I just made this bread and although mine looks more dense than yours, it is good. I was going to make it again using a little less water to see if I can get more rise, but then I read your comment about you not eating this bread because your keto bread is more weight loss friendly. So I shouldn’t eat this since I’m trying to lose weight? I’ve been keto-adapted for over a year, but I’ve only lost 62 pounds:( Thank you for your recipes and all of the research you do! Don’t think I could stick with this way of eating without being able to cook delicious food!
Just made my 3rd loaf. My technique has been improving each time so I am getting a better result! I had never baked anything before like this and there is an art involved. But the deliciousness has never been absent… the mixture of these ingredients has been amazing. Just going from Salvador Dali bread to Leonardo Divinci for style is the new goal!

I am disappointed with my first effort but remain undaunted. I did not use the J Robb psyllium but did grind it up as finely as I could and otherwise followed the recipe exactly. I am an experienced baker so I’m not giving up and will try using less water next time. I want to use as many ingredients as I can find in my small town in order to vote with my dollars for more healthy foods so I will try a few more times before special ordering.
BMI (body mass index), an alternate measure of obesity that is used by many healthcare practitioners; it is calculated by taking: (Weight in pounds X 705) / (height in inches squared); for example: (150 pounds X 705) / (67 inches X 67 inches) = a BMI of 23.5. An adult with a BMI greater than 30 is considered obese. This calculation does not, however, describe where the excess weight is on the body.
Because the population of the U.S. is aging, and because metabolic syndrome is more likely the older you are, the American Heart Association (AHA) has estimated that metabolic syndrome soon will become the main risk factor for cardiovascular disease, ahead of cigarette smoking. Experts also think that increasing rates of obesity are related to the increasing rates of metabolic syndrome.
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. 
Cinnamon supplements may modestly improve blood sugar in people with type 2 diabetes whose blood sugar is not well controlled with medication. In addition, one small study found that a branded cinnamon extract reduced fasting blood sugar by an average of about 10 mg/dL in prediabetic men and women with metabolic syndrome. Keep in mind, however, that only certain varieties of cinnamon have been shown to have this effect, and long-term safety studies have not been conducted.

