Finally, exogenous ketones have been shown to decrease the levels of triglycerides and free fatty acids in the blood after one drink 107 ,106 ,11. There is also early data showing that ketone ester consumption decreases cholesterol biosynthesis in rodents, an effect which appeared to be conserved in humans114. It is unclear at this stage what the long term effects of exogenous ketone consumption on blood lipids and cholesterol would be, but this is an area of promising research. 

And the one thing to keep in mind is that your bread will likely fall slightly post bake. Blame it on the lack of starch (keto flours are notoriously heavy and moist) and certain missing proteins (think gluten). Just keep in mind that we’re baking at ridiculously high altitude here, so if our loaf was still nearly double it’s volume after cooling- odds are yours will be even better!
Did you hear the news? I have a new cookbook out called Keto Instant Pot Recipes book! But this is not just any Instant Pot cookbook. This keto cookbook has a ton recipes with BOTH Instant Pot directions AND slow cooker directions! I also started an Instagram account on my favorite Keto Instant Pot Recipes and giveaways called @KetoInstantPotRecipes! 
Soooooo fluffy, yummy and versatile! I just made it for the first time. Been making the coconut flour mug bread the past couple of days but this is so less dense. Grilled a couple of pieces and HOLY HELL it’s amazing! Love your site and your recipes. Coconut flour wraps (love wrapping my salad) are next! Neither bread has affected my keto either. I’m also 100% Paleo. Swapping out the cream for ghee in the coconut mug bread works really well!
170. Garbow J. R., Doherty J. M., Schugar R. C., et al. Hepatic steatosis, inflammation, and ER stress in mice maintained long term on a very low-carbohydrate ketogenic diet. American Journal of Physiology-Gastrointestinal and Liver Physiology. 2011;300(6):G956–G967. doi: 10.1152/ajpgi.00539.2010. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
More recently a community of researchers and athletes have emerged who feel that following a ketogenic diet offers a performance advantage, especially to endurance sports where athletes are more likely to run out of stored carbohydrate during the event. However the evidence remains inconclusive and research is ongoing to provide a definitive answer to as to if a ketogenic diet offers a performance advantage.    
If you divide the dough in 3 you’ll cook the bread for 90 seconds on high, but if you cook it all together you’ll want to do 150 seconds (2 1/2 minutes). Either way, it’ll come out looking pale and spongy (and not very appetizing at all tbh!). But worry not, just wait for it to cool down until just lightly warm (it continues to cook guys!), and then you’ll definitely want to give it a toast to get some texture on.
^ Jump up to: a b c Vemuri VK, Janero DR, Makriyannis A (March 2008). "Pharmacotherapeutic targeting of the endocannabinoid signaling system: drugs for obesity and the metabolic syndrome". Physiology & Behavior. 93 (4–5): 671–86. doi:10.1016/j.physbeh.2007.11.012. PMC 3681125. PMID 18155257. The etiology of many appetitive disorders is characterized by a pathogenic component of reward-supported craving, be it for substances of abuse (including alcohol and nicotine) or food. Such maladies affect large numbers of people as prevalent socioeconomic and healthcare burdens. Yet in most instances drugs for their safe and effective pharmacotherapeutic management are lacking despite the attendant medical needs, collateral adverse physical and psychological effects, and enormous global market potential. The endocannabinoid signaling system plays a critical role in motivational homeostasis as a conduit for reward stimuli and a positive modulator of brain reward circuits. Endocannabinoid-system hyperactivity through CB1 receptor transmission is considered contributory to a range of appetitive disorders and, hence, is a major focus of contemporary pharmaceutical research.
In addition to eating small meals at night, it's best to limit dishes piled high with pasta, rice, sugar, and other carbs. “When you focus on whole-food carbs spread throughout the day, the less pressure there's going to be on your pancreas to constantly chug out insulin,” Wright says. You want your blood sugar to roll like hills over the course of the day rather than spike like mountain peaks and plummet to valleys, she adds.
