PGC-1α coactivates all three known PPAR isoforms (PPARα, PPARδ, and PPARγ) . Although each isoform is expressed in a variety of tissues, PPARα is prominently expressed in the liver, PPARδ in skeletal muscle, the heart, and the pancreas, and PPARγ in adipose [286, 296]. PGC-1α was discovered and named based on its promotion of brown adipose differentiation through coactivation of PPARγ and subsequent induction of mitochondrial biogenesis and UCP1 expression . However, it is the PGC-1α coactivation of PPARα that is responsible for the upregulated transcription of many of the enzymes responsible for increased ketogenesis and fatty acid metabolism in response to a ketogenic diet . Consistent with the role of PGC-1α in inducing mitochondrial biogenesis, it also shifts skeletal muscle fiber composition towards type I [298, 299] and type IIa , which are more oxidative. AMPK also contributes to fiber type changes and is required for the transition of highly glycolytic, type IIb fibers to more oxidative, type IIa fibers . Although PGC-1α is primarily known for inducing transcription of nuclear DNA, it may also, in conjunction with SIRT1, induce expression of mtDNA .
The ketogenic diet: The ketogenic diet could affect cancer by a similar mechanism to calorie restriction and fasting. Of the 29 animal studies that have examined ketogenic diet and cancer, 72% of them have demonstrated an anti tumor effect. There have been a small number of case studies of the safety and efficacy of the ketogenic diet in humans. The results have been largely positive, for example following a ketogenic diet helped to stabilise tumour growth and alter tumor metabolism96 ,97 ,98. There is an absence of fully randomised clinical trials in humans, but 24 case studies have been published; one recent appraisal of the case study data said that “ a probabilistic argument shows that the available data strengthen the belief in the anti-tumor effect hypothesis (of the ketogenic diet) at least for some individuals"99.
PGC-1α is also influenced by p38 MAPK, which is well known for being involved in development  and adaptation  in skeletal muscle. PGC-1α is activated by p38 MAPK [283, 303] through phosphorylation , which prevents repression  by blocking interaction with the p160 myb binding protein . In addition, expression of PGC-1α is increased by p38 MAPK [305, 306], and the overlap in bioenergetic and antioxidant signaling is further indicated based on p38 MAPK activation by AMPK [307–309], oxidative stress [310–314], and β-adrenergic signaling [280, 315, 316].
Hello, may I ask if someone has some experience week fasting for 14 days? I was told that the food which should be started taken after 14 days of fasting has to be in very simple and in slow amount. Unfortunately 1-2 days after fasting I am allowed to take only bouillon out of buckwheat, barley, from the 3rd day buckwheat mush, and only from 5th day milk or sour cream, oil since 11th day. Can anyone advice how should I adopt this come back food path to Ketogenic diet? Thank you in advance, Maria
Under conditions of abundant glucose (and sufficient insulin sensitivity) the brain is primarily converting glucose to pyruvate (left side of figure). Pyruvate is then shuttled into the mitochondria and converted into acetyl CoA with the help of a very important enzyme called pyruvate dehydrogenase (PDH). I’m going to come back to this enzyme, in part II of this series, because this is where the story gets very interesting. Acetyl CoA (which is also a direct byproduct of fatty acid breakdown) is then combined with oxaloacetate and so begins the Krebs Cycle, which generates all the reducing agents to feed the ETC and generate massive amounts of ATP.
I was a Corpsman (not a corpse-man as some recent somewhat fanatical president would say), and I can tell you many stories of Marines and Sailors who maintained restrictive diets (aka picky eaters). Most obvious was lack of sustaining energy (hypoglycemia) at mile 15 (with 80lbs of gear including a 6.5lb rifle and 200 rnds of ammo, etc.) and depletion of essential vitamins, electrolyte imbalance. They were always the first to collapse and have to hear me scold “see I told you so.” An IV of D5W usually does the trick (D is for dextrose, OMG!)
