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?
Many different supplements may help lower or control blood sugar in people with prediabetes or type 2 diabetes who experience hyperglycemia (when blood glucose rises higher than normal). These supplements are discussed below. More details about each, including dosage, drug interactions, potential side effects, and ConsumerLab.com's reviews of products on the market, can be found by clicking on the links.
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.
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But that doesn't mean it could never, ever happen—in fact, it actually did happen to one women on a "no-carbohydrate" diet, according to a 2006 case report in the New England Journal of Medicine. According to the case report, the woman was on a strict low-carb regimen for four years (she ate fewer than 20 grams of carbs a day—20 grams per day is the minimum on the keto diet, but most people eat 50 grams per day), but her ketoacidosis cleared up after she was put on a diet with normal carbohydrate intake.
Metabolic syndrome has been shown to be associated with an increased risk of cataract in several observational studies (Table 19.2). Paunksnis et al. reported an association between metabolic syndrome and cataract among middle-aged European men and women.16 In the Blue Mountains Eye Study (BMES), metabolic syndrome was associated with an increased risk of all subtypes of cataract including cortical, nuclear, and posterior subcapsular cataract (PSC) among elderly Australians.17 In a population of Malay adults in Singapore, a significant association between metabolic syndrome and cataract was also found.13 A dose–response relationship was also observed between an increasing number of metabolic syndrome components and cataract. Among the subtypes, cortical cataract showed a positive association with metabolic syndrome.13 Lindblad et al. examined a large, population-based cohort of Swedish women who participated in the Swedish Mammography Cohort and found that a combination of three components of metabolic syndrome, including raised waist circumference, diabetes, and hypertension, increased the risk of cataract extraction by 68% compared to those without any of these components.15 In addition, metabolic syndrome increased the risk of cataract extraction by approximately three-fold among women aged less than 65 years. Galeone et al. found that metabolic syndrome was associated with a two-fold increased risk of cataract extraction in a clinic-based study in Italy.14 Further, a significant linear trend in risk was also reported with an increasing number of metabolic syndrome components.
Also frequently seen with metabolic syndrome are tendencies for excessive blood clotting and inflammation. While obvious symptoms may be absent, these features are a warning of an increased likelihood of clogged arteries, heart disease, stroke, diabetes, kidney disease, and even premature death. If left untreated, complications from diseases associated with untreated metabolic syndrome can develop in as few as 15 years. Those who have metabolic syndrome and also smoke tend to have an even poorer prognosis.
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Admittedly, I started my journey on this path in 2009, with a deep dive into ketosis in the Spring of 2011, but it seemed so obscure! (For a timeline of what I did, I think I covered it somewhere in this talk…yes I’m too lazy to actually confirm this by skimming through it.) All told I spent approximately 3 years in the strictest state of nutritional ketosis (NK) with one very memorable deviation when I had 6 or 7 full-sized and upsettingly decadent desserts circa September 2013. I believe the diet helped me transition from metabolic syndrome to metabolic health and I certainly thought it could benefit other people. This nutritional state could gain some steam, I thought.
Losing weight is 80% diet. Volek and Phinney did a study where they put people on a High fat (65-80% of calories from fat, 50-75 grams protein and low carb) and had one group do no exercise, one do resistance training and one to resistance training and cardio. All 3 groups lost the same amount of weight on average. But the resistance training group lost almost entirely fat while preserving muscle mass, which is important. So I always advocate some resistance training. 🙂
I actually clicked on the story just to see if they included anything about it’s use in managing chronic migraine. I have chronic migraine, basically intractable. Nothing has helped. I’ve tried medications, meditations, and everything in between including a bunch of dietary changes. Keto is my next consideration. I’m happy to hear it helped you! Thanks for sharing
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.
© 2019 Maria Mind Body Health. Disclaimer: Some links in posts are affiliate links. If you click on a link and make a purchase, I may receive a commission but your price will not change. All products that I link to I use personally and contain no ingredients that we don't recommend for optimum health. The information contained on this site is not intended to diagnose, treat, cure, or prevent any medical condition and is not to be used as a substitute for the care and guidance of a physician.
