thanks for your reply, maria! i can’t figure out why mine tastes so vinegar-y while no one else has had this problem. could it be the type of vinegar i’m using? It’s trader joe’s organic ACV. could i just reduce the amount of vinegar? or, in your baking experience, do you think i could i use lemon juice as the acid in place of the vinegar (or a mix of the two)? i think i could stand a lemon taste better than a vinegar taste…
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“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.”
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Hi Anita, I double checked my carton egg whites. 3/4 cup of egg whites is equivalent to 4 large whole eggs, not 4 large egg whites. Mine has a chart for converting whole eggs, and the conversion for egg whites only is below the chart. It says 2 tablespoons of liquid egg whites are equivalent to the egg white of 1 whole egg. So, 12 large egg whites would be 24 tablespoons, or 1 1/2 cups as written in the recipe. Hope this helps!
Nice and firm. Baked it on the recommended temp, added 6 or 7 minutes. Pressed the middle and it was great. I let it cool. What was nice about it was obviously it’s low carb bread…hurray for that, but it cut well. Got 18 slices easily about 1/2 inch thick without breakage. Most importantly, it wasn’t greasy, or almond tasting overload, just delicious.
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Sounds weird? Yeah I thought so too! Ok let me explain. When at room temperature I’m fairly certain you’ll all agree it tastes like a lovely corn (free) bread. Dense, but soft and lightly crumbly (and I’m fairly certain that with a cornbread extract some good stuff will happen). But then when you warm it up, it goes softer again and reminds me of a lovely sweet bun.
Ketosis is a sensitive state so as soon as you increase your carb intake above your carb tolerance, you’re out! You probably don’t want to continuously weigh and count your food for the rest of your life. So even if you stick to the approved list of ketogenic food, there is no guarantee that you will be in ketosis without interruption. That’s OK. Now if you’re in ketosis to manage cancer or epilepsy, that’s a different story obviously.
The goal of the ketogenic diet is to keep you in this fat-burning metabolic state of ketosis. This is achieved by following a very low-carbohydrate, high-fat diet that includes only moderate amounts of protein. Foods like bread, cereal, processed snacks and sugary drinks are therefore off the table, while fattier foods like butter, grass-fed beef, fish and also non-starchy veggies take center stage, providing the majority of daily calories (as much as 70–80 percent).
You’ll recall, from the point I made above, that my brain requires about 400 to 500 kcal of glucose per day (100 to 120 gm).  You’ll also recall (from the video, above) that I can store about 100 to 120 gm of glucose in my liver.  While I can store much more in my muscles, (on the order of about 300 to 350 gm), because muscles lack the enzyme glucose-6-phosphatase, glucose stored in muscle as glycogen is unable to re-enter the bloodstream and is meant for the muscle and the muscle alone to use.  In other words, muscle glycogen is a stranded asset of glucose in the body to be used only by the muscle.
^ Lawrie 2014, pp. 92-. "A much delayed onset of rigor mortis has been observed in the muscle of the whale (Marsh, 1952b). The ATP level and the pH may remain at their high in vivo values for as much as 24h at 37ºC. No adequate explanation of this phenomenon has yet been given; but the low basal metabolic rate of whale muscle (Benedict, 1958), in combination with the high content of oxymyoglobin in vivo (cf 4.3.1), may permit aerobic metabolism to continue slowly for some time after the death of the animal, whereby ATP levels can be maintained sufficiently to delay the union of actin and myosin in rigor mortis."
I waited awhile to try this, certain it would be blah but decided to give it a go. I did add a pinch of salt and I used Brummel and brown butter, made with yogurt, as it lowered the fat and calories. toasted and spread some sugar free strawberry preserves. really good! texture took a bit to get used to but so excited to be able to eat bread! not on keto but recently diagnosed as diabetic so bread is a nono bc of all the carbs.
Going from a standard-American diet to a well-formulated low-carb or ketogenic diet is a health upgrade. However, it usually comes with unpleasant but temporary symptoms of carbohydrate withdrawal, also known as the keto flu. This is easily addressed by using Nutrita to properly follow a ketogenic diet or simply by familiarizing yourself with basic electrolyte management.
You’ve got a few options here. Erythritol (Lakanto is awesome here), Xylitol (non-corn though to avoid tummy troubles!) and allulose are my top choices (no aftertaste at all!). Pyure is also a good one for muffins and quick breads, particularly if you’re trying to limit your sugar alcohol consumption (it’s added stevia makes it twice as sweet as sugar… i.e. you add half!).
I think next time I will either use less psyllium or less egg. I had to halve the recipe and I used a bit more egg and water by accident. Next time I’ll try it with coconut flour since I think as a very “dry” flour it works best with flours/meals that are very “wet” like flax meal and psyllium. They cancel each other out in the end it seems. I’ll also bake it a bit longer because the crust is yummy!

