Therefore the combustion enthalpy (∆H) of each fuel is an important factor in the energy it can provide to the cell. When expressed as the energy per 2 carbons in the molecule, ketones (BHB) have a higher combustion enthalpy (∆H) than pyruvate, lactate and glucose (see table). This means that the amount of energy that could possibly be transferred to ATP is higher than for those other substrates:

Hello from Jakarta, Indonesia! I just tried your recipe coz i was making an eggs bennedict & needed something for “bread”. Your recipe was BY FAR the easiest to make & quite tasty! Initially i was worried about the “eggy” taste, but didn’t happen. I think i will be making this often… i will pre-measure the 30gr of almond flour & cut up 10gr of butter pieces for easier assembly in the mornings. Cheers!

Our bodies need sugar to make energy for the cells. Without it, we cannot do basic functions. When we eat foods with glucose, insulin pairs with it to allow it to enter into the cell wall. If the insulin is not there, then the glucose molecule can’t get through the wall and cannot be used. The extra glucose hangs out in the bloodstream which is literally high blood sugar.
Insulin is a hormone that allows glucose to move into tissue cells, where is it is used for energy production. Insulin then prompts the liver to either store the remaining excess blood glucose as glycogen (for short-term energy storage) and/or to use it to produce fatty acids (which then become triglycerides). In people with insulin resistance, additional insulin must be released by the pancreas to overcome the tissue cells' resistance and allow glucose to enter the cells. This resistance and response to resistance can lead to increased insulin and glucose concentrations in the blood. Over time, increased glucose levels can harm blood vessels and organs such as the kidneys. Increased insulin levels can increase sodium retention by the kidneys, resulting in increases in blood pressure (which can lead to hypertension).

Thank you Mira for your quick reply. I didn’t make it that same day but I just made a batch now and they are excellent! I really enjoyed them. I made the recipe times 10 for 12 large muffin slots in the muffin tin. I’m thinking of shaping a larger round of batter on a parchment lined pan next time and after baking, carefully cutting in half to make 2 rounds to make a pizza crust. Thank you so much!!!


Despite continuous advances in the medical world, obesity continues to remain a major worldwide health hazard with adult mortality as high as 2.8 million per year. The majority of chronic diseases like diabetes, hypertension, and heart disease are largely related to obesity which is usually a product of unhealthy lifestyle and poor dietary habits. Appropriately tailored diet regimens for weight reduction can help manage the obesity epidemic to some extent. One diet regimen that has proven to be very effective for rapid weight loss is a very-low-carbohydrate and high-fat ketogenic diet.[1][2][3]
Heat a large non-stick skillet over medium heat.  Mix all of the ingredients for the pancakes into a small bowl.  Spray the skillet with cooking spray and spoon the batter into 4 round pancakes in the skillet.  Let the pancakes cook until bubbles start to form in the batter around the side.  Flip and continue to cook on the other side until the center on the pancake springs back when lightly touched.
The handheld devices that are available for home testing (such as FreeStyle by Abbott, or KetoMojo) require a small droplet of blood (obtained by a finger prick with a lancet) to be placed on a testing strip. A new testing strip must be used each time a reading is taken. The machine delivers a numerical blood BHB measurement in the unit milli molar (mM) after ~8 seconds. 
This “lazy” keto bread recipe is anything but boring: Crumbling the butter directly into the dough creates moist and tender biscuits for all your sweet and savory recipes. Plus, this recipe takes 30 minutes from start to finish and keeps each biscuit macro-friendly at 3 net carbs. Stay more Bulletproof and use the sour cream and whey protein swaps suggested in the recipe, plus avoid eating flaxseed too often.

