So, now, I’ve got another loaf in the oven. I doubled the salt, ground up the Psyllium Husk in my Blend Tec (instead of the shoddy thing I used the first time) and reduced the baking soda to 3 tsp. I also (accidentally) ended up with 1 egg yolk in there. Hopefully, that won’t cause too much of an issue. I weighed all my ingredients and I’m hopeful that this batch will give me the results I am looking for. I would *love* a grilled cheese sandwich for a quick-fix dinner with my keto plan. 🙂 Thanks for the recipe. I’ll let you know how this batch turns out.


This breakfast casserole by I Breathe I’m Hungry packs all of the delicious flavors of a Monte Cristo sandwich (a ham and cheese sandwich dipped in French toast batter, fried, and served with syrup) without the carbs. The recipe layers cream cheese keto pancakes, Canadian bacon, and cheese, and is served warm with sugar-free syrup. Sounds like ooey-gooey perfection, doesn’t it? One serving provides 32 grams of protein and just 4.5 grams of net carbs.
Metabolic syndrome promotes coronary heart disease through several mechanisms. It increases the thrombogenicity of circulating blood, in part by raising plasminogen activator type 1 and adipokine levels, and it causes endothelial dysfunction. [14] Metabolic syndrome may also increase cardiovascular risks by increasing arterial stiffness. [15] Additional mechanisms include oxidative stress, [16] which has been associated with numerous components of metabolic syndrome. [17]
Ketogenic and low-carbohydrate diets greatly increase reliance on fat oxidation [78–89], which would logically be expected to increase mitochondrial respiration and mtROS production and, in turn, induce mitohormesis. Furthermore, mtROS produced through RET appears to have particular relevance to hormetic adaptation, including increased lifespan [90]. Nutritional ketosis is likely to increase RET by altering the FADH2 to NADH ratio. As the primary source of acetyl CoA shifts from glycolysis to β-oxidation and ketolysis, this ratio increases, more than doubling for β-oxidation of longer-chain fatty acids. Electrons from FADH2 reduce the CoQ pool through complex II and ETF-QO, thereby increasing RET [91, 92]. This induction of RET by alteration of substrate availability can also be influenced by configuration of mtETC complexes into supercomplexes [90]. The greater potential for mtROS production through RET is consistent with evidence of mitochondria producing more H2O2 during oxidation of palmitoyl carnitine versus pyruvate [93, 94]. Furthermore, succinate is generated during ketolysis by succinyl-CoA:3-oxoacid CoA-transferase (SCOT), which also promotes RET by reducing the CoQ pool through complex II. Demonstrating the likely role of RET in mitohormesis, particularly within the context of nutritional ketosis, extension of lifespan in C. elegans through BHB treatment is dependent on both complex I function and expression of bioenergetic and antioxidant proteins [95].

A ketogenic diet also has been shown to improve blood sugar control for patients with type 2 diabetes, at least in the short term. There is even more controversy when we consider the effect on cholesterol levels. A few studies show some patients have increase in cholesterol levels in the beginning, only to see cholesterol fall a few months later. However, there is no long-term research analyzing its effects over time on diabetes and high cholesterol.

Hello, I’m sure you must roll your eyes at getting yet another post about glitches when making this bread. Unlike the first loaf I made I had four loaves turn out gummy. it still makes reasonable toast but I’d like to avoid this the next time I make the bread. I used your recommended almond flour, and I really ground the psyllium. However in narrowing things down there are two factors that may have contributed to the problem: 1) I mixed up two loaves at a time and I wonder if the dough was too heavy for my mixer and did not combine sufficiently. 2) I may have let a very small amount of yolk fall into the whites. Would either of these caused the gummy texture? Thanks for this amazing website. We purchased all your books and find them a wealth of information. Liz

When preparing keto bread recipes, look out for low-carb ingredients that could contribute to brain fog and inflammation. Skip recipes that require conventional dairy or yeast, and avoid eating common keto bread ingredients like psyllium husk, xanthan gum, and nuts or nut butters too often — these can contain mold or irritate your gut. Grass-fed butter, ghee, and coconut flour are the few exceptions that will still produce a stellar loaf.
First I tried using coconut flour only. The batter was very thick and pasty and the resulting bread was very firm and dry, like a really dry biscuit. It did, however, keep its shape well and toasted up evenly golden-brown in a skillet with oil. I thought about trying again with more liquid, but that wouldn’t solve its fatal flaw: the strong, overwhelming coconut flavor. Even chicken and sun-dried tomato pesto could barely cover it up.