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
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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  and SIRT1 . In a variety of organisms, tissues, and cell types, FOXO3a increases mitochondrial biogenesis and expression of TFAM , 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) , thioredoxins [287, 323], Prx3 [287, 334], Prx5 , and metallothioneins I and II , 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 , 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 . FOXO3a also induces expression of LKB1  and NAMPT , indicating a feed-forward cycle of activation with AMPK and sirtuins. Like PGC-1α, FOXO3a transcriptional activity is inhibited by insulin through PKB .
The goal of the ketogenic diet is to keep you in this fat-burning metabolic state of ketosis. This is achieved by following a very low-carbohydrate, high-fat diet that includes only moderate amounts of protein. Foods like bread, cereal, processed snacks and sugary drinks are therefore off the table, while fattier foods like butter, grass-fed beef, fish and also non-starchy veggies take center stage, providing the majority of daily calories (as much as 70–80 percent).
Once inside the mitochondrion, the dominant way that the bound fatty acids are used as fuel in cells is through β-oxidation, which cleaves two carbons off of the acyl-CoA molecule in every cycle to form acetyl-CoA. Acetyl-CoA enters the citric acid cycle, where it undergoes an aldol condensation with oxaloacetate to form citric acid; citric acid then enters the tricarboxylic acid cycle (TCA), which harvests a very high energy yield per carbon in the original fatty acid.
Ketosis is deliberately induced by use of a ketogenic diet as a medical intervention in cases of intractable epilepsy. Other uses of low-carbohydrate diets remain controversial. Carbohydrate deprivation to the point of ketosis has been argued to have both negative and positive effects on health. Ketosis can also be induced following periods of fasting (starvation), and after consumption of ketogenic fats (such as medium chain triglycerides) or exogenous ketones.
I tried this recipe today and I’m blown away. I haven’t started Keto yet but I am soon. I’ve been trying recipes out, and I truly didn’t expect this to come out right the first time because I’ve never whipped egg whites or folded them into anything. I’m a terrible baker. It was so easy! Even my toddler and husband loves this! I didn’t use the sweetener and love the way it tastes!
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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.
Considering the high rates of obesity now facing most developed nations — along with an increased risk for health conditions like diabetes or heart problems as a result — researchers have been anxiously working on how to suppress appetite and achieve weight loss in a healthy, sustainable manner. The keto diet has emerged over the past several decades as one potential answer to this large-scale weight loss problem. (1)
So, if I’m deprived of a dietary source of glucose, I depend solely on my liver to release glycogen (a process known as hepatic glucose output, or HGO). How long can HGO supply my brain with sufficient glucose? It depends on a few things that impact both the “source” and the “sink” of glucose. Other competing sinks for glucose (e.g., activity level, thermogenic needs) and sources (e.g., glycerol and gluconeogenic amino acid availability) can make a difference for a while. But, in a state of starvation we’ve only got about one to three days before we’re in trouble. If our brain doesn’t get a hold of something else, besides glucose, we will die quite unceremoniously.
If you need to lose weight, find an eating plan you can stick with. “Whatever results in lasting weight loss for you is the best approach for you,” Wright says. “If you make over-restrictive changes you can't maintain, as soon as you tire of that diet, you will fall back to what you did previously, gain weight, and raise your risk of type 2 diabetes.”
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Hi John, You could possible try a hand mixer in a bowl instead of the food processor, but I haven’t tried it, so can’t vouch for the results. Most likely the bread would not be as tall because the mixer would completely deflate the first half of the egg whites when you add them to the batter. The second half should be folded so that part will be find. If you try with a bowl and hand mixer, let me know how that goes.