Hi, I’ve made this recipe twice and LOVE the taste. However, both times the bread would rise so high in the oven, but as soon as I take it out to cool it deflated and middle sink down. What could’ve gone wrong? Over mixing? I did switch coconut flour to all almond flour instead. Could that be a problem? Please help as I’m anxious to make another batch. Thank you.
So I made my own coconut-flour from flaked coconut(according to a recipe I found on line). Psyllium Husk i managed to find only in whole husks form so I grind it up to a powder in a blender. I understand now it sounds like a recipe for disaster but I don’t have another choice (getting the ingredients from the internet will take about 2 weeks and until then it is all I have).
The difference between ketosis and ketoacidosis is the level of ketones in the blood. Ketosis is a physiological adaptation to a low carbohydrate environment like fasting or a ketogenic diet. There are situations (such as treatment-resistant epilepsy) where ketosis can be beneficial to health. Ketoacidosis is an acute life-threatening state requiring prompt medical intervention; its most common form is diabetic ketoacidosis where both glucose and ketone levels are significantly elevated.
I’m following the ketogenic diet and I find it very easy, pleasant and varied. I can even say that my diet today is more varied than the previous one. I do not intend to leave this diet and I cannot really see why. My initial focus was not to lose weight, I’ve always been lean, but to feel better, well disposed. And I got it! I am very pleased, I have read a lot about it (including scientific literature) and I have influenced other people who need to lose weight or improve some aspects of their health. But from the beginning I went on my own way, without the help of a nutritionist because I did not want to suffer the influence of others’ ideas.
Some research suggests that ketogenic diets might help lower your risk of heart disease. Other studies show specific very-low-carb diets help people with metabolic syndrome, insulin resistance, and type 2 diabetes. Researchers are also studying the effects of these diets on acne, cancer, polycystic ovary syndrome (PCOS), and nervous system diseases like Alzheimer's, Parkinson's, and Lou Gehrig's disease.
KBs can cross the BBB but not in a homogenous manner. For example, past experiments have demonstrated that BHB utilization is different in various brain areas (Hawkins and Biebuyck, 1979). Areas without BBB, hypothalamic regions and the lower cortical layers have a higher BHB metabolism compared to the lower one of the basal ganglia (Hawkins and Biebuyck, 1979). Also the metabolic meaning of the three KBs is different: while the main KB produced in the liver is AcAc, the primary circulating ketone is BHB. The third one, acetone, is produced by spontaneous decarboxylation of AcAc, and it is the cause of the classic “fruity breath.” Acetone does not have any metabolic functions, but it can be used as a clinical diagnostic marker. BHB acid is not, strictly speaking, a KB because the ketone moiety has been reduced to a hydroxyl group. Under normal conditions the production of free AcAc is negligible and this compound, transported via the blood stream, is easily metabolized by various tissues including skeletal muscles and the heart. In conditions of overproduction, AcAc accumulates above normal levels and a part is converted to the other two KBs. The presence of KBs in the blood and their elimination via urine causes ketonemia and ketonuria. Apart from being the fundamental energy supply for CNS, glucose is necessary for the replenishment of the quota of oxaloacetate, since this intermediate of the tricarboxylic acid cycle (TCA) is labile at body temperature and cannot be accumulated in the mitochondrial matrix. Hence it is necessary to refurnish the TCA with oxaloacetate via the anaplerotic cycle that derives it from glucose through ATP dependent carboxylation of pyruvic acid by pyruvate carboxylase (Jitrapakdee et al., 2006). This pathway is the only way to create oxaloacetate in mammals. Once produced by the liver, KBs are used by tissues as a source of energy (Fukao et al., 2004; Veech, 2004; McCue, 2010): initially BHB is converted back to AcAc that is subsequently transformed into Acetoacetyl-CoA that undergoes a reaction producing two molecules of Acetyl-CoA to be used in the Krebs cycle (Figure ​(Figure22).

This bread does have quite a few ingredients, but you’ll find that most are staple paleo and keto pantry ingredients. In the list below you’ll find details on several ingredients and possible subs. But if possible, please do try and make this recipe without any subs. As out of the 18 permutations we tried, this one really was terrific and the absolute best.