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Prediabetes: When blood glucose (also called blood sugar) levels are higher than normal and not yet high enough to be diagnosed with diabetes. That’s an A1C of 5.7 percent to 6.4 percent (a way to estimate your 3-month average blood sugar reading), a fasting blood glucose level of 100 to 125 mg/dl, or an OGTT (oral glucose tolerance test) two hour blood glucose of 140 to 199 mg/dl.

My first attempt of this bread leaves something to be desired. It looked great when it came out of the oven but as it cooled it caved a bit; and when I took it out of the pan when it had cooled, I realized that the bottom inch looked undercooked, very wet. After reading ALL of Maria’s remarks to other folks who have had problems (I am not alone), I will try again adding less water next time. For now I will use the loaf I just made and turn it into croutons or bagel chips as suggested by Ellen (thanks for sharing some positives from a negative). Maria, I applaud you for your endless patience with all of us all who keep asking the same questions over and over again.


As will be discussed in the following sections, many of the signaling proteins involved in regulating antioxidant defense also regulate oxidative phosphorylation and fat oxidation. There is abundant evidence (Table 1) showing ketogenic and low-carbohydrate diets to increase expression, content, or activity of many targets of these signaling proteins, further indicating increased oxidative capacity. It is particularly striking that ketogenic or low-carbohydrate diets upregulate expression of proteins associated with each of the five mtETC complexes.
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First of all, thanks for the recipe. I tried it yesterday with coconut flour and egg whites, and I failed miserably. It rose 5 or 6 times in volume and then collapsed like the world economy. Also, it was very moist on the inside. I’ll try the almond flour version with half the baking powder and full eggs this time, but I’m having trouble wrapping my head around measurements. If 1 and 1/2 cup of almond flour is 5oz, how can 1/2 cup of coconut flour be 2.5oz (equalling 7.5oz for 1 and 1/2 cup)? If anything, almond flour is more dense, not less.
Lose a pound. Or four. You don’t need to be supermodel skinny to improve your blood sugar. If you lose 7 percent of your weight, you’ll improve your insulin resistance. That will lower your blood sugar across the board, and dramatically reduce after-meal spikes. How much weight is that, really? Well, it depends on how much you weigh, of course. If you tip the scales at 200 pounds, 7 percent is 14 pounds. You could easily shed that in six months, simply by eating fewer bites per meal. I know we were taught as children to clean our plates, but it’s far better to throw some food away than to eat more than we need to. It’s only wasteful to eat what our bodies don’t need.

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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.
Ketones may also be important, or even necessary, for the bioenergetic signaling associated with mitohormesis. As will be discussed later, peroxisome proliferator-activated receptor α (PPARα) is a nuclear receptor that is responsible for many of the bioenergetic adaptations associated with nutritional ketosis and mitohormesis [120]. In mice, a ketogenic diet (% energy: 90 fat, 0 carbohydrate, and 10 protein) increased blood BHB concentration to 1-2 mM and upregulated expression of numerous PPARα targets in the liver [37]. However, in mice fed a nonketogenic low-carbohydrate diet (% energy: 75 fat, 15 carbohydrate, and 10 protein), which did not raise blood concentration of BHB, the increased expression of PPARα targets did not occur [37], implying that induction of PPARα signaling by a ketogenic diet is dependent on ketones. This response may be, at least in part, a result of the epigenetic effects of BHB. In addition to HDAC inhibition, BHB also influences gene expression through β-hydroxybutyrylation of histone lysine residues [121]. In the livers of mice subjected to prolonged fasting, this β-hydroxybutyrylation has been associated with upregulation of PPAR signaling, oxidative phosphorylation, fatty acid metabolism, the proteasome, and amino acid metabolism related to redox balance [121]. Upregulation of these pathways is largely influenced by β-hydroxybutyrylation of the histone residue H3K9 [121], which is also involved in the upregulation of antioxidant defense through BHB-induced HDAC inhibition [103]. This potential for BHB to influence expression of both mitochondrial and antioxidant genes through a common histone residue is further indication of the overlap between bioenergetics and antioxidant defense and suggests that if mitohormesis is indeed induced during nutritional ketosis, induction may be dependent on ketones and may therefore not occur during a low-carbohydrate diet that is not ketogenic.

