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.
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 . Hypoadiponectinemia also appears to be a predictor for the future development of metabolic syndrome in obese individuals [109,110].
In addition, as early as in 2008, the Swedish Board of Health and Welfare examined and approved advice on LCHF within the health care system. Advice on LCHF is, according to the Swedish Board of Health and Welfare’s review, in accordance with science and proven knowledge. In other words, certified healthcare professionals, who give such advice (for example myself) can feel completely confident.
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:
Independent of nutritional ketosis, increased dietary fat intake increases expression of UCP2 and UCP3 in muscle , and fatty acids facilitate uncoupling through UCP2 [143, 144], UCP3 [94, 143, 144], and ANT . Given the high fat intake that is characteristic of a ketogenic diet, it is logical to expect nutritional ketosis to increase mitochondrial uncoupling.
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Hi Jodi, I haven’t tried that, but don’t think it would work well for this recipe. First, yeast needs sugar (for it to consume – it’s not typically in the end result), so you’d need to add that. But also, just with how we are making the bread fluffy with beaten egg whites, I don’t think yeast would work. If you want to try adding yeast to a low carb bread, I would do it with this low carb bread recipe instead.
I am so frustrated. I have made the rolls a dozen times and they vary in results but always come out acceptable. I truly enjoy them. However, no matter what I do I cannot get the darn loaf to work! I am specific with ingredients, I have tried leaving the loaf in the oven to cool, I have tried taking it out. I make sure the water is at a rolling boil. I tried different sized pans…just doesn’t work. The only difference I can think of is the loaf pan. I am wondering if I were to just form the dough into a loaf without the restriction of a pan, would it come out better? It wouldn’t be as pretty but it might work.
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The use of lifestyle interventions to treat and prevent chronic disease is attractive because of their potential to lower medical costs and produce more robust and holistic improvements in health. Ketogenic diets have been studied sporadically for more than 100 years, but over the last 15 years, a growing number of researchers have contributed to what is now a critical mass of discoveries that link the process of keto-adaptation to a broad range of health benefits [10–33]. Early clinical research focused on the use of “extreme” versions of ketogenic diets to treat seizures, but recent research indicates that benefits related to the management of epilepsy, weight loss, metabolic syndrome, and type 2 diabetes can be achieved with an approach that is less restrictive in carbohydrate and protein, and therefore more satisfying, sustainable, and feasible for the general population. A “well-formulated” ketogenic diet is generally characterized by a total carbohydrate intake of less than 50 g/d and a moderate protein intake of approximately 1.5 g/d per kg of reference weight . This typically increases circulating β-hydroxybutyrate (BHB) and acetoacetate (ACA) from concentrations that are typically less than 0.3 mM into the range of nutritional ketosis, which for BHB, we define as 0.5–3 mM . This range is below the typical 5–10 mM range for BHB that occurs during prolonged fasting, and well below concentrations characteristic of ketoacidosis [34, 35]. From the perspective of meeting energy demands, the reduced carbohydrate and moderate protein intakes necessarily make ketogenic diets high in fat. Despite this contradiction with mainstream dietary guidelines, ketogenic diets may be beneficial for many health conditions, particularly the previously mentioned conditions related to mitochondrial impairment, which includes obesity [10, 11], diabetes [12–14], cardiovascular disease [15–17], cancer [15, 18–26], neurodegenerative diseases [19, 20, 27–30], and even aging [31–33, 36, 37].
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290. Vega R. B., Huss J. M., Kelly D. P. The coactivator PGC-1 cooperates with peroxisome proliferator-activated receptor alpha in transcriptional control of nuclear genes encoding mitochondrial fatty acid oxidation enzymes. Molecular and Cellular Biology. 2000;20(5):1868–1876. doi: 10.1128/mcb.20.5.1868-1876.2000. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
A well-formulated ketogenic diet, besides limiting carbohydrates, also limits protein intake moderately to less than 1g/lb body weight, unless individuals are performing heavy exercise involving weight training when the protein intake can be increased to 1.5g/lb body weight. This is to prevent the endogenous production of glucose in the body via gluconeogenesis. However, it does not restrict fat or overall daily calories. People on a ketogenic diet initially experience rapid weight loss up to 10 lbs in 2 weeks or less. This diet has a diuretic effect, and some early weight loss is due to water weight loss followed by a fat loss. Interestingly with this diet plan, lean body muscle is largely spared. As a nutritional ketosis state sustains, hunger pangs subside, and an overall reduction in caloric intake helps to further weight loss.
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 . 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 . 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 . 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 . 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) .
Metabolic syndrome (metabolic syndrome X, insulin resistance syndrome, dysmetabolic syndrome, hypertriglyceridaemic waist, obesity syndrome, Reaven syndrome) is the name for a group of risk factors that increase the risk for ischaemic heart disease (IHD), diabetes and stroke (Fig. 23.1). The metabolic syndrome is diagnosed when at least three of the IHD risk factors listed in Table 23.1 are present. Whether the syndrome, which affects possibly 25% of the US population, is a specific syndrome, and nothing more than the sum of its parts, is controversial.