^ Jump up to: a b c Clemente FJ, Cardona A, Inchley CE, Peter BM, Jacobs G, Pagani L, Lawson DJ, Antão T, Vicente M, Mitt M, DeGiorgio M, Faltyskova Z, Xue Y, Ayub Q, Szpak M, Mägi R, Eriksson A, Manica A, Raghavan M, Rasmussen M, Rasmussen S, Willerslev E, Vidal-Puig A, Tyler-Smith C, Villems R, Nielsen R, Metspalu M, Malyarchuk B, Derenko M, Kivisild T (October 2014). "A Selective Sweep on a Deleterious Mutation in CPT1A in Arctic Populations". American Journal of Human Genetics. 95 (5): 584–589. doi:10.1016/j.ajhg.2014.09.016. PMC 4225582. PMID 25449608.
On the contrary, in the brain, as mentioned above, the increase of AMPK activity leads to higher food intakes. But the effect of AMPK in the brain is more complicated; mice lacking AMPKa2 in pro-opiomelanocortin neurons develop obesity, while the deficiency of AMPKa2 in agouti-related protein neurons results in an age-dependent phenotype. Thus, the conclusion is that even while AMPK is a regulator of hypothalamic functions, it does not act as a signal for energy deficit or excess (Claret et al., 2007). However, the picture is more complex than this (Figure ​(Figure3);3); BHB induces AgRP expression while increasing ATP and inhibiting AMPK phosphorylation (Cheng et al., 2008). Moreover, Laeger and colleagues have recently demonstrated that under physiological conditions BHB decreases AMPK phosphorylation and AgRP mRNA expression in GT1-7 hypothalamic cells (Laeger et al., 2012).
A high proportion of energy from ketone oxidation is transferred to the electron transport chain at the start (as NADH+), in comparison to the energy from fat, where a high proportion is transferred ‘downstream’ (as FADH). This means that, even though there is a high amount of ‘potential energy’ in a fat molecule, less of this can be transferred to ATP.   
I would like to point out that the metric conversion of 3/4 cup to 90g coconut flour as stated in your recipe is incorrect. Should be 84g per package labeling (Bob’s Red Mill). Unfortunately I made my first batch with 90g of coconut flour, and it was definitely not “pourable”. More like scoopable. I will try again with correct amount but thought I would point so you can update the recipe. Thank you!
sdLDL. This is a measurement of the number of small dense low-density lipoprotein molecules a person has. LDL varies in size, and the smaller denser molecules, which tend to form when elevated triglycerides and VLDL are present in the blood, are thought to be more aggressive in causing atherosclerosis. This test is now commercially available, but is not performed by many laboratories and is not ordered frequently. Its ultimate clinical utility has yet to be determined. It may be evaluated in a LDL particle testing.
As the rate of oxidative phosphorylation approaches the capacity of the mtETC, Δp will increase and facilitate mtROS production [53]. Higher oxidative capacity should therefore decrease the potential for mtROS production and subsequent oxidative damage. Furthermore, greater oxidative capacity may compensate for the resulting decrease in efficiency of ATP production associated with increased mitochondrial uncoupling. Since oxidative phosphorylation occurs exclusively in mitochondria, mitochondrial density is a key determinant of oxidative capacity [154].
The use of lifestyle interventions to treat and prevent chronic disease is attractive because of their potential to lower medical costs and produce more robust and holistic improvements in health. Ketogenic diets have been studied sporadically for more than 100 years, but over the last 15 years, a growing number of researchers have contributed to what is now a critical mass of discoveries that link the process of keto-adaptation to a broad range of health benefits [10–33]. Early clinical research focused on the use of “extreme” versions of ketogenic diets to treat seizures, but recent research indicates that benefits related to the management of epilepsy, weight loss, metabolic syndrome, and type 2 diabetes can be achieved with an approach that is less restrictive in carbohydrate and protein, and therefore more satisfying, sustainable, and feasible for the general population. A “well-formulated” ketogenic diet is generally characterized by a total carbohydrate intake of less than 50 g/d and a moderate protein intake of approximately 1.5 g/d per kg of reference weight [34]. This typically increases circulating β-hydroxybutyrate (BHB) and acetoacetate (ACA) from concentrations that are typically less than 0.3 mM into the range of nutritional ketosis, which for BHB, we define as 0.5–3 mM [35]. This range is below the typical 5–10 mM range for BHB that occurs during prolonged fasting, and well below concentrations characteristic of ketoacidosis [34, 35]. From the perspective of meeting energy demands, the reduced carbohydrate and moderate protein intakes necessarily make ketogenic diets high in fat. Despite this contradiction with mainstream dietary guidelines, ketogenic diets may be beneficial for many health conditions, particularly the previously mentioned conditions related to mitochondrial impairment, which includes obesity [10, 11], diabetes [12–14], cardiovascular disease [15–17], cancer [15, 18–26], neurodegenerative diseases [19, 20, 27–30], and even aging [31–33, 36, 37].
Ok, My last question before I try it for the 5th time. Thank you for taking the time to answer!! I know you say grind it more, but here is my dilemma. You says yours weighs 90 grams for 10 tablespoons. So, i weighed mine out (I grind in a high power vitamix) my 10 tablespoons weight 115 grams…so mine is more dense than yours. I’m torn, should I actually grind less? Buy another brand? Maybe Frontier? Thanks for any help. I am so frustrated not having a bread sub for my grain free family 🙁 I tried protein bread but I have this awful aversion to cream cheese taste and can’t seem to get over it 🙁 Even if I could just get a baguette or roll to work out I’d be so happy! I get my hubby’s hopes up every time it bakes because it smells so good! Thanks again!

Where does nutrition info come from? Nutrition facts are provided as a courtesy, sourced from the USDA Food Database. You can find individual ingredient carb counts we use in the Low Carb & Keto Food List. Carb count excludes sugar alcohols. Net carb count excludes both fiber and sugar alcohols, because these do not affect blood sugar in most people. We try to be accurate, but feel free to make your own calculations.

Hi James, Thank you for sharing. Most likely this wasn’t fully cooked if it stuck to the parchment paper, as I never have to grease it, but I did add a note to the post that you could do that to be on the safe side. I think the previous recipe and post were not clear enough on how to make sure that it’s done, so I updated them and hope that will help. I’d love to know if that made a difference if you try it again. But, this bread is more similar to fluffy pre-sliced white bread than a crusty bread, so I still would not expect a crust. If you are looking for a crusty bread, try this almond flour bread instead.
Fortunately, since peaking in 2001-2002, the overall prevalence of metabolic syndrome in the United States has fallen, primarily due to decreases in the prevalences of hypertriglyceridemia and hypertension—and in spite of increases in the prevalences of hyperglycemia and obesity/waist circumference. [27]  Data from the 2009-2010 National Health and Nutrition Examination Survey (NHANES) showed that the age-adjusted prevalence of metabolic syndrome had fallen to approximately 24% in men and 22% in women. [28]