Many athletes would not consider following a ketogenic diets due to the limited evidence of a performance enhancing effect, the risk of side effects having a negative impact on performance and the difficulty in maintaining the lifestyle changes required to stay in ketosis. Exogenous ketones offer a method to deliver some of the benefits of ketone metabolism without requiring athletes to follow a strict ketogenic diet. Taking exogenous ketones creates a metabolic state that would not normally occur naturally: the state of having full carbohydrate stores as well as elevated ketones.
There is one exception to exercising with diabetes. If your blood sugar is too high (such as over 240) and you are spilling ketones into your urine, then exercise is only going to increase your blood sugar. You can buy a dipstick urine test to check for ketones, but the best thing to do would be to talk to your doctor about what is safe for you to do.
As is in the case of GABA, the intracellular reactive oxygen species (ROS) hypothesis works against the hunger-suppressive role of KD: it has been demonstrated that the hypothalamic ROS increase through NADPH oxidase is required for the eating-inhibitory effect of insulin (Jaillard et al., 2009); moreover it has been demonstrated that there is a ROS-dependent signaling pathway within the hypothalamus that regulates the energy homeostasis, and that activation of ROS-sensitive mechanisms could be sufficient to promote satiety (Benani et al., 2007). On the other side, KBs decreases mitochondrial production of ROS by increasing NADH oxidation in the mitochondrial respiratory chain (Maalouf et al., 2007).
Whey protein isolate. This one is pretty much a must if you’re baking the bread in a pan (say as opposed to muffins), as it will ensure your bread doesn’t collapse post-bake. Having said that, you can sub it with more almond flour and bake it in a muffin pan (smaller baked goods have don’t require as much structure). Not exactly the same, but works well.
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.

I read through aaaaallllll the comments for research before I made this bread, one thing I noticed when making your protein buns was – when I used 2 teaspoons of baking powder they deflated when exiting the oven. When I reduced the BP to 1.5 teaspoons, they turned out fine. I made two batches with 2 tsp of BP – they turned out like raisins, and 2 batches with 1.5 tsp of BP and they turned out fine. No one posting mentioned adjusting the baking powder – perhaps that would help in this recipe since deflating is a problem, maybe there is too much chemical loft for the non-gluten structure to handle?
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).
By dramatically shifting energy metabolism towards ketogenesis and fatty acid oxidation, ketogenic diets are likely to have a profound effect on mitochondrial function. However, despite the rapidly growing amount of research on ketogenic diets and their effects on various disease states, only a small amount of this research has focused on mitochondrial function or oxidative stress. The well-established increase in fat oxidation induced by a ketogenic diet [7, 8] clearly indicates prominent connection with mitochondrial function and, in turn, oxidative stress and mitohormesis [5, 6, 9]. Therefore, the purpose of this review is to describe the current, but limited, understanding of how ketogenic diets may affect mitochondrial function and resistance to oxidative stress, particularly within the context of extending human healthspan.
Dr. Campos, it is so discouraging to see that you disparage the ketogenic diet based on your assumption that it is very heavy in poor quality processed meats. No diet that relies on processed foods can be viewed as “healthy”. Become better informed by getting up to speed with what Jeff Volek, RD, PhD, calls a “well-formulated ketogenic diet.” Also, learn more about the potential of the diet to slow cancer progression (my specialty). You owe it to your patients who are depending on you for advice. Present them with facts, not opinions.
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In the absence of acetyl CoA (several ways this can happen, including substrate shortage, as I’m describing here) we evolved a cool trick.  Our liver can make – out of fat or protein, though we much prefer to use fat so we can spare our protein and prevent severe muscle wasting – something called beta-hydroxybutyrate, one of the 3 ketone bodies I described above.

