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!!!


Hands down, the absolute best low carb bread recipe ever!!! I made it last night and I am blown away!!! I’ve tried a lot of low carb bread recipes trying to find something close to the “carby” bread I once loved, and you have solved my dilemma. This bread is better than the carb-laden kind (in my opinion) and I am so happy to be able to enjoy toast, sandwiches and any other idea that comes to my mind for utilizing this bread. I can’t wait to make another batch because I didn’t leave this one in quite long enough, but I am certain of it’s potential! God bless you.
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Pizza for breakfast? You betchya! This recipe by All Day I Dream About Food slashes carbs by subbing in cauliflower for the standard wheat flour crust, and racks up plenty of fats and protein with toppings like cheese, sausage, eggs, and avocado. It’s as gooey and crispy as your favorite pizza pie, but costs you a slim 5.43 grams of net carbs a serving. Perfect for relaxing weekend mornings or keto-friendly brunch.
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The yeast in this low carb and keto bread ensures a wonderful texture and taste. Now, how much your bread will rise (and fall!) post-bake depends quite a bit on your altitude. But note that you still won’t get that gummy and wet texture here of most low carb breads. Plus, as mentioned, we’re baking at over 7,000 feet (Mexico City here!!), so if we can make this keto sandwich bread work so can you.
^ Hochachka PW, Storey KB (February 1975). "Metabolic consequences of diving in animals and man". Science. 187 (4177): 613–21. Bibcode:1975Sci...187..613H. doi:10.1126/science.163485. PMID 163485. In the terminal stages of prolonged diving, however, even these organs must tolerate anoxia for surprisingly long times, and they typically store unusually large amounts of glycogen for this purpose.
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.

The yeast in this low carb and keto bread ensures a wonderful texture and taste. Now, how much your bread will rise (and fall!) post-bake depends quite a bit on your altitude. But note that you still won’t get that gummy and wet texture here of most low carb breads. Plus, as mentioned, we’re baking at over 7,000 feet (Mexico City here!!), so if we can make this keto sandwich bread work so can you.