I made this bread today and love it! The only problem I have is that the bread is very moist on the inside. The crust is perfect. I baked it at 350 for 70 mins and the bottom of the bread was a little moist as well as the inside. I measured all of my ingredients as your instructions say. Please help. This is the best bread I’ve made in the 2 years we have been eating wheat free.
I could go on for days about how a good diet can keep your blood sugar in control. To receive the most efficient information, set up a meeting with a dietician to look at your specific needs and you recent sugar readings. They can provide you with recipes and tools which make it easier for you to know exactly what you are putting into your body. 40 states in the United States require insurance companies to cover a meeting with a dietician for those with diabetes. Check with your insurance to see if this benefit is available for you.
It is known that different dietary components exert some effects on gut microbiome composition, mainly in relation to obesity and inflammatory states. In general, a Mediterranean diet has a positive effect while a high-protein diet seems to have detrimental effects due to putrefaction phenomena (Lopez-Legarrea et al., 2014; Flint et al., 2015). Few data are available at this time about the effects of KD on gut microbiota. For example, a study by Crawford et al. (2009) investigated the regulation of myocardial ketone body metabolism by the gut microbiota and demonstrated that, during fasting, the presence of gut microbiota improved the supply of ketone bodies to the heart where KBs were oxidized. In the absence of a microbiota, low levels of KB was associated with a related increase in glucose utilization, but heart weight was still significantly reduced. The myocardial-mass reduction was completely reversed in germ-free mice feeded with a ketogenic diet. Regarding food control we can hypothesize that the particular metabolic state of ketosis could provide some benefit to weight and food control via synergic actions between butyrate production by gut bacteria and circulating high blood ketones (Sanz et al., 2015).
317. Jornayvaz F. R., Jurczak M. J., Lee H. Y., et al. A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain. American Journal of Physiology-Endocrinology and Metabolism. 2010;299(5):E808–E815. doi: 10.1152/ajpendo.00361.2010. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Even without the gluten of a traditional tortilla, this keto bread recipe creates a soft and pliable alternative perfect for all your favorite taco fillings. Almond and coconut flours keep carbs to a minimum, while xanthan gum holds everything together. Each tortilla tallies up to 2 net carbs, and takes only five minutes to cook. No Bulletproof substitutions needed — just avoid eating xanthan gum too often.
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 . 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 .
This bread does have quite a few ingredients, but you’ll find that most are staple paleo and keto pantry ingredients. In the list below you’ll find details on several ingredients and possible subs. But if possible, please do try and make this recipe without any subs. As out of the 18 permutations we tried, this one really was terrific and the absolute best.
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.
^ Jump up to: a b Cardona A, Pagani L, Antao T, Lawson DJ, Eichstaedt CA, Yngvadottir B, Shwe MT, Wee J, Romero IG, Raj S, Metspalu M, Villems R, Willerslev E, Tyler-Smith C, Malyarchuk BA, Derenko MV, Kivisild T (2014). "Genome-wide analysis of cold adaptation in indigenous Siberian populations". PLOS One. 9 (5): e98076. Bibcode:2014PLoSO...998076C. doi:10.1371/journal.pone.0098076. PMC 4029955. PMID 24847810.
