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.

Insulin is the medication that will bring blood glucose down the fastest. Someone who uses mealtime insulin can take correction doses to lower blood glucose. This requires a thorough understanding of when to inject, how often to give correction doses, and how much insulin to use. You will need to work with your doctor or diabetes educator to learn how to do this.


Metabolic syndrome between pregnancies increases the risk of recurrent preeclampsia, according to a retrospective cohort study of 197 women who had preeclampsia during their first pregnancy. Of the 197 women, 40 (20%) had metabolic syndrome between pregnancies. Of these 40 women, 18 (45%) had preeclampsia during their second pregnancy, compared with 27 (17%) of the 157 women without metabolic syndrome between pregnancies. The risk of recurrent preeclampsia increased with the number of components of the metabolic syndrome present. [68, 69]

Proof the yeast. This involves mixing dry active yeast with water that’s just warm to touch (between 105-110°F to be precise) and maple syrup or honey for 7 minutes until foamy. And before you scream sugar (!!) remember that the yeast will feed on such sugar to emit carbon dioxide, so it doesn’t affect the carb count at all. And yes, this is a scientific fact.
Interestingly, one study showed that weightlifters on a ketogenic diet lost lean body mass, but this did not lead to a decrease in performance [16]. This suggests that the measured reduction of lean body mass was not due to a loss in actual muscle tissue, but probably due to a loss of water and glycogen content in the muscles. Muscles can be made to look bigger or achieve ‘the pump’ by eating lots of carbs which fills them with water and glycogen.
So how does this work? A quick run-through: The first tip was to eat low carb. This is because a low-carb diet lowers your levels of the fat-storing hormone insulin, allowing your fat deposits to shrink and release their stored energy. This tends to cause you to want to consume less calories than you expend – without hunger – and lose weight. Several of the tips mentioned above are about fine-tuning your diet to better this effect.
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The involvement of the endocannabinoid system in the development of metabolic syndrome is indisputable.[33][34][35] Endocannabinoid overproduction may induce reward system dysfunction[34] and cause executive dysfunctions (e.g., impaired delay discounting), in turn perpetuating unhealthy behaviors.[medical citation needed] The brain is crucial in development of metabolic syndrome, modulating peripheral carbohydrate and lipid metabolism.[33][34]

Theresa, Thanks so much for your comment! We aren’t sure what you mean though; our recipe above calls for 2 cups (224g) of almond flour, which is the same measurement you mentioned from the brand you use (112g per 1 cup X 2 cups = 224g). It may be helpful to reach out to a particular almond flour manufacturer if you have a product-specific question. We hope this helps and happy keto baking!
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.
Rick, Yes, I would try baking it longer if it’s coming out gummy. If it’s starting to brown too much outside, but the inside doesn’t seem to be fully cooked, you could cover it with foil to prevent over-browning. Another trick I sometimes use is to leave the bread in the oven to cool once it’s done baking (sometimes covering the loaf with foil to prevent over-browning). I hope these tips help!
Some research suggests that ketogenic diets might help lower your risk of heart disease. Other studies show specific very-low-carb diets help people with metabolic syndrome, insulin resistance, and type 2 diabetes. Researchers are also studying the effects of these diets on acne, cancer, polycystic ovary syndrome (PCOS), and nervous system diseases like Alzheimer's, Parkinson's, and Lou Gehrig's disease.
For those with gummy results, don’t throw away the bread. I found toasting it in oven on 425 works better than toaster and makes the bread edible if your loaf did come out gummy. Also, by accident, I left a piece in oven and preheated oven later for something else I was making and found my extremely crispy toasted bread which made a GREAT baguette! Now I’m making a bunch like this to eat with different creamed cheese spreads! The only real success I’ve had making this bread is in sub or roll form, otherwise, I too experienced some dense/gummy results, moreso, using the coconut flour recipe though.
Insulin resistance also may increase your risk for metabolic syndrome. Insulin resistance is a condition in which the body can’t use its insulin properly. Insulin is a hormone that helps move blood sugar into cells where it’s used for energy. Insulin resistance can lead to high blood sugar levels, and it’s closely linked to overweight and obesity. Genetics (ethnicity and family history) and older age are other factors that may play a role in causing metabolic syndrome.

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.