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Several additional rodent studies have shown ketogenic diets to increase protein content of UCPs. However, since mitochondrial function was not measured in these studies, it is not known if uncoupling was affected by these changes in UCP content. In obese mice fed a ketogenic diet (0.4% of energy as carbohydrate), expression of UCP1 and UCP2 increased in adipose and the liver, respectively [148]. Similarly, expression of UCP1 has increased in brown adipose of mice fed a low-carbohydrate diet (18.5% of energy) supplemented with ketone esters (6% w/v) [149]. The increase in hepatic UCP2 expression during a ketogenic diet has been demonstrated by other studies as well [37, 150, 151]. Ketogenic diets also induce expression of UCP3 in skeletal muscle. In rats fed a ketogenic diet (% energy: 78.1 fat, 0 carbohydrate, and 21.9 protein) for 8 weeks, UCP3 expression increased in the soleus but not the extensor digitorum longus, which is consistent with the soleus containing mostly oxidative, type I muscle fibers [152]. In humans, glycogen depleting exercise followed by two days of a low-carbohydrate diet (0.7 g/kg body mass) increased UCP3 expression in the vastus lateralis [153].
Embarrassing admission: I remember exactly where I was sitting in a clinic at Johns Hopkins in 2002 explaining to (admonishing, really) a patient who was on the Atkins diet how harmful it was because of DKA.  I am so embarrassed by my complete stupidity and utter failure to pick up a single scientific article to fact check this dogma I was spewing to this poor patient. If you’re reading this, sir, please forgive me. You deserved a smarter doctor.
First of all, almond flour bread will never have EXACTLY the same texture as wheat bread because it lacks the gluten. It will be slightly softer. But. Baking with almond flour is never an exact science. If your almond flour is coarser, just add an extra couple of tbsp next time and the bread will be firmer. Or try reducing the amount of water so it dries out more. I would not recommend changing the amount of egg (unless you used extra large eggs). Hope this helps!
^ Ringberg TM, White RG, Holleman DF, Luick JR (1981). "Body growth and carcass composition of lean reindeer (Rangifer tarandus tarandusL.) from birth to sexual maturity" (PDF). Canadian Journal of Zoology. 59 (6): 1040–1044. doi:10.1139/z81-145. ISSN 0008-4301. Body growth and carcass composition were measured in lean reindeer during the juvenile growth period between birth and 3 years of age. Mean carcass weight in these lean reindeer was 56 ± 4% of body weight and the deposition of body muscle and bone mass was linearly correlated with body weight after the 1st month of age. The weight of the brain relative to body weight and carcass weight declined, while the relative changes in heart, liver, kidneys, parotid glands, and tissues of the gastrointestinal tract were small after the neonatal period. The extractable fat content in carcasses increased from 4.4 to 11.4% of wet weight or approximately 100 g fat at birth and 3.5 kg fat in adult reindeer. Fat-free dry matter represented a constant percentage (18–20%) of wet carcass weight independent of body weight after the neonatal period, while a significant inverse relationship between carcass fat and body water was found.
The ARC exerts opposing actions on food intake responding not only to leptin and insulin, but also to gut hormones (the most studied are ghrelin and, recently, PYY). The neurophysiological pathways suggest that feeding is regulated by a feedback loop, where the hypothalamus provides the long-term regulatory input to the NTS, which acts as a setpoint (Williams et al., 2001).
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. 
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.[24] 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.[25][26]
The metabolic syndrome is the name of a cluster of risk factors that, when they appear together, dramatically raise your risk of heart disease, heart failure, stroke and diabetes, as well as other non-cardiovascular conditions. Like smoking, it’s one of the strongest predictors of heart disease. “Nearly one in three Americans have metabolic syndrome. Many people don’t recognize that they have the condition and underestimate the risks it presents,” says Chiadi E. Ndumele, M.D., M.H.S. , cardiologist at the Johns Hopkins Ciccarone Center for the Prevention of Heart Disease. “Understanding that you have metabolic syndrome in the first place can help motivate you to make the needed changes.” 
