Ketone esters (BHB-BD) could help to accelerate glycogen resynthesis32. After exercise that depletes muscle glycogen, the muscle uses carbohydrate from the diet to replenish these stores. An experiment was carried out where athletes undertook depletive exercise and then were given a ketone drink (or carbohydrate placebo) as well as glucose intravenously to maintain a high blood level (10mM). In this experiment, when the recovery drink contained ketone ester, more glucose was infused in order to maintain blood glucose at 10 mM, and muscle glycogen levels were 50% higher. However, the evidence is not conclusive: another study. 31 found that adding ketone ester to a protein and carbohydrate recovery drink did not enhance the normal rate of glycogen re-synthesis.  

Before we get started, here’s a short recap of the tips so far: The first and most crucial piece of advice was to choose a low-carb diet. The next were eating when hungry, eating real food, eating only when hungry, measuring progress wisely, being persistent, avoiding fruit, beer and artificial sweeteners, review your medications, stressing less and sleeping more, eating less dairy and nut products, stocking up on vitamins and minerals, using intermittent fasting and finally, exercising smart.
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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 [90]. 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 [90]. 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 [95].


Within the healthcare system people with type 2 diabetes are still often given advice on blood sugar-raising foods. It is not uncommon to receive nice, colored folders, like the Swedish one above. In this folder it’s stated that foods that raise blood sugar slowly are good for you. Examples of such foods are said to be fruit, rice, pasta, potatoes and bread!

In a subsequent series of experiments, glucose metabolism in C. elegans was inhibited by knockdown of the insulin receptor, insulin-like growth factor 1 (IGF-1) receptor, and insulin receptor substrate 1 (IRS-1) [73]. Consistent with the previous study [72], inhibition of glucose metabolism increased mitochondrial respiration concomitant with ROS-dependent increases in lifespan, stress resistance, and antioxidant enzyme activity. However, in this case, detection of ROS was mitochondria-specific, and repeated measures allowed for changes in antioxidant enzyme activities to be evaluated more closely in relation to the timing of changes in mtROS. Compared to controls, inhibition of glucose metabolism resulted in higher mitochondrial O2 consumption at 12 h, higher mtROS production at 24 h, and higher activities of SOD and catalase at 48 h, suggesting a dependence of antioxidant activity on mtROS and a dependence of mtROS on mitochondrial respiration. The most striking result is the lower mtROS at 120 h, indicating that the initial increase in mtROS and subsequent increase in antioxidant enzyme activity ultimately lowered net mtROS production to a level lower than controls, which is the proposed explanation for the more than twofold increase in lifespan. As with the previous study, this demonstration of mitohormesis is further supported by the changes in ROS production, antioxidant enzyme activity, and lifespan having been prevented with antioxidant treatment.
Keep in mind that the ketogenic diet takes into account net grams of carbohydrates, not simply total grams. Net carbohydrates are the amount of carbohydrates left over after you subtract grams of fiber from total grams of carbohydrates. For example, if vegetables you’re eating have 5 grams of carbohydrates total, but 3 grams come from fiber, the total number of net carbohydrates is only 2 grams, which is the number you add to your daily total.
The most common reason that any bread falls is that it needed to bake for longer. That being said, I’ll be perfectly honest – sometimes this keto bread recipe falls anyway, even despite doing everything else right. Fortunately this isn’t a huge deal because it still tastes delicious – IF you baked it for long enough and the center is cooked through.
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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:
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).
Basically, carbohydrates are the primary source of energy production in body tissues. When the body is deprived of carbohydrates due to reducing intake to less than 50g per day, insulin secretion is significantly reduced and the body enters a catabolic state. Glycogen stores deplete, forcing the body to go through certain metabolic changes. Two metabolic processes come into action when there is low carbohydrate availability in body tissues: gluconeogenesis and ketogenesis.[4][5]
In essence, it is a diet that causes the body to release ketones into the bloodstream. Most cells prefer to use blood sugar, which comes from carbohydrates, as the body’s main source of energy. In the absence of circulating blood sugar from food, we start breaking down stored fat into molecules called ketone bodies (the process is called ketosis). Once you reach ketosis, most cells will use ketone bodies to generate energy until we start eating carbohydrates again. The shift, from using circulating glucose to breaking down stored fat as a source of energy, usually happens over two to four days of eating fewer than 20 to 50 grams of carbohydrates per day. Keep in mind that this is a highly individualized process, and some people need a more restricted diet to start producing enough ketones.
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Hi Jen, It sounds like it needed to bake for longer – this is why it sunk and was still moist. The timing varies by ovens and even different pans. I hope you’ll try it again and just keep it in there for longer. You can cover the top if it starts to brown too much. For the one you made, depending on how moist it was in the middle, you may be able to salvage it somewhat by pan frying the slices.
Staphylococcus or staph is a group of bacteria that can cause a multitude of diseases. Staph infections can cause illness directly by infection or indirectly by the toxins they produce. Symptoms and signs of a staph infection include redness, swelling, pain, and drainage of pus. Minor skin infections are treated with an antibiotic ointment, while more serious infections are treated with intravenous antibiotics.
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All of the factors associated with metabolic syndrome are interrelated. Obesity and lack of exercise tend to lead to insulin resistance. Insulin resistance has a negative effect on lipid production, increasing VLDL (very low-density lipoprotein), LDL (low-density lipoprotein – the "bad" cholesterol), and triglyceride levels in the blood and decreasing HDL (high-density lipoprotein – the "good" cholesterol). This can lead to fatty plaque deposits in the arteries which, over time, can lead to cardiovascular disease and strokes. Insulin resistance also leads to increased insulin and glucose levels in the blood. Excess insulin increases sodium retention by the kidneys, which increases blood pressure and can lead to hypertension. Chronically elevated glucose levels in turn damage blood vessels and organs, such as the kidneys. 