AGAIN I tried the protein bread, this time I even bought Jay Robb whey protein even though I have a huge container of whey protein, I thought I needed to try to do exactly what you were doing ;). And AGAIN my bread flopped. I whipped the egg whites very STIFF but as soon as I add the protein it breaks them down and it turns to a thick liquid. I bake it anyway and it comes out probably half the size of yours and there are spots through out that look dense like it’s not done. I love the bread and I need a bread substitute to feel satisfied. I’ll keep trying. sighhhhh.
When you eat out at a nice place, what comes first? Oh, right. The so-perky-you-want-to-strangle-her girl named Brittany whose pleasure it is to serve you today. But I was talking about the meal itself. Most non-fast-food meals start out with a good salad. What could be healthier? Salads are generally low in both calories and carbohydrates. That means they are good for controlling blood sugar and controlling waistline expansion. An added bonus: if you get filled up with salad, you’ll be less hungry when it comes to the rest of the meal—so you’ll eat less of the stuff that’s “bad” for your blood sugar log. Eating less of that other stuff will help you with Tip Number 4.
Metabolic syndrome is similarly prevalent in men (24%) and women (22%), after adjusting for age. [28] However, several considerations are unique to women with metabolic syndrome, including pregnancy, use of oral contraceptives, and polycystic ovarian syndrome. [43] Metabolic syndrome and polycystic ovarian syndrome share the common feature of insulin resistance; they therefore share treatment implications as well. [44] Cardiometabolic risk is thought to be elevated in both groups. [45]
My point here is that the warnings about the ketogenic principles are well taken and well documented. My concern is implications that this is a fad. I don’t use the word diet with my patients and I’m concerned that the principles behind the label and the real results that these readers have commented on might get minimized. I have found it best to encourage patients to read authors like: Stephen Phinney, Jeff Volek, Patricia Daly, and Charles Gant and the be partners with their doctors and check blood work as they move along. I am not for or against the article. If ketogenic principles offer people enduring, satisfying, and cohesive change then why not read about its potential and flexilbity?
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I have made this bread and as everybody knows it is wonderful. I have one problem though, my son loved it but the next day he told me he was gasy and a bit painful. I know that fiber causes some gas but I was wondering if you know from your experience with so many people, if this will go away after a while or does it mean that he shouldn’t eat any psyllium husk anymore…
I read through aaaaallllll the comments for research before I made this bread, one thing I noticed when making your protein buns was – when I used 2 teaspoons of baking powder they deflated when exiting the oven. When I reduced the BP to 1.5 teaspoons, they turned out fine. I made two batches with 2 tsp of BP – they turned out like raisins, and 2 batches with 1.5 tsp of BP and they turned out fine. No one posting mentioned adjusting the baking powder – perhaps that would help in this recipe since deflating is a problem, maybe there is too much chemical loft for the non-gluten structure to handle?
The coordinated effects of AMPK, SIRT1, and SIRT3 are primarily mediated through PGC-1α, which is activated through phosphorylation by AMPK [242, 265] and deacetylation by SIRT1 [77, 242, 266–269]. SIRT3 also increases PGC-1α activity [270], possibly through cAMP response element binding protein (CREB) [271, 272], but the exact mechanism has not been elucidated. In addition to phosphorylating PGC-1α, activated AMPK also increases PGC-1α expression [260, 273–276]. Activation of β2-adrenergic receptors [277–280] and the adiponectin AdipoR1 receptor [281] also increase PGC-1α expression, independently of AMPK activation [278, 281]. PGC-1α activity is increased by oxidative stress [76, 77, 282–284], possibly through activation of AMPK [259, 260] or p38 mitogen-activated protein kinase (MAPK) [283, 284], or inhibition of glycogen synthase kinase 3β, which inhibits PGC-1α through phosphorylation [77, 283]. In contrast, insulin decreases PGC-1α activity through phosphorylation by PKB [285]. Once activated, PGC-1α interacts with the PPAR family of nuclear receptors [286] and the FOXO family of transcription factors [287] to influence expression of a variety of bioenergetic and antioxidant proteins. PGC-1α most notably increases transcription of proteins involved in mitochondrial biogenesis and respiration [76, 242, 265, 267, 269, 274, 279, 282, 285, 288–293] but also increases transcription of antioxidant proteins including SOD1 [76], SOD2 [76, 282, 289, 292–294], catalase [282], GPx [76, 294], thioredoxins [282, 283, 292], TRXR [282, 292], Prx3 [282, 292], and Prx5 [282, 292], as well as the mitochondrial uncoupling proteins UCP2 [76, 265, 282, 288, 294], UCP3 [76, 265, 294], and ANT [76, 295].