As you could probably figure out I love my cast iron skillets, but my second favorite piece of cookware is definitely the Instant Pot, followed by my smoker/grill combo but I’m getting off track.  Anyway, if you’ve never made hard boiled eggs in the Instant Pot, no offense… but you’re doing it wrong.  This post from SkinnyTaste covers all the details to make perfect hard-boiled (or soft-boiled) eggs every time that are the absolute easiest to peel.  

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!
If there’s one thing keto dieters miss when they're trying to enjoy brunch, it’s those damn roasted potatoes. Yet you can dig into these "potatoes"—a.k.a. turnips—by Cast Iron Keto. They have so much flavor from paprika, garlic powder, salt, and pepper and only 4 grams of net carbs—you won’t even miss the real thing. Pair with eggs, fish, or meat for extra protein, and you’re set. (Though there is some bacon already!)
Both sleep deprivation and stress can cause elevated levels of the stress hormone cortisol, which raises blood sugar. Aim for seven to nine hours of sleep per night, and adopt stress-busting habits such as exercise, meditation, or yoga. One study found that nursing students who did meditation and yoga experienced lower blood sugar spikes after meals. If you're ready to start your meditation practice, check out mindbodygreen's 14-Day Guide to meditation with mbg Collective member Light Watkins.
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! 🙂 🙂
We’ve longed been told that calorie restriction, increasing exercise and reducing dietary fat intake are the keys to weight loss. But, if you’ve ever attempted to control your weight by subsisting on fewer calories — especially from mostly bland “diet foods”— you’re already probably aware that this typically produces minimal results and is extremely hard to stick with long-term or consistently.

