“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.”
To conclude, athletes may consider adopting a ketogenic diet in the hope of improving endurance, well being and body composition but unless the diet is well formulated they risk causing fatigue, under fuelling and ultimately compromising performance. There is currently insufficient scientific research to definitively support the use of ketogenic diet for athletes to improve performance, although beneficial effects on fat oxidation, body composition and well-being have been described. However, the anecdotal reports of success and the increasing number of pro and elite athletes claiming to be experimenting with the ketogenic diet is compelling. Furthermore, people who are training and competing at a sub elite level may have a greater net benefit from the effects of the diet on recovery, wellness and body composition that may outweigh the loss of top end power resulting from the diet. Finally, it is unknown if there would be a beneficial effect of following the ketogenic diet but adding in strategic carbohydrate refeeds around more intense training and competition periods. Given the popularity of the ketogenic diet, one hopes these questions will be addressed in the near future. 
The most common reason that any bread falls is that it needed to bake for longer. That being said, I’ll be perfectly honest – sometimes this keto bread recipe falls anyway, even despite doing everything else right. Fortunately this isn’t a huge deal because it still tastes delicious – IF you baked it for long enough and the center is cooked through.

143. Echtay K. S., Winkler E., Frischmuth K., Klingenberg M. Uncoupling proteins 2 and 3 are highly active H+ transporters and highly nucleotide sensitive when activated by coenzyme Q (ubiquinone) Proceedings of the National Academy of Sciences. 2001;98(4):1416–1421. doi: 10.1073/pnas.98.4.1416. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
^ Jump up to: a b c Clemente FJ, Cardona A, Inchley CE, Peter BM, Jacobs G, Pagani L, Lawson DJ, Antão T, Vicente M, Mitt M, DeGiorgio M, Faltyskova Z, Xue Y, Ayub Q, Szpak M, Mägi R, Eriksson A, Manica A, Raghavan M, Rasmussen M, Rasmussen S, Willerslev E, Vidal-Puig A, Tyler-Smith C, Villems R, Nielsen R, Metspalu M, Malyarchuk B, Derenko M, Kivisild T (October 2014). "A Selective Sweep on a Deleterious Mutation in CPT1A in Arctic Populations". American Journal of Human Genetics. 95 (5): 584–589. doi:10.1016/j.ajhg.2014.09.016. PMC 4225582. PMID 25449608.
Most of these benefits occur due to the decrease in dietary carbohydrate intake; it is largely unknown what role ketones themselves play in the efficacy of the diet. Because of this, it is unclear how exogenous ketones could be used to help treat diabetes. One effect that is consistently reported is that ketone ester and ketone salt drinks and infusions lower blood glucose and lipid levels 11,106 ,107. It is also possible that exogenous ketones have a positive effect on insulin sensitivity; ketone ester supplementation increased insulin sensitivity in rodents by 73%108. It is possible that exogenous ketones could be used alongside diet and lifestyle changes to help control blood in diabetes, but further research must be done before this can be realised. 
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.
Agree with post regarding salt omitted salt, grilled it first time. It definitely reminds me of corn muffins texture. This morning make recipe added 1 T. of swerve brown sugar and dash or cinnamon,nutmeg and chopped walnuts OMG. It was great topped with cream cheese frosting(cream cheese,butter ,vanilla and swerve confection .Thanks can’t wait to try pumpkin spice next time I’m craving carrot cake thanks so much!
Russel Wilder first used the ketogenic diet to treat epilepsy in 1921. He also coined the term "ketogenic diet." For almost a decade, the ketogenic diet enjoyed a place in the medical world as a therapeutic diet for pediatric epilepsy and was widely used until its popularity ceased with the introduction of antiepileptic agents. The resurgence of the ketogenic diet as a rapid weight loss formula is a relatively new concept the has shown to be quite effective, at least in the short run.

Notably, it can take several months to become fully ‘keto-adapted’ and performance can decline in the short term as these adaptations occur. It is also likely that individual responses to the diet vary. These factors make design and interpretation of sports science studies challenging and leave the door open for continued disagreement between scientists on each side of the debate. If you want to find out what each side has to say, we would recommend reading the comprehensive reviews by Louise Burke (who dislikes the use of the ketogenic diet)27 and Volek and Phinney (who promote the use of ketogenic diet)28. 
Patterns can be great because they help you figure out what is causing undesirable blood sugar values. A good way to track of it is to keep a journal of all of the food you eat, activities you do and your blood sugar levels for 1 week. During this week, check your sugar before and after you eat, as well as in between meals. Also document any insulin that you give yourself.