289. Kukidome D., Nishikawa T., Sonoda K., et al. Activation of AMP-activated protein kinase reduces hyperglycemia-induced mitochondrial reactive oxygen species production and promotes mitochondrial biogenesis in human umbilical vein endothelial cells. Diabetes. 2006;55(1):120–127. doi: 10.2337/diabetes.55.1.120. [PubMed] [CrossRef] [Google Scholar]
Look no further for keto breakfast recipes: This may be the only list you’ll ever need. There’s something for everyone here, including paleo, egg-free, dairy-free, vegetarian, vegan, and Whole30 options. (Only enjoy coffee or tea in the morning? We got you covered there, too.) Best of all? These recipes are all under 10 net carbs per serving — and most are much lower than that.
Rookie experiment, I tried to add 1/4 C of Almond Flour to the Coconut based recipe 1st time all whites and 2 T less, ground psyllium – rise was high, then sunk down quite a bit & was still gummy. 2nd attempt 1 C egg whites and 4 whole eggs, looked a bit better, but the loaf didn’t rise a lot. Not too gummy though. 2nd one tasted better according to husband. Help! London.
Physical inactivity is a predictor of CVD events and related mortality. Many components of metabolic syndrome are associated with a sedentary lifestyle, including increased adipose tissue (predominantly central); reduced HDL cholesterol; and a trend toward increased triglycerides, blood pressure, and glucose in the genetically susceptible. Compared with individuals who watched television or videos or used their computers for less than one hour daily, those who carried out these behaviors for greater than four hours daily have a twofold increased risk of metabolic syndrome.[27]
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Excess abdominal fat leads to excess free fatty acids in the portal vein, increasing fat accumulation in the liver. Fat also accumulates in muscle cells. Insulin resistance develops, with hyperinsulinemia. Glucose metabolism is impaired, and dyslipidemias and hypertension develop. Serum uric acid levels are typically elevated (increasing risk of gout), and a prothrombotic state (with increased levels of fibrinogen and plasminogen activator inhibitor I) and an inflammatory state develop.
The effects of a ketogenic diet on cholesterol and triglycerides is complex. It is dependant on the exact composition of the diet, the genetic and physical characteristics of the individuals studied and other hormonal and environmental factors. Therefore, blood lipid changes whilst on the ketogenic diet can vary between individuals. This means that it is advisable to track your personal levels by having a blood test before starting the ketogenic diet and to follow this with regular testing to monitor any changes.  
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I also had the problem of gumminess. I watched your video and did as you did…I didn’t make any replacements or anything. I didn’t use Jay Robb psyllium. Mine came from a bulk bin somewhere (and I ground it into powder myself), did that make a difference? the loaf was purple but i don’t care about color, i just want it to taste good and not vinegar-y and not gummy!! thanks so much for any suggestions!
The World Health Organization (WHO) was the first to publish an internationally accepted definition for metabolic syndrome in 1998, but the criteria that have received the most widespread acceptance and use in the United States are those established in 2002 as guidelines in the third report of the National Cholesterol Education Program expert panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III).
Thanks for this article. I just started a Keto diet so found it appropriate to my current lifestyle. Though I don’t believe your bottom line is strong enough since you simply stating that the diet is “hard to follow” and food is “notoriously unhealthy” without evidence going deeper into why those “notoriously unhealthy” foods are worse than keeping carbohydrate-heavy food that are addictive and give the body a quick sugar high for energy. I believe “hard to follow” is your opinion only, since acceptable Keto foods are found at all restaurants easily and also all grocery stores. All the foods you mention: “rich in very colorful fruits and vegetables, lean meats, fish, whole grains, nuts, seeds, olive oil, and lots of water” are all Keto-friendly. Many people have been on a Keto-diet for years. A healthy lifestyle is a healthy mindset change and making right choices – it’s not going to be easy.
The last point I’ll make on the starving patient is that, as you can see in the figure below, the glucose level normalizes at about 65-70 mg/dL (about 3.7 mM) within days of fasting, despite no sources of exogenous glucose.  Why?  Because with so much fat being converted into B-OHB and acetoacetic acid by the liver, a significant amount of glycerol (the 3-carbon backbone of triglycerides) is liberated and converted by the liver into glycogen.  As an aside, this is why someone in nutritional ketosis – even if eating zero carbohydrates – still has about 50-70% of a normal glycogen level, as demonstrated by muscle biopsies in such subjects.
If someone has already had a heart attack, their LDL ("bad") cholesterol should be reduced below 70mg/dl. A person who has diabetes has a heart attack risk equivalent to that of someone who has already one and so should be treated in the same way. If you have metabolic syndrome, a detailed discussion about lipid therapy is needed between you and your doctor, as each individual is unique.
Moreover, in the above study of Sumithran et al. (2013), ketosis maintains post-prandial secretion of CCK as previously demonstrated by other researchers (Chearskul et al., 2008). Note that the orexigenic effect of BHB is blocked by transection of the common hepatic branch of the vagus nerve (Langhans et al., 1985). The hepatic branch contains fibers from the proximal small intestine, stomach and pancreas, and is sensitive to CCK (Horn and Friedman, 2004); ghrelin signals to brain are also transmitted via vagus nerve (Habara et al., 2014). Thus, the effects of ketosis on these two appetite-related hormones could be one of the many factors related to the effects of such nutritional regimen on food control.

Optimally, the management approach results in weight loss based on a healthy diet and regular physical activity, which includes a combination of aerobic activity and resistance training, reinforced with behavioral therapy. Metformin, an insulin sensitizer, or a thiazolidinedione (eg, rosiglitazone, pioglitazone) may be useful. Weight loss of ≈ 7% may be sufficient to reverse the syndrome, but if not, each feature of the syndrome should be managed to achieve recommended targets; available drug treatment is very effective.