Although convincing, the bulk of evidence in relation to the inhibitory effects of ketosis on appetite is still anecdotal. Preliminary scientific reports seem to support this phenomenon, and the evidence shows that KD is more effective, at least in the short/medium-term, on fat loss (Paoli, 2014). It was demonstrated that diet-induced weight loss leads to changes in energy expenditure and in appetite-regulating hormones that facilitate weight regain and the return to initial energy homeostasis (Sumithran et al., 2011). This response to alteration of energy balance nullifies the success of many dietary approaches. It is well-known that the long-term success of a nutritional approach is defined by the amount of weight regain and is the main problem regarding the so-called weight cycling or “yo-yo” effect (Jeffery, 1996). A recent study by our group has demonstrated that a brief ketogenic period, if followed by a longer period of correct Mediterranean diet could avoid this yo-yo effect (Paoli et al., 2013). During the ketogenic period subjects reported less hunger, confirming previous studies (Nickols-Richardson et al., 2005; Johnston et al., 2006; Johnstone et al., 2008) on hunger-suppression effect of ketogenic diet. Despite these clinical findings, the mechanisms of action of ketosis on appetite reduction are still not completely understood. Clinical results are suggestive of both direct and indirect (via modifications of hunger-related hormones concentration) actions of KBs on appetite (Sumithran et al., 2013).
I have AS and am on a no starch diet to control the pain, which works very well for me. So I’m wondering if you have any idea how much starch is in the PH before I order it only to have the iodine test turn it black for starch, which would mean I can’t use and I’d have to throw it out? I can mix up my own baking powder without corn starch and all of the other ingredients are safe for me to eat, so my only concern is the PH. It looks so delicious and I’ve yet to find a truly tasty starch free bread recipe.
188. Tomas E., Tsao T. S., Saha A. K., et al. Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: acetyl-CoA carboxylase inhibition and AMP-activated protein kinase activation. Proceedings of the National Academy of Sciences. 2002;99(25):16309–16313. doi: 10.1073/pnas.222657499. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
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).

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.

Target organ damage occurs through multiple mechanisms in metabolic syndrome. The individual diseases leading to metabolic syndrome produce adverse clinical consequences. For example, hypertension in metabolic syndrome causes left ventricular hypertrophy, progressive peripheral arterial disease, and renal dysfunction. [12] However, the cumulative risk for metabolic syndrome appears to cause microvascular dysfunction, which further amplifies insulin resistance and promotes hypertension. [13]
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.

Another process also happens during ketosis that helps keep your body energized, and it’s called gluconeogenesis. This occurs when glycerol (created during beta-oxidation) get’s converted into glucose that your body can use for energy. Protein in your diet can also be converted to glucose in small amounts. So as you can see, essentially your body is able to create its own source of necessary glucose without getting it from carbohydrate foods. The human body is very efficient, and it knows just how to convert other macronutrients (protein and fat) into useable molecules that can be dispersed throughout the body as needed.
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Metabolic syndrome is a burgeoning global problem. Approximately one fourth of the adult European population is estimated to have metabolic syndrome, with a similar prevalence in Latin America. [25] It is also considered an emerging epidemic in developing East Asian countries, including China, Japan, and Korea. The prevalence of metabolic syndrome in East Asia may range from 8-13% in men and from 2-18% in women, depending on the population and definitions used. [29, 30, 31]
Ok I will try this with the physillium since no sub will work. 🙂 I have a Q though-I read that too much physillium may interfere with how medicines work-my son is on 5 seizure meds, and we are going keto to help with his seizures. This looks like a good and tasty bread to replace his beloved loaf…what would you say is a safe amount for him to eat daily or weekly? Any resources on daily physillium allowances for kids so I can adapt his servings? THanks! 🙂 🙂
tips for making this bread with coconut flour and those getting purple results! i made half the recipe and made the following changes: 3/4 cups of water, 1 teaspoon baking powder, 1/2 teaspoon baking soda. my bread which previously came out purple and with very dense patches came up much fluffier and with more bread like ‘holes’ and also had the colour of normal brown bread! i baked it in a small loaf and the bread rose a lot but the top half was basically a tunnel. the rest of it is good ‘bread’ though! 🙂

