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.
Eating some protein, fiber, and healthy fat with all of your meals can help stabilize blood sugar and manage your appetite, especially when your meal also contains carbohydrate-dense foods like high-sugar fruits (mangos, grapes, cherries) or starchy vegetables (potatoes). Each of these nutrients helps balance blood sugar on its own, but they’re even better together. We love a good kale salad topped with avocado and grass-fed steak.
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More definitive evidence that metabolic syndrome per se predisposes to coronary heart disease and cerebrovascular disease has been reported. Thus a twofold to fourfold increase in subsequent cardiovascular events has been described in men and women with metabolic syndrome (modified WHO criteria) even in the absence of type 2 diabetes or impaired glucose tolerance.234-236 Qualitatively, similar results have been obtained when metabolic syndrome was defined by ATP III criteria237,238 (Fig. 43-9). In a compilation of multiple studies, the presence of metabolic syndrome had a greater impact on the risk for developing diabetes (fivefold) than ASCVD (twofold).22,182,199 In addition, where studied, the rate of cardiovascular events was higher in patients who had diabetes and metabolic syndrome than in individuals with only metabolic syndrome.22,239
Glucose-sensitive neurons have been identified in a number of CNS regions including the metabolic control centers of the hypothalamus. Medeiros et. al. have used patch-clamp electrophysiology to examine whether neurons in a specific specialized region known as the subfornical organ (SFO), an area where the blood-brain barrier is not present, are also glucose sensitive or not. These experiments demonstrated that SFO neurons are glucose-responsive and that SFO is an important sensor and integrative center of circulating signals of energy status (Medeiros et al., 2012).
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).
Scoop out dough with a spatula and place onto a large sheet of plastic wrap. Cover the dough in plastic wrap and knead a few times with the dough inside the plastic wrap until you have a uniform dough ball. Lightly coat your hands with oil and divide dough into 8 equal parts. Roll each dough between your palms until it forms a smooth round ball. Place dough balls onto baking sheet, spaced 2 inches apart.
Mohanraj, R., & Sivasankar, S. (2014, June). Sweet Potato (Ipomoea batatas [L.] Lam) – a valuable medicinal food: A review. Journal of Medicinal Food, 17(7), 733–741. Retrieved from https://www.researchgate.net/profile/Remya_Mohanraj2/publication/263096030_Sweet_Potato_Ipomoea_batatas_L_Lam_-_A_Valuable_Medicinal_Food_A_Review/links/54ee2b8b0cf2e55866f22c1a.pdf
Ketones are a special type of fat that can stimulate the pathways that enhance the growth of new neural networks in the brain. A ketogenic diet is one that is high in fats, and this diet has been a tool of researchers for years, used notably in a 2005 study on Parkinson’s patients finding an improvement in symptoms after just 28 days. The improvements were on par with those made possible via medication and brain surgery. Other research has shown the ketogenic diet to be remarkably effective in treating some forms of epilepsy, and even brain tumors.
Why is the keto diet good for you? A keto diet is one that prioritizes fats and proteins over carbohydrates. It can help reduce body weight, acne, and the risk of cancer. Find out about the mechanisms through which it achieves these benefits and the research that supports it. This MNT Knowledge Center article also discusses the risks of the diet. Read now
Acetyl-CoA can be metabolized through the TCA in any cell, but it can also undergo a different process in liver cells: ketogenesis, which produces ketone bodies. Ketone bodies are also produced in mitochondria, and usually occur in response to low blood glucose levels. When glucose levels are low, oxaloacetate is diverted away from the TCA cycle and is instead used to produce glucose de novo (gluconeogenesis). But when oxaloacetate is unavailable to condense with acetyl-CoA, acetyl-CoA cannot enter the cycle, and so the body has evolved an alternative way to harvest energy from it.
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) .
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We can say that no species, including humans, could have survived for millions of years without the ability to withstand brief periods of hunger or starvation (Amen-Ra, 2006). These periods of fasting are themselves ketogenic (McCue, 2010) during which the concentrations of insulin and glucose decrease while that of glucagon increases in the attempt to maintain normal blood glucose levels. When the body passes from a condition of food abundance to one of deprivation (or else via VLCKD simulated deprivation), there is, with a slight delay, an increase in the concentration of free FAs as well as KB in the blood. Thus, from this point of view KD could be compared to caloric restriction for fasting. These manipulations of nutrients, both in quantity and quality, seem to not only act on blood glucose/KB level but also to promote changes in metabolic pathways and cellular signaling. How this kind of metabolic condition (ketosis) can affect satiety and hunger mechanisms is still a matter of debate.
In contrast to most other diet plans, remaining in ketosis doesn’t require counting calories, measuring portions or dealing with hunger pangs for the sake of eating as little as possible. In fact, most people feel satisfied and energized while in ketosis and find that they can go for longer periods without the need to eat (which is why intermittent fasting is commonly practiced with a keto diet).
^ 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.
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Patterns can be great because they help you figure out what is causing undesirable blood sugar values. A good way to track of it is to keep a journal of all of the food you eat, activities you do and your blood sugar levels for 1 week. During this week, check your sugar before and after you eat, as well as in between meals. Also document any insulin that you give yourself.
