Type I diabetes is usually treated by insulin injections, that replace the body’s own insulin production. In Type I diabetics, lowering dietary carbohydrate consumption can reduce the need to inject insulin to lower blood sugar101. However, because they do not release any insulin Type I diabetics can be at risk of developing a complication called “Diabetic Ketoacidosis” (DKA). DKA occurs because, alongside its effects on glucose, insulin has other effects in the body. Insulin normally inhibits the release of fat (lipolysis) from adipose tissue. In Type I diabetics, the lack of insulin can lead to high levels of lypolysis, high levels of fatty acids in the blood, this then drives rapid and uncontrolled liver ketone production. The symptoms of DKA are weakness, confusion and deep gasping breathing. In order to avoid developing DKA while following a ketogenic diet, Type I diabetics should seek medical supervision and closely monitor their glucose and ketone levels if reducing their dietary carbohydrate intake. 
Nutritional ketosis may facilitate PGC-1α activity through multiple mechanisms. Since PGC-1α is activated by AMPK and SIRT1, nutritional ketosis may initiate PGC-1α activity through these enzymes. As previously mentioned, catecholamines and adiponectin facilitate PGC-1α activity by promoting its expression, and insulin inhibits PGC-1α through downstream phosphorylation, all independent of AMPK. As previously discussed, a ketogenic diet may increase catecholamines and adiponectin and is well known to decrease insulin, indicating that nutritional ketosis may directly facilitate PGC-1α activity through these hormones. Supporting these potential mechanisms, a ketogenic or low-carbohydrate diet has increased expression, protein content, and activation of PGC-1α [149, 231, 317], as well as expression of its target PPARα [87, 148]. Furthermore, in skeletal muscle of mice following a ketogenic diet, the resulting increases in O2 consumption and expression of genes related to fat oxidation appear to be dependent on PGC-1α [157]. Ketones likely contribute to this signaling as well based on the recent observation that the increased hepatic expression of PPARα targets induced by a ketogenic diet did not occur with a nonketogenic low-carbohydrate diet [37].
Finally made this recipe, is my second bread recipe I’ve made and the top is nice but the inside always feels moist … I am putting it in the oven a bit more to see if it dries out, is that the texture that it should have because of the butter or what? I liked the flavor! Just not sure of how is supposed to be inside. I haven’t watched the video yet. Thanks!!
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.
In regard to the practicality of BHB signaling, many of the outcomes described above, including HDAC inhibition, were achieved with BHB concentrations within the range of 0.6–2 mM [37, 103, 105, 108, 109, 111, 112, 116], which is well within the physiological range of nutritional ketosis for humans and even suggests potential benefit at low to moderate levels.
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! 🙂 🙂
The previous definitions of the metabolic syndrome by the International Diabetes Federation[40] and the revised National Cholesterol Education Program are very similar and they identify individuals with a given set of symptoms as having metabolic syndrome. There are two differences, however: the IDF definition states that if body mass index (BMI) is greater than 30 kg/m2, central obesity can be assumed, and waist circumference does not need to be measured. However, this potentially excludes any subject without increased waist circumference if BMI is less than 30. Conversely, the NCEP definition indicates that metabolic syndrome can be diagnosed based on other criteria. Also, the IDF uses geography-specific cut points for waist circumference, while NCEP uses only one set of cut points for waist circumference regardless of geography. These two definitions are much more similar than the original NCEP and WHO definitions.
The Mediterranean diet is palatable and easily sustained. In addition, recent studies have shown that when compared to a low fat diet, people on the Mediterranean diet have a greater decrease in body weight, and also had greater improvements in blood pressure, cholesterol levels, and other markers of heart disease -- all of which are important in evaluating and treating metabolic syndrome.

Nutritional ketosis is a natural metabolic state in which your body adapts to burning fat rather than carbohydrates as its primary fuel. It is clinically proven to directly reduce blood sugar (as measured by HbA1c), improve insulin sensitivity (as measured by HOMA-IR) and reduce inflammation (as measured by white blood cell count and CRP). Nutritional ketosis can be induced by following a ketogenic diet. Learn more in our FAQ below!
Last point of background: Everything I’ve just presented is based on data from starving subjects.  If one restricts carbohydrate intake, typically to less than about 20-50 gm/day (dependent on timing and carbohydrate composition), and maintains modest but not high protein intake (because protein is gluconeogenic – i.e., protein in excess will be converted to glycogen by the liver), one can induce a state referred to as “nutritional ketosis” with similar physiology to what I’ve just presented without resorting to starvation.  Why you’d do this is something I will discuss later.
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].
I was well aware of the dearth of mainstream knowledge of NK, and particularly the conflation of NK with diabetic ketoacidosis (DKA), a pathologic state that results from the complete or near absence of insulin, which is what prompted my writing and desire to share my journey. And I was once in the wanker category of folks who spoke with “authority” about ketosis, despite knowing somewhere between zero and nothing on the topic. I remember exactly where I was sitting in a clinic at Johns Hopkins in 2002 during my residency explaining to (admonishing, really) a patient who was on the Atkins diet how harmful it was because of DKA. Not only that, the ketogenic diet could be seen as the antithesis of a “healthy” diet by conventional standards. I could see how this was a difficult proposition for many to acknowledge.
