As previously mentioned, numerous studies have demonstrated a profound increase in fat oxidation in response to ketogenic and low-carbohydrate diets. Some studies have even shown an increase in O2 consumption [148, 155–158]. However, fats contain fewer oxygen atoms per carbon than carbohydrates, thereby necessitating greater O2 intake to produce the same amount of energy [159]. Furthermore, since β-oxidation and ketolysis produce a greater proportion of FADH2 to NADH, the resulting decrease in passage of electrons through complex I decreases potential for ATP production per unit of O2 consumption [160]. Increased O2 consumption in response to a ketogenic diet may therefore merely be an effect of the differences in the metabolism and molecular structures of fat and carbohydrate rather than a true indication of increased capacity for oxidative phosphorylation. However, in rat hearts perfused with glucose, the addition of ketones has decreased O2 consumption [161]. This discrepancy may be related to variations in mitochondrial uncoupling. Either way, several studies have shown ketogenic diets to increase mitochondrial content, and numerous studies have shown these diets to increase expression, content, or activity of mitochondrial proteins involved in oxidative phosphorylation and fat oxidation. Compared to O2 consumption alone, these findings provide more conclusive support for an increase in oxidative capacity in response to nutritional ketosis.
Many neurological conditions share a common feature of impaired brain energy metabolism. It isn’t always clear if this impairment is the cause or the effect of the disease, but nonetheless, interventions that even partially restore or improve brain energy metabolism could help to prevent, slow or even reverse some conditions of the brain. Because ketones can: 1) get into the brain; 2) undergo metabolism by a distinct pathway that bypasses glucose metabolism, providing ketones by either following a ketogenic diet or by taking exogenous ketones could impact the natural course of some neurological conditions. 

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.
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 [157]. 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 [37].
I just made this today. If I lived in London and could hug you, I would! You have NO idea how many recipes I’ve tried for almond flour bread and they never come out right or taste very good. This recipe is amazing! Since I can’t use psyllium due to an allergy to it, I used ground flax seed meal instead. OMG, this bread is delicious! I used the small loaf pan like you did and it came out perfect. It rose above the pan and is a perfect loaf. I let it completely cool, cut it with a bread knife and it did NOT fall apart, something so many of these type of breads do. AND it does NOT taste eggy which has been another problem I’ve dealt with. The loaf is so pretty! I can’t wait to experiment with different spices or herbs in this bread. Another plus for me is that since the slices are smaller than regular bread, it helps with calorie control when putting things on it for a sandwich. I have a strong wheat intolerance and don’t do well with grains in general so I’m always looking for alternative recipes. Thank you from the bottom of my heart. You just made my day!!!!

In skeletal muscle, impaired mitochondrial function contributes to age-associated atrophy, impaired contraction, and insulin resistance [2]. While exercise provides a direct stimulus for mitochondrial adaptation in muscle, with great potential to prevent or treat the aforementioned conditions, the global effects of exercise on bioenergetic homeostasis may lead to mitochondrial adaptations in other tissues as well. Based on this, exercise has the potential to influence any condition for which impairments in global energy metabolism or local mitochondrial function are a contributing factor, which is arguably the case for a majority of chronic diseases. Exercise is therefore an excellent adjunct to nutritional ketosis because it facilitates β-oxidation and ketogenesis by increasing energy demand and depleting glycogen storage, which is likely to augment the signaling induced by nutritional ketosis.
I am disappointed with my first effort but remain undaunted. I did not use the J Robb psyllium but did grind it up as finely as I could and otherwise followed the recipe exactly. I am an experienced baker so I’m not giving up and will try using less water next time. I want to use as many ingredients as I can find in my small town in order to vote with my dollars for more healthy foods so I will try a few more times before special ordering.