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In controlled studies on exercise-trained humans and animals, ketogenic diets have been shown to increase fat oxidation [8, 167] and expression or activity of carnitine palmitoyltransferase [167, 168] and β-HAD [168, 172], demonstrating that nutritional ketosis induces adaptation beyond exercise. Similarly, in a study comparing the independent and combined effects of exercise and a ketogenic diet on rats, the combination resulted in greater β-HAD and citrate synthase activities in skeletal muscle and higher maximal O2 consumption than either intervention alone, further indicating the potential for exercise to magnify adaptations induced by nutritional ketosis .
Eating whole grains has been shown to cause blood sugar levels to rise more slowly after a meal and reduce the risk of type 2 diabetes. The fiber in whole grains slows the digestion of carbs, reducing the demand for insulin. Whole grains also contain antioxidants and anti-inflammatory nutrients that may also play a role in helping prevent diabetes.
The situation for Type II diabetics is different because some insulin production remains and some cells of the body can still respond to insulin. It is worth noting that insulin sensitivity can be different between the different tissues of the body such as liver, adipose tissue and muscle. A small amount of insulin release can help to prevent development of DKA unless the body is totally insulin resistant. Insulin resistance is a term used to indicate that for a given amount of insulin, the cells of the body are less responsive and take up less glucose. This means that blood glucose levels remain higher for longer when insulin resistant Type II diabetics eat a carbohydrate rich meal. Over time, the pancreas secretes more insulin to compensate for reduced insulin sensitivity, which can damage the insulin producing (beta) cells. Furthermore, having high blood glucose can lead to a number of side effects:
Like many variables in diet, health, and disease, it behooves us to look beyond the bumper sticker explanation. I want to highlight a couple of posts I wrote, to attempt to provide a little more nuance and understanding to the subject: “Ketosis — advantaged or misunderstood state?” Parts I and II. Part I follows below. I’m hoping to write more on the topic in the not-too-distant future since there’s been a number of intriguing papers published recently (certainly since 2012). But I also wanted to bring these back into focus in light of the information I’m seeing more of on the interwebz. (You can also visit the Ketosis section of the site to view more articles on the subject.)
4.) Fill the dough into a loaf tin lined with baking paper. If you don’t use a silicone loaf pan line ALL SIDES with parchment paper so the bread will release easily. Smooth the top, but don’t press down too much – keep as much air in the dough as possible. Bake at 180 Celsius / 350 Fahrenheit for about 45 minutes or until a knife inserted comes out clean!
In particular, eat a healthy diet that includes fruits, vegetables, and whole grains. Exercise is also important when it comes to preventing this condition. Regular physical activity will reduce your blood pressure, blood sugar, and cholesterol levels. The key is to try to maintain a healthy weight. Talk to your doctor before beginning an exercise program or radically changing your diet.
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 . 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 . 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 .
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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
I just tried this recipe in my kitchen. OMG thank you so so much for this wonderful idea! The only thing I think I will try next time is to add just a dash or so of salt to the mug before microwaving (although it already tastes great!). I think it will be fun to experiment with adding some different seasonings or herbs to the batter before baking it, too, just for variety.
The metabolic theory states that the root cause of cancer is a defect in mitochondrial energy production or ‘an irreversible injuring in respiration’91. Once the cells ability to produce energy is compromised, this is hypothesised to lead to the subsequent accumulation of changes that make the cell cancerous92. A key change is decreased mitochondrial glucose metabolism in cancer cells. Cancer cells ferment glucose to lactate (which happens outside of the mitochondria) at a much higher rate than normal cells93, in a change called ‘The Warburg Effect.’ This implicates damage to the mitochondria and failure in energy production as a central process of cancer progression.
Luckily, DKA has some pretty glaring signs, so someone experiencing it can get help ASAP—symptoms include rapid and heavy breathing, having to pee a lot, and thirst that can’t be quenched, says Klett. As things progress, they’ll also “get confused, become delirious, and eventually have cardiovascular collapse because the blood pH gets so low,” and their organs will stop functioning properly. So again, treatment is necessary.
Overweight individuals with metabolic syndrome, insulin resistance, and type 2 diabetes are likely to see improvements in the clinical markers of disease risk with a well-formulated very-low-carbohydrate diet. Glucose control improves due to less glucose introduction and improved insulin sensitivity. In addition to reducing weight, especially truncal obesity and insulin resistance, low-carb diets also may help improve blood pressure, blood glucose regulation, triglycerides, and HDL cholesterol levels. However, LDL cholesterol may increase on this diet.
Many athletes would not consider following a ketogenic diets due to the limited evidence of a performance enhancing effect, the risk of side effects having a negative impact on performance and the difficulty in maintaining the lifestyle changes required to stay in ketosis. Exogenous ketones offer a method to deliver some of the benefits of ketone metabolism without requiring athletes to follow a strict ketogenic diet. Taking exogenous ketones creates a metabolic state that would not normally occur naturally: the state of having full carbohydrate stores as well as elevated ketones.
One of the foods that people tell us they miss most after going keto is bread. (And cookies or cakes, but you get the idea.) We get it, bread is undeniably comfort food. Growing up, it wasn’t unheard of to eat toast for breakfast, a sandwich for lunch, and maybe even a slice of buttered bread along with dinner. Not only is that ton of carbs, but it’s also a lot of empty calories when we could have been eating real-food alternatives, like this bread made from nutrient-dense ingredients!