The hypothalamus is the brain's main center responsible for hunger/satiety (H/S) control. In the theory that Mayer proposed more than 60 years ago, he assigned a central role to glucose levels in the H/S control: the so-called “glucostatic theory” (Mayer, 1955). Mayer suggested that depletion of carbohydrate availability leads to hunger, and the hypothalamic centers with receptors sensitive to glucose levels might be involved in the short-term regulation of energy intake (Mayer, 1955). The “feeding center” in the lateral hypothalamic area (LHA), according to the glucostatic theory, reacts to the between-meal fall of blood glucose and stimulates food intake. The LHA contains glucose-inhibited neurons that are stimulated by hypoglycemia, a process crucial to mediating the hyperphagia normally induced by hypoglycemia. The subsequent post-prandial hyperglycemia activates the “satiety center” in the ventromedial hypothalamus (VMH), which contains glucose-excited neurons and inhibits both “feeding center” and food intake.
The goal of the ketogenic diet is to keep you in this fat-burning metabolic state of ketosis. This is achieved by following a very low-carbohydrate, high-fat diet that includes only moderate amounts of protein. Foods like bread, cereal, processed snacks and sugary drinks are therefore off the table, while fattier foods like butter, grass-fed beef, fish and also non-starchy veggies take center stage, providing the majority of daily calories (as much as 70–80 percent).
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Perturbations in bioenergetic homeostasis induce signal transduction that leads to upregulation of mitochondrial capacity and antioxidant defense. Three key enzymes involved in the sensing of these perturbations and the subsequent induction of signal transduction are AMP-activated protein kinase (AMPK) and silent mating type information regulation 2 homologues 1 and 3 (SIRT1 and SIRT3).
The gastrointestinal tract (GIT) plays a central role in the control of energy balance. Many molecules produced by the GIT exert hunger or satiety effects on the brain. Ghrelin is a peptide produced mainly by the stomach's oxyntic cells that stimulates ghrelin secretion in the hypophysis and has some neuroendocrine activities. However, its orexigenic properties are the most relevant to us and ghrelin is the only known peripheral orexigenic hormone (Date, 2012). Cholecystokinin (CCK) is a peptide produced mainly in the duodenum and jejunum that acts on the vagus nerve and directly on the hypothalamic nuclei. CCK is an anorexigenic factor and it reduces food intake, meal size and duration (Murphy et al., 2006). Three other related hormones are pancreatic polypeptide (PP), amylin, and peptide YY (PYY). PP is a peptide produced by the endocrine pancreas in relation to the caloric content of meals, and it reduces food intake both in rodents and humans. Amylin is a peptide co-secreted with insulin; its main effect on food control is a reduction of meal sizes and food intake (Murphy et al., 2006). Peptide YY (PYY) is produced in the gut and is similar to PP. PYY is stored in intestinal cells and released into the circulation as PYY3−36, a truncated form of PYY. The release of PYY3−36 is dependent on a meal's caloric and fat content (Veldhorst et al., 2008). The glucagon-like peptide 1 (GLP-1) is produced by the cleavage of pro-glucagon gene in the intestine. It acts as incretin at a pancreatic level, promoting insulin secretion and as neuro hormone on hypothalamic nuclei, inducing satiety (Valassi et al., 2008).
If you can't shake a hankering for a good old-fashioned McDonald's Egg McMuffin, this keto-friendly take on the classic from Peace, Love, and Low Carb will scratch that same itch. Use mason jar rings to cook the eggs into perfect bun-like circles, then layer it up with sausage and cheddar cheese. To upgrade way past drive-thru status (and add a dose of healthier fat), throw some avocado in there.
Finally, an important consideration is the effect of the ketogenic diet on blood lipids. This is because the levels of various lipids in the blood have been shown to predict the likelihood of cardiovascular disease. Lipids and cholesterol are carried through the blood in biochemical assemblies called ‘lipoproteins,’ because they do not dissolve in water. There are two broad classes of lipoproteins in the blood: high density lipoprotein (HDL) and low density lipoprotein (LDL). HDL is thought of as more ‘healthy’ (H = ‘Healthy’) because it responsible for moving cholesterol and lipids from the peripheral tissues into the liver for metabolism. LDL is demonised as bad cholesterol (L = ‘Lethal’), levels are elevated after a fatty meal and elevated LDL is associated with cholesterol build up in the arteries. 
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!