In skeletal muscle, oxidative capacity and mitochondrial content are related to fiber type. Compared to type II fibers, type I fibers have larger mitochondria  with greater oxidative enzyme content . While fiber type is plastic, particularly in response to endurance exercise, transformation from oxidative, slow-twitch fibers (type I) to glycolytic, fast-twitch fibers (type II) is unlikely to occur [372, 373]. Type II fibers, however, can shift in humans from highly glycolytic (type IIx) to more oxidative (type IIa) . Compared to type IIx fibers, type IIa fibers have greater citrate synthase activity, indicating greater mitochondrial content . The relevance of oxidative capacity and fiber type to oxidative stress has been demonstrated by greater mitochondrial respiration with less H2O2 production in permeabilized fibers from rat muscle consisting primarily of type I or IIa fibers versus type IIb fibers . Although muscle fiber-type transformation has been well characterized in response to exercise, this appears to not be the case for ketogenic diets. However, in rats, β-hydroxyacyl-CoA dehydrogenase (β-HAD) has been shown to increase most prominently in glycolytic, type IIb fibers following 4 weeks of a ketogenic diet (% energy: 70 fat, 6 carbohydrate, and 24 protein) , suggesting transition of these fibers towards type IIa fibers and, in turn, indicating potential for nutritional ketosis to promote a more oxidative muscle fiber composition.
I love how simple this recipe is and how quickly they bake! My oven is broken and only goes to 350, so I had to adjust the bake time and think I slightly overbooked them as they were a bit dry. I followed some of the comments’ recommendations and used half egg whites and half whole eggs (I made 4) and did not find them eggy. They were light and fluffy, but a bit bland. I added rosemary to 2 and garlic powder, cheddar cheese and parsley to 2. I just eyeballed the additions and found them bland. Next time I will add more herbs/cheese. I did butter them and found they soaked up the butter – again maybe because they were dry? I will definitely make these again. Thanks again for a great quick and easy recipe!
Blood tests often report the level of total cholesterol (HDL + LDL) as well as the levels of each type independently. It is possible that the relative abundance (ratio) of HDL: LDL is more important to predict the occurrence of cardiovascular disease that the total cholesterol level109. Whilst the ketogenic diet can cause an increase in total cholesterol, the ratio of healthy HDL : less healthy LDL generally increases (i.e more HDL)110 whilst following a ketogenic diet. In contrast, whilst total cholesterol tends to be lower whilst following a low fat diet, the ratio of HDL:LDL tends to be lower (i.e more LDL)21.
^ Hochachka PW, Storey KB (February 1975). "Metabolic consequences of diving in animals and man". Science. 187 (4177): 613–21. Bibcode:1975Sci...187..613H. doi:10.1126/science.163485. PMID 163485. In the terminal stages of prolonged diving, however, even these organs must tolerate anoxia for surprisingly long times, and they typically store unusually large amounts of glycogen for this purpose.
I want to say thank you. I don’t always have time to bake, and this is a life saver, of sorts. My brother is diabetic, and his doctor recommended a low-carb diet; I’m diabetic also, and gluten intolerant. This bread has the most wonderful taste and texture, and is so quick and easy, I’ve already committed the recipe to memory. Even my SO, who is neither gluten free nor diabetic, likes the taste and texture. I did cut down the salt, because like some others, I found the 1/4 teaspoon to be too salty. Other than that, raves and kudos!! We are thrilled, and planning all the different ways we’re going to use this bread. Many thanks!!