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Another product of elevated levels of free FA is polyunsaturated FA (PUFA). The potential ability of PUFA to block seizure activity in the brain is speculated to be associated with KD. Some mechanisms are thought to be a direct inhibition of voltage-gated sodium and calcium channels, modulation of a lipid-sensitive potassium channel, the activity of the sodium pump to limit neuronal excitability, or the induction of expression and activity of proteins in the mitochondria, thereby inducing a neuroprotective effect by partially inhibiting the production of reactive oxygen species (ROS) (Bough and Rho, 2007; Paoli et al., 2014).
It is important to note that these herbs and spices are intended to support blood sugar maintenance and are not meant to replace diabetes/hyperglycemic medications. Research does show benefits to incorporating these herbs and spices, so enjoy incorporating them daily into your favorite recipes for a boost of flavor and blood sugar-lowering benefit.
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Well my Bread wasn’t tall enough for say sandwich stuff, and I am not sure if I did anything wrong, I know I used the wrong sized bread pan so that is one thing. However, I couldn’t believe how great it tasted, it was more like a moist custard shortbread. The texture and color were perfect. I cut some thick slices and buttered both sides cooked them in a pan. I spread some sugar-free preserves on top, wow is that good. I may not have made it as intended but I can’t complain. The flavor is amazing.
Metabolic syndrome is not merely a single disease but a collection of pathological conditions (i.e., abdominal obesity, insulin resistance, dyslipidemia, hyperglycemia, and hypertension) that increase the risk of developing diabetes and cardiovascular diseases. Low adiponectin levels directly correlate with the development of metabolic syndrome after adjusting for age, sex, and BMI [106,107]. In a study of Japanese adults, an increase in the number of metabolic syndrome components was associated with decreasing adiponectin levels [108]. Hypoadiponectinemia also appears to be a predictor for the future development of metabolic syndrome in obese individuals [109,110].
I have been making Maria’s bread in my convection oven for a while and I had to lower the temp considerably to make sure it didn’t burn on the outside (even with a shorter baking time). I have a “portable” convection oven and I had always assumed that convection was the way to go for baking. Then I read some more about it and saw that convection is best for meats, etc. but not for baking, and I tried using the ‘normal” baking setting. My bread was MUCH better baked on normal. I used the temperature in the recipe and the timing and it came out perfect. No monkeying around with settings or duration.
Fanatic? Someone with T2D, a disease usually claimed to be progressive and a never ending stream of problems and medications, was REVERSED. That’s something to shout from the rooftops. The drop in medication use alone, but the big pharma companies would prefer that people’s stories of reversing (well, putting it into remission) T2D get called fanatical instead of insightful.
β-hydroxybutyrate and, in some cases, acetoacetate contribute to protection against oxidative stress by decreasing production of mitochondrial reactive oxygen species (mtROS), by increasing expression or protein content of antioxidant enzymes through histone deacetylase (HDAC) inhibition, and by directly scavenging the hydroxyl radical (•OH). Upregulation of antioxidant enzymes through HDAC inhibition includes manganese superoxide dismutase (SOD2), catalase, and metallothionein II and is likely mediated by the transcription factor forkhead box O 3a (FOXO3a).
The only issue with keto, is really that I’m afraid that it might be hard to up my calories to a maintenance weight now that I’ve gotten a taste preference for the rich assortment of foods with no carbs in them. I’m satisfied with less calories than I will need after my excess fat is burned off… but , maybe I bet my body will send more hunger signs once there isn’t anymore body fat in the cupboard to use instead of what goes down my throat.
Toasting it did no good as it had that “plastic” smell that Mizzsingbabe mentioned. I tried cutting a very thin piece, loading it with butter, garlic powder, salt and grilling in cast iron fry pan, then broiling it but still cannot get past the plastic/smell taste. So I wasted 3 cups of (not cheap) almond flour along with all the other ingredients.
For those, like myself, wanting a low-carb real bread I would recommend a proper low-carb yeast bread recipe with vital wheat gluten (the vast majority of people have zero gluten sensitivity, so the gluten-free fad is at best a waste and at worst a scam). Such breads have approx 1.5-2 grams more net carbs per 40g slice (5-6 grams total net carbs) than this recipe and I think it’s worth it.

In recent times there has been an exponential increase in the rates of obesity and diabetes. Popular opinion has blamed (in turn) overconsumption of fat, overconsumption of carbs and sugar and overconsumption of calories. Whilst the overall calorie balance is a crucial factor that cannot be overlooked, it is also the case that different macronutrients in the diet (especially carbs and fat) have different effects on the body when consumed.  
Although the hunger-reducing effect of KD is well-documented, its main mechanisms of action are still elusive. The global picture is complicated by the contradictory role of ketosis on anorexigenic and orexigenic signals (summarized in Figure ​Figure4).4). Ketones (mainly BHB) can act both orexigenically or anorexigenically. In the orexigenic mechanism, it increases the circulating level of adiponectin, increasing brain GABA and AMPK phosphorylation and decreasing brain ROS production. The anorexigenic mechanism triggers a main normal glucose meal response, increasing circulating post-meal FFA (thus reducing cerebral NPY), maintaining CCK meal response and decreasing circulating ghrelin. It can be postulated that the net balance of the contrasting stimuli results in a general reduction of perceived hunger and food intake. More studies are needed to explore the mechanism of potential beneficial effects of KD on food control.

But comprehensive transcriptional profiling of glucose-sensing neurons is challenging, as glucokinase (Gck) and other key proteins that transduce glucose signals are expressed at low levels. Glucose also exerts a hormonal-like action on neurons; electrophysiological recordings demonstrated, for example, that hypoglycemia activates growth hormone-releasing hormone (GHRH) neurons, suggesting a mechanistic link between low blood glucose levels and growth hormone release (Stanley et al., 2013).

