If for any reason you get a fail…a spongy loaf , or one with a buble don’t throw it away. Cut off the top bubble and cut into squares or triangles then taost for great pita like chips…cube the bottom sprinkle on some spices and toast or rebake for croutons…I have had my successes and failures wih this loaf but the ingredients are too expensive to waste…another idea would be to toast the bottom after you slice the top off and then add butter, garlic and cheese for a good garlic bread.
Meanwhile, the KD induces a ketosis that is not a pathological but physiological condition occurring on a daily basis. Hans Krebs was the first to use the term “physiological ketosis” despite the common view of it as oxymoron (Krebs, 1966); this physiological condition, i.e., ketosis, can be reached through fasting or through a drastically reduced carbohydrate diet (below 20 g per day). In these conditions, glucose reserves become insufficient both for normal fat oxidation via the supply of oxaloacetate in the Krebs cycle and for the supply of glucose to the central nervous system (CNS) (Felig et al., 1969; Owen et al., 1969) (Figure ​(Figure1).1). It is well-known that the CNS cannot use FAs as an energy source because free FAs cannot cross the blood-brain barrier (BBB). This is why the brain normally uses only glucose. After 3–4 days without carbohydrate intake (KD or fasting) the CNS must find alternative energy sources as demonstrated by Cahill et al. (Owen et al., 1967, 1969; Felig et al., 1969; Cahill, 2006). These alternative energy sources are the ketones bodies (KBs): acetoacetate (AcAc), β-hydroxybutyric acid (BHB) and acetone and the process of their formation occurring principally in the mitochondrial matrix in the liver is called ketogenesis (Fukao et al., 2004). Usually the concentration of KB is very low (<0.3 mmol/L) compared to glucose (≅ 4 mmol) (Veech, 2004; Paoli et al., 2010). Since glucose and KB have a similar KM for glucose transport to the brain the KB begin to be utilized as an energy source by the CNS when they reach a concentration of about 4 mmol/L (Veech, 2004), which is close to the KM for the monocarboxylate transporter (Leino et al., 2001).
It looks and smells beautiful when baking. The bottom of my loaves is heavy and dense. The top rises and makes an air pocket. As a result, it’s just not really pleasant to eat with it being so dense and solid even though it tastes good. The few good pieces at the very ends were yummy. I really don’t know what to do. Almond flour is expensive to be going through it like this. 🙁
But without carbs, sandwiches aren’t available either, and if there’s one thing followers of these diets miss the most, it’s got to be bread. Luckily, enterprising food-lovers following a keto diet have figured out a work-around. It’s called “90 Second Keto Bread” and it’s popping up all over the internet. Think of it like a mug cake version of a biscuit that happens to look a lot like an English muffin.
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]
Weighed my ingredients…used Jay Robb Psyllium ground down to half the amount exactly…used almond flour from nuts.com….used All Whites 100% Egg Whites. Bread fell about one minute after I took it out of the oven. Do you cool yours out of the pan or in it? Does that matter? Could that be the problem? Or could it be my vinegar? Have had it a few months…does it get old? Help!!! I promised my husband if he let me spend all this $ on ingredients I could give him a nice loaf of bread for sandwiches! So disappointed! But determined!
The Service offers health, fitness and nutritional information and is designed for educational purposes only. You should not rely on this information as a substitute for, nor does it replace professional medical advice, diagnosis, or treatment. If you have any concerns or questions about your health, you should always consult with a physician or other health-care professional.
Today was my second attempt at making “Amazing Bread”. Maybe I needed to bake it longer, but both times, it turned out gooey. The texture was not like bread at all, but more like a dumpling. I was able to slice it and I am hoping that toasting it will make it edible since I do not want to throw it out. I weighed every ingredient by the gram and used psyllium husk POWDER.
Recently, many of my patients have been asking about a ketogenic diet. Is a ketogenic diet safe? Would you recommend it? Despite the recent hype, a ketogenic diet is not something new. In medicine, we have been using it for almost 100 years to treat drug-resistant epilepsy, especially in children. In the 1970s, Dr. Atkins popularized his very-low-carbohydrate diet for weight loss that began with a very strict two-week ketogenic phase. Over the years, other fad diets incorporated a similar approach for weight loss.
Most people who have metabolic syndrome already have a closely related condition called insulin resistance, which is when the body stops responding to insulin (a hormone produced in the pancreas). After the food we eat is converted into a type of sugar called glucose, insulin is what enables the glucose to enter the body’s cells and be used as energy. For someone who is insulin resistant, however, the glucose builds up in the blood, setting the stage for damage.
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].
224. Noakes M., Foster P. R., Keogh J. B., James A. P., Mamo J. C., Clifton P. M. Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk. Nutrition & Metabolism. 2006;3:p. 7. doi: 10.1186/1743-7075-3-7. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
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In the United States, metabolic syndrome has a high prevalence in African Americans, particularly African American women, and this has been attributed to the higher prevalence of obesity, hypertension, and diabetes in this population. [40] However, the highest age-adjusted prevalence of metabolic syndrome in the United States is found in Mexican Americans, approximately 31.9% of whom had the condition (compared with 27% of the general population) in a 1988-1994 survey. [41]