You've probably heard of the keto diet, the trendy weight loss plan that advocates for cutting down carbs and upping your fat intake. (That means no to pastries and pasta, and yes to meat, eggs, and heart-healthy oils.) If your morning routine of the past involved bagels, toast, or oatmeal, trying to come up with keto breakfast ideas can feel like a rude awakening. With so many carb-heavy a.m. foods, it's arguably the hardest meal to find ketogenic diet-approved substitutes for — especially when you're staring right in the face of a donut on your morning coffee run.
Similarly, several studies have demonstrated that up to half or more of patients undergoing PD have metabolic syndrome, and at least one study has demonstrated a significant increase in the prevalence with initiation of PD therapy. The only study that made a head-to-head comparison concluded that metabolic syndrome was significantly more prevalent in patients undergoing PD compared with in-center HD. These observations have raised concerns that PD therapy itself may contribute to the development of metabolic syndrome. However, the prevalence of metabolic syndrome in patients undergoing in-center HD in the only study with head-to-head comparison was substantially lower than in other studies. Moreover, there are two challenges with the diagnosis of metabolic syndrome in patients undergoing PD. First, the intraperitoneal instillation of dialysate with PD results in an increase in waist circumference, an important component for the diagnosis of metabolic syndrome. Second, there is continuous systemic absorption of glucose from intraperitoneal dialysate, and hence, patients undergoing PD are never in a postabsorptive state. This results in overestimation of fasting glucose and lipid parameters. Finally, the results from studies examining the association of metabolic syndrome with cardiovascular events or all-cause mortality have been inconsistent. This is not surprising because the individual components of metabolic syndrome themselves do not portend a higher risk for death or cardiovascular events in patients with ESRD, including among those undergoing PD.
Enter these delightfully low carb Keto Silver Dollar Pancakes. They give you all the fluffy scrumptious-ness you’ve come to expect from a pancake without all those daunting carbs. Aside from being low carb they’re easy to make as well. They’re actually no more difficult to make than standard pancakes. Just mix all the ingredients together and pour them into a pan. Simple, painless and oh so tasty!
Forget Atkins and Paleo — the new low-carb diet du jour is called keto, as in ketogenic. Although there are many similarities between these diets, a keto diet is all about restricting carbohydrates and increasing healthy fats. The goal is to force your body’s metabolism into ketosis, which means it burns fat instead of glucose — because without carbs, glucose isn’t readily available.
The exact cause of metabolic syndrome is not known. Many features of the metabolic syndrome are associated with "insulin resistance." Insulin resistance means that the body does not use insulin efficiently to lower glucose and triglyceride levels. Insulin resistance is a combination of genetic and lifestyle factors. Lifestyle factors include diet, activity and perhaps interrupted sleep patterns (such as sleep apnea).
Love how quick and easy these are to whip up and they’re really satisfying to eat. Made them tonight to use as hamburger buns; sliced them in half and grilled them and they worked great. I think the coconut gives them some sweetness that reminds me of cornbread (I used a coconut/almond milk blend for the liquid). I think we’ll be making a lot of these!
The gut-brain link is important not only for the hormones produced by the gut, but also for the long-term body weight regulation. Studies in mice indicate that the gut microbiome influences both sides of the energy balance by contributing to nutrient absorption and regulating host genes that affect adiposity [however there are conflicting reports (Parks et al., 2013; Schele et al., 2013)]. However, it remains uncertain just how important gut microbiota are for nutrient absorption in humans. A cohort study has demonstrated that the nutrient load is a key variable that can influence the gut/fecal bacterial content over short time frames. Furthermore, the observed associations between gut microbes and nutrient absorption indicates a possible role of the human gut microbiota in the regulation of the nutrient intake and utilization (Jumpertz et al., 2011).
The goal of metabolic syndrome treatment is to reduce the risk of heart disease and diabetes by controlling the associated problematic health conditions (high blood pressure, high cholesterol, diabetes, insulin resistance). “A study in which 53 percent of people had metabolic syndrome at the start found that over three years, intensive lifestyle changes—mainly diet and exercise—resulted in the lowest risk of developing diabetes and the lowest risk of developing metabolic syndrome in those who didn’t have it,” Ndumele says. Recommended changes include:
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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.


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I tried this with the Psyllium husk powder I had (Konsyl) and it was too gummy. It looks like the Jay Robb is out of stock everywhere. If you had success with this bread using a different brand, would you share with me what brand worked? I could taste in the crust that this will be wonderful once I get the right psyllium. Thanks, everyone! I’m excited to nail this.
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To Make Sure You Get the Best Rise: Make sure your baking powder and yeast are fresh. Let your egg whites come to room temperature before using. Cook for the recommended amount of time (and make sure your oven is properly calibrated). Measure all ingredients carefully (we recommend weighing the dry ingredients). Try to avoid the temptation to slice it while it's hot because this can cause the loaf to fall. 
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