In addition to BHB inducing upregulation of antioxidant defense, ketones have direct antioxidant capacity. BHB scavenges •OH, as does ACA, although to a lesser extent [108]. The applicability of this antioxidant capacity has been investigated in vitro and in vivo in the context of hypoglycemia. In cultured hippocampal neurons, treatment with BHB or ACA decreased ROS during hypoglycemia induced through inhibition of glycolysis, and in hypoglycemic rats, infusion of BHB decreased hippocampal lipid peroxidation [108].
Formation of O2•− at complexes I and III primarily occurs in the mitochondrial matrix, but some of the O2•− produced at complex III is produced in the intermembrane space [63]. Within the matrix, O2•− is rapidly dismutated into hydrogen peroxide (H2O2) by manganese superoxide dismutase (SOD2) [41, 53]. Some O2•− may escape into the mitochondrial intermembrane space [64] and cytosol [65], where copper/zinc superoxide dismutase (SOD1) can dismutate it into H2O2 [41]. The large majority of mitochondrial H2O2 is removed by peroxiredoxin (Prx) 3, followed by much smaller contributions from Prx5 and glutathione peroxidases (GPx) 1 and 4 [66]. GPx also removes other peroxides, including lipid hydroperoxides [41]. Catalase is another antioxidant enzyme capable of removing H2O2 but is primarily located in peroxisomes and is therefore unlikely to directly remove mitochondrial H2O2 [41, 66]. However, H2O2 can be transported out of mitochondria [67], and it is possible that the majority of mitochondrial H2O2 is removed in the cytosol. Since Prxs and GPxs rely on NADPH for recycling of their cofactors (thioredoxins and glutathione, resp.) [41], and since NADH is required for recycling of NADPH [68], activity of these enzymes would decrease availability of NADH for oxidative phosphorylation. Therefore, transport of H2O2 out of mitochondria for removal in the cytosol may be a more likely defense mechanism [67], implying a more important role of catalase and other antioxidant enzymes outside of mitochondria. Despite the lower reactivity of H2O2, it is still reactive and can oxidize metal ions, particularly iron, to form the hydroxyl radical (•OH), which readily damages DNA, lipids, and proteins [41]. •OH is scavenged by metallothioneins I and II [69, 70] and glutatathione [71], indicating that these antioxidant proteins may be important defenses against byproducts of unaddressed mtROS. Other important antioxidant enzymes include glutamate-cysteine ligase (GCL), which is the rate-limiting step in glutathione synthesis, and glutathione reductase (GSR) and thioredoxin reductase (TRXR), which recycle glutathione and thioredoxin, respectively, to their reduced forms [41].
^ Ringberg TM, White RG, Holleman DF, Luick JR (1981). "Body growth and carcass composition of lean reindeer (Rangifer tarandus tarandusL.) from birth to sexual maturity" (PDF). Canadian Journal of Zoology. 59 (6): 1040–1044. doi:10.1139/z81-145. ISSN 0008-4301. Body growth and carcass composition were measured in lean reindeer during the juvenile growth period between birth and 3 years of age. Mean carcass weight in these lean reindeer was 56 ± 4% of body weight and the deposition of body muscle and bone mass was linearly correlated with body weight after the 1st month of age. The weight of the brain relative to body weight and carcass weight declined, while the relative changes in heart, liver, kidneys, parotid glands, and tissues of the gastrointestinal tract were small after the neonatal period. The extractable fat content in carcasses increased from 4.4 to 11.4% of wet weight or approximately 100 g fat at birth and 3.5 kg fat in adult reindeer. Fat-free dry matter represented a constant percentage (18–20%) of wet carcass weight independent of body weight after the neonatal period, while a significant inverse relationship between carcass fat and body water was found.
Hi Maria, I love your bread recipes but can’t get over the one thing, the gritty texture you get in one every couple bites due to the psyllium husk, I have tried different brands and all have it. I haven’t tried Jay Robs yet. But have you tried ground up chia seeds instead by any chance? I read somewhere to just add twice the amount of water. Thanks
188. Tomas E., Tsao T. S., Saha A. K., et al. Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: acetyl-CoA carboxylase inhibition and AMP-activated protein kinase activation. Proceedings of the National Academy of Sciences. 2002;99(25):16309–16313. doi: 10.1073/pnas.222657499. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