Physical inactivity is a predictor of CVD events and related mortality. Many components of metabolic syndrome are associated with a sedentary lifestyle, including increased adipose tissue (predominantly central); reduced HDL cholesterol; and a trend toward increased triglycerides, blood pressure, and glucose in the genetically susceptible. Compared with individuals who watched television or videos or used their computers for less than one hour daily, those who carried out these behaviors for greater than four hours daily have a twofold increased risk of metabolic syndrome.[27]
How to test for diabetes at home Diabetes is a condition that can dominate what a person eats and how they live their life. However, measures are now available allowing people can test for diabetes at home. Learn how a test for diabetes can be performed at home and how to interpret test results. Which blood glucose monitor should people choose? Read now

Choose whole grains such as brown rice and whole-wheat bread instead of white rice and white bread. Whole-grain foods are rich in nutrients compared with more processed foods. Whole grains are higher in fiber, so the body absorbs them more slowly. They do not cause a rapid spike in insulin, which can trigger hunger and cravings. The 2015-2020 Dietary Guidelines from the USDA recommend that at least half of your grains be whole-grains.
Type II diabetics can reduce their risk of developing these complications by keeping blood glucose levels within a healthy range (4.5 - 6.5 mM). This can be achieved using insulin injections, but using insulin is not without side effects (i.e hypoglycemia requiring assistance and weight gain)101. Therefore dietary carbohydrate restriction is likely to be a good lifestyle change to help with diabetes management,. Companies such as Virta Health are popularising this approach to diabetes management and pioneering the use of technology to improve compliance. The benefits of carbohydrate restriction include:
Optimally, the management approach results in weight loss based on a healthy diet and regular physical activity, which includes a combination of aerobic activity and resistance training, reinforced with behavioral therapy. Metformin, an insulin sensitizer, or a thiazolidinedione (eg, rosiglitazone, pioglitazone) may be useful. Weight loss of ≈ 7% may be sufficient to reverse the syndrome, but if not, each feature of the syndrome should be managed to achieve recommended targets; available drug treatment is very effective.
The beautiful part of good science is its self-correcting nature. The ugly part is this self-correcting nature often moves at a glacial pace—and it’s not linear. We often view history century-by-century and see what amounts to continual progress in medicine. But we live our lives—and consume information—day-by-day, exposed to the peaks and valleys of medical wisdom.
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This poses a real evolutionary dilemma.  We need an enormous amount of energy just to not die, but the single most important organ in our body (also quite energy hungry in its own right) can’t access the most abundant source of energy in our body (i.e., fat) and is, instead, almost solely dependent on the one macronutrient we can’t store beyond a trivial amount (i.e., glucose). Obviously our species wouldn’t be here today if this were the end of the story. But, to understand how we survived requires one more trip down biochemistry memory lane.  In the figure below (also included and described in the video) I gloss over a pretty important detail.
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208. Steinberg G. R., Watt M. J., McGee S. L., et al. Reduced glycogen availability is associated with increased AMPKα2 activity, nuclear AMPKα2 protein abundance, and GLUT4 mRNA expression in contracting human skeletal muscle. Applied Physiology, Nutrition, and Metabolism. 2006;31(3):302–312. doi: 10.1139/h06-003. [PubMed] [CrossRef] [Google Scholar]
Insulin is a hormone that allows glucose to move into tissue cells, where is it is used for energy production. Insulin then prompts the liver to either store the remaining excess blood glucose as glycogen (for short-term energy storage) and/or to use it to produce fatty acids (which then become triglycerides). In people with insulin resistance, additional insulin must be released by the pancreas to overcome the tissue cells' resistance and allow glucose to enter the cells. This resistance and response to resistance can lead to increased insulin and glucose concentrations in the blood. Over time, increased glucose levels can harm blood vessels and organs such as the kidneys. Increased insulin levels can increase sodium retention by the kidneys, resulting in increases in blood pressure (which can lead to hypertension).
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]
Heat a large non-stick skillet over medium heat.  Mix all of the ingredients for the pancakes into a small bowl.  Spray the skillet with cooking spray and spoon the batter into 4 round pancakes in the skillet.  Let the pancakes cook until bubbles start to form in the batter around the side.  Flip and continue to cook on the other side until the center on the pancake springs back when lightly touched.
Several other rodent studies provide additional evidence of ketogenic diets upregulating antioxidant defense, but without enough data to convincingly attribute the results to mitohormesis. Content of SOD2 has increased in the livers of mice fed a ketogenic diet (% energy: 89 fat, <1 carbohydrate, and 10 protein), which occurred in conjunction with increased median lifespan and decreases in tumors and age-associated losses of physical and cognitive performance [36]. In addition, activity of GCL and the protein content of its two subunits increased in the hippocampal homogenate of rats fed a ketogenic diet (Bio-Serv F3666) for 3 weeks [97]. This was in conjunction with higher levels of reduced glutathione (GSH) and lower ROS production in hippocampal mitochondria. The ketogenic diet also increased resistance to mtDNA damage in hippocampal mitochondria exposed to H2O2 [97]. Consistent with these results, total antioxidant capacity and activities of GPx and catalase were increased in hippocampal homogenate of rats fed a ketogenic diet (% energy: 86 fat, <1 carbohydrate, and 13 protein) for 8 weeks [98]. Furthermore, in cortical homogenate of rats induced with traumatic brain injury, a ketogenic diet increased cytosolic and mitochondrial protein contents of NAD(P)H:quinone oxidoreductase 1 (NQO1) and SOD1, as well as mitochondrial protein content of SOD2, and also prevented mitochondrial oxidative damage (indicated by 4-HNE) [99].
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^ Jump up to: a b c Taboulet P, Deconinck N, Thurel A, Haas L, Manamani J, Porcher R, Schmit C, Fontaine JP, Gautier JF (April 2007). "Correlation between urine ketones (acetoacetate) and capillary blood ketones (3-beta-hydroxybutyrate) in hyperglycaemic patients". Diabetes & Metabolism. 33 (2): 135–9. doi:10.1016/j.diabet.2006.11.006. PMID 17320448.
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]
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For the eggs, beat the 4 eggs in a medium sized bowl until whites and yolks are combined.  Heat a medium skillet (I used the same skillet as the pancakes) over medium-low heat.  Add the butter and then the beaten eggs. Let the eggs cook until the edges begin to set.  push the eggs with a rubber spatula scraping the bottom of the pan.  scrape occasionally to get large folds of soft scrambled eggs.  When the eggs are just set and still a little runny, remove from the heat.  
Maya, this is a beautiful looking bread. I’m going to try it, but before I do, I’d like to know if you have ever tried doubling the recipe. It seems that it would work–based on the fact that my almond flour bread that I have made for years uses 3 1/4 cups flour, and turns out pretty well. (I’m pretty content with my recipe, but admit that yours looks better due to the whiteness and it appears to have more air bubbles, indicating it’s probably lighter.) If I don’t hear from you, I’ll probably go ahead and double it, and use a 9×5 pan–wish me luck.