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.
It is known that different dietary components exert some effects on gut microbiome composition, mainly in relation to obesity and inflammatory states. In general, a Mediterranean diet has a positive effect while a high-protein diet seems to have detrimental effects due to putrefaction phenomena (Lopez-Legarrea et al., 2014; Flint et al., 2015). Few data are available at this time about the effects of KD on gut microbiota. For example, a study by Crawford et al. (2009) investigated the regulation of myocardial ketone body metabolism by the gut microbiota and demonstrated that, during fasting, the presence of gut microbiota improved the supply of ketone bodies to the heart where KBs were oxidized. In the absence of a microbiota, low levels of KB was associated with a related increase in glucose utilization, but heart weight was still significantly reduced. The myocardial-mass reduction was completely reversed in germ-free mice feeded with a ketogenic diet. Regarding food control we can hypothesize that the particular metabolic state of ketosis could provide some benefit to weight and food control via synergic actions between butyrate production by gut bacteria and circulating high blood ketones (Sanz et al., 2015).
Additional evidence, although independent of mitohormesis, further supports the induction of NFE2L2 activity by nutritional ketosis. Succinate is a byproduct of ketolysis and is oxidized to fumarate by succinate dehydrogenase. Therefore, the increased presence of ketones and increased rate of ketolysis during nutritional ketosis are likely to increase fumarate, which can succinylate cysteine residues of proteins [363]. In particular, fumarate can succinylate Keap1, thereby allowing NFE2L2 to enter the nucleus to induce transcription [364, 365]. In the retinas of rats injected with BHB, the nuclear content of NFE2L2 and the total homogenate content of SOD2 and GCL increased in conjunction with increased fumarate concentration [366]. BHB injection also decreased retinal ROS production and degeneration following induction of ischemia, and this protection was dependent on NFE2L2 [366]. These effects were observed at blood concentrations of BHB between 1 and 2 mM, which is consistent with nutritional ketosis.

Lipodystrophic disorders in general are associated with metabolic syndrome. Both genetic (e.g., Berardinelli-Seip congenital lipodystrophy, Dunnigan familial partial lipodystrophy) and acquired (e.g., HIV-related lipodystrophy in patients treated with highly active antiretroviral therapy) forms of lipodystrophy may give rise to severe insulin resistance and many of metabolic syndrome's components.[27]


Looking back on my earlier posts on ketosis—and explaining what I eat, for example—makes me both chuckle and cringe. I remember how bizarre the diet seemed to many readers and the general public at the time. I also remember digging into the literature and learning, for example, that my alma mater, Johns Hopkins had been using the ketogenic diet to treat pediatric epilepsy for almost a century…and being so embarrassed about admonishing that patient I saw in my residency.
How long does it take to get into ketosis? This will depend on a few factors, including how strictly you limit your carb intake and also certain variables that are mostly out of your control, like your genetics, medical history, body composition and energy needs. If you’re consistently eating from food list, you should be able to see results and improvements within a short couple of weeks.
This website is for informational and educational purposes only. Statements have not been approved by the FDA. The reader assumes full responsibility for consulting a qualified health professional before starting a new diet or health program. All nutritional information is estimated using an online program, it is the users responsibility to verify the accurecy of this information. The writer(s) and publisher(s) of this site are not responsible for adverse reactions, effects, or consequences resulting from the use of any recipes or suggestions herein or procedures undertaken hereafter.

It’s well known that adherence to the prescribed diet is usually low and self-reported food intake is very unreliable. So there’s no way to guarantee that the participants strictly adhered to the diet. Because it requires a lot of discipline and planning to stay in ketosis for a long time without interruption, it won’t be possible to perform a long-term study that guarantees uninterrupted ketosis using old study methods. This may change soon with improved self-tracking devices.
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Moreover, in the above study of Sumithran et al. (2013), ketosis maintains post-prandial secretion of CCK as previously demonstrated by other researchers (Chearskul et al., 2008). Note that the orexigenic effect of BHB is blocked by transection of the common hepatic branch of the vagus nerve (Langhans et al., 1985). The hepatic branch contains fibers from the proximal small intestine, stomach and pancreas, and is sensitive to CCK (Horn and Friedman, 2004); ghrelin signals to brain are also transmitted via vagus nerve (Habara et al., 2014). Thus, the effects of ketosis on these two appetite-related hormones could be one of the many factors related to the effects of such nutritional regimen on food control.