In some cases epilepsy cannot be treated successfully using anticonvulsant medications. In some cases where drugs have failed, the ketogenic diet has been widely documented to deliver transformative seizure control, reducing frequency by anywhere between 40-90%43. Whilst the exact mechanisms underlying the beneficial effect of the ketogenic diet are unclear, the hypothesised mechanisms include:
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In rats fed a ketogenic diet (Bio-Serv F3666) for 22 days, mitochondrial density (determined by electron microscopy) in the hippocampus increased in conjunction with increased transcription of 39 of the 42 mitochondrial proteins analyzed [162]. Similarly, mitochondrial content (mtDNA copy number) increased in skeletal muscle of mice fed a ketogenic diet (Research Diets D05052004; % energy: 89.5 fat, 0.1 carbohydrate, and 10.4 protein) for 10 months [163]. Higher mtDNA copy number was also observed in skeletal muscle of rats fed a high-fat, low-carbohydrate diet (% energy: 60 fat, 20 carbohydrate, and 20 protein) for 4 weeks in conjunction with daily injections of heparin (0.5 U/g) to increase circulation of fatty acids [87]. In humans, after just 3 days of a low-carbohydrate, high-fat diet (% energy: 50 fat, 34 carbohydrate, and 16 protein), fat oxidation significantly increased and 49% of the variance was explained by mtDNA content [79]. Despite this, the content of mtDNA did not change significantly, but this was expected given the brief duration of the diet.
Glucose. Usually a fasting glucose test is performed but, in some cases, a healthcare practitioner may also order a post prandial glucose (after a meal) or a GTT (glucose tolerance test – several glucose tests that are taken before and at timed intervals after a glucose challenge). The goal of glucose testing is to determine whether a person has diabetes or a decreased ability to process glucose (impaired glucose tolerance), which can eventually result in diabetes.
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The longest studies/follow-ups for ketogenic diets are about 10 years long and have shown it to be safe [3, 4, 5, 6]. Studies that carefully keep people in metabolic wards to strictly monitor food intake and biomarkers are always short because they are very costly and laborious. Moreover, most participants are not able or willing to participate for a long time in a study that supervises food intake around the clock. For these reasons, these kinds of studies are always of short duration, a few weeks maximum.
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This is a classic breakfast for a reason: It's delicious, and the steak and eggs each pack a monster punch of protein to keep you fueled up till lunch. Next time you're grilling up steak at night, cook a little extra with incredible keto breakfast leftovers in mind. Tasteaholic's take uses sirloin, a leaner cut of beef, but feel free to use what you have on hand.
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The use of lifestyle interventions to treat and prevent chronic disease is attractive because of their potential to lower medical costs and produce more robust and holistic improvements in health. Ketogenic diets have been studied sporadically for more than 100 years, but over the last 15 years, a growing number of researchers have contributed to what is now a critical mass of discoveries that link the process of keto-adaptation to a broad range of health benefits [10–33]. Early clinical research focused on the use of “extreme” versions of ketogenic diets to treat seizures, but recent research indicates that benefits related to the management of epilepsy, weight loss, metabolic syndrome, and type 2 diabetes can be achieved with an approach that is less restrictive in carbohydrate and protein, and therefore more satisfying, sustainable, and feasible for the general population. A “well-formulated” ketogenic diet is generally characterized by a total carbohydrate intake of less than 50 g/d and a moderate protein intake of approximately 1.5 g/d per kg of reference weight [34]. This typically increases circulating β-hydroxybutyrate (BHB) and acetoacetate (ACA) from concentrations that are typically less than 0.3 mM into the range of nutritional ketosis, which for BHB, we define as 0.5–3 mM [35]. This range is below the typical 5–10 mM range for BHB that occurs during prolonged fasting, and well below concentrations characteristic of ketoacidosis [34, 35]. From the perspective of meeting energy demands, the reduced carbohydrate and moderate protein intakes necessarily make ketogenic diets high in fat. Despite this contradiction with mainstream dietary guidelines, ketogenic diets may be beneficial for many health conditions, particularly the previously mentioned conditions related to mitochondrial impairment, which includes obesity [10, 11], diabetes [12–14], cardiovascular disease [15–17], cancer [15, 18–26], neurodegenerative diseases [19, 20, 27–30], and even aging [31–33, 36, 37].
91. Speijer D. Oxygen radicals shaping evolution: why fatty acid catabolism leads to peroxisomes while neurons do without it: FADH(2)/NADH flux ratios determining mitochondrial radical formation were crucial for the eukaryotic invention of peroxisomes and catabolic tissue differentiation. Bioessays. 2011;33(2):88–94. doi: 10.1002/bies.201000097. [PubMed] [CrossRef] [Google Scholar]
“Individuals vary in their blood ketone levels (i.e., beta-hydroxybutyrate – aka BOHB) over the course of a day and from day to day. This can be due to variations in dietary carbohydrate and protein from meal to meal and from day to day…Additional factors that increase blood BOHB are endurance exercise and also after consuming fats containing medium chain triglycerides (MCT) such as butter, coconut oil, or purified MCT oil. In contrast, there is often a steep drop in BOHB after high intensity exercise, the mechanism for which has yet to be proven. This post-sprint drop in BOHB tends to be temporary (lasting for an hour or two), which means that it’s cause is very different from the days-long drop in blood BOHB that one sees after a large carb meal.”