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]
A little more than 9.2% of pregnant women have gestational diabetes. It is very common that all women are tested during their pregnancy. If you haven’t yet, bring it up to your physician’s attention. The cause is really unknown, but doctors believe that it is because the extra hormones that are released during pregnancy hinder the insulin sensitivity and increase the need for more insulin. It is very important to keep blood sugar levels under control because high blood sugars can lead to complications such as:

Your first dietary step towards more balanced blood sugar: ditching (most of) the packaged foods and focusing on high-quality whole foods such as vegetables, fruits, whole grains, beans, nuts, seeds, and quality meats and fish. Many processed foods are high in sugar, refined grains and carbs, and artificial ingredients and flavorings, while being low in blood-sugar-stabilizing fiber and protein. Of course, it’s also important to be realistic. You’re probably not going to be able to nix packaged foods completely, so just make a point to select those that are made from mostly whole-food ingredients, like a bar that lists just nuts, seeds, and dried fruit on its label.
Recent research indicates prolonged chronic stress can contribute to metabolic syndrome by disrupting the hormonal balance of the hypothalamic-pituitary-adrenal axis (HPA-axis).[23] A dysfunctional HPA-axis causes high cortisol levels to circulate, which results in raising glucose and insulin levels, which in turn cause insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension, with direct effects on the bone, causing "low turnover" osteoporosis.[24] HPA-axis dysfunction may explain the reported risk indication of abdominal obesity to cardiovascular disease (CVD), type 2 diabetes and stroke.[25] Psychosocial stress is also linked to heart disease.[26]
In addition to the downstream bioenergetic and antioxidant signaling induced by sirtuins, they directly facilitate ketogenesis and β-oxidation. SIRT1 [254] and SIRT3 [255] deacetylate 3-hydroxy-3-methylglutaryl CoA (HMG CoA) synthase, which is the rate-limiting enzyme for ketogenesis [256], resulting in increased levels of β-hydroxybutyrate [255]. In addition, SIRT3 deacetylates and increases activity of long-chain acyl-CoA dehydrogenase (LCAD) [257], which participates in β-oxidation and therefore supports ketogenesis. SIRT3 has a similar influence on medium-chain acyl-CoA dehydrogenase (MCAD) as well [258]. Since sirtuins facilitate ketogenesis, which then facilitates sirtuin activation, nutritional ketosis may promote, to some extent, a feed-forward cycle of sirtuin activity.
A study on hippocampal mitochondrial function in rats more directly supports the induction of mitohormesis by a ketogenic diet. After the first day of the diet (Bio-Serv F3666), H2O2 production by isolated mitochondria was increased [96]. After the third day, mitochondrial levels of oxidized glutathione (GSSG) and hippocampal levels of 4-hydroxy-2-nonenal (4-HNE) were also increased, further indicating an increase in oxidative stress. However, at completion of the first week, upregulation of antioxidant signaling occurred, indicated by increased nuclear content and transcriptional activity of nuclear factor erythroid-derived 2-like 2 (NFE2L2), which persisted through the remainder of the study. By the third week, mitochondrial H2O2 production decreased to below baseline [96]. In the liver, content of reduced acetyl CoA, which is indicative of mitochondrial redox status, decreased after three days of the ketogenic diet, but increased relative to the control diet after three weeks, indicating an initial increase in oxidative stress followed by a decrease [96]. This was in conjunction with changes in NFE2L2 nuclear content and transcriptional activity similar to those observed in the hippocampus. As with the previously described C. elegans experiments, the time course of these observations is a strong indication of mitohormesis, and the similarity in results between the liver and hippocampus suggests that a ketogenic diet can induce mitohormesis in a variety of tissues.
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).
Hi Leo, almond flour bread will always taste of almond flour – there’s no way around it. Since there is no way you can make bread with almond flour using only one egg – it would simply not hold together – it sounds like you’ll have to look for a substitute that is more to your taste. Thank you for taking the time to comment on this recipe, and I hope you find other recipes on my site that are more to your liking 🙂