Has anyone tried this using a substitute for the eggs/egg whites? My husband seems to be sensitive to eggs (not sure which part, to be honest) and we’ve been making most recipes using agar agar as a substitute (for either whites or whole eggs) but this only works if the egg is a binder. I’m guessing that they are a leavening agent in the bread (please correct me if I’m wrong!) and I don’t know if agar would work in this recipe. I do have VersaWhip 600 – anyone ever tried that in a bread recipe?
4. Tapia P. C. Sublethal mitochondrial stress with an attendant stoichiometric augmentation of reactive oxygen species may precipitate many of the beneficial alterations in cellular physiology produced by caloric restriction, intermittent fasting, exercise and dietary phytonutrients: “Mitohormesis” for health and vitality. Medical Hypotheses. 2006;66(4):832–843. doi: 10.1016/j.mehy.2005.09.009. [PubMed] [CrossRef] [Google Scholar]
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As the rate of oxidative phosphorylation approaches the capacity of the mtETC, Δp will increase and facilitate mtROS production . Higher oxidative capacity should therefore decrease the potential for mtROS production and subsequent oxidative damage. Furthermore, greater oxidative capacity may compensate for the resulting decrease in efficiency of ATP production associated with increased mitochondrial uncoupling. Since oxidative phosphorylation occurs exclusively in mitochondria, mitochondrial density is a key determinant of oxidative capacity .
Hi Kristi, I’m glad you liked the taste! Sorry it didn’t rise for you. It’s hard to say what happened without being in the kitchen with you. Were the peaks in the egg whites not firm enough, or did they fall too much when folding with the rest of the batter? That is the main culprit I can think of, as the egg whites are a big part of what creates the volume in this bread.
The ARC exerts opposing actions on food intake responding not only to leptin and insulin, but also to gut hormones (the most studied are ghrelin and, recently, PYY). The neurophysiological pathways suggest that feeding is regulated by a feedback loop, where the hypothalamus provides the long-term regulatory input to the NTS, which acts as a setpoint (Williams et al., 2001).
Ketone salts did not improve performance 35 ,36. There are two recent published studies of ketone salts on athletes.. Performance was compared between ketone salts vs. carbohydrate in a 4 minute cycling time trial and a 150 kJ ( ~10 mins) cycling time trial. In the 4 minute trial there was no change in performance, and in the 150 kJ test, performance was decreased by 7%. Reasons for the difference in findings could be: Lower levels of blood BHB levels (which peaked at 0.6 mM and 0.8 mM in these studies) meaning far less BHB was present than in the ketone ester study. The ketone salt was given without carbohydrate and so there was no additive effect of ketones + carbohydrate as seen in the ketone ester study. The tests used were short and highly reliant on anaerobic (glycolytic) metabolism, therefore ketones did not offer an advantage.
The longest studies/follow-ups for ketogenic diets are about 10 years long and have shown it to be safe [3, 4, 5, 6]. Studies that carefully keep people in metabolic wards to strictly monitor food intake and biomarkers are always short because they are very costly and laborious. Moreover, most participants are not able or willing to participate for a long time in a study that supervises food intake around the clock. For these reasons, these kinds of studies are always of short duration, a few weeks maximum.
To encourage ketone production, the amount of insulin in your bloodstream must be low. The lower your insulin, the higher your ketone production. And when you have a well-controlled, sufficiently large amount of ketones in your blood, it’s basically proof that your insulin is very low – and therefore, that you’re enjoying the maximum effect of your low-carbohydrate diet. That’s what’s called optimal ketosis.
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We’ve been on the Keto journey since the end of February last year and this is my favourite bread recipe so far, I just made a loaf and it turned out great. I don’t have a food processor so I did use my blender and for ingredients I only used the almond flour, coconut flour, baking powder, butter, salt, 8 egg whites (all I had left in the fridge) and the only optional ingredient I added was stevia. The texture was still really nice without the extra ingredients which is a nice option and this tasted like a regular loaf of bread, I’ll definitely be making this again!!
Additional evidence, although disparate and primarily based on neuronal mitochondrial function related to epileptic seizures, further supports the potential for nutritional ketosis to induce mitohormesis . Much of this is based on signal transduction, antioxidant defense, and oxidative capacity, all of which will be discussed in proceeding sections.
In addition to the downstream bioenergetic and antioxidant signaling induced by sirtuins, they directly facilitate ketogenesis and β-oxidation. SIRT1  and SIRT3  deacetylate 3-hydroxy-3-methylglutaryl CoA (HMG CoA) synthase, which is the rate-limiting enzyme for ketogenesis , resulting in increased levels of β-hydroxybutyrate . In addition, SIRT3 deacetylates and increases activity of long-chain acyl-CoA dehydrogenase (LCAD) , which participates in β-oxidation and therefore supports ketogenesis. SIRT3 has a similar influence on medium-chain acyl-CoA dehydrogenase (MCAD) as well . Since sirtuins facilitate ketogenesis, which then facilitates sirtuin activation, nutritional ketosis may promote, to some extent, a feed-forward cycle of sirtuin activity.