Brain glucose and KB uptake was investigated in rats subjected to mild experimental ketonemia induced by 2 weeks on the KD or by 48 h fasting. To test this, researchers developed a carbon-11 labeled AcAc (11)C-AcAc for PET use. They found in rats that after 10 days of KD (11)C-AcAc brain uptake increased up to 8-fold, an increase comparable to those measured after 48 h of fasting (Pifferi et al., 2008).
Another mechanism that could be involved in food-regulation during KD is the gamma aminobutyric acid (GABA) and glutamate regulation. Wu et al. demonstrated that GABAergic signaling from the NPY/AgRP neurons to the parabrachial nucleus (located in the dorsolateral part of the pons) is involved in many regulatory sensory stimuli including taste and gastric distension, regulate feeding behavior. GABA signaling seems to prevent animals from anorexia when AgRP neurons were destroyed (Wu et al., 2009). These findings are yet another contradictory aspect of KDs and food behavior; ketosis should increase the availability of glutamate (via diminution of transamination of glutamate to aspartate) and therefore increase GABA and glutamine levels; moreover, in ketosis, the brain imports a huge amount of acetate and converts it through glia into glutamine (an important precursor of GABA) (Yudkoff et al., 2008). The result of these mechanisms, together with the increased mitochondrial metabolism and flux through the TCA cycle, is an increased synthesis of glutamine and a “buffering” of glutamate. These results are not consistent with the well-documented anorexigenic effect of KDs, and therefore the GABA hypothesis cannot be taken into account despite the mild euphoria often reported during a KD that is probably due to the action of BHB (Brown, 2007) and can help to reduce appetite.
Jenkins, D. J. A., Kendall, C. W. C., Augustin, L. S. A., Mitchell, S., Sahye-Pudaruth, S., Mejia, S. B., … Josse, R. G. (2012, November 26). Effect of legumes as part of a low glycemic index diet on glycemic control and cardiovascular risk factors in type 2 diabetes mellitus: A randomized controlled trial. JAMA Internal Medicine, 172(21), 1653–1660. Retrieved from
This was my first time baking anything EVER and it turned out perfectly! I do find that the bread does taste a tad “eggy” but it’s soft and a perfect replacement for sandwich bread. I can finally have grilled cheese sandwiches again!! Next time around, I’ll double the recipe because the bread was smaller than expected. Thanks for this amazing recipe!
Some people may ask: Why not just have liposuction of the abdomen and remove the large amount of abdominal fat that is a big part of the problem? Data thus far shows no benefit in liposuction on insulin sensitivity, blood pressure, or cholesterol. As the saying goes, "If it's too good to be true, it probably is." Diet and exercise are still the preferred primary treatment of metabolic syndrome.
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β-hydroxybutyrate and, in some cases, acetoacetate contribute to protection against oxidative stress by decreasing production of mitochondrial reactive oxygen species (mtROS), by increasing expression or protein content of antioxidant enzymes through histone deacetylase (HDAC) inhibition, and by directly scavenging the hydroxyl radical (•OH). Upregulation of antioxidant enzymes through HDAC inhibition includes manganese superoxide dismutase (SOD2), catalase, and metallothionein II and is likely mediated by the transcription factor forkhead box O 3a (FOXO3a).

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Ratliff J., Mutungi G., Puglisi M. J., Volek J. S., Fernandez M. L. (2009). Carbohydrate restriction (with or without additional dietary cholesterol provided by eggs) reduces insulin resistance and plasma leptin without modifying appetite hormones in adult men. Nutr. Res. 29, 262–268. 10.1016/j.nutres.2009.03.007 [PubMed] [CrossRef] [Google Scholar]

Fathead dough is a low carb/keto dough that is made out of cream cheese, mozzarella cheese, eggs and a flour substitute. It started out as a pizza crust recipe published by Tom Naughton while he was creating the movie Fat Head. The recipe became an internet viral sensation and has since been adapted and modified for recipes beyond pizza crust, such as breadsticks, bread rolls and bagels.