The coordinated effects of AMPK, SIRT1, and SIRT3 are primarily mediated through PGC-1α, which is activated through phosphorylation by AMPK [242, 265] and deacetylation by SIRT1 [77, 242, 266–269]. SIRT3 also increases PGC-1α activity , possibly through cAMP response element binding protein (CREB) [271, 272], but the exact mechanism has not been elucidated. In addition to phosphorylating PGC-1α, activated AMPK also increases PGC-1α expression [260, 273–276]. Activation of β2-adrenergic receptors [277–280] and the adiponectin AdipoR1 receptor  also increase PGC-1α expression, independently of AMPK activation [278, 281]. PGC-1α activity is increased by oxidative stress [76, 77, 282–284], possibly through activation of AMPK [259, 260] or p38 mitogen-activated protein kinase (MAPK) [283, 284], or inhibition of glycogen synthase kinase 3β, which inhibits PGC-1α through phosphorylation [77, 283]. In contrast, insulin decreases PGC-1α activity through phosphorylation by PKB . Once activated, PGC-1α interacts with the PPAR family of nuclear receptors  and the FOXO family of transcription factors  to influence expression of a variety of bioenergetic and antioxidant proteins. PGC-1α most notably increases transcription of proteins involved in mitochondrial biogenesis and respiration [76, 242, 265, 267, 269, 274, 279, 282, 285, 288–293] but also increases transcription of antioxidant proteins including SOD1 , SOD2 [76, 282, 289, 292–294], catalase , GPx [76, 294], thioredoxins [282, 283, 292], TRXR [282, 292], Prx3 [282, 292], and Prx5 [282, 292], as well as the mitochondrial uncoupling proteins UCP2 [76, 265, 282, 288, 294], UCP3 [76, 265, 294], and ANT [76, 295].
Toasting it did no good as it had that “plastic” smell that Mizzsingbabe mentioned. I tried cutting a very thin piece, loading it with butter, garlic powder, salt and grilling in cast iron fry pan, then broiling it but still cannot get past the plastic/smell taste. So I wasted 3 cups of (not cheap) almond flour along with all the other ingredients.
Although mitohormesis has not been studied comprehensively in higher-level organisms, its occurrence is supported by compelling evidence in lower-level organisms. For example, inhibition of glycolysis in C. elegans increased fat oxidation (based on nematode triglyceride content) and mitochondrial O2 consumption, which was followed by increases in ROS production at day 2 and catalase activity at day 6 . The increase in catalase activity occurred in conjunction with increases in lifespan and resistance to the mitochondrial stressors sodium azide and paraquat. However, antioxidant treatment (N-acetylcysteine) decreased the elevation of ROS at day 2 and eliminated the resistance to sodium azide and paraquat treatments, indicating a requirement of ROS as a stimulus .
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Impaired mitochondrial function often results in excessive production of reactive oxygen species (ROS) and is involved in the etiology of many chronic diseases, including cardiovascular disease, diabetes, neurodegenerative disorders, and cancer. Moderate levels of mitochondrial ROS, however, can protect against chronic disease by inducing upregulation of mitochondrial capacity and endogenous antioxidant defense. This phenomenon, referred to as mitohormesis, is induced through increased reliance on mitochondrial respiration, which can occur through diet or exercise. Nutritional ketosis is a safe and physiological metabolic state induced through a ketogenic diet low in carbohydrate and moderate in protein. Such a diet increases reliance on mitochondrial respiration and may, therefore, induce mitohormesis. Furthermore, the ketone β-hydroxybutyrate (BHB), which is elevated during nutritional ketosis to levels no greater than those resulting from fasting, acts as a signaling molecule in addition to its traditionally known role as an energy substrate. BHB signaling induces adaptations similar to mitohormesis, thereby expanding the potential benefit of nutritional ketosis beyond carbohydrate restriction. This review describes the evidence supporting enhancement of mitochondrial function and endogenous antioxidant defense in response to nutritional ketosis, as well as the potential mechanisms leading to these adaptations.
Whether ketosis is taking place can be checked by using special urine test strips. The strips have a small pad on the end, which the user dips in a fresh urine specimen. Within seconds, the strip changes color to indicate the level of acetoacetate ketone bodies, which reflects the degree of ketonuria, which, in turn, gives a rough estimate of the level of hyperketonemia in the body (see table below). Alternatively, some products targeted to diabetics such as the Abbott Precision Xtra or the Nova Max can be used to take a blood sample and measure the β-hydroxybutyrate ketone levels directly. Normal serum reference ranges for ketone bodies are 0.5–3.0 mg/dL, equivalent to 0.05–0.29 mmol/L.