A stack of pancakes might sound like the opposite of a keto-friendly breakfast, but where there's a will, there's a way. These ones from A Big Man's World are made with the perfect combination of almond flour, coconut flour, and eggs for a result so fluffy, you'll hardly be able to tell they're low in carbs. The blueberries add a touch of sweetness (but they contain sugar, so be careful about the portions).
Finally, exogenous ketones have been shown to decrease the levels of triglycerides and free fatty acids in the blood after one drink 107 ,106 ,11. There is also early data showing that ketone ester consumption decreases cholesterol biosynthesis in rodents, an effect which appeared to be conserved in humans114. It is unclear at this stage what the long term effects of exogenous ketone consumption on blood lipids and cholesterol would be, but this is an area of promising research. 
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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.
^ Greenberg CR, Dilling LA, Thompson GR, Seargeant LE, Haworth JC, Phillips S, Chan A, Vallance HD, Waters PJ, Sinclair G, Lillquist Y, Wanders RJ, Olpin SE (April 2009). "The paradox of the carnitine palmitoyltransferase type Ia P479L variant in Canadian Aboriginal populations". Molecular Genetics and Metabolism. 96 (4): 201–7. doi:10.1016/j.ymgme.2008.12.018. PMID 19217814.

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The FOXO family of transcription factors is highly conserved and promotes longevity and resistance to cellular stress. Although there are a variety of FOXO isoforms with varying tissue distribution [318–320], FOXO3a has been the most thoroughly studied in relation to energy sensing, mitochondrial function, and antioxidant defense. Similar to PGC-1α, FOXO3a is activated through phosphorylation by AMPK [321–323] and deacetylation by SIRT1 [324, 325] and SIRT3 [326–329], and its transcriptional activity is at least partly dependent on AMPK [322] and SIRT1 [325]. In a variety of organisms, tissues, and cell types, FOXO3a increases mitochondrial biogenesis and expression of TFAM [329], but is more known for increasing expression of antioxidant and repair proteins, including SOD2 [287, 330, 331], catalase [287, 330, 332, 333], glutathione S-transferase (GST) [322], thioredoxins [287, 323], Prx3 [287, 334], Prx5 [287], and metallothioneins I and II [322], as well as UCP2 [287, 322] and the DNA repair enzyme growth arrest and DNA damage-inducible 45 (GADD45) [322, 324, 335, 336]. FOXO3a is also activated by oxidative stress [324, 331, 333], possibly in a SIRT1-dependent manner [324], and likely mediated through c-Jun N-terminal protein kinase (JNK), which allows FOXOs to translocate to the nucleus by promoting dissociation of 14-3-3 [337, 338]. Furthermore, FOXO3a and SIRT3 interact in mitochondria to induce mitochondrial gene expression in an AMPK-dependent manner [339]. FOXO3a also induces expression of LKB1 [340] and NAMPT [341], indicating a feed-forward cycle of activation with AMPK and sirtuins. Like PGC-1α, FOXO3a transcriptional activity is inhibited by insulin through PKB [331].
Instead of a complicated keto bread recipe, this breakfast sandwich from Hey Keto Mama gets creative and simple by using spicy pork sausage patties in place of an English muffin or bagel. An egg plus a sriracha and cheese mixture are sandwiched in between, along with any veggies of choice (a slice of tomato and spinach would fit right in). To lighten it up, swap in turkey sausage patties and use just egg whites instead of the whole egg.
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 [287], 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 [325]. In muscle, expression of many of the bioenergetic and antioxidant proteins previously discussed is dependent on PGC-1α [265]. Upstream, activation of PGC-1α is dependent on AMPK [242] and SIRT1 [242, 269] and partly dependent on SIRT3 [270]. Furthermore, activation of SIRT1 is dependent on AMPK [242], 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 [95], 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 [73]. 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 [346] and the activities of AMPK [259, 260], SIRT3 [329], p38 MAPK [311, 312], PGC-1α [76, 77, 260, 283], FOXO3a [324], and NFE2L2 [368] 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).

