. Another possibility is that ketone metabolism decreases mitochondrial damage caused by oxidative stress in the brain52. Individuals with AD tend to have increased mitochondrial oxidative stress, which can worsen brain energy production and increase plaque and tangle formation53.  

In low carb and keto baking, we’re concerned with two things: 1) keeping carbs low, and 2) still achieving a baked good that has great flavor and texture (because if we can’t gag it down there’s just no point, right? Lol). Low carb bread recipes are usually gluten free and grain free (although we’ve seen a couple that use oat fiber), but then the challenge is to get creative to get the right combination of ingredients to yield something that rises properly and tastes good.
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