The notion that metabolic syndrome, or its surrogate markers hyperinsulinemia and insulin resistance, antedate and contribute to the pathogenesis of coronary heart disease, diabetes, and at least some cases of hypertension was proposed many years ago.21,35 Coronary heart disease in the setting of metabolic syndrome can to a great extent be attributed to dyslipidemia (increased dense LDL cholesterol, diminished HDL cholesterol, and hypertriglyceridemia)231 as well as to elevations in blood pressure and blood glucose and the presence of a procoagulant, proinflammatory state.22,228 In addition, some studies suggest that hyperinsulinemia and insulin resistance, as well as hyperglycemia, may be independent risk factors.51 Whether elevated FFA levels or a dysregulation of intracellular fatty acid metabolism contribute to atherosclerosis by directly altering the function of endothelium (see the section entitled “Vascular Endothelial Cells and Atherogenesis”) or other cells in the vascular wall remains to be determined. Relevant to this discussion, low levels of adiponectin are associated with an increased risk for coronary heart disease in humans,155 whereas, as noted earlier, overexpression of adiponectin or its globular subunit diminishes the severity of atherosclerosis in ApoE–/– mice.232,233


Populations living further north had much less edible vegetation available for gathering. Thankfully for us, animals that lived in these areas ate the vegetation inedible to us, effectively transforming it into fatty meat we could hunt and enjoy. These people most certainly relied on high levels of fat and protein, thus likely spending most of their time in ketosis.

Like you say on your show, I am a foodie and hate it when recipes on websites turn out tasting bleh. This bread has a great texture. After making it a few times plain now, I added some sesame seeds to the batter and that turned out great too. I make an open faced breakfast sandwich with a slice of this almond flour bread, plenty of cream cheese and scrambled eggs. Paired with coffee. So tasty, that I can’t tell it isn’t a regular scrumptious egg sandwich.
You can find a mixed bag of studies in rodents; sometimes the ketogenic diet is amazing sometimes it’s terrible. The main reason why is because there are many kinds of ketogenic diets; what fats were used? how processed is the food and what was the method of processing? were these genetically manipulated mice or wild type? were they fed ad lib (to their hearts content), forced fed (hypercaloric) or had their calories restricted?
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According to most experts on the ketogenic diet, technically nutritional ketosis is defined by serum ketone levels (the amount of ketones in the blood) that fall between 0.5 to 3.0 mM. (3) Some believe that 1.5 – 3 mmol/L is “optimal ketosis,” which might contribute to the most weight loss. Every person is a bit different in terms of what exact macronutrient ratio will keep them in this range, while also allowing them to feel their best in terms of energy levels and other symptoms. You can experiment with different carb amounts while testing to see how this affects your ketone levels, aiming to remain in nutritional ketosis (0.5 to 3.0 mM), as long as you feel well doing so. Try to test at the same time each day for consistency and avoid testing right after exercise.

Insulin resistance also may increase your risk for metabolic syndrome. Insulin resistance is a condition in which the body can’t use its insulin properly. Insulin is a hormone that helps move blood sugar into cells where it’s used for energy. Insulin resistance can lead to high blood sugar levels, and it’s closely linked to overweight and obesity. Genetics (ethnicity and family history) and older age are other factors that may play a role in causing metabolic syndrome.
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.
Last point of background: Everything I’ve just presented is based on data from starving subjects.  If one restricts carbohydrate intake, typically to less than about 20-50 gm/day (dependent on timing and carbohydrate composition), and maintains modest but not high protein intake (because protein is gluconeogenic – i.e., protein in excess will be converted to glycogen by the liver), one can induce a state referred to as “nutritional ketosis” with similar physiology to what I’ve just presented without resorting to starvation.  Why you’d do this is something I will discuss later.
^ Vancampfort D, Correll CU, Wampers M, Sienaert P, Mitchell AJ, De Herdt A, Probst M, Scheewe TW, De Hert M (July 2014). "Metabolic syndrome and metabolic abnormalities in patients with major depressive disorder: a meta-analysis of prevalences and moderating variables". Psychological Medicine. 44 (10): 2017–28. doi:10.1017/S0033291713002778. PMID 24262678.
Sorry, I realized I should have clarified which kind of freshly milled flours. Specifically, wheat, rye and spelt. I have been using freshly milled flour for over a year now and my family loves it. I have recently bought 3 of your books and I am learning all kinds of wonderful new things, but I am having a hard time letting go of freshly milled flour completely. Your thoughts on the subject would be much appreciated!
Make nonstarchy vegetables the star of your plate, taking up half of it. “For anybody at risk of diabetes, it's important to take your vegetable intake to the next level,” Wright says. “Balancing your plate with half vegetables will fill you up without loading you down with tons of carbs.” Credit the fiber and water in the vegetables for helping keep you satisfied.