Ketone esters (BHB-BD) decreases muscle protein breakdown30. Exercise triggers the breakdown of some muscle proteins in order to top up metabolic processes inside the cell. This results in a rise in ‘branched chain amino acid’ levels inside the muscle after exercise. Taking a ketone ester drink before exercise decreased the exercise-induced rise in muscle branched chain amino acid levels. This could help to protect muscle during exercise. 
People who have metabolic syndrome typically have apple-shaped bodies, meaning they have larger waists and carry a lot of weight around their abdomens. It's thought that having a pear-shaped body — that is, carrying more of your weight around your hips and having a narrower waist — doesn't increase your risk of diabetes, heart disease and other complications of metabolic syndrome.
Before we begin, a disclaimer in order: If you want to actually understand this topic, you must invest the time and mental energy to do so.  You really have to get into the details.  Obviously, I love the details and probably read 5 or 6 scientific papers every week on this topic (and others).  I don’t expect the casual reader to want to do this, and I view it as my role to synthesize this information and present it to you. But this is not a bumper-sticker issue.  I know it’s trendy to make blanket statements – ketosis is “unnatural,” for example, or ketosis is “superior” – but such statements mean nothing if you don’t understand the biochemistry and evolution of our species.  So, let’s agree to let the unsubstantiated statements and bumper stickers reside in the world of political debates and opinion-based discussions.  For this reason, I’ve deliberately broken this post down and only included this content (i.e., background) for Part I.
These breakfast egg muffins from Hurry The Food Up just might be the ultimate meal prep food. They take only 25 minutes to throw together, and three muffins provides 20 grams of protein for under 300 calories. You can also change up your mix-ins with different cheeses, vegetables, and seasonings. Freeze them for later or keep them in your fridge for the week — chances are, it won't be long before you need to make another batch.
Various strategies have been proposed to prevent the development of metabolic syndrome. These include increased physical activity (such as walking 30 minutes every day),[48] and a healthy, reduced calorie diet.[49] Many studies support the value of a healthy lifestyle as above. However, one study stated these potentially beneficial measures are effective in only a minority of people, primarily due to a lack of compliance with lifestyle and diet changes.[12] The International Obesity Taskforce states that interventions on a sociopolitical level are required to reduce development of the metabolic syndrome in populations.[50]
Nuclear factor erythroid-derived 2-like 2 (NFE2L2 or NRF2) is a transcription factor that has a prominent role in antioxidant signaling and also influences mitochondrial bioenergetics. The NFE2L2 abbreviation is used in this review to avoid confusion with nuclear respiratory factor 2, which despite being a different protein, has overlapping function with NFE2L2 and shares the same NRF2 abbreviation [349]. Although the mechanisms of NFE2L2 signaling are not fully elucidated [350], oxidative stress has a clear role in interacting with cysteine residues of Kelch-like ECH-associated protein 1 (Keap1), which decreases proteasomal degradation of NFE2L2 and thereby allows entry of NFE2L2 into the nucleus to induce transcription [351–355]. Although the influence of PGC-1α on antioxidant enzyme expression is not dependent on NFE2L2 [76, 356], PGC-1α increases NFE2L2 expression [357], indicating that NFE2L2 activity is influenced by perturbations in both energy and redox homeostasis. NFE2L2 primarily increases expression of antioxidant enzymes, including SOD1 [358], SOD2 [358], catalase [358–361], GPx [360], NQO1 [354, 359–362], GCL [359–361], GST [362], GSR [359–361], and Prx1 [352], but also increases expression of proteins involved in mitochondrial biogenesis and bioenergetics including NRF-1, NRF-2, TFAM, cytochrome c oxidase, and citrate synthase [358].
The sirtuin isoforms SIRT1 [232, 233] and SIRT3 [234–236] are nicotinamide adenine dinucleotide- (NAD+) dependent deacetylases associated with longevity. Many reactions are regulated by the redox state of NAD+ and its phosphorylated form, NADP+. Among these reactions, a prominent role of reduced NADP+ (i.e., NADPH) is to support reductive biosynthesis and antioxidant defense, requiring the NADP+/NADPH ratio to be kept low [237]. In contrast, the NAD+/NADH ratio is kept high to support energy metabolism [237], thereby linking sirtuin function to bioenergetic status [238]. Although sirtuins are inhibited by high concentrations of NADH, their activity is influenced more by absolute NAD+ concentration than the NAD+/NADH ratio [238].
The findings of a stable (Chearskul et al., 2008) or slightly increased response (Sumithran et al., 2013) of post-prandial FFA after KD can be viewed in the nutrient-static context. Elevated circulating FFA may actually reduce food intake and glucose production through actions on specific hypothalamic neurons (Obici et al., 2003). It has been suggested that this effect could be mediated by the increase of cellular concentration of long-chain FAs-CoA in the arcuate nuclei of the hypothalamus (Obici et al., 2003).
Last point of background: Everything I’ve just presented is based on data from starving subjects.  If one restricts carbohydrate intake, typically to less than about 20-50 gm/day (dependent on timing and carbohydrate composition), and maintains modest but not high protein intake (because protein is gluconeogenic – i.e., protein in excess will be converted to glycogen by the liver), one can induce a state referred to as “nutritional ketosis” with similar physiology to what I’ve just presented without resorting to starvation.  Why you’d do this is something I will discuss later.
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.[27]

β-hydroxybutyrate and, in some cases, acetoacetate contribute to protection against oxidative stress by decreasing production of mitochondrial reactive oxygen species (mtROS), by increasing expression or protein content of antioxidant enzymes through histone deacetylase (HDAC) inhibition, and by directly scavenging the hydroxyl radical (•OH). Upregulation of antioxidant enzymes through HDAC inhibition includes manganese superoxide dismutase (SOD2), catalase, and metallothionein II and is likely mediated by the transcription factor forkhead box O 3a (FOXO3a).
One of the foods that people tell us they miss most after going keto is bread. (And cookies or cakes, but you get the idea.) We get it, bread is undeniably comfort food. Growing up, it wasn’t unheard of to eat toast for breakfast, a sandwich for lunch, and maybe even a slice of buttered bread along with dinner. Not only is that ton of carbs, but it’s also a lot of empty calories when we could have been eating real-food alternatives, like this bread made from nutrient-dense ingredients!
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