Hey Maya!! This is the 2nd recipe I’ve tried off your website and again I love it!! Turned out really well. I can have sandwiches again or a quick piece Of toast when I’m in a hurry to get out the door. I was skeptical about the xanthan gum since I tried a recipe using psyllium husk powder. I did not like it. I can’t taste the xanthan gum so I have no problem using it going forward. Thanks again for the recipe!!!

No-sugar diet plan: What you need to know Eliminating sugar from the diet can help prevent weight gain, diabetes, heart disease, and other problems. Whether cutting sugar out of the diet completely or simply cutting back, we have eight important tips for following a no-sugar diet, and some advice about fruits and other natural foods that contain sugar. Read now


I so miss bread fresh from the oven (I’m going to be adding the yeast)! You are absolutely correct about beaten egg whites creating air pockets. My family has always made buttermilk pancakes from scratch and we always separate the eggs, beat the whites to soft peaks and fold them in at the last minute. The pancakes rise beautifully! Have you tried this with your keto pancakes?
Hunger and satiety are two important mechanisms involved in body weight regulation. Even though humans can regulate food intake by will, there are systems within the central nervous system (CNS) that regulate food intake and energy expenditure. This complex network, whose control center is spread over different brain areas, receives information from adipose tissue, the gastrointestinal tract (GIT), and from blood and peripheral sensory receptors. The actions of the brain's hunger/satiety centers are influenced by nutrients, hormones and other signaling molecules. Ketone bodies are the major source of energy in the periods of fasting and/or carbohydrate shortage and might play a role in food intake control.
Hi Mindy, That sounds very odd. The salted butter is probably why it was too salty, but I think one of your ingredients must have gone bad, because the bread shouldn’t have a bitter or sour taste at all. Or did you use baking soda instead of baking powder? That would taste both bitter and sour, so that could be it. It needs to be baking powder, not baking soda. Hope you’ll try again!
In a separate post, I explained the difference between nutritional ketosis (NK) and diabetic ketoacidosis (DKA). If this distinction is not clear, I’d suggest giving this separate post a quick skim for a refresher.  DKA is a pathologic (i.e., harmful) state that results from the complete or near absence of insulin.  This occurs in the setting of type 1 diabetes or very end-stage type 2 diabetes, and often as the result of a physiologic insult (e.g., an infection) where the patient is not receiving sufficient insulin to bring glucose into his cells.  A person with a normal pancreas, regardless of how long he fasts (including the fellow I reference above who fasted for 382 days!) or how much he restricts carbohydrates, can not enter DKA because even a trace amount of insulin will keep B-OHB levels below about 7 or 8 mM, well below the threshold to develop the pathologic acid-base abnormalities associated with DKA. Let me reiterate, it is physiologically impossible to induce DKA in anyone that does not have T1D or very, very, very late-stage T2D with pancreatic “burnout.”
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This is now my go to for lo-carb bread recipe. It is SO EASY! I made it last weekend, Instead of Xanthan gum I used konjac root powder, it worked just fine, my baking time was more like 50 minutes and I did cover the top loosely with foil for the first 15 minutes so the top wouldn’t brown so quickly (maybe why my cooking time was so long?) I also added a pinch of Bakers yeast (brewers yeast is NOT gluten free) just for flavor and stevia 3/4 T. This bread makes really good grilled cheese or avocado toast! Very yummy! Thanks for this recipe!
Hi Maria- I am a 3 year cancer survivor. I had been following basically a paleo diet, but often fell off the wagon where sugar was concerned. In the last year I was diagnosed with ulcerative colitis and chrohn’s disease. My naturopath recommended I follow the keto-adaptive diet. I was very excited to make your amazing bread, but I wonder if the psyllium powder would be bad for my intestinal issues? Hope not!

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.


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]
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].
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]
If you’ve been looking for what is definitively the best keto bread recipe on the internet, then you’ve come to the right place. How do I know it’s the best? Well, I’ve tried just about every keto bread recipe over the past three years and decided that nothing was good enough. There’s a couple that are good, but I wanted perfection! The best part about this recipe is that it’s simple, and once you have it down, you can replicate this keto friendly bread any time you want. I’ve been making a low carb loaf every Sunday for the past few weeks and would recommend that to anyone. It’s so nice to have a loaf of bread at your disposal when you’re on a low carb diet. It almost feels like cheating. Check out this recipe and start making the best keto bread you’ve ever tried today!
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