Ketones may also have effects in neurons beyond their use as an energy source. Preliminary work shows ketones can affect neurotransmitter release, reduce inflammation in the brain and reduce damage caused by oxidative stress8. Whilst the strength of the clinical evidence supporting the use of ketosis varies according to the condition, future work should look to explore the efficacy and underlying mechanisms further. Ketosis (by diet or by exogenous ketones) could offer an intervention that has good efficacy, but without the side effects profile of many drugs currently in use. It should be noted that the use of ketogenic diet or exogenous ketones in the conditions discussed below is still classified as ‘experimental’ in the most part and so individuals should not their alter medication or diet without full medical supervision.  
Humans have always relied on ketones for energy when glucose sources were scarce (i.e. no fruits available during winter). It is a normal state of metabolism. In fact, most babies are born in a state of ketosis. However, with abundant sources of carbohydrate, people rarely access ketosis and it becomes a dormant metabolic pathway.Our ancestors likely had frequent periods of time when high carbohydrate food wasn’t immediately available. For this reason, our bodies are amazing at adapting to burning of ketones for fuel.

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.
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Maria, I made your bread using NOW psyllium, it tastes more like a loaf of real bread than anything I’ve tried. It’s lots better than the pricey Low Carb Bread Company loaves that I have been buying on Netrition. I had previously tried a similar recipe that had coconut flour, and even though I added quite a bit of onion powder, the coconut flavor was still distinguishable, and I’m not a fan.
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.