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.
^ Yiu H. Hui (February 1985). Principles and issues in nutrition. Wadsworth Health Sciences Division. p. 91. Retrieved 2014-05-19. Eskimos actually consume more carbohydrates than most nutritionists have assumed. Because Eskimos frequently eat their meat raw and frozen, they take in more glycogen than a person purchasing meat with a lower glycogen content in a grocery store. The Eskimo practice of preserving a whole seal or bird carcass under an intact whole skin with a thick layer of blubber also permits some proteins to ferment into carbohydrates.
In 1977 and 1978, Gerald B. Phillips developed the concept that risk factors for myocardial infarction concur to form a "constellation of abnormalities" (i.e., glucose intolerance, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and hypertension) associated not only with heart disease, but also with aging, obesity and other clinical states. He suggested there must be an underlying linking factor, the identification of which could lead to the prevention of cardiovascular disease; he hypothesized that this factor was sex hormones.[66][67]
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In addition, metabolic syndrome has been implicated in the pathophysiology of several other diseases, including obstructive sleep apnea. Breast cancer has also been linked to metabolic syndrome, possibly through dysregulation of the plasminogen activator inhibitor-1 (PAI-1) cycle. [64] Additional studies have linked metabolic syndrome with cancers of the colon, gallbladder, kidney, and, possibly, prostate gland. [65] Evidence is emerging of an association with psoriasis. [66, 67]
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).
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After a period of time, your body becomes adapted to using ketones as fuel instead of glucose. Your muscles begin to learn to convert acetoacetate into a ketogenic substance called beta-hydroxybutyrate, or BHB. BHB then becomes the new preferred ketogenic source of energy, including to fuel all brain activity. What is not needed is expelled from the body as waste.
In addition to increased mitochondrial demand and mtROS production, there are several other commonalities in the mechanisms through which exercise and nutritional ketosis induce adaptive signaling. Exercise-induced activation of AMPK is greater when the exercise is performed in a glycogen depleted state [209–211, 382, 383], and exercise-induced activation of p38 MAPK [315] and PGC-1α [277–279] occurs at least partly through β-adrenergic signaling. Although changes in NAD+ and NADH are difficult to measure and are complicated by conflicting results, exercise is also likely to increase sirtuin activation by increasing the NAD+ to NADH ratio [402].
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.

Parkinson’s disease (PD) is caused by death of neurons in a region of the brain called the ‘substantia nigra.’ As well as loss of neurons, those that survive accumulate misfolded proteins called “Lewy Bodies,” exhibit increased inflammation and impaired mitochondrial function. PD is most common in individuals over the age of 60 and is primarily characterised by poor control of movement (shaking, rigidity etc). Neuronal death leads to decreased levels of a neurotransmitter called dopamine, which is a key factor in the deterioration of motor function. Current treatments for PD centre on replacing dopamine using a drug called L-DOPA, which is a precursor to dopamine. This drug treats the symptoms of PD but not the underlying cause. 