By dramatically shifting energy metabolism towards ketogenesis and fatty acid oxidation, ketogenic diets are likely to have a profound effect on mitochondrial function. However, despite the rapidly growing amount of research on ketogenic diets and their effects on various disease states, only a small amount of this research has focused on mitochondrial function or oxidative stress. The well-established increase in fat oxidation induced by a ketogenic diet [7, 8] clearly indicates prominent connection with mitochondrial function and, in turn, oxidative stress and mitohormesis [5, 6, 9]. Therefore, the purpose of this review is to describe the current, but limited, understanding of how ketogenic diets may affect mitochondrial function and resistance to oxidative stress, particularly within the context of extending human healthspan.
Formation of O2•− at complexes I and III primarily occurs in the mitochondrial matrix, but some of the O2•− produced at complex III is produced in the intermembrane space [63]. Within the matrix, O2•− is rapidly dismutated into hydrogen peroxide (H2O2) by manganese superoxide dismutase (SOD2) [41, 53]. Some O2•− may escape into the mitochondrial intermembrane space [64] and cytosol [65], where copper/zinc superoxide dismutase (SOD1) can dismutate it into H2O2 [41]. The large majority of mitochondrial H2O2 is removed by peroxiredoxin (Prx) 3, followed by much smaller contributions from Prx5 and glutathione peroxidases (GPx) 1 and 4 [66]. GPx also removes other peroxides, including lipid hydroperoxides [41]. Catalase is another antioxidant enzyme capable of removing H2O2 but is primarily located in peroxisomes and is therefore unlikely to directly remove mitochondrial H2O2 [41, 66]. However, H2O2 can be transported out of mitochondria [67], and it is possible that the majority of mitochondrial H2O2 is removed in the cytosol. Since Prxs and GPxs rely on NADPH for recycling of their cofactors (thioredoxins and glutathione, resp.) [41], and since NADH is required for recycling of NADPH [68], activity of these enzymes would decrease availability of NADH for oxidative phosphorylation. Therefore, transport of H2O2 out of mitochondria for removal in the cytosol may be a more likely defense mechanism [67], implying a more important role of catalase and other antioxidant enzymes outside of mitochondria. Despite the lower reactivity of H2O2, it is still reactive and can oxidize metal ions, particularly iron, to form the hydroxyl radical (•OH), which readily damages DNA, lipids, and proteins [41]. •OH is scavenged by metallothioneins I and II [69, 70] and glutatathione [71], indicating that these antioxidant proteins may be important defenses against byproducts of unaddressed mtROS. Other important antioxidant enzymes include glutamate-cysteine ligase (GCL), which is the rate-limiting step in glutathione synthesis, and glutathione reductase (GSR) and thioredoxin reductase (TRXR), which recycle glutathione and thioredoxin, respectively, to their reduced forms [41].
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.
Patients with metabolic syndrome can have several disorders of coagulation that make it easier for blood clots to form within blood vessels. These blood clots are often a precipitating factor in developing heart attacks. Patients with metabolic syndrome should generally be placed on daily aspirin therapy to help prevent such clotting events. You should speak to a doctor, of course, before starting any new medication regimen.
Hi John, You could possible try a hand mixer in a bowl instead of the food processor, but I haven’t tried it, so can’t vouch for the results. Most likely the bread would not be as tall because the mixer would completely deflate the first half of the egg whites when you add them to the batter. The second half should be folded so that part will be find. If you try with a bowl and hand mixer, let me know how that goes.
There is one exception to exercising with diabetes. If your blood sugar is too high (such as over 240) and you are spilling ketones into your urine, then exercise is only going to increase your blood sugar. You can buy a dipstick urine test to check for ketones, but the best thing to do would be to talk to your doctor about what is safe for you to do.

