Nutritional ketosis is a natural metabolic state in which your body adapts to burning fat rather than carbohydrates as its primary fuel. It is clinically proven to directly reduce blood sugar (as measured by HbA1c), improve insulin sensitivity (as measured by HOMA-IR) and reduce inflammation (as measured by white blood cell count and CRP). Nutritional ketosis can be induced by following a ketogenic diet. Learn more in our FAQ below!
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Ketone esters (BHB-BD) lowers blood lactic acid 30. Lactic acid build up occurs during exercise as a result of burning carbohydrate at a high rate without enough oxygen. Blood lactic acid levels during exercise were 30% lower after ketone ester drinks compared to carbohydrate drinks. This is because high blood levels of BHB from the ketone ester drink slow down carbohydrate use and increase oxygen efficiency, which could decrease blood lactic acid levels. 


Carbohydrates need to be consistent. You don’t want to eat all of your daily carb count in one meal. That will cause your blood sugar to spike, and then drop during the other meals. Giving your body a steady amount of carbohydrates will provide a stable amount of energy. It will also help your body make enough insulin to keep your blood sugar at a healthy number.
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Maria, I made this bread today – weighed my ingredients carefully and followed instructions. My only adaptation was adding a little liquid Stevia, cinnamon, and raisins right before putting into the bread pan. It raised nicely but fell a little while cooling and is pretty heavy, although tastes great. Any help on what I did wrong? (I’m not sure my water was boiling enough – it was just starting to bubble, not full rolling boil, when I added it. Would that make the difference?)
I finally made this recipe. (I have made many of your others and use them often.) It did fall slighty but I was still able to slice it after it cooled. It was also purple, which is just fine with me. I toasted in the oven this morning and it was nice and crisp. I can’t tell you have happy I was to dip it in my fried egg this morning. Thanks, Maria, for all you do!

In controlled studies on exercise-trained humans and animals, ketogenic diets have been shown to increase fat oxidation [8, 167] and expression or activity of carnitine palmitoyltransferase [167, 168] and β-HAD [168, 172], demonstrating that nutritional ketosis induces adaptation beyond exercise. Similarly, in a study comparing the independent and combined effects of exercise and a ketogenic diet on rats, the combination resulted in greater β-HAD and citrate synthase activities in skeletal muscle and higher maximal O2 consumption than either intervention alone, further indicating the potential for exercise to magnify adaptations induced by nutritional ketosis [156].
How can ketosis help reduce your risk various health concerns? It comes down to the benefits of stabilizing your blood sugar and decreasing glucose intake and usage. As glucose enters your blood, your pancreas sends out insulin to pick up the sugar and carry it to your cells so they can use it as energy. However, when your cells have used or stored all the glucose that they can, what remains is converted into glycogen to be stored in the liver and muscles OR converted into triglycerides, the storage form of fat.
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!
Hi John, You could possible try a hand mixer in a bowl instead of the food processor, but I haven’t tried it, so can’t vouch for the results. Most likely the bread would not be as tall because the mixer would completely deflate the first half of the egg whites when you add them to the batter. The second half should be folded so that part will be find. If you try with a bowl and hand mixer, let me know how that goes.
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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.
The ketogenic diet can compromise high intensity sprint performance: High intensity exercise performance is heavily reliant on the ability to produce energy via anaerobic respiration (glycolysis), which requires carbohydrate as a substrate. Following a ketogenic diet causes a decrease in the amount/activity of the enzymes in the glycolysis pathway that decreases the rate that the pathway can proceed24. This could explain the decrease in anaerobic sprint performance consistently seen with athletes following a ketogenic diet 25 ,23. 
NOTE:  Make sure to weigh your ingredients to ensure it rises properly and doesn’t get hallow and gummy.  Also, if you do weigh and grind your psyllium and still have a problem, try grinding the psyllium again.  We have a batch of psyllium that we ground and didn’t work.  Stay really wet.  So we ground it again and it works great!  Also, if your loaf looks nice and big but then deflates after removed from the oven, try reducing the baking powder to 3 teaspoons.
Weight loss is the primary reason my patients use the ketogenic diet. Previous research shows good evidence of a faster weight loss when patients go on a ketogenic or very low carbohydrate diet compared to participants on a more traditional low-fat diet, or even a Mediterranean diet. However, that difference in weight loss seems to disappear over time.
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!