This bread does have quite a few ingredients, but you’ll find that most are staple paleo and keto pantry ingredients. In the list below you’ll find details on several ingredients and possible subs. But if possible, please do try and make this recipe without any subs. As out of the 18 permutations we tried, this one really was terrific and the absolute best.
Have breakfast within an hour or two of waking up and then eat a snack or meal every three to six hours after that, says Rebecca Denison, RD, doctor of integrative medicine and diabetes educator at Greater Baltimore Medical Center’s Geckle Diabetes and Nutrition Center. This will add up to three to six total meals and snacks daily. It takes about four to six hours for your body to digest a meal. “You want to eat just a teeny bit before you actually need it so that your body doesn’t have to figure out how to keep your blood sugar stable,” Denison explains.
^ 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.
Carbohydrates need to be consistent. You don’t want to eat all of your daily carb count in one meal. That will cause your blood sugar to spike, and then drop during the other meals. Giving your body a steady amount of carbohydrates will provide a stable amount of energy. It will also help your body make enough insulin to keep your blood sugar at a healthy number.
Additional evidence, although independent of mitohormesis, further supports the induction of NFE2L2 activity by nutritional ketosis. Succinate is a byproduct of ketolysis and is oxidized to fumarate by succinate dehydrogenase. Therefore, the increased presence of ketones and increased rate of ketolysis during nutritional ketosis are likely to increase fumarate, which can succinylate cysteine residues of proteins [363]. In particular, fumarate can succinylate Keap1, thereby allowing NFE2L2 to enter the nucleus to induce transcription [364, 365]. In the retinas of rats injected with BHB, the nuclear content of NFE2L2 and the total homogenate content of SOD2 and GCL increased in conjunction with increased fumarate concentration [366]. BHB injection also decreased retinal ROS production and degeneration following induction of ischemia, and this protection was dependent on NFE2L2 [366]. These effects were observed at blood concentrations of BHB between 1 and 2 mM, which is consistent with nutritional ketosis.
The handheld devices that are available for home testing (such as FreeStyle by Abbott, or KetoMojo) require a small droplet of blood (obtained by a finger prick with a lancet) to be placed on a testing strip. A new testing strip must be used each time a reading is taken. The machine delivers a numerical blood BHB measurement in the unit milli molar (mM) after ~8 seconds. 
Metabolic syndrome (metabolic syndrome X, insulin resistance syndrome, dysmetabolic syndrome, hypertriglyceridaemic waist, obesity syndrome, Reaven syndrome) is the name for a group of risk factors that increase the risk for ischaemic heart disease (IHD), diabetes and stroke (Fig. 23.1). The metabolic syndrome is diagnosed when at least three of the IHD risk factors listed in Table 23.1 are present. Whether the syndrome, which affects possibly 25% of the US population, is a specific syndrome, and nothing more than the sum of its parts, is controversial.
Ok I will try this with the physillium since no sub will work. 🙂 I have a Q though-I read that too much physillium may interfere with how medicines work-my son is on 5 seizure meds, and we are going keto to help with his seizures. This looks like a good and tasty bread to replace his beloved loaf…what would you say is a safe amount for him to eat daily or weekly? Any resources on daily physillium allowances for kids so I can adapt his servings? THanks! 🙂 🙂
Embarrassing admission: I remember exactly where I was sitting in a clinic at Johns Hopkins in 2002 explaining to (admonishing, really) a patient who was on the Atkins diet how harmful it was because of DKA.  I am so embarrassed by my complete stupidity and utter failure to pick up a single scientific article to fact check this dogma I was spewing to this poor patient. If you’re reading this, sir, please forgive me. You deserved a smarter doctor.
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Comments are welcomed and encouraged. The purpose of comments on our site is to expand knowledge, engage in thoughtful discussion, and learn more from readers.Criticism and skepticism can be far more useful than praise and unflinching belief.There’s an art and science to critical thinking and how to conduct yourself. There’s a multitude of fallacious appeals we could spell out, but a good rule of thumb is not to attack the person, attack the ideas. Don’t look for the flaws in the person, look for the flaws in the hypothesis. Let’s keep the brawling to movies depicting minor league hockey teams and political “news” shows.Thank you for adding to the discussion.
Eat 15 g less carbohydrates at your next meal. While skipping meals is not a healthy option for individuals with high blood sugar, decreasing the number of carbohydrates consumed at the next meal can help force your body to use the excess sugar. Check your blood sugar an hour after the meal and if your sugar level has decreased but is still high, decrease the next meal by 30 g of carbohydrates.
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.
Thank you for the recipe. I was going to give up gluten free bread making but your recipe made my day! I used ghee instead of butter as I was too lazy to melt butter. It rose prettily in the oven. Such a nice loaf of bread. Definitely not eggy and it even has the fluffiness of bread. I would like to double the recipe and make it in a 1 lb loaf pan. Do you think that’s feasible? Many thanks,