Hi I made the Easy paleo keto bread 5 ingredients. It was moist, texture was good but it didn’t turn out completely white, more like a pale yellow and the crust was overdone. I opted for honey as my sweetner because this bread is for my nephew who has autism and we want to keep it as natural as possible. I baked the bread exactly at 325 for 40mins uncovered and then another 40mins covered (tent). What could I do next time to achieve a white bread with golden crust?
Ketogenic and low-carbohydrate diets greatly increase reliance on fat oxidation [78–89], which would logically be expected to increase mitochondrial respiration and mtROS production and, in turn, induce mitohormesis. Furthermore, mtROS produced through RET appears to have particular relevance to hormetic adaptation, including increased lifespan [90]. Nutritional ketosis is likely to increase RET by altering the FADH2 to NADH ratio. As the primary source of acetyl CoA shifts from glycolysis to β-oxidation and ketolysis, this ratio increases, more than doubling for β-oxidation of longer-chain fatty acids. Electrons from FADH2 reduce the CoQ pool through complex II and ETF-QO, thereby increasing RET [91, 92]. This induction of RET by alteration of substrate availability can also be influenced by configuration of mtETC complexes into supercomplexes [90]. The greater potential for mtROS production through RET is consistent with evidence of mitochondria producing more H2O2 during oxidation of palmitoyl carnitine versus pyruvate [93, 94]. Furthermore, succinate is generated during ketolysis by succinyl-CoA:3-oxoacid CoA-transferase (SCOT), which also promotes RET by reducing the CoQ pool through complex II. Demonstrating the likely role of RET in mitohormesis, particularly within the context of nutritional ketosis, extension of lifespan in C. elegans through BHB treatment is dependent on both complex I function and expression of bioenergetic and antioxidant proteins [95].
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.
This recipe is like having last night's cake for breakfast — except it's fiber-filled chia seed pudding instead. This dessert-like breakfast from Healthy Sweet Eats is hardly a disappointing substitute, though. Fresh cherries add sweetness, while whole almonds add crunch (and more fiber). Plus, it's made with strongly brewed coffee to give you an extra jolt of caffeine with your usual cup of java.
Thank you Mira for your quick reply. I didn’t make it that same day but I just made a batch now and they are excellent! I really enjoyed them. I made the recipe times 10 for 12 large muffin slots in the muffin tin. I’m thinking of shaping a larger round of batter on a parchment lined pan next time and after baking, carefully cutting in half to make 2 rounds to make a pizza crust. Thank you so much!!!
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.
Moreover, recent studies show that the Inuit have evolved a number of rare genetic adaptations that make them especially well suited to eat large amounts of omega-3 fat.[57][58][59] And earlier studies showed that the Inuit have a very high frequency—68% to 81% in certain arctic coastal populations—of an extremely rare autosomal recessive mutation of the CPT1A gene—a key regulator of mitochondrial long-chain fatty-acid oxidation[60][61]—which results in a rare metabolic disorder known as carnitine palmitoyltransferase 1A (CPT1A) deficiency and promotes hypoketotic hypoglycemia—low levels of ketones and low blood sugar.[62] The condition presents symptoms of a fatty acid and ketogenesis disorder.[62] However, it appears highly beneficial to the Inuit[60] as it shunts free fatty acids away from liver cells to brown fat, for thermogenesis.[63][64] Thus the mutation may help the Inuit stay warm by preferentially burning fatty acids for heat in brown fat cells.[64] In addition to promoting low ketone levels, this disorder also typically results in hepatic encephalopathy (altered mental state due to improper liver function), enlarged liver and high infant mortality.[65] Inuit have been observed to have enlarged livers with an increased capacity for gluconeogenesis, and have greater capacity for excreting urea to remove ammonia, a toxic byproduct of protein breakdown.[57][66][67][68] Ethnographic texts have documented the Inuit's customary habit of snacking frequently [69] and this may well be a direct consequence of their high prevalence of the CPT1A mutation[70] as fasting, even for several hours, can be deleterious for individuals with that allele, particularly during strenuous exercise.[57][70] The high frequency of the CPT1A mutation in the Inuit therefore suggests that it is an important adaptation to their low carbohydrate diet and their extreme environment.[57][60][70]
Make this keto bread pizza base crispy and thin, or roll it into a thicker, fluffier crust — no matter how you prepare it, this recipe cuts out all dairy, grains, and gluten for a total of 6 net carbs. Coconut flour and psyllium creates a firm texture, while apple cider vinegar lends a tangy flavor. To stay more Bulletproof, avoid eating garlic and psyllium husk too often.
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