As described throughout the previous sections, there are many instances of codependencies and feed-forward loops in bioenergetic and antioxidant signal transduction, which supports the well-known potential for metabolic stimuli, such as diet or exercise, to have a profound physiological influence. Given the central role of mitochondria in oxidative phosphorylation and ROS production, the overlap between bioenergetic and antioxidant signaling is not surprising and is possibly an outcome of evolution favoring efficiency. PGC-1α is at the center of this overlapping and complex network of codependencies. The likely role of PGC-1α as a coactivator of FOXO3a indicates a possible dependence of FOXO3a transcriptional activity on PGC-1α , indicating FOXO3a as a central mediator as well. Furthermore, FOXO3a induces transcription of PGC-1α [287, 322, 367], and formation and antioxidant transcriptional activity of the PGC-1α-FOXO3a complex are partly dependent on interaction with SIRT1 . In muscle, expression of many of the bioenergetic and antioxidant proteins previously discussed is dependent on PGC-1α . Upstream, activation of PGC-1α is dependent on AMPK  and SIRT1 [242, 269] and partly dependent on SIRT3 . Furthermore, activation of SIRT1 is dependent on AMPK , which may also be the case for SIRT3. AMPK and PGC-1α are therefore two key factors, with critical supporting roles of the sirtuins, in the signal transduction linking bioenergetics to antioxidant defense. Further supporting the relevance of this linkage to nutritional ketosis, expression of AMPK, SIRT1, FOXO3a, and NFE2L2 is required for extension of lifespan in C. elegans by exogenous BHB , and expression of AMPK, p38 MAPK, and NFE2L2 is required for the extension of lifespan, also in C. elegans, by mitohormesis induced through inhibition of glucose metabolism . The induction of AMPK [259, 260], SIRT3 [263, 329], p38 MAPK [310–313], PGC-1α [76, 77, 260, 282, 283], FOXO3a [324, 331, 333], and NFE2L2 [358–360] activity by oxidative stress also makes this signaling highly relevant to mitohormesis [263, 282, 360], especially given that activation of these proteins has been shown to decrease mitochondrial or cellular ROS [76, 263, 282, 289, 323, 332, 334, 356, 359, 367]. Furthermore, mitochondrial biogenesis  and the activities of AMPK [259, 260], SIRT3 , p38 MAPK [311, 312], PGC-1α [76, 77, 260, 283], FOXO3a , and NFE2L2  are increased by H2O2, more specifically associating this signaling with mitohormesis. Given that AMPK and sirtuins are upstream of the majority of this signaling and that AMPK and sirtuin activities are stimulated by both bioenergetic and oxidative stressors, these stressors are likely the primary signals through which nutritional ketosis may induce the mitochondrial and antioxidant adaptations characteristic of mitohormesis (Figure 2).
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.
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Concussion (a mild form of TBI), is defined as a short term impairment of brain function caused by impact. Symptoms include dizziness, confusion and headache. When the brain suffers a concussive impact this triggers an acute cascade of cellular events that can eventually cause chronic problems. Firstly, immediately after impact there are changes to the concentrations of ions and neurotransmitters in and outside of the neurones. For example, the cells release potassium and glutamate (excitatory neurotransmitter); this can cause neuronal damage instantly64. The disruption to the equilibrium of substances within the brain must be corrected, which requires the action of the ATP dependant ion pumps in the cell membranes. In order to produce enough ATP the brain has a transient period of high glucose metabolism (within 30 minutes of impact), which is followed by a period of glucose metabolic depression that can last anywhere from 5 days to several months, depending on severity65. In this time the brain is starved of energy when it is unable to metabolise glucose, which can cause long term damage. Severe or repeated impacts can lead to development of conditions such as chronic traumatic encephalopathy (CTE).
Clinical results suggest both direct and indirect actions of ketones via modifications of various hunger-related hormones concentrations. While it’s not completely clear how ketosis reduces appetite, studies have found that ketosis is effective at lowering food intake and regulating appetite by altering levels of the hunger hormones including cholecystokinin (CCK) and ghrelin. At the same, ketone bodies seem to affect the hypothalamus region in the brain, positively impact leptin signals, and avoid slowing down the metabolism like most other diets do. (5)
Therefore the combustion enthalpy (∆H) of each fuel is an important factor in the energy it can provide to the cell. When expressed as the energy per 2 carbons in the molecule, ketones (BHB) have a higher combustion enthalpy (∆H) than pyruvate, lactate and glucose (see table). This means that the amount of energy that could possibly be transferred to ATP is higher than for those other substrates:
I don’t usually cook making things from scratch. Glad I did this to replace high carb bread! Made my first bread plain this am in microwave using all the ingredients with 1 sub – olive oil no butter. Worked Great! Toasted it and had it with sliced egg, bacon and mayo instead of butter. Nice and firm and the taste, Fabulous! Very satisfying. Thanks for sharing this and making it so easy for us guys that don’t cook from scratch. Appreciate it much 🙂
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).