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Would highly recommend listening to Tim Noakes and his trail in Cape Town – he was pretty much the trigger for me to switch to LCHF and now I am starting to educate myself on what I need to follow a path that works for me. The information on Verta is giving me more information to enable me to ask my Dr for what I want – I know this will be an uphill battle and this information will help me avoid getting railroaded into the so called norms. It also give the Dr a way out because then I am asking him to help me go down a certain path that he is not responsible for recommending if it bucks the system.
Fasting: As with caloric restriction, any benefits of fasting are likely to stem from the lowering of glucose, and insulin plus the elevation of ketone bodies. However, fasting may not be a good fit for patients who are already subject to a huge physiologic stress, particularly when being treated with chemotherapy or radiotherapy. Patients are frequently immunocompromised and may also experience muscle wastage (cachexia). However, fasting may sensitise cells to the effects of chemotherapy95, so a short fast prior to a treatment cycle could potentiate the drug’s efficacy. 
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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. 


I can’t find an 8×4 pan in the local stores, so while I wait for one to be shipped I went ahead and made these into hamburger bun shape. I don’t have a kitchen scale so I just measured everything super precise and got great results. I only have NOW brand psyllium husk powder so yes, they are an odd shade of purple but they taste great so I don’t care. What I really wanted was a vessel for butter and it made for a great snack before bed- which I know I’m not supposed to have but I was too curious to wait until morning! 🙂 Thanks for the update on this recipe, it made all the difference!
Triglycerides are a common form of fat that we digest. Triglycerides are the main ingredient in animal fats and vegetable oils. Elevated levels of triglycerides are a risk factor for heart disease, heart attack, stroke, fatty liver disease, and pancreatitis. Elevated levels of triglycerides are also associated with diseases like diabetes, kidney disease, and medications (for example, diuretics, birth control pills, and beta blockers). Dietary changes, and medication if necessary can help lower triglyceride blood levels.

The fact that the diagnostic criteria for metabolic syndrome vary between ethnic populations is testimony to significant nuances in the manifestation of metabolic syndrome in these groups. The original metabolic syndrome criteria were derived in mostly Caucasian populations, and some have argued for modification of individual criteria for specific ethnic subgroups, as has been done with waist circumference for patients of Asian origin. [39]
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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.