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I made the bread on Sunday and we loved it. When I made up the dough, I started out with less water because it’s really humid here and it was a wet, drizzly day. I had to use a different psyllium husk because I can’t get Jay Robb here (I’ll have to order some). It was Walmart’s equate brand (I was desperate to try the recipe right away), so my bread was purple, but nobody minded. I had to grind almonds myself and ended up adding an extra tablespoon of psyllium to get my dough to the same texture as Maria’s in the video, but it baked up perfectly. It was delicious, but I did notice an odd smell. Is that the psyllium, maybe? I’m on a strict diet to get my blood sugar back down to normal, so this bread is such a treat. Thanks so much for sharing this with us.
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.
In type 2 diabetes the body has an increasingly harder time to handle all the sugar in the blood. Large amounts of the blood sugar-lowering hormone insulin are produced, but it’s still not enough, as insulin sensitivity decreases. At the time of being diagnosed with type 2 diabetes, people usually have ten times more insulin in their bodies than normal. As a side effect, this insulin stores fat and causes weight gain, something that has often been in progress for many years before the disease was diagnosed.
People suffering from diabetes and taking insulin or oral hypoglycemic agents suffer severe hypoglycemia if the medications are not appropriately adjusted before initiating this diet. The ketogenic diet is contraindicated in patients with pancreatitis, liver failure, disorders of fat metabolism, primary carnitine deficiency, carnitine palmitoyltransferase deficiency, carnitine translocase deficiency, porphyrias, or pyruvate kinase deficiency. People on a ketogenic diet rarely can have a false positive breath alcohol test. Due to ketonemia, acetone in the body can sometimes be reduced to isopropanol by hepatic alcohol dehydrogenase which can give a false positive alcohol breath test result.
Add yeast and maple syrup (to feed the yeast, see notes) to a large bowl. Heat up water to 105-110°F, and if you don't have a thermometer it should only feel lightly warm to touch. Pour water over yeast mixture, cover bowl with a kitchen towel and allow to rest for 7 minutes. The mixture should be bubbly, if it isn't start again (too cold water won't activate the yeast and too hot will kill it).
The beautiful part of good science is its self-correcting nature. The ugly part is this self-correcting nature often moves at a glacial pace—and it’s not linear. We often view history century-by-century and see what amounts to continual progress in medicine. But we live our lives—and consume information—day-by-day, exposed to the peaks and valleys of medical wisdom.
Fanatic? Someone with T2D, a disease usually claimed to be progressive and a never ending stream of problems and medications, was REVERSED. That’s something to shout from the rooftops. The drop in medication use alone, but the big pharma companies would prefer that people’s stories of reversing (well, putting it into remission) T2D get called fanatical instead of insightful.
How can ketosis help reduce your risk various health concerns? It comes down to the benefits of stabilizing your blood sugar and decreasing glucose intake and usage. As glucose enters your blood, your pancreas sends out insulin to pick up the sugar and carry it to your cells so they can use it as energy. However, when your cells have used or stored all the glucose that they can, what remains is converted into glycogen to be stored in the liver and muscles OR converted into triglycerides, the storage form of fat.
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So, now, I’ve got another loaf in the oven. I doubled the salt, ground up the Psyllium Husk in my Blend Tec (instead of the shoddy thing I used the first time) and reduced the baking soda to 3 tsp. I also (accidentally) ended up with 1 egg yolk in there. Hopefully, that won’t cause too much of an issue. I weighed all my ingredients and I’m hopeful that this batch will give me the results I am looking for. I would *love* a grilled cheese sandwich for a quick-fix dinner with my keto plan. 🙂 Thanks for the recipe. I’ll let you know how this batch turns out.
I waited awhile to try this, certain it would be blah but decided to give it a go. I did add a pinch of salt and I used Brummel and brown butter, made with yogurt, as it lowered the fat and calories. toasted and spread some sugar free strawberry preserves. really good! texture took a bit to get used to but so excited to be able to eat bread! not on keto but recently diagnosed as diabetic so bread is a nono bc of all the carbs.