More recently, other hypothalamic appetite control regions have been identified, including those in the arcuate nucleus (ARC), the periventricular nucleus (PVN) and the dorsomedial hypothalamic nucleus (DMH) (Valassi et al., 2008). These are sites of convergence and integration of many central and peripheral signals, not just macronutrients, that are involved in food intake and energy expenditure mechanisms, e.g., a group of neurons in the ARC stimulating food intake via neuropeptide Y (NPY) and agouti gene-related protein (AGRP). These neurons interact with those producing the anorexigenic pro-opiomelanocortin (POMC) and the cocaine/amphetamine-regulated transcript (CART) (Williams et al., 2001). Thus, a more comprehensive, unified model should include macronutrients as well as many single amino acids and other signaling molecules.
Ketosis is the result of following the ketogenic diet, which is why it’s also sometimes called “the ketosis diet.” Ketosis takes place when glucose from carbohydrate foods (like grains, all sources of sugar or fruit, for example) is drastically reduced, which forces the body to find an alternative fuel source: fat. Although dietary fat (especially saturated fat) often gets a bad name, provoking fear of weight gain and heart disease, it’s also your body’s second preferred source of energy when carbohydrates are not easily accessible.
309. Lemieux K., Konrad D., Klip A., Marette A. The AMP-activated protein kinase activator AICAR does not induce GLUT4 translocation to transverse tubules but stimulates glucose uptake and p38 mitogen-activated protein kinases alpha and beta in skeletal muscle. FASEB Journal. 2003;17(12):1658–1665. doi: 10.1096/fj.02-1125com. [PubMed] [CrossRef] [Google Scholar]
The BBB, largely formed by the brain capillary endothelial cells, provides a protective barrier between the systemic blood and the extracellular environment of the CNS. Passage of FAs from the blood to the brain may occur either by diffusion or by proteins that facilitate their transport. Studies indicate that FATP-1 and FATP-4 are the predominant FA transport proteins expressed in the BBB based on human and mouse expression studies (Mitchell et al., 2011).
Keto is not hard to follow at all. See, this is why I took my diet and nutrition into my own hands. I have PCOS and the ketogenic diet has worked wonders for me. I’m finally pregnant at the age of 32 and after 11 years of marriage because the ketogenic diet made me lose over 100 lbs and brought my insulin resistance under control. I feel better than I’ve ever felt. Sometimes doctors don’t seem to know as much as they should, or as much as they assume they do, and that’s pretty disturbing. Just like they’re still using the old school and very inaccurate BMI charts that are just pure bs. I’ll just take care of myself outside of certain situations involving illness or injury. I’m doing great on my own.
A ketogenic diet could be an interesting alternative to treat certain conditions, and may accelerate weight loss. But it is hard to follow and it can be heavy on red meat and other fatty, processed, and salty foods that are notoriously unhealthy. We also do not know much about its long-term effects, probably because it’s so hard to stick with that people can’t eat this way for a long time. It is also important to remember that “yo-yo diets” that lead to rapid weight loss fluctuation are associated with increased mortality. Instead of engaging in the next popular diet that would last only a few weeks to months (for most people that includes a ketogenic diet), try to embrace change that is sustainable over the long term. A balanced, unprocessed diet, rich in very colorful fruits and vegetables, lean meats, fish, whole grains, nuts, seeds, olive oil, and lots of water seems to have the best evidence for a long, healthier, vibrant life.
These cake-like donuts have the perfect crumb and light crunch from a dusting of cinnamon “sugar.” Plus, with only 3 net carbs per donut, you can sneak an extra one to dunk in your coffee without the guilt. Swap in coconut milk for almond milk, and make sure you use grass-fed butter and non-GMO erythritol to keep this keto breakfast recipe Bulletproof.
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^ Jump up to: a b Gatta-Cherifi, Blandine; Cota, Daniela (2015). "Endocannabinoids and Metabolic Disorders". Endocannabinoids. Handbook of Experimental Pharmacology. 231. pp. 367–91. doi:10.1007/978-3-319-20825-1_13. ISBN 978-3-319-20824-4. PMID 26408168. The endocannabinoid system (ECS) is known to exert regulatory control on essentially every aspect related to the search for, and the intake, metabolism and storage of calories, and consequently it represents a potential pharmacotherapeutic target for obesity, diabetes and eating disorders. ... recent research in animals and humans has provided new knowledge on the mechanisms of actions of the ECS in the regulation of eating behavior, energy balance, and metabolism. In this review, we discuss these recent advances and how they may allow targeting the ECS in a more specific and selective manner for the future development of therapies against obesity, metabolic syndrome, and eating disorders.