Lower fasting blood glucose: Fasting blood glucose gives a good snapshot of insulin sensitivity. In a healthy person, fasting blood glucose is , in pre-diabetes , and in diabetics this can exceed . A clinical study comparing a low calorie ketogenic diet to a low calorie diet showed that following the ketogenic diet resulted in lower blood glucose and lipid levels even if subjects were maintained at a constant weight 102 ,103.
Hi Howard, You’re right that this bread doesn’t rise much – the volume comes mostly from whipping the egg whites. If the whites fell too much, the bread might not be tall enough. But even if they didn’t, it might still be shorter than some other tall bread loaves. Feel free to multiply the recipe by 1.5 if you prefer a taller loaf. I’m glad you liked the flavor and texture!
Clinical trials of various ketogenic agents have shown promising outcomes in AD. Recently, a case report was published describing a dramatic improvement in cognitive function in a patient consuming daily drinks of a ketone ester of beta-hydroxybutyrate-butanediol54. This corroborates evidence from animal studies of AD, which showed behavioural and anatomical improvements in AD mice treated with the same ketone ester55. Also, medical foods containing medium chain triglycerides can give an acute improvement in cognitive scores in AD patients 56 ,57. The effectiveness of this treatment was found to depend on the absence of a gene variant that has been associated to increased chance of AD, called APOE4. Finally, following a ketogenic diet for 6 weeks improved the symptoms of mild cognitive impairment58. It is still early days, but the use of ketogenic diets and exogenous ketones may help to improve the quality of life of patients with dementia and their caregivers.             
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).
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 [36]. 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 [97]. 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 [97]. 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 [98]. 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) [99].
In the absence of acetyl CoA (several ways this can happen, including substrate shortage, as I’m describing here) we evolved a cool trick.  Our liver can make – out of fat or protein, though we much prefer to use fat so we can spare our protein and prevent severe muscle wasting – something called beta-hydroxybutyrate, one of the 3 ketone bodies I described above.
Maria – I’ve tried making this loaf twice and each time it’s still gummy! I use the same Nuts.com almond flour and Jay Robb psyllium husk powder, and weigh everything. The first time, I baked 60m and let cool completely. The loaf shrunk down and was gummy all in the center, like it was undercooked. This time, I baked 115m (after slicing at 75m and finding it gummy), and it shrunk down immediately after removing from the oven and is still gummy! Any advice? I want large, fluffy, non-gummy slices like you!
Usually, there are no immediate physical symptoms. Medical problems associated with the metabolic syndrome develop over time. If you are unsure if you have metabolic syndrome, see your healthcare provider. He or she will be able to make the diagnosis by obtaining the necessary tests, including blood pressure, lipid profile (triglycerides and HDL), and blood glucose.
I still have trouble finding it palatable with savory sandwitches, though. I wanted to try the receipe with gluten free oat flour or using other more neutral flours or starches that don’t contain that much PUFA’s and are more heat stable (vs. almond), since I do OK with carbs on training days. The amount of flour will still be quit low in this receipe.
After being in ketosis for a while, you may notice being able to tolerate a bit more carbs. If you so desire, gradually increase them and check for changes in your ketone levels and how you feel, look and perform (as Robb Wolf fond of saying). You could start by eating dairy products again. But beware if you’re highly insulin resistant, milk and yogurt can have enough carbs to kick you out of ketosis.
When your carb intake is that low, your body can't burn glucose (a.k.a the sugar from carbs) for energy like it normally would. So instead, it burns fat for energy, a process that then releases ketones as a byproduct, says Eric Klett, M.D. an endocrinologist and associate professor of medicine and nutrition at the University of North Carolina at Chapel Hill. (This process explains why people on the keto diet see such crazy weight-loss results.)
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The clinical relevance of nutritional ketosis to mitochondrial function is further indicated by promotion of ketogenic diets for treatment of mitochondrial disorders [19, 20, 26, 30, 247, 403]. The most prominent example is the study of mitochondrial adaptations as a mechanism for the well-known antiseizure effect of ketogenic diets [19, 29, 33, 162, 247, 403–405]. As previously discussed, the dramatic shift in energy metabolism and subsequent increase in circulating ketones induced by a ketogenic diet can enhance mitochondrial function and endogenous antioxidant defense. The primary mechanism behind these adaptations appears to be the increased demand for fat oxidation resulting from carbohydrate restriction. However, ketones themselves have important metabolic and signaling effects that enhance mitochondrial function and endogenous antioxidant defense, implying that a well-formulated ketogenic diet should have greater benefit than a nonketogenic low-carbohydrate diet. Regardless of the mechanism(s), the potential outcomes imply protection against chronic disease through improved mitochondrial function and, in turn, decreased potential for oxidative stress and subsequent pathology. However, further research is needed to better understand how nutritional ketosis influences mitochondrial function across different tissues and how these influences relate to human disease. Future research should also focus on further differentiation of the effects of carbohydrate restriction from the direct effects of ketones.
A sustainable exercise program, for example 30 minutes five days a week is reasonable to start, providing there is no medical contraindication. (If you have any special concerns in this regard, check with your doctor first.) There is a beneficial effect of exercise on blood pressure, cholesterol levels, and insulin sensitivity, regardless of whether weight loss is achieved or not. Thus, exercise in itself is a helpful tool in treating metabolic syndrome.
Schele E., Grahnemo L., Anesten F., Hallen A., Backhed F., Jansson J. O. (2013). The gut microbiota reduces leptin sensitivity and the expression of the obesity-suppressing neuropeptides proglucagon (Gcg) and brain-derived neurotrophic factor (Bdnf) in the central nervous system. Endocrinology 154, 3643–3651. 10.1210/en.2012-2151 [PubMed] [CrossRef] [Google Scholar]
Metabolic syndrome (also known as metabolic syndrome X) is a grouping of cardiac risk factors that result from insulin resistance (when the body's tissues do not respond normally to insulin). A person with metabolic syndrome has a greatly increased risk of developing type 2 diabetes, cardiovascular disease and premature death. In fact, another name for metabolic syndrome is pre-diabetes.
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 [9]. Much of this is based on signal transduction, antioxidant defense, and oxidative capacity, all of which will be discussed in proceeding sections.
Another aspect of mitochondrial function influenced by ketones is the mitochondrial permeability transition pore (mPTP). Prolonged opening of the mPTP is one of the mechanisms through which mtROS can induce cellular injury and promote disease [114]. In neurons isolated from rat brain slices, treatment with BHB + ACA has decreased the mtROS production, mPTP opening, and cell death induced by H2O2 [115]. This protective effect was duplicated with catalase, even in conjunction with diamide-induced opening of the mPTP, indicating that the protective effect of BHB and ACA is at least partly due to defense against ROS [115]. In a mouse model of epilepsy, this decrease in mPTP opening was found to be induced exclusively by BHB, and in a manner dependent on the cyclophilin D subunit of the mPTP [116]. BHB in combination with ACA also appears to promote opening of mitochondrial ATP-sensitive K+ (mtKATP) channels [117], which in heart mitochondria is known to protect against Ca+ overload [118] and dissipate membrane potential (ΔΨ) [119]. Since high ΔΨ promotes mtROS production, dissipation of ΔΨ through mtKATP channels may partly explain the potential for ketones to decrease mtROS production. However, opening of mtKATP channels by pinacidil decreases mitochondrial ATP production [119], which is consistent with dissipation of ΔΨ and suggests a compromise between ATP and mtROS production.
On a keto diet, carbs provide only about 5 percent of daily calories, compared to anywhere between 40–60 percent on a “standard diet.” Reducing carbohydrate consumption this drastically means that the majority of empty calories from highly processed foods must be eliminated from your diet, including things like white bread and rolls, pasta, rice or other grains, sugar-sweetened beverages, desserts, etc. These are the same foods that tend to cause fluctuating blood sugar levels, cravings for more carbs and sugar, low energy and contribute to overeating in general.