Attempt #4 or 5, I lost count 🙂 I measured everything by weight (ounces and grams as you listed) not by cups or tsps, etc. Put in oven at 375 since I don’t have convection and the previous attempts didn’t rise. This one rose beautifully! Nice beautiful color! Cooked 80 minutes. Let cool completely in my 8×4 metal loaf pan. Several hours later, I decided to take out of pan and cut a slice. It caved a little in on the sides, it looks similar to your 12 oz water picture, but it is wet. I’m not sure you’d call it gummy but definitely too much moisture again. And, I thought I finally had one! Back to the testing…I’ve gone thru 1/2 my Honeyville 5 lb bag and haven’t had one successful loaf yet 🙁
Hi Maria! Just wanted to say I love this recipe and I found a way to make similar single servings quickly that look like english muffins! I just use a greased ramekin and combine 2 tbsp almond flour, 2 tsp psyllium husk (or 1 tsp powder), pinch of salt and baking powder. Then stir in 2 tbsp + 2 tsp egg whites, 2 tbsp water, 1 tsp olive oil and 1/8 tsp apple cider vinegar. Microwave for 1 min then flip out onto a plate and microwave for another 30 sec. Toast and top with whatever you’d like! 🙂
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.
Hi Diane, the bread should not be moist in the middle now should it fall apart. I don’t think substituting the butter for coconut oil could have been the reason for the problem – they have similar consistencies and can normally be subbed for one another without problem. The only thing I can think of is that you may need to bake it for longer. Ovens do vary and maybe it was the case that it was just not done. I hope this helps 🙂
My first try at this recipe –lower half was gummy. Crust tasted amazing to I’m eating the ends as toast. I’m too frugal to throw away 3 cups of almond flour, so I cubed up the rest of the loaf, put it in to bake at 350 for 30 minutes or so. Cubes are great on salad -taste like toasted almond/sesame. Now I’m making savory bread pudding with about 2 cups of the cubes (6 eggs, 3/4c almond milk, 1/4c cream, cooked bacon bits, shallots, basil and chives). Baking in muffin tins. Will be taking them for lunches.
Back in the really old days (like in the Paleolithic), life had some challenges. Like saber-tooth tigers. What happened when your ancient ancestors encountered a saber-tooth cat? I imagine they threw their hands up in the air, screamed, and ran like hell. To assist in the running like hell, their bodies would dump sugar into their blood for extra energy. To this day, our bodies still do that. The problem is that the modern saber-tooth tiger is the overdue electric bill, the dropped cell phone call, the dinnertime telemarketer, and the annoying neighbor. You can’t run away from any of these tigers. The extra sugar just sits in your body. But you can learn to defeat this ancient biological fight-or-flight response by learning how to relax. You’ll need to make time for you. It might be a warm bubble bath in the evening, a good book at lunch, aromatherapy candles, or even kickboxing. Take that, saber-tooth tiger. Bam!

Among the chronic and degenerative diseases in which impaired mitochondrial function is a contributing factor, many respond favorably to lifestyle interventions focused on diet and exercise. The therapeutic potential of nutritional ketosis stands out in this regard. For example, in just the first 10 weeks of an ongoing clinical trial with hundreds of type 2 diabetics following a ketogenic diet, glycated hemoglobin (HbA1c) decreased to below the diagnostic threshold in more than a third of patients, and prescription medication was reduced or eliminated for more than half of patients [12]. Convincing arguments for a ketogenic diet to be the default treatment for diabetes are a decade old [13] and have continued to gain support since then [14]. Similar arguments are developing for obesity [10, 11], neurodegenerative diseases [19, 20, 27–30], cardiovascular disease [15–17], cancer [18–26], and even aging [31, 32]. Although the mechanisms through which a ketogenic diet may improve these conditions expand beyond mitochondrial function, the great extent to which nutritional ketosis increases reliance on mitochondrial metabolism strongly suggests that mitochondrial adaptation is a central factor.


More recently, other hypothalamic appetite control regions have been identified, including those in the arcuate nucleus (ARC), the periventricular nucleus (PVN) and the dorsomedial hypothalamic nucleus (DMH) (Valassi et al., 2008). These are sites of convergence and integration of many central and peripheral signals, not just macronutrients, that are involved in food intake and energy expenditure mechanisms, e.g., a group of neurons in the ARC stimulating food intake via neuropeptide Y (NPY) and agouti gene-related protein (AGRP). These neurons interact with those producing the anorexigenic pro-opiomelanocortin (POMC) and the cocaine/amphetamine-regulated transcript (CART) (Williams et al., 2001). Thus, a more comprehensive, unified model should include macronutrients as well as many single amino acids and other signaling molecules.