Ketogenic diets have become popular in recent decades for their demonstrated positive effects on weight loss (Bueno et al., 2013), though the precise mechanism of action is not fully understood (Paoli, 2014). In fact there is contradictory data about KD in mice and rats. In fact, there are contradictory data about KD in mice and rats. For example whilst a huge amount of data confirm that KD in humans is effective in weight reduction, improving lipidemia and glucose tolerance (Bueno et al., 2013), it has been recently demonstrated that a long-term KD (22 weeks) caused dyslipidemia, a pro-inflammatory state, hepatic steatosis, glucose intolerance and a reduction in beta and alpha cell mass, all without weight loss in mice (Ellenbroek et al., 2014). Two considerations should be made: (1) the induction of ketosis and the response to ketosis in humans and mice are quite different and (2) mice and humans have different life spans, and results obtained in mice after several weeks on the diet can correspond to months on the diet in humans (Demetrius, 2005, 2006).
Theoretically, supplying ketones during this period of compromised glucose metabolism could prevent the energy deficit and reduce the likelihood of long-term brain damage. This could be because ketones can act as an alternative, highly energy efficient substrate7. Additionally, the antioxidant, antiinflammatory33 and anti-apoptosis properties of ketones (i.e ketones prevent the opening of the mitochondrial permeability transition pore, which causes cell death66) could protect against neuronal loss and damage. 
Everyone loves a bagel, lox and eggs for breakfast. While lox and eggs are keto-approved, bagels can cost you 48 grams of carbs or more depending on the seasonings or flavor. These keto bagels by Keto Connecthave only 3 grams of net carbs a serving and don’t skimp on flavor, thanks to everything bagel seasoning. This blogger uses cream cheese, almond flour and cheese to provide good protein and fat, with 10 grams and 15 grams respectively.

In the previously described C. elegans experiments demonstrating mitohormesis, knockout of the NFE2L2 homologue SKN-1 attenuated the increases in antioxidant enzyme activity and lifespan [73], indicating that mitohormesis may, at least in part, be dependent on NFE2L2 signaling. Similarly, a ketogenic diet (Bio-Serv F3666) increased nuclear content of NFE2L2 and expression of its target NQO1 in the hippocampi of rats, all of which occurred after an initial increase in mtROS [96]. This increase in NFE2L2 content appears to have mediated the subsequent decrease in mtROS to a level below baseline [96], thereby further indicating a likely role of NFE2L2 in the induction of mitohormesis during a ketogenic diet.
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.  
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[…] One of the things I’ve grown to love over the years is fried eggs with runny yolks. They’ve become a regular breakfast for me on the weekends. However, when I do regular low carb high fat meals, I like to have toast to dip into the egg yolks. Psyllium low carb bread seems to be all the rage right now, so I came up with this coconut flour psyllium husk bread that is perfect with my morning eggs. I’m not really sure who started the low carb psyllium bread trend, but one of the first breads I’ve found was Maria Emmerich’s Amazing Bread. […]
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Hi Cindy, nut flour breads do not rise as much as wheat breads. Also, I used a small bread tin in the post – if you use a regular size bread pan your bread will end up flatter. What you can try next time is to try to keep the dough nice and fluffy, trying to keep as much air inside as possible (for example, not press it into the pan as much as you can). You could also try to whisk the egg whites until they’re stiff and fold them under last, which will make your dough lighter (=more air). I hope this helps