The ketogenic diet: The ketogenic diet could affect cancer by a similar mechanism to calorie restriction and fasting. Of the 29 animal studies that have examined ketogenic diet and cancer, 72% of them have demonstrated an anti tumor effect. There have been a small number of case studies of the safety and efficacy of the ketogenic diet in humans. The results have been largely positive, for example following a ketogenic diet helped to stabilise tumour growth and alter tumor metabolism96 ,97 ,98. There is an absence of fully randomised clinical trials in humans, but 24 case studies have been published; one recent appraisal of the case study data said that “ a probabilistic argument shows that the available data strengthen the belief in the anti-tumor effect hypothesis (of the ketogenic diet) at least for some individuals"99. 


Looking back on my earlier posts on ketosis—and explaining what I eat, for example—makes me both chuckle and cringe. I remember how bizarre the diet seemed to many readers and the general public at the time. I also remember digging into the literature and learning, for example, that my alma mater, Johns Hopkins had been using the ketogenic diet to treat pediatric epilepsy for almost a century…and being so embarrassed about admonishing that patient I saw in my residency.
One hypothesised contributor to neuronal death is insufficient energy production, secondary to impaired mitochondrial function. However, it is unclear if this is in fact a cause or effect of PD. Whatever the case may be, patients with PD have been shown to have impaired mitochondrial energy production in the brain59 and lower brain glucose utilisation60. Another factor may be neuro-inflammation, which is also common in PD, and is thought to lead to further accumulation of Lewy Bodies and neuronal death.
AMP competes with ATP for binding to the γ regulatory subunit of AMPK [177, 178] and by doing so, greatly increases AMPK activity, but only in the presence of an upstream kinase such as liver kinase B1 (LKB1) [179]. This binding of AMP to the γ subunit appears to promote AMPK activity through at least two mechanisms: facilitated phosphorylation of the α subunit [180–183] and inhibition of dephosphorylation by protein phosphatases 2Cα and 2Ac [179, 181, 183, 184]. ADP also binds to the γ subunit of AMPK to inhibit dephosphorylation [183, 185, 186] and possibly facilitate phosphorylation [185]. This is important to the energy sensing sensitivity of AMPK based on the much higher physiological concentration of ADP compared to AMP [186]. Data on changes in AMP and ADP levels in response to a ketogenic diet are lacking. However, the decreased availability of carbohydrate and increased mitochondrial uncoupling (previously described) during nutritional ketosis suggest a decline in ATP production, at least until compensatory adaptations occur. A decline in ATP implies a relative increase in AMP and ADP, which would facilitate AMPK phosphorylation and activation. In addition, ketogenic diets are commonly reported to have a satiating effect [187], which may further increase the AMP and ADP to ATP ratios through spontaneous caloric restriction.

It is common for there to be a development of visceral fat, after which the adipocytes (fat cells) of the visceral fat increase plasma levels of TNF-α and alter levels of a number of other substances (e.g., adiponectin, resistin, and PAI-1). TNF-α has been shown not only to cause the production of inflammatory cytokines, but also possibly to trigger cell signaling by interaction with a TNF-α receptor that may lead to insulin resistance.[31] An experiment with rats fed a diet with 33% sucrose has been proposed as a model for the development of metabolic syndrome. The sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance. The progression from visceral fat to increased TNF-α to insulin resistance has some parallels to human development of metabolic syndrome. The increase in adipose tissue also increases the number of immune cells present within, which play a role in inflammation. Chronic inflammation contributes to an increased risk of hypertension, atherosclerosis and diabetes.[32]
You've probably heard of the keto diet, the trendy weight loss plan that advocates for cutting down carbs and upping your fat intake. (That means no to pastries and pasta, and yes to meat, eggs, and heart-healthy oils.) If your morning routine of the past involved bagels, toast, or oatmeal, trying to come up with keto breakfast ideas can feel like a rude awakening. With so many carb-heavy a.m. foods, it's arguably the hardest meal to find ketogenic diet-approved substitutes for — especially when you're staring right in the face of a donut on your morning coffee run.

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.