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!
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]
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Ketogenesis is the pathway that forms ketone bodies from fatty acids. Starvation (specifically low levels of blood insulin and glucose) triggers ketogenesis in the liver cells’ mitochondria. Two molecules of acetyl-CoA from the breakdown of fatty acids are condensed via acetyl-CoA transferase to form acetoacetyl-CoA; a third is added to form 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) in a reaction catalysed by HMG-CoA synthase. HMG-CoA lyase then splits this to re-generate acetyl-CoA and form one molecule of AcAc. Beta-hydroxybutyrate (BHB) is formed from reduction of AcAc by BHB-dehydrogenase enzyme, and acetone results from spontaneous, non-enzymatic decarboxylation of AcAc. Acetone is a volatile molecule which is primarily excreted in the breath, although some evidence suggests that a small amount can be metabolised and oxidised4.
Exogenous ketones: Very little is known about the effects of exogenous ketones on cancer. However, as exogenous ketones can also lower blood sugar and elevate BHB they could be helpful by a similar mechanism to the ketogenic diet. Exogenous ketones may even be preferable to the ketogenic diet, as patients can eat a wider range of palatable and calorically dense food to maintain their strength during treatment. One animal study showed that ketone ester supplementation (acetoacetate diester) decreased tumour size and prolonged the survival of mice with metastatic cancer100. 
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Acetone is a molecule that results from the breakdown of acetoacetate. Acetone is commonly referred to as a ‘waste product’ as it is less readily used as energy compared to BHB (although some studies have shown that acetone can be oxidised as a fuel4. That said, some evidence suggests that it is responsible for the antiseizure effects of ketogenic diets so in may not be completely inert. At low levels acetone in the breath corresponds well to levels of ketones in the blood 12,13, however this is not the case as blood BHB levels increase 13 and if the increase is rapid, such as with exogenous ketone consumption11. 

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.
It is still unclear what is the very first step that occurs in a normal cell becoming cancerous. Two theories that explain the development of cancer are the ‘somatic mutation’ theory, and the ‘metabolic theory.’ The somatic mutation theory states that the first event in cancer is a gene mutation due to environmental damage or a mistake in the DNA replication and repair processes. This gene mutation initiates a cascade of events that subsequently leads to tumour growth. Popular opinion favoured the somatic mutation theory for many years, leading to a large body of research describing the different genetic mutations of cancer cells, and ambitious projects to sequence the ‘Cancer Genome.’ From the compelling simplicity of the somatic mutation theory, an increasingly complicated picture has emerged as more than 100 oncogenes and 30 tumor suppressor genes have been identified, leading researchers to look for alternative explanations. 
How, exactly, does our body take pyruvate (from glucose) or acetyl CoA (from fat) and generate so much ATP?  The answer lies in the beauty of the Krebs Cycle, which feeds into a process called the electron transport chain (or ETC), I alluded to above.  Since the adage ‘you can’t get something for nothing’ is as true in biochemistry as it appears to be in life, to get all that ATP (i.e., stored energy in the form of the phosphate bond), we need to give up something.  What the ETC does give up, as its name suggests, is electrons.  Through a series of redox reactions the ETC trades the stored energy held by electrons going from higher to lower energy states in exchange for the chemical energy stored in the bonds of the third phosphate group on an ATP molecule.
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 [270], 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 [281] 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 [285]. Once activated, PGC-1α interacts with the PPAR family of nuclear receptors [286] and the FOXO family of transcription factors [287] 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 [76], SOD2 [76, 282, 289, 292–294], catalase [282], 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].
I made this bread several times by grinding the jay robb psyllium husks, but never got a good loaf. Then I bought the now brand psyllium husk powder and it worked without turning purple. I did have to weigh everything and cook it about an hour and a half or longer. When I cooked it the first time it sank in the middle. If you don’t have a vitamin or blend tech this is the way to go.
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A high proportion of energy from ketone oxidation is transferred to the electron transport chain at the start (as NADH+), in comparison to the energy from fat, where a high proportion is transferred ‘downstream’ (as FADH). This means that, even though there is a high amount of ‘potential energy’ in a fat molecule, less of this can be transferred to ATP.   
Angie, I’m happy to hear you and your hubby enjoyed the taste, but sorry to hear the bread was flat! The egg whites don’t need to be whipped for this recipe, but I’ll try to help you troubleshoot…first I would check to make sure that your baking powder is fresh. Also, did you use the full cup of egg whites? Did you make any ingredient substitutions or adjustments? Did you use a 9 by 5-inch loaf pan? Did you cook it at 350F and is your oven properly calibrated? Did you bake it for the amount of time the recipe calls for? I hope this helps!
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