In skeletal muscle, oxidative capacity and mitochondrial content are related to fiber type. Compared to type II fibers, type I fibers have larger mitochondria [370] with greater oxidative enzyme content [371]. 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) [373]. Compared to type IIx fibers, type IIa fibers have greater citrate synthase activity, indicating greater mitochondrial content [374]. 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 [375]. 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) [165], 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.
Most breakfast foods are very high in carbohydrates, which is exactly what you don’t want on a ketogenic diet. If you can do a mental shift as to what foods are classified as breakfast, you will spare yourself a lot of headaches. No matter what you’ve been told in the past, any food can be eaten for breakfast. A bowl of beanless chili made with ground beef, pulled pork, or baked salmon can all be “breakfast foods.”

So how does this work? A quick run-through: The first tip was to eat low carb. This is because a low-carb diet lowers your levels of the fat-storing hormone insulin, allowing your fat deposits to shrink and release their stored energy. This tends to cause you to want to consume less calories than you expend – without hunger – and lose weight. Several of the tips mentioned above are about fine-tuning your diet to better this effect.


Dr. Campos, it is so discouraging to see that you disparage the ketogenic diet based on your assumption that it is very heavy in poor quality processed meats. No diet that relies on processed foods can be viewed as “healthy”. Become better informed by getting up to speed with what Jeff Volek, RD, PhD, calls a “well-formulated ketogenic diet.” Also, learn more about the potential of the diet to slow cancer progression (my specialty). You owe it to your patients who are depending on you for advice. Present them with facts, not opinions.


The graph below, also from the Cahill and Veech paper, shows the blood chemistry of a person starving for 40 days.  Within about 3 days, a starving person’s level of glucose stops falling.  Within about 10 days they reach a steady-state equilibrium with B-OHB levels exceeding glucose levels and offsetting most of the brain’s need for glucose. In fact, the late George Cahill did an experiment many years ago (probably would never get IRB approval to do such an experiment today) to demonstrate how ketones can offset glucose in the brain. Subjects with very high levels of B-OHB (about 5-7 mM) were injected with insulin until glucose levels reached 1 mM (about 19 mg/dL)!  A normal person would fall into a coma at glucose levels below about 40 mg/dL and die by the time blood glucose reached 1 mM.  These subjects were completely asymptomatic and 100% neurologically functional.
Ketosis could benefit patients with PD, as ketones provide an alternative energy source to the brain and also have antiinflammatory effects. Several research groups have shown that the ketogenic diet can have manifold beneficial effects in animal models of PD: alleviating motor symptoms, reducing inflammation, decreasing neuronal loss 61 ,62. Also, an in vitro model of PD (neurons in culture treated with a drug called MPTP) was used to demonstrate that addition of 4 mM of BHB was protective against neurodegeneration52. An early study of the ketogenic diet in PD patients reported very promising results: patients improved their clinical PD ‘score,’ as classified by factors including tremor, balance and mood 63. Whilst there are promising results, further clinical studies are required to demonstrate if the ketogenic diet or exogenous ketones (either alone or in combination) are a tolerable and efficacious intervention for PD.            
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)
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Parkinson’s disease (PD) is caused by death of neurons in a region of the brain called the ‘substantia nigra.’ As well as loss of neurons, those that survive accumulate misfolded proteins called “Lewy Bodies,” exhibit increased inflammation and impaired mitochondrial function. PD is most common in individuals over the age of 60 and is primarily characterised by poor control of movement (shaking, rigidity etc). Neuronal death leads to decreased levels of a neurotransmitter called dopamine, which is a key factor in the deterioration of motor function. Current treatments for PD centre on replacing dopamine using a drug called L-DOPA, which is a precursor to dopamine. This drug treats the symptoms of PD but not the underlying cause. 