So, there you have it—ten simple things you can do to lower your blood sugar. Notice anything special about these tips? Right! There’s nothing special about them at all. They aren’t bizarre. They aren’t difficult. You don’t have to change your entire life. These are things you can integrate into the daily life you already live now. And once they become habits—healthy habits—you’ll have taken blood sugar management into your own hands.
Although mitochondrial ROS (mtROS) are generally considered harmful, which is certainly the case at high concentrations, modest levels stimulate necessary biological processes such as proliferation, differentiation, and immunity [3]. Adaptations that enhance resistance to oxidative stress are also induced by mtROS [3], possibly decreasing net ROS production during basal metabolism. This adaptive response is called mitohormesis [4–6] and is a promising mechanism through which lifestyle interventions that enhance mitochondrial function may, in turn, enhance resistance to chronic and degenerative diseases.
The approximate prevalence of the metabolic syndrome in patients with coronary artery disease (CAD) is 50%, with a prevalence of 37% in patients with premature coronary artery disease (age 45), particularly in women. With appropriate cardiac rehabilitation and changes in lifestyle (e.g., nutrition, physical activity, weight reduction, and, in some cases, drugs), the prevalence of the syndrome can be reduced.[27]

Hi Howard, You’re right that this bread doesn’t rise much – the volume comes mostly from whipping the egg whites. If the whites fell too much, the bread might not be tall enough. But even if they didn’t, it might still be shorter than some other tall bread loaves. Feel free to multiply the recipe by 1.5 if you prefer a taller loaf. I’m glad you liked the flavor and texture!
So, there you have it—ten simple things you can do to lower your blood sugar. Notice anything special about these tips? Right! There’s nothing special about them at all. They aren’t bizarre. They aren’t difficult. You don’t have to change your entire life. These are things you can integrate into the daily life you already live now. And once they become habits—healthy habits—you’ll have taken blood sugar management into your own hands.
This book is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to the Creative Commons license, and any changes made are indicated.
Ketone esters (BHB-BD) lowers blood lactic acid 30. Lactic acid build up occurs during exercise as a result of burning carbohydrate at a high rate without enough oxygen. Blood lactic acid levels during exercise were 30% lower after ketone ester drinks compared to carbohydrate drinks. This is because high blood levels of BHB from the ketone ester drink slow down carbohydrate use and increase oxygen efficiency, which could decrease blood lactic acid levels. 
These Keto Breakfast Fat Bombs are a true lifesaver for frantic (Monday) mornings.  Personally, when I wake up in the morning after my alarm clock gives out a warning I don’t think I’ll ever make it on time.  By the time I grab my books and give myself a look, I’m at the corner just in time to see the bus fly by…wait no, scratch that…that’s Zach Morris, not me. Either way, I’m sure we’ve all had those mornings where we were saved by the bell, so let these little bacon covered bites of heavenly deliciousness make your mornings more calm*, I guess you could say you’re saved by the (fat) bomb.
People with type 1 diabetes do not produce enough insulin, so their bodies are unable to regulate ketones, which can lead to a dangerous environment. Always consult with your doctor if you have diabetes before changing your diet, and look out for warning signs of ketoacidosis including: excessive thirst, increased urination, nausea, vomiting, abdominal pain, shortness of breath, weakness, fatigue and confusion.
Menopause is the time in a woman's life when menstrual periods permanently stop, also called the "change of life." Menopause symptoms include hot flashes, night sweats, irregular vaginal bleeding, vaginal dryness, painful intercourse, urinary incontinence, weight gain, and emotional symptoms such as mood swings. Treatment of menopausal symptoms varies, and should be discussed with your physician.
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As with other sources of oxidative stress, mtROS can damage enzymes and cell membranes and subsequently facilitate the pathogenesis of chronic disease [41]. Oxidative damage to mitochondrial DNA (mtDNA) is of particular concern because of its proximity to the electron transport chain (mtETC). Furthermore, compared to nuclear DNA, mtDNA is more prone to oxidative damage and is not repaired as effectively [42–45], although this has been debated based on more recent evidence [46–50]. Unrepaired mtDNA damage leads to mitochondrial dysfunction, which is implicated in the pathogenesis of a variety of chronic diseases [51] and associated with shorter lifespan [52]. Therefore, while moderate levels of mtROS have important roles in signaling and health, protection against excessive levels is also important.

The SS providing information to the brain mainly send information to the nucleus of the solitary tract (NTS). These signals are generated in the GIT and abdominal viscera, as well as in the oral cavity and provide information about mechanical and chemical properties of food. The information is transmitted via vagal and spinal nerve to the NTS. The ASs arrive to the median eminence through ARC or through the blood-brain barrier (BBB). All these afferents are integrated in a complex and not fully understood network.