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Ketoacidosis occurs mainly in people with type 1 diabetes if they do not take insulin. In diabetic ketoacidosis (DKA), blood sugar and ketones rise to dangerous levels, which disrupts the blood’s delicate acid-base balance. People in ketoacidosis feel extremely ill and experience profound dehydration, vomiting, abdominal pain, and weakness. DKA requires hospitalization so that IV fluids and insulin can be given to gradually and safely lower blood sugar.
Ketone bodies are acidic, but acid-base homeostasis in the blood is normally maintained through bicarbonate buffering, respiratory compensation to vary the amount of CO2 in the bloodstream, hydrogen ion absorption by tissue proteins and bone, and renal compensation through increased excretion of dihydrogen phosphate and ammonium ions.[9] Prolonged excess of ketone bodies can overwhelm normal compensatory mechanisms, defined as acidosis if blood pH falls below 7.35.

Type I diabetes is usually treated by insulin injections, that replace the body’s own insulin production. In Type I diabetics, lowering dietary carbohydrate consumption can reduce the need to inject insulin to lower blood sugar101. However, because they do not release any insulin Type I diabetics can be at risk of developing a complication called “Diabetic Ketoacidosis” (DKA). DKA occurs because, alongside its effects on glucose, insulin has other effects in the body. Insulin normally inhibits the release of fat (lipolysis) from adipose tissue. In Type I diabetics, the lack of insulin can lead to high levels of lypolysis, high levels of fatty acids in the blood, this then drives rapid and uncontrolled liver ketone production. The symptoms of DKA are weakness, confusion and deep gasping breathing. In order to avoid developing DKA while following a ketogenic diet, Type I diabetics should seek medical supervision and closely monitor their glucose and ketone levels if reducing their dietary carbohydrate intake. 
Hi Amber, Yes, the baking powder and egg whites do help it rise a bit, just not as much as regular bread. It’s hard to say what went wrong, if anything. Everyone’s palate is a little different, so it’s possible you just didn’t like it, or maybe something didn’t go as it should have. It could be that the batter and whites weren’t folded together quite enough?
Hi, I’ve made this recipe twice and LOVE the taste. However, both times the bread would rise so high in the oven, but as soon as I take it out to cool it deflated and middle sink down. What could’ve gone wrong? Over mixing? I did switch coconut flour to all almond flour instead. Could that be a problem? Please help as I’m anxious to make another batch. Thank you.
Metabolic syndrome is a serious health condition that affects about 23 percent of adults and places them at higher risk of cardiovascular disease, diabetes, stroke and diseases related to fatty buildups in artery walls. The underlying causes of metabolic syndrome include overweight and obesity, physical inactivity, genetic factors and getting older.