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.
It’s a habit to enjoy a brie cheese for desert instead of a piece of chocolate cake but each are favored deserts in France. I’m personally more satisfied after a 350 calorie sized wedge of brie than the same number of calories of cake.. which will give me sugar crash and .. really I’d like two slices of cake(I’ve got a sweet tooth that once I get going it wants to keep being fed)
I’m so glad you love it, Tanya! Yes, $17 sounds like a lot for xanthan gum. I use this one here. Swerve is sweeter than erythritol, so you’d need less of it – I have a conversion chart here. You’re absolutely right about the xanthan gum and texture – it will make the bread more chewy. It will still be more of a “light and fluffy” bread, but definitely less muffin-like with the xanthan gum. I haven’t tried add-ins yet – let me know how it goes if you try!
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.
314. Wadley G. D., Nicolas M. A., Hiam D. S., McConell G. K. Xanthine oxidase inhibition attenuates skeletal muscle signaling following acute exercise but does not impair mitochondrial adaptations to endurance training. American Journal of Physiology-Endocrinology and Metabolism. 2013;304(8):E853–E862. doi: 10.1152/ajpendo.00568.2012. [PubMed] [CrossRef] [Google Scholar]
If for any reason you get a fail…a spongy loaf , or one with a buble don’t throw it away. Cut off the top bubble and cut into squares or triangles then taost for great pita like chips…cube the bottom sprinkle on some spices and toast or rebake for croutons…I have had my successes and failures wih this loaf but the ingredients are too expensive to waste…another idea would be to toast the bottom after you slice the top off and then add butter, garlic and cheese for a good garlic bread.
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We’ve now arrived at tip number 16. If you’re still having trouble losing weight, despite following the 15 pieces of advice listed above, it might be a good idea to bring out the heavy artillery: optimal ketosis. Many people stalling at weight plateaus while on a low carb diet have found optimal ketosis helpful. It’s what can melt the fat off once again.
Metabolic syndrome promotes coronary heart disease through several mechanisms. It increases the thrombogenicity of circulating blood, in part by raising plasminogen activator type 1 and adipokine levels, and it causes endothelial dysfunction. [14] Metabolic syndrome may also increase cardiovascular risks by increasing arterial stiffness. [15] Additional mechanisms include oxidative stress, [16] which has been associated with numerous components of metabolic syndrome. [17]
The popular belief that high-fat diets cause obesity and several other diseases such as coronary heart disease, diabetes, and cancer has not been observed in recent epidemiological studies. Studies carried out in animals that were fed high-fat diets did not show a specific causal relationship between dietary fat and obesity. On the contrary, very-low-carbohydrate and high-fat diets such as the ketogenic diet have shown to beneficial to weight loss.
Add mozzarella and cream cheese to a large microwave-safe bowl. Cover the cream cheese with mozzarella (this will prevent the cream cheese from overheating and making a mess in your microwave). Melt in the microwave at 30 second intervals. After each 30 seconds, stir cheese until cheese is completely melted and uniform and resembles a dough in appearance (see photo for reference). This should only take around 1 minute total cooking time. Do not try to microwave the full time at once because some of the cheese will overcook. You can also melt the cheeses over the stove in a double boiler.
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.
I had the same effect but I used the same pan. The issue I had was the egg whites. I beat them with a mixer for 2 minutes with the cream of tartar and still couldn’t get them whipped. I’d say they were half whipped. I gave up and put them in the loan pan anyway. The bread looked the same and tasted great but it was somewhat spongy. I’m wondering if the egg whites really wouldn’t whip because I didn’t realize they had to be room temp. The bread is great but it won’t hold up for sandwiches. Any tips on egg whipping? I felt egg defeated today!
Metabolic syndrome is similarly prevalent in men (24%) and women (22%), after adjusting for age. [28] However, several considerations are unique to women with metabolic syndrome, including pregnancy, use of oral contraceptives, and polycystic ovarian syndrome. [43] Metabolic syndrome and polycystic ovarian syndrome share the common feature of insulin resistance; they therefore share treatment implications as well. [44] Cardiometabolic risk is thought to be elevated in both groups. [45]
Apart from administering insulin, the fastest way to lower your blood glucose is to engage in physical activity. Exercise results in an increased sensitivity to insulin. It causes your muscle cells to take up more glucose, leaving less of it to circulate in your bloodstream during and after the physical activity (which means a lower blood glucose when you test). Frequent, regular exercise is very important to good blood glucose control no matter what type of diabetes you have. Research has shown that it is vital in warding off long-term complications like neuropathy, retinopathy, and heart and kidney diseases. Don't forget to check with a doctor, though, before making any major changes to your exercise routine. And, if you have type 1 diabetes and your glucose is 250 mg/dl or higher, check for urine ketones. You should not exercise if ketones are present.
Drug treatment may be necessary to address other aspects of metabolic syndrome. Hypertension should be treated. Statins may be prescribed to treat unhealthy lipid levels. Some healthcare practitioners also recommend aspirin to decrease the risk of inappropriate blood clots. Some may prescribe medications to increase insulin sensitivity (although there is not widespread agreement on this).

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.

Gluconeogenesis is the endogenous production of glucose in the body, especially in the liver primarily from lactic acid, glycerol, and the amino acids alanine and glutamine. When glucose availability drops further, the endogenous production of glucose is not able to keep up with the needs of the body and ketogenesis begins in order to provide an alternate source of energy in the form of ketone bodies. Ketone bodies replace glucose as a primary source of energy. During ketogenesis due to low blood glucose feedback, stimulus for insulin secretion is also low, which sharply reduces the stimulus for fat and glucose storage. Other hormonal changes may contribute to the increased breakdown of fats that result in fatty acids. Fatty acids are metabolized to acetoacetate which is later converted to beta-hydroxybutyrate and acetone. These are the basic ketone bodies that accumulate in the body as a ketogenic diet is sustained. This metabolic state is referred to as "nutritional ketosis." As long as the body is deprived of carbohydrates, metabolism remains in the ketotic state. The nutritional ketosis state is considered quite safe, as ketone bodies are produced in small concentrations without any alterations in blood pH. It greatly differs from ketoacidosis, a life-threatening condition where ketone bodies are produced in extremely larger concentrations, altering blood ph to acidotic a state.