Ketone esters (BHB-BD) lowers glycogen use30. During exercise, the muscle breaks down stored carbohydrate (glycogen) to provide a fuel for the working muscle. When a ketone ester drink was taken pre-workout, the muscle used far less glycogen compared to when the pre-workout drink contained carbohydrate. The high levels of blood ketones meant that the muscle used ketones as a fuel before needing to use glycogen. Reducing reliance on muscle glycogen could improve performance and decrease the time for muscle glycogen to fully recover between exercise bouts.
This keto bread recipe delivers sweet heat with no corn whatsoever — instead, it uses a blend of coconut flour and sweetener to capture the same taste and texture for about 3 net carbs per serving. Add fresh cranberries and jalapeño slices for a fun twist that pairs well with holiday meals. To keep this recipe more Bulletproof, use grass-fed butter, swap almond milk with full-fat canned coconut milk, and skip the peppers if you have a nightshade sensitivity.
Dr. Campos, it is unfortunate that you retain the medical community’s negative stance on the ketogenic diet, probably picked up in medical school when you studied ketoacidosis, in the midst of an obesity and type II diabetes epidemic that is growing every year, especially among populations who will never see the Harvard Health Letter. The medical community has failed in reversing this trend, especially among children, and the public is picking up the tab, in the form of higher health insurance premiums to treat chronic metabolic diseases which doctors cannot cure. The ketogenic diet does not bid its adherents to eat unhealthy processed meats, and the green leafy vegetables that it emphasizes are important in a number of nutritional deficiencies. People lose weight on the ketogenic diet, they lose their craving for sugar, they feel more satiety, they may become less depressed, their insulin receptors sensitivity is improved, and these are all the good outcomes you fail to mention. There is a growing body of research which demonstrates the neuroprotective effects of the ketogenic diet to slow cancer progression, as well as diseases like Parkinson’s and Alzheimer’s, for which there are no effective medical treatments. Please respect your patients by providing them with evidence-based medical outcomes, not opinions.

Nutrition: What is it and why is it important? Nutrition is the supply of materials that organisms and cells require to live. Humans need seven major types of nutrients to function. A nutritionist studies nutrients, how the body uses them, and the relationship between a person’s diet and their health. Here, learn more about nutrients and what a nutritionist does. Read now
Instead of a complicated keto bread recipe, this breakfast sandwich from Hey Keto Mama gets creative and simple by using spicy pork sausage patties in place of an English muffin or bagel. An egg plus a sriracha and cheese mixture are sandwiched in between, along with any veggies of choice (a slice of tomato and spinach would fit right in). To lighten it up, swap in turkey sausage patties and use just egg whites instead of the whole egg.
Consistent with the mechanisms described above, changes in AMPK in response to a ketogenic or low-carbohydrate diet have been reported in several studies. In rodents, a ketogenic diet (Bio-Serv F3666) has increased AMPK activity in skeletal muscle [150] and AMPK phosphorylation in the liver [230], and a low-carbohydrate diet (18.5% of energy) supplemented with ketone esters (6% w/v) increased AMPK content in brown adipose [149]. In humans, a nonketogenic low-carbohydrate diet (% energy: 50 fat, 30 carbohydrate, and 20 protein) has increased AMPK phosphorylation in skeletal muscle [231].
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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