Yolks are great. Make a healthified custard, or a custard ice cream (Maria has recipies for both). I’m a diabetic and I got that way eating “real” food, not manufatured food. I baked. All from scratch, all homemade. But that meant traditional sugar and wheat flour. I had developed a number of reduced carb recipies on my own, but Maria’s recipies go all the way with better success than I would have guessed possible. (I still yearn for a good, two-day rise wheat and yeast bread — But I know allow myself this only once a quarter. It is not good for you.) I’m excited to try this. So far my favorite has been her psyllium powder/egg/boiling water version pizza crust. A homemade pizza made with this tastes as good as any pizza.
While there have not been large studies that show the relationship between the ketogenic diet and cancer, we will be publishing a case study about that topic. The author failed to comment that pediatric patients with epilepsy are on the diet for usually about 2 years with no harmful effects. Before the false studies about heart disease and fat, the low carb diet was a respected way to lose weight. Studies into our metabolism show we can use both fat and carbohydrate as fuel. So stepping away from our high carb diet- I am sorry to say that we eat more carbs since the 70s with most of it processed and we now use high fructose corn syrup to sweeten products and we have a wide spread childhood obesity problem. If cholesterol is a concern try plant sterols and stenals to block cholesterol from the receptors in the body. So much more can be said about a keto diet than this article states
Normally, the body breaks down carbohydrates, fat, and (sometimes) proteins to provide energy. When carbohydrate is consumed in the diet, some is used immediately to maintain blood glucose levels, and the rest is stored. The hormone that signals to cells to store carbohydrate is insulin. The liver stores carbohydrate as glycogen, this is broken down and released between meals to keep blood glucose levels constant. Muscles also store glycogen, when broken down this provides fuel for exercise. Most cells in the body can switch readily between using carbohydrates and fat as fuel. Fuel used depends on substrate availability, on the energy demands of the cell and other neural and hormonal signals. 
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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.
AMPK is activated through phosphorylation of the Thr172 residue of the AMPK α catalytic subunit [174–176], and this phosphorylation is largely regulated by molecules related to bioenergetic homeostasis including AMP, ADP, catecholamines, adiponectin, glycogen, and insulin. In general, AMPK is activated by energy deficit and induces signaling that upregulates energy production. AMP and ADP are direct byproducts of energy depletion while adiponectin and catecholamines serve as endocrine signals to increase energy production, often in response to energy depletion. In contrast, indications of energy surplus, such as glycogen and insulin, inhibit activation of AMPK. Nutritional ketosis increases the aforementioned factors that activate AMPK and decreases those that inhibit AMPK, suggesting that nutritional ketosis is similar to caloric restriction in inducing a signal of energy depletion.
Research shows that Western diet habits are a factor in development of metabolic syndrome, with high consumption of food that is not biochemically suited to humans.[21] Weight gain is associated with metabolic syndrome. Rather than total adiposity, the core clinical component of the syndrome is visceral and/or ectopic fat (i.e., fat in organs not designed for fat storage) whereas the principal metabolic abnormality is insulin resistance.[22] The continuous provision of energy via dietary carbohydrate, lipid, and protein fuels, unmatched by physical activity/energy demand creates a backlog of the products of mitochondrial oxidation, a process associated with progressive mitochondrial dysfunction and insulin resistance.
The distribution of adipose tissue appears to affect its role in metabolic syndrome. Fat that is visceral or intra-abdominal correlates with inflammation, whereas subcutaneous fat does not. There are a number of potential explanations for this, including experimental observations that omental fat is more resistant to insulin and may result in a higher concentration of toxic free fatty acids in the portal circulation. [21]
Independent of nutritional ketosis, increased dietary fat intake increases expression of UCP2 and UCP3 in muscle [142], and fatty acids facilitate uncoupling through UCP2 [143, 144], UCP3 [94, 143, 144], and ANT [145]. Given the high fat intake that is characteristic of a ketogenic diet, it is logical to expect nutritional ketosis to increase mitochondrial uncoupling.
Adiponectin increases AMPK activity in skeletal muscle [188, 189] and the liver [189] by promoting Thr172 phosphorylation, likely in response to an increase in the AMP to ATP ratio [189]. Similarly, α-adrenergic signaling increases AMPK activity in skeletal [190] and cardiac muscle [191], and β-adrenergic signaling increases AMPK activity in adipose [192, 193], all through promotion of Thr172 phosphorylation. While activation through β-adrenergic signaling appears to involve the AMP to ATP ratio [192], α-adrenergic signaling appears to work independently of AMP and ATP [190]. Increases in adiponectin have been observed during ketogenic or low-carbohydrate diets, although primarily in obese individuals [194–196]. BHB induces adiponectin secretion in adipocytes [197], indicating that the level of nutritional ketosis may be an important determinant of the extent to which ketogenic diets influence AMPK activity through adiponectin. In regard to catecholamines, epinephrine increases during fasting, and this appears to be dependent on carbohydrate restriction [198], implying that epinephrine is likely to be elevated during nutritional ketosis. Consistent with this, dietary carbohydrate restriction increases catecholamines at rest [155, 199] and in response to exercise [155, 199–202]. This may be, at least in part, a result of glycogen depletion [200, 203], suggesting both direct and indirect effects of glycogen on AMPK activity. The potential for nutritional ketosis to increase catecholamines is further supported by the dependency of the antiseizure effects of ketogenic diets on norepinephrine [204].
While it is believed that carbohydrate intake after exercise is the most effective way of replacing depleted glycogen stores,[72][73] studies have shown that, after a period of 2–4 weeks of adaptation, physical endurance (as opposed to physical intensity) is unaffected by ketosis, as long as the diet contains high amounts of fat, relative to carbohydrates.[74] Some clinicians refer to this period of keto-adaptation as the "Schwatka imperative" after Frederick Schwatka, the explorer who first identified the transition period from glucose-adaptation to keto-adaptation.[75]
The approximate prevalence of the metabolic syndrome in patients with coronary artery disease (CAD) is 50%, with a prevalence of 37% in patients with premature coronary artery disease (age 45), particularly in women. With appropriate cardiac rehabilitation and changes in lifestyle (e.g., nutrition, physical activity, weight reduction, and, in some cases, drugs), the prevalence of the syndrome can be reduced.[27]
This paleo keto bread recipe makes a delicious option for coconut lovers. For a low-fuss loaf, blend coconut flour with ingredients like eggs, coconut oil, and salt — then bake away for a sturdy bread with only 1.3 net carbs per serving. Make this recipe totally nut-free (and more Bulletproof) by swapping almond milk with full-fat canned coconut milk.
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