184. Davies S. P., Helps N. R., Cohen P. T., Hardie D. G. 5′-AMP inhibits dephosphorylation, as well as promoting phosphorylation, of the AMP-activated protein kinase. Studies using bacterially expressed human protein phosphatase-2C alpha and native bovine protein phosphatase-2AC. FEBS Letters. 1995;377(3):421–425. doi: 10.1016/0014-5793(95)01368-7. [PubMed] [CrossRef] [Google Scholar]


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.
The FOXO family of transcription factors is highly conserved and promotes longevity and resistance to cellular stress. Although there are a variety of FOXO isoforms with varying tissue distribution [318–320], FOXO3a has been the most thoroughly studied in relation to energy sensing, mitochondrial function, and antioxidant defense. Similar to PGC-1α, FOXO3a is activated through phosphorylation by AMPK [321–323] and deacetylation by SIRT1 [324, 325] and SIRT3 [326–329], and its transcriptional activity is at least partly dependent on AMPK [322] and SIRT1 [325]. In a variety of organisms, tissues, and cell types, FOXO3a increases mitochondrial biogenesis and expression of TFAM [329], but is more known for increasing expression of antioxidant and repair proteins, including SOD2 [287, 330, 331], catalase [287, 330, 332, 333], glutathione S-transferase (GST) [322], thioredoxins [287, 323], Prx3 [287, 334], Prx5 [287], and metallothioneins I and II [322], as well as UCP2 [287, 322] and the DNA repair enzyme growth arrest and DNA damage-inducible 45 (GADD45) [322, 324, 335, 336]. FOXO3a is also activated by oxidative stress [324, 331, 333], possibly in a SIRT1-dependent manner [324], and likely mediated through c-Jun N-terminal protein kinase (JNK), which allows FOXOs to translocate to the nucleus by promoting dissociation of 14-3-3 [337, 338]. Furthermore, FOXO3a and SIRT3 interact in mitochondria to induce mitochondrial gene expression in an AMPK-dependent manner [339]. FOXO3a also induces expression of LKB1 [340] and NAMPT [341], indicating a feed-forward cycle of activation with AMPK and sirtuins. Like PGC-1α, FOXO3a transcriptional activity is inhibited by insulin through PKB [331].
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My first try at this recipe –lower half was gummy. Crust tasted amazing to I’m eating the ends as toast. I’m too frugal to throw away 3 cups of almond flour, so I cubed up the rest of the loaf, put it in to bake at 350 for 30 minutes or so. Cubes are great on salad -taste like toasted almond/sesame. Now I’m making savory bread pudding with about 2 cups of the cubes (6 eggs, 3/4c almond milk, 1/4c cream, cooked bacon bits, shallots, basil and chives). Baking in muffin tins. Will be taking them for lunches.
In relation to overall caloric intake, carbohydrates comprise around 55% of the typical American diet, ranging from 200 to 350 g/day. The vast potential of refined carbohydrates to cause harmful effects were relatively neglected until recently. A greater intake of sugar-laden food is associated with a 44% increased prevalence of metabolic syndrome and obesity and a 26% increase in the risk of developing diabetes mellitus. In a 2012 study of all cardiometabolic deaths (heart disease, stroke, and type 2 diabetes) in the United States, an estimated 45.4% were associated with suboptimal intakes of 10 dietary factors. The largest estimated mortality was associated with high sodium intake (9.5%), followed by low intake of nuts and seeds (8.5%), high intake of processed meats (8.2%), low intake of omega-3 fats (7.8%), low intake of vegetables 7.6%), low intake of fruits (7.5%), and high intake of artificially sweetened beverages (7.4%). The lowest estimated mortality was associated with low polyunsaturated fats (2.3%) and unprocessed red meats (0.4%). In addition to this direct harm, excess consumption of low-quality carbohydrates may displace and leave no room in the diet for healthier foods like nuts, unprocessed grains,  fruits, and vegetables.

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.
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. 

Hi Kristi, I’m glad you liked the taste! Sorry it didn’t rise for you. It’s hard to say what happened without being in the kitchen with you. Were the peaks in the egg whites not firm enough, or did they fall too much when folding with the rest of the batter? That is the main culprit I can think of, as the egg whites are a big part of what creates the volume in this bread.

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!

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