While entering into ketosis it’s common to notice certain signs and symptoms of your body changing. These have been nicknamed by some “the keto flu.” While implementing the ketogenic diet can be challenging at first, commonly causing some side effects that can last for 1–2 weeks (or potentially more), these typically go away with time. Symptoms usually decrease as your body get’s more accustomed to being in ketosis, but in the meantime you might find that you experience:
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The sausage for this keto breakfast sandwich is pretty straight forward.  I used half a pound of store bought breakfast sausage.  I formed it into 2 patties and cooked them in my cast iron skillet.  Cook it on medium-high heat and don’t touch it until it forms a crust.  Try to ignore the splatters all over the stovetop, unless you’re OCD like me and you wipe it away while everything is still cooking.  Then wipe again, and again.
In addition to the seaweed and glycogen carbohydrates mentioned above, the Inuit can access many plant sources. The stomach contents of caribou contain a large quantity of partially digested lichens and plants, which the Inuit once considered a delicacy. They also harvested reindeer moss and other lichens directly. The extended daylight of the arctic summer led to a profusion of plant life, and they harvested plant parts including berries, roots and stems, as well as mushrooms. They preserved some gathered plant life to eat during winter, often by dipping it in seal fat.[71]
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Fantastic! So easy to make. Not sure if I didn’t mix mine well enough, but it had a couple of “air holes” in it after baking. Did not matter…tastes great. I made a grilled cheese out of two of the slices…delicious! I can’t wait to try some of the ideas from the comments: adding herbs and/or spices, adding cinnamon and stevia, etc. Seems the possibilities are endless.
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The Inuit are often cited as an example of a culture that has lived for hundreds of years on a low-carbohydrate diet.[42] However, in multiple studies the traditional Inuit diet has not been shown to be a ketogenic diet.[43][44][45][46] Not only have researchers been unable to detect any evidence of ketosis resulting from the traditional Inuit diet, but the ratios of fatty-acid to glucose were observed at well below the generally accepted level of ketogenesis.[44][47][45][46] Furthermore, studies investigating the fat yields from fully dressed wild ungulates, and the dietary habits of the cultures who rely on them, suggest that they are too lean to support a ketogenic diet.[48][49] With limited access to fat and carbohydrates, cultures such as the Nunamiut Eskimos—who relied heavily on caribou for subsistence—annually traded for fat and seaweed with coastal-dwelling Taremiut.[48]
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Some people may ask: Why not just have liposuction of the abdomen and remove the large amount of abdominal fat that is a big part of the problem? Data thus far shows no benefit in liposuction on insulin sensitivity, blood pressure, or cholesterol. As the saying goes, "If it's too good to be true, it probably is." Diet and exercise are still the preferred primary treatment of metabolic syndrome.
The graph below, also from the Cahill and Veech paper, shows the blood chemistry of a person starving for 40 days.  Within about 3 days, a starving person’s level of glucose stops falling.  Within about 10 days they reach a steady-state equilibrium with B-OHB levels exceeding glucose levels and offsetting most of the brain’s need for glucose. In fact, the late George Cahill did an experiment many years ago (probably would never get IRB approval to do such an experiment today) to demonstrate how ketones can offset glucose in the brain. Subjects with very high levels of B-OHB (about 5-7 mM) were injected with insulin until glucose levels reached 1 mM (about 19 mg/dL)!  A normal person would fall into a coma at glucose levels below about 40 mg/dL and die by the time blood glucose reached 1 mM.  These subjects were completely asymptomatic and 100% neurologically functional.
The metabolic syndrome quintuples the risk of type 2 diabetes mellitus. Type 2 diabetes is considered a complication of metabolic syndrome. In people with impaired glucose tolerance or impaired fasting glucose, presence of metabolic syndrome doubles the risk of developing type 2 diabetes.[28] It is likely that prediabetes and metabolic syndrome denote the same disorder, defining it by the different sets of biological markers.
What is the link between ketones and diabetes? Ketone is a chemical produced by the body when fats are broken down for energy. Ketone testing is important for people with diabetes, because high levels can lead to diabetic ketoacidosis (DKA), when acid levels become too high in the blood and the person loses consciousness. Find out when and why to do ketone testing. Read now
Nice and firm. Baked it on the recommended temp, added 6 or 7 minutes. Pressed the middle and it was great. I let it cool. What was nice about it was obviously it’s low carb bread…hurray for that, but it cut well. Got 18 slices easily about 1/2 inch thick without breakage. Most importantly, it wasn’t greasy, or almond tasting overload, just delicious.

Schele E., Grahnemo L., Anesten F., Hallen A., Backhed F., Jansson J. O. (2013). The gut microbiota reduces leptin sensitivity and the expression of the obesity-suppressing neuropeptides proglucagon (Gcg) and brain-derived neurotrophic factor (Bdnf) in the central nervous system. Endocrinology 154, 3643–3651. 10.1210/en.2012-2151 [PubMed] [CrossRef] [Google Scholar]
Hi James, Thank you for sharing. Most likely this wasn’t fully cooked if it stuck to the parchment paper, as I never have to grease it, but I did add a note to the post that you could do that to be on the safe side. I think the previous recipe and post were not clear enough on how to make sure that it’s done, so I updated them and hope that will help. I’d love to know if that made a difference if you try it again. But, this bread is more similar to fluffy pre-sliced white bread than a crusty bread, so I still would not expect a crust. If you are looking for a crusty bread, try this almond flour bread instead.

Has anyone tried this using a substitute for the eggs/egg whites? My husband seems to be sensitive to eggs (not sure which part, to be honest) and we’ve been making most recipes using agar agar as a substitute (for either whites or whole eggs) but this only works if the egg is a binder. I’m guessing that they are a leavening agent in the bread (please correct me if I’m wrong!) and I don’t know if agar would work in this recipe. I do have VersaWhip 600 – anyone ever tried that in a bread recipe?
I’m just starting a new low carb diet and I love your channel. You have so many great and easy recipes but I will definitely be trying this bread out. I love burgers, and was sad I won’t be able to have a bun anymore. I tried a different recipe before and it just tasted like eggs. This looks like it will work much better for me. I may try and make a few batches all at once in the oven and then freeze it for later. Rock on! \m/
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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.
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