The ketogenic diet is high-fat and low-carb, and if you pay attention to food and nutrition trends, then you already know that creative recipes for this weight-loss plan are all over social media. If you've gone keto or are thinking of trying it, check out these tasty morning meal ideas to help you stay full, score energy, and leave you feeling satisfied.

141. Khailova L. S., Prikhodko E. A., Dedukhova V. I., Mokhova E. N., Popov V. N., Skulachev V. P. Participation of ATP/ADP antiporter in oleate- and oleate hydroperoxide-induced uncoupling suppressed by GDP and carboxyatractylate. Biochimica et Biophysica Acta. 2006;1757(9-10):1324–1329. doi: 10.1016/j.bbabio.2006.04.024. [PubMed] [CrossRef] [Google Scholar]
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.

I have been on a low carb keto diet for more than a year. As T2DM my A1C dropped from 9% to 5.4% & I discontinued meds. All my lipids improved even with ample healthy saturated fat. More than a year now so I wonder why this would be a short term improvement when its obvious that I will not go back to a high A1C and taking 3 diabetes medications including sulphonylureas. It is clear from this article that you lack the necessary experience that would be gained from wholeheartedly trying the diet or monitoring patients doing it properly like me. I would be probably be facing my first amputation if I believed the negativity in your article. So for people with diabetes who may be dissuaded by your article. Ignore it and take back your health by restricting carbs (<25 g a day) or as low as you reasonably can below 130g while being satisfied that you are getting adequate nutrition.
Like you say on your show, I am a foodie and hate it when recipes on websites turn out tasting bleh. This bread has a great texture. After making it a few times plain now, I added some sesame seeds to the batter and that turned out great too. I make an open faced breakfast sandwich with a slice of this almond flour bread, plenty of cream cheese and scrambled eggs. Paired with coffee. So tasty, that I can’t tell it isn’t a regular scrumptious egg sandwich.

[Guideline] Skyler JS, Bergenstal R, Bonow RO, et al. Intensive glycemic control and the prevention of cardiovascular events: implications of the ACCORD, ADVANCE, and VA Diabetes Trials: a position statement of the American Diabetes Association and a Scientific Statement of the American College of Cardiology Foundation and the American Heart Association. J Am Coll Cardiol. 2009 Jan 20. 53(3):298-304. [Medline].
So rather than giving one-size-fits-all dietary advice or weaponizing the word “balanced” it might be better if the medical community suggested that there are Individual differences that need to be considered. This might also help those lay folk who have had success with one dietary lifestyle or another also realize that what’s valid for them may not be good advice for others.
Just made this and as a normal bread lover, I am very impressed! But do have a question. Can you over cook this? Mine seems a bit light inside, like a teenie bit mooshy, and can’t see it holding up in a sandwich. The temp was at 200 inside but I had already had it in for like 50 minutes longer than the posted time and I could still hear a little squish but didn’t want to over cook.

These fluffy, colorful pancakes from The Big Man’s World satisfy any cravings for a decadent, comfort food breakfast without totally sabotaging ketosis. Made with almond flour and coconut flour instead of the conventional stuff, these pillowy cakes are much higher in fats, protein, and fiber than your average stack—and at 2.1 grams of net carbs per serving, much lower in carbs. Did we mention they’re also vegan and take just 10 minutes to whip up?


You are right. It’s not 2g it’s 4g per mug bread. We use 30 grams of almond flour which is 6g carbs and 1g from the egg which is 4g net carbs. I’ve corrected it. My earlier calculation was with ‘Trader Joe’s Almond Flour’. Bob’s Red Mill is what’ I’ve used now. Also almond flour = ground almonds which have 10g net carbs per 100g so we’re anyway looking at 3g net carbs for 30 grams of almond flour plus the .7g from the egg. So 4g is about right.
Many neurological conditions share a common feature of impaired brain energy metabolism. It isn’t always clear if this impairment is the cause or the effect of the disease, but nonetheless, interventions that even partially restore or improve brain energy metabolism could help to prevent, slow or even reverse some conditions of the brain. Because ketones can: 1) get into the brain; 2) undergo metabolism by a distinct pathway that bypasses glucose metabolism, providing ketones by either following a ketogenic diet or by taking exogenous ketones could impact the natural course of some neurological conditions. 
Keto Bread Recipe - Four Ways - quick and simple way to make low carb, individual keto bread rolls, in ramekins and just a few healthy ingredients. You can either bake it in the microwave for 90 seconds or in the oven for 10-15 minutes. The the-easiest, the-best kept bread recipe I've ever tried. There are four different options available - you can make cheese keto bread,  broccoli ketogenic bread, bacon and spinach and feta. And of course you can leave it as it is, if you prefer plain kept bread  rolls.
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