I would like to point out that the metric conversion of 3/4 cup to 90g coconut flour as stated in your recipe is incorrect. Should be 84g per package labeling (Bob’s Red Mill). Unfortunately I made my first batch with 90g of coconut flour, and it was definitely not “pourable”. More like scoopable. I will try again with correct amount but thought I would point so you can update the recipe. Thank you!
Ketolysis is the process of breaking down ketones to ultimately provide energy through the Krebs Cycle and mitochondrial oxidative (using oxygen) phosphorylation. Ketone bodies are broken down in the mitochondria of virtually all tissues in the body. The liver is a notable exception, being unable to utilise ketones as a fuel because liver cells lack acetyl-CoA thiolase, a key enzyme in the ketone oxidative pathway. BHB enters the mitochondria of the cell through a monocarboxylate transporter, undergoes conversion to acetoacetate by BHB dehydrogenase and then addition of a CoA group from succinyl-CoA by 3-oxo-acid transferase. The resulting acetoacetyl-CoA acts a substrate for the formation of two molecules of acetyl-CoA in a reaction catalysed by acetyl-CoA thiolase. Acetyl-CoA is then available to condense with oxaloacetate and enter the Krebs cycle.
Dr. Campos, it is unfortunate that you retain the medical community’s negative stance on the ketogenic diet, probably picked up in medical school when you studied ketoacidosis, in the midst of an obesity and type II diabetes epidemic that is growing every year, especially among populations who will never see the Harvard Health Letter. The medical community has failed in reversing this trend, especially among children, and the public is picking up the tab, in the form of higher health insurance premiums to treat chronic metabolic diseases which doctors cannot cure. The ketogenic diet does not bid its adherents to eat unhealthy processed meats, and the green leafy vegetables that it emphasizes are important in a number of nutritional deficiencies. People lose weight on the ketogenic diet, they lose their craving for sugar, they feel more satiety, they may become less depressed, their insulin receptors sensitivity is improved, and these are all the good outcomes you fail to mention. There is a growing body of research which demonstrates the neuroprotective effects of the ketogenic diet to slow cancer progression, as well as diseases like Parkinson’s and Alzheimer’s, for which there are no effective medical treatments. Please respect your patients by providing them with evidence-based medical outcomes, not opinions.
If you are someone who has struggled with the roller coaster of blood sugar management, I have some good news! Research shows that there are common herbs and spices, likely ones that you already have in your kitchen, that have some potential positive effects on improving blood sugar. Today, I’m breaking down some of the superstar herbs and spices that data has indicated may help with blood sugar management.
When preparing keto bread recipes, look out for low-carb ingredients that could contribute to brain fog and inflammation. Skip recipes that require conventional dairy or yeast, and avoid eating common keto bread ingredients like psyllium husk, xanthan gum, and nuts or nut butters too often — these can contain mold or irritate your gut. Grass-fed butter, ghee, and coconut flour are the few exceptions that will still produce a stellar loaf.
Sigh…..Made it with high hopes and boy did it smell good! I used all your brands and weighed it all, but I wound up with a loaf that did sink, which I don’t care if it sinks, but it was still gelatinous and wet on the inside. I hate wasting so much almond flour, but I will try again. What would you recommend I change? Decrease the water? It puffed up so beautifully and my husband told me it’s a good crust, lol. I cubed up the whole loaf and I’m trying to make it in to croutons now but I’m unsure those wet little cubes will ever dry out. This is my first flop. I have LOVED all your other recipes so far! Thank you!
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A reduced availability of dietary carbohydrates leads to an increased liver production of KBs. The liver cannot utilize KBs because it lacks the mitochondrial enzyme succinyl-CoA: 3-ketoacid (oxoacid) CoA transferase (SCOT) necessary for activation of acetoacetate to acetoacetyl CoA. KBs are utilized by tissues, in particularly by brain. KBs enter the citric acid cycle after being converted to acetyl CoA by hydroxybutyrate dehydrogenase (HBD), succinyl-CoA: 3–CoA transferase (SCOT), and methylacetoacetyl CoA thiolase (MAT). Modified from Owen (2005), Paoli et al. (2014).
White mulberry (Moruns alba or Morus indica) has been traditionally used in Asia to help treat type 2 diabetes, and there is some preliminary evidence to support this use. Mulberry leaf extract (species not given) may lessen increases in blood sugar after ingestion of table sugar in healthy people and people with type 2 diabetes (Mudra, Diabetes Care 2007). Among people with type 2 diabetes, taking 1 gram of powdered white mulberry leaf three times daily (after breakfast, lunch and dinner) for four weeks was found to lower fasting blood sugar by 27%, while taking 5 mg of the anti-diabetes drug glibenclamide lowered fasting blood sugar by only 8% (Andallu, Clin Chim Acta 2001).
I’m discouraged to see that nowhere in the article nor in the comments is there a mention of a diet’s best fit to genetics. Consider if someone is an APOE E2 carrier and/or has certain polymorphisms of the APO5 gene. These are quite rare in Okinawa but much more prevalent in the USA (12% of the population). According to a number of well-designed studies, these genetic characteristics point to a higher fat, lower carbohydrate diet as beneficial and even a “moderate” carb diet as problematic.

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).

In order to best investigate the efficiency of different fuels, one needs a closed system, where the substrate conditions can be changed and the oxygen consumption and work done can be accurately measured. Isolated (ex-vivo) animal hearts are the best model to study these variables, as it is easy to manipulate the fuel provided (i.e glucose, ketones), to measure the oxygen use and also the amount of work (how much fluid is pumped). 