Hi Al, I’m glad you liked the taste and am honored you chose my site for your first ever comment! 🙂 I haven’t tried this recipe in a bread machine. Most likely the biggest issue with your bread being flat is that you didn’t fold the egg whites in – breaking them down would definitely make the bread flat. I haven’t tried adding yolks as most people want their bread less egg-y, not more. I’d have some concerns about the bread being too “wet” by adding them though, even if you like an eggy taste. A better option might be to brush the top with yolks for color.
LOVE this bread. As a pregnant type 1 diabetic, I was looking for something to toast. I’ve tried multiple different recipes from other sites, and the bread is always so crumbly that you can never spread anything on it. This one is AMAZING! I may have to experiment with more water so that it comes out less dense, but soooo happy to prevent blood sugar spikes with future sandwiches. I can even foresee being able to have traditional burgers again (not just wrapped in lettuce). My husband bakes his own “normal” bread, and now I get bread too and its even easier to make than his 🙂
Kumar, R., Chhatwal, S., Arora, S., Sharma, S., Singh, J., Singh, N., … Khurana, A. (2013, January 19). Antihyperglycemic, antihyperlipidemic, anti-inflammatory and adenosine deaminase–lowering effects of garlic in patients with type 2 diabetes mellitus with obesity. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, 6, 49–56. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3554227/

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Brain glucose and KB uptake was investigated in rats subjected to mild experimental ketonemia induced by 2 weeks on the KD or by 48 h fasting. To test this, researchers developed a carbon-11 labeled AcAc (11)C-AcAc for PET use. They found in rats that after 10 days of KD (11)C-AcAc brain uptake increased up to 8-fold, an increase comparable to those measured after 48 h of fasting (Pifferi et al., 2008).

I’m discouraged to see that nowhere in the article nor in the comments is there a mention of a diet’s best fit to genetics. Consider if someone is an APOE E2 carrier and/or has certain polymorphisms of the APO5 gene. These are quite rare in Okinawa but much more prevalent in the USA (12% of the population). According to a number of well-designed studies, these genetic characteristics point to a higher fat, lower carbohydrate diet as beneficial and even a “moderate” carb diet as problematic.
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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
A combination of baking soda, lemon juice, and baking powder eliminates the need for yeast in this bubbly keto bread recipe. With tons of Italian seasonings, olive oil, and flaky salt sprinkled on top, you’ll want to include this loaf with every meal. Each generous slice is 3 net carbs — and to stay more Bulletproof, simply avoid eating garlic and xanthan gum too often.
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