Like many variables in diet, health, and disease, it behooves us to look beyond the bumper sticker explanation. I want to highlight a couple of posts I wrote, to attempt to provide a little more nuance and understanding to the subject: “Ketosis — advantaged or misunderstood state?” Parts I and II. Part I follows below. I’m hoping to write more on the topic in the not-too-distant future since there’s been a number of intriguing papers published recently (certainly since 2012). But I also wanted to bring these back into focus in light of the information I’m seeing more of on the interwebz. (You can also visit the Ketosis section of the site to view more articles on the subject.)
Just made my 3rd loaf. My technique has been improving each time so I am getting a better result! I had never baked anything before like this and there is an art involved. But the deliciousness has never been absent… the mixture of these ingredients has been amazing. Just going from Salvador Dali bread to Leonardo Divinci for style is the new goal!
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.
A good low carb breakfast can set the tone for the rest of the day, so we make sure it’s delicious and satisfying! Whether it’s a quick Bulletproof coffee to get your day started or a full blown bacon, egg and cheese, pancake Sunday breakfast, everybody loves the first meal of the day. Our full collection of keto breakfast recipes should inspire you to mix breakfast up a bit and try to include new things in your morning routine.
The discovery of many appetite-related hormones provided molecular basis for appetite control, decreasing the relevance of the metabolites hypothesis (Karatsoreos et al., 2013). Recently, Sumithran et al. demonstrated that there is a long-term persistence of changes in some peripheral hormones involved in food control (Sumithran et al., 2011). In this study, they found a significant difference in mean levels of many food intake-related hormones 1 year after the cessation of weight loss via the hypocaloric diet. There was a long lasting decrease of anorexigenic compounds: leptin, PYY, cholecystokinin, insulin, and pancreatic peptide and an increase of the orexigenic molecule ghrelin. Moreover, they found that hunger remained elevated 1 year after diet cessation. In a successive study the same group investigated hunger-related hormones after 8 weeks of KD, demonstrating that during ketosis the increase of ghrelin (a strong stimulator of appetite) was suppressed (Sumithran et al., 2013). These results are consistent with those of Ratliff et al (Ratliff et al., 2009), who found no significant change in fasting plasma ghrelin after 12 weeks of VLCD.
One side effect of ketosis that some people experience is the keto rash. It is rare but can be very irritating. The keto rash occurs in the armpits, chest, and back. These areas are red and itching. There are several theories about the causes of the rash. Because it is found in regions where sweat accumulates, the most plausible explanation is that acetone in the sweat irritates the skin. [7].
I love this recipe! Thanks for sharing, my 1st batch came out awesome, my 2nd batch, like others have described came out a bit dry and started breaking apart. So I added about a tablespoon of hot water at a time till I got the texture that I wanted and it didnt fall apart after I added a bit more water. This dough texture reminds me a lot of corn dough that is used to make tamales. So if you've made tamales this might be easy for you to make. I also took another user's advise and used a corn tortilla press, that made spreading it an easy. Definitely a redo. Already made 2 batches one with chorizo and egg the other with pepperoni, marinara and cheese and the kids love them!
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Increased reliance on mitochondrial respiration will increase the flow of electrons through the mtETC and, in turn, increase the potential for mtROS formation. Although oxidative stress is traditionally viewed as harmful, a modest increase in ROS is now established as a signaling stimulus that induces hormetic adaptation [3]. In regard to mitohormesis and mtROS, such adaptation is largely centered around antioxidant defense [4–6], making mitohormesis an attractive target for the prevention and treatment of chronic disease.
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Try to be patient. Although some people get into ketosis relatively quickly, it can take others a while. Unfortunately, people who are insulin resistant often have a longer journey. Put in a solid month of consistent keto eating, and try to ramp up your physical activity, if possible. Within four weeks, you should definitely be in ketosis and experiencing its benefits.
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