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Hi Tammy, I still have to try the muffin tin method to ive you a better response. Why don’t you make the recipe using exact ingredients for one bread multiplied x 9-10 and divide between 12 muffin tin slots? I think this will work better. This way we are not changing the amount of eggs. If you use less eggs, the bread will be more dry, since it is gluten-free.
The Mediterranean diet is palatable and easily sustained. In addition, recent studies have shown that when compared to a low fat diet, people on the Mediterranean diet have a greater decrease in body weight, and also had greater improvements in blood pressure, cholesterol levels, and other markers of heart disease -- all of which are important in evaluating and treating metabolic syndrome.
Theoretically, supplying ketones during this period of compromised glucose metabolism could prevent the energy deficit and reduce the likelihood of long-term brain damage. This could be because ketones can act as an alternative, highly energy efficient substrate7. Additionally, the antioxidant, antiinflammatory33 and anti-apoptosis properties of ketones (i.e ketones prevent the opening of the mitochondrial permeability transition pore, which causes cell death66) could protect against neuronal loss and damage. 
I love this low carb pancake recipe because it makes fluffy pancakes and the batter is thick enough to make perfectly round pancakes that make the perfect bread for this breakfast sandwich.  Hold your hats, folks, because everything in this recipe is perfect!  I added a little sugar free maple syrup to the batter to sweeten them up.  I cook them on medium heat and wait to flip until little bubbles start to form around the edges.

When you eat more food than your body needs, it’s converted to triglycerides and stored inside your fat cells. The more often you keep consuming large amounts of glucose through carbohydrate foods, the less your body needs to tap into existing sources (your fat cells or stored glycogen in your liver and muscles) for energy, so your newly added fat cells remain intact and, therefore, weight loss is much more difficult.


The clinical relevance of nutritional ketosis to mitochondrial function is further indicated by promotion of ketogenic diets for treatment of mitochondrial disorders [19, 20, 26, 30, 247, 403]. The most prominent example is the study of mitochondrial adaptations as a mechanism for the well-known antiseizure effect of ketogenic diets [19, 29, 33, 162, 247, 403–405]. As previously discussed, the dramatic shift in energy metabolism and subsequent increase in circulating ketones induced by a ketogenic diet can enhance mitochondrial function and endogenous antioxidant defense. The primary mechanism behind these adaptations appears to be the increased demand for fat oxidation resulting from carbohydrate restriction. However, ketones themselves have important metabolic and signaling effects that enhance mitochondrial function and endogenous antioxidant defense, implying that a well-formulated ketogenic diet should have greater benefit than a nonketogenic low-carbohydrate diet. Regardless of the mechanism(s), the potential outcomes imply protection against chronic disease through improved mitochondrial function and, in turn, decreased potential for oxidative stress and subsequent pathology. However, further research is needed to better understand how nutritional ketosis influences mitochondrial function across different tissues and how these influences relate to human disease. Future research should also focus on further differentiation of the effects of carbohydrate restriction from the direct effects of ketones.

Metabolic syndrome is a collection of heart disease risk factors that increase your chance of developing heart disease, stroke, and diabetes. The condition is also known by other names including Syndrome X, insulin resistance syndrome, and dysmetabolic syndrome. According to a national health survey, more than 1 in 5 Americans has metabolic syndrome. The number of people with metabolic syndrome increases with age, affecting more than 40% of people in their 60s and 70s.
We have solid evidence showing that a ketogenic diet reduces seizures in children, sometimes as effectively as medication. Because of these neuroprotective effects, questions have been raised about the possible benefits for other brain disorders such as Parkinson’s, Alzheimer’s, multiple sclerosis, sleep disorders, autism, and even brain cancer. However, there are no human studies to support recommending ketosis to treat these conditions.
Although resting skeletal muscle is less metabolically active than the heart, kidneys, brain, or liver, it rivals even the brain in being the body's most metabolically demanding tissue when considered relative to total tissue mass [369]. Physical activity can greatly increase this demand, making exercise a practical and powerful way to induce bioenergetic adaptations.
First I tried using coconut flour only. The batter was very thick and pasty and the resulting bread was very firm and dry, like a really dry biscuit. It did, however, keep its shape well and toasted up evenly golden-brown in a skillet with oil. I thought about trying again with more liquid, but that wouldn’t solve its fatal flaw: the strong, overwhelming coconut flavor. Even chicken and sun-dried tomato pesto could barely cover it up.
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Also that’s absolutely wrong information about microwaves. Breast milk is not microwaved because of the uneven heating which can cause ‘hot spots’ which will lead to your baby’s mouth being burned. It does nothing to the nutrition of the milk itself or the proteins. There is a lot of fear mongering about microwaves and most people don’t understand the basic principle of how it works. It’s like people who blindly say there are ‘chemicals’ in food not realizing that everything is a chemical compound, even drinking water. So don’t worry 🙂


Rick, Yes, I would try baking it longer if it’s coming out gummy. If it’s starting to brown too much outside, but the inside doesn’t seem to be fully cooked, you could cover it with foil to prevent over-browning. Another trick I sometimes use is to leave the bread in the oven to cool once it’s done baking (sometimes covering the loaf with foil to prevent over-browning). I hope these tips help!
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