I am so frustrated. I have made the rolls a dozen times and they vary in results but always come out acceptable. I truly enjoy them. However, no matter what I do I cannot get the darn loaf to work! I am specific with ingredients, I have tried leaving the loaf in the oven to cool, I have tried taking it out. I make sure the water is at a rolling boil. I tried different sized pans…just doesn’t work. The only difference I can think of is the loaf pan. I am wondering if I were to just form the dough into a loaf without the restriction of a pan, would it come out better? It wouldn’t be as pretty but it might work.
Probiotics are an obvious supplement for digestive health, but they may play an important role in lowering blood sugar, too. One small study found that people who were following a heart-health DASH diet and also consumed probiotics experienced a decrease in fasting blood sugar and hemoglobin A1C levels (a marker for testing long-term blood sugar levels). Start by adding healthy, probiotic-rich foods to your diet such as kefir, plain yogurt, sauerkraut, kimchi, or even a little low-sugar kombucha. And, to help probiotic bacteria to thrive, eat plenty of prebiotic foods such as fiber-rich leafy greens and vegetables.
When you are choosing types of exercise, pick activities which are going to be enjoyable for you. When you perform activities that you enjoy, you have a better chance of sticking with them. You can occasionally change up the exercises that you do to prevent yourself from getting tired of following the same routine. Great examples of fun exercises are swimming, walking with a friend, or a dance class.
NRF-1 and NRF-2 are transcription factors that increase expression of TFAM [342], which is required for full initiation of mtDNA transcription [343–345] and hence mitochondrial biogenesis. PGC-1α induces expression of NRF-1 and NRF-2 and facilitates TFAM expression by coactivating NRF-1 [288]. Oxidative stress increases this signaling [346, 347] in conjunction with increased mitochondrial biogenesis [346]. AMPK also contributes to mitochondrial biogenesis, but by inducing mitochondrial fission through phosphorylation of mitochondrial fission factor (MFF) [348], which is in addition to and independent of AMPK's role in activating PGC-1α.
Try to be patient. Although some people get into ketosis relatively quickly, it can take others a while. Unfortunately, people who are insulin resistant often have a longer journey. Put in a solid month of consistent keto eating, and try to ramp up your physical activity, if possible. Within four weeks, you should definitely be in ketosis and experiencing its benefits.
One particular concern to be aware of is the risk for ketoacidosis, which especially applies to diabetics. Ketoacidosis is a dangerous metabolic state in which excessive amounts of ketones are produced. In mostly healthy individuals, ketosis is regulated by insulin, which is the hormone that controls the creation of ketone bodies and regulates the flow of fatty acids into the blood.
As the rate of oxidative phosphorylation approaches the capacity of the mtETC, Δp will increase and facilitate mtROS production [53]. Higher oxidative capacity should therefore decrease the potential for mtROS production and subsequent oxidative damage. Furthermore, greater oxidative capacity may compensate for the resulting decrease in efficiency of ATP production associated with increased mitochondrial uncoupling. Since oxidative phosphorylation occurs exclusively in mitochondria, mitochondrial density is a key determinant of oxidative capacity [154].
Contact your doctor and ask if you should change or increase your medication dosage, if you are taking a medication for diabetes. Despite the perception you may have that your blood sugar instability is becoming worse, Diabetes Health explains that the medication adjustment may just be dividing the dosage and taking it more often. Additionally, infection and illnesses can make your body less efficient at processing sugar, resulting in higher blood sugar levels temporarily.
Hi Maria- I am a 3 year cancer survivor. I had been following basically a paleo diet, but often fell off the wagon where sugar was concerned. In the last year I was diagnosed with ulcerative colitis and chrohn’s disease. My naturopath recommended I follow the keto-adaptive diet. I was very excited to make your amazing bread, but I wonder if the psyllium powder would be bad for my intestinal issues? Hope not!
Glycogen influences AMPK activity by binding to a glycogen binding domain on the β regulatory subunit of AMPK [205, 206]. In human and rodent skeletal muscle, AMPK activity is lower when glycogen is bound to this domain [207, 208] and higher when muscle is depleted of glycogen [209–212]. In direct contrast to the effect of AMP and ADP, glycogen inhibits the phosphorylation of AMPK by upstream kinases such as LKB1 [213]. Although muscle glycogen concentration has recently been demonstrated to be similar in ultra-endurance athletes regardless of a ketogenic or high-carbohydrate diet [8], concentrations generally decrease in response to dietary carbohydrate restriction [156, 166, 173, 214–221]. Furthermore, the long-term adaptations to nutritional ketosis that may enable some athletes to replenish glycogen at a normal rate may not apply to less physically active individuals.
Our keto bread recipe has a beautiful golden crust. It has great structure with a lovely rise and perfect bread-like crumb. It slices well for sandwiches or toasting, but you don’t have to toast or grill it to make it taste good. Sliced with a smear of salted butter is keto perfection. And it actually tastes like bread, not eggs or almonds or coconut. Additionally, this bread will keep well wrapped in the fridge for up to a week!
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