The last point I’ll make on the starving patient is that, as you can see in the figure below, the glucose level normalizes at about 65-70 mg/dL (about 3.7 mM) within days of fasting, despite no sources of exogenous glucose.  Why?  Because with so much fat being converted into B-OHB and acetoacetic acid by the liver, a significant amount of glycerol (the 3-carbon backbone of triglycerides) is liberated and converted by the liver into glycogen.  As an aside, this is why someone in nutritional ketosis – even if eating zero carbohydrates – still has about 50-70% of a normal glycogen level, as demonstrated by muscle biopsies in such subjects.
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.
More specific to mitochondrial function, treatment with BHB + ACA (1 mM each) has decreased O2•− production in isolated rat neuronal mitochondria following glutamate exposure [109]. This occurred in conjunction with decreased NADH levels, suggesting that ketones may additionally decrease mtROS production by enhancing electron transport along the mtETC after NADH oxidation and, in turn, decreasing mitochondrial Δp and associated O2•− production. The observed decrease in mitochondrial O2•− production occurred independently of glutathione [109], but in isolated and stunned hearts from guinea pigs, treatment with 5 mM ACA increased GSH and the NADPH/NADP+ ratio [110], suggesting that glutathione may be involved to some extent.
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.
Look, the good doctor is right – he only forgot to stress “portion control” which is why many fanatical dieters are so kee-jerk reactive to any discussion – odds are you over ate like a hog before your keto diet, and are weak and insecure in your diet plans. Eat EVERYTHING in small amounts, and you will live long and prosper. The only thing to avoid are processed foods. Cook your meals from scratch using quality ingredients.
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Similarly, several studies have demonstrated that up to half or more of patients undergoing PD have metabolic syndrome, and at least one study has demonstrated a significant increase in the prevalence with initiation of PD therapy. The only study that made a head-to-head comparison concluded that metabolic syndrome was significantly more prevalent in patients undergoing PD compared with in-center HD. These observations have raised concerns that PD therapy itself may contribute to the development of metabolic syndrome. However, the prevalence of metabolic syndrome in patients undergoing in-center HD in the only study with head-to-head comparison was substantially lower than in other studies. Moreover, there are two challenges with the diagnosis of metabolic syndrome in patients undergoing PD. First, the intraperitoneal instillation of dialysate with PD results in an increase in waist circumference, an important component for the diagnosis of metabolic syndrome. Second, there is continuous systemic absorption of glucose from intraperitoneal dialysate, and hence, patients undergoing PD are never in a postabsorptive state. This results in overestimation of fasting glucose and lipid parameters. Finally, the results from studies examining the association of metabolic syndrome with cardiovascular events or all-cause mortality have been inconsistent. This is not surprising because the individual components of metabolic syndrome themselves do not portend a higher risk for death or cardiovascular events in patients with ESRD, including among those undergoing PD.
Acetyl-CoA can be metabolized through the TCA in any cell, but it can also undergo a different process in liver cells: ketogenesis, which produces ketone bodies.[27] Ketone bodies are also produced in mitochondria, and usually occur in response to low blood glucose levels.[28] When glucose levels are low, oxaloacetate is diverted away from the TCA cycle and is instead used to produce glucose de novo (gluconeogenesis). But when oxaloacetate is unavailable to condense with acetyl-CoA, acetyl-CoA cannot enter the cycle, and so the body has evolved an alternative way to harvest energy from it.
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Contact your doctor and ask if you should change or increase your medication dosage, if you are taking a medication for diabetes. Despite the perception you may have that your blood sugar instability is becoming worse, Diabetes Health explains that the medication adjustment may just be dividing the dosage and taking it more often. Additionally, infection and illnesses can make your body less efficient at processing sugar, resulting in higher blood sugar levels temporarily.
High blood sugar levels, or hyperglycemia, is a condition in which glucose concentrations in the blood are too high. This condition is commonly found in individuals who have diabetes and is caused when the body does not produce enough of or is resistant to the effects of the hormone insulin. When high blood sugar is left untreated, it can lead to organ and tissue damage, coma and death. Monitoring your blood sugar levels is a good way to address high sugar immediately and there are several ways to lower sugar levels in the blood.
Insulin resistance. Insulin is a hormone that helps your body use glucose -- a simple sugar made from the food you eat -- as energy. In people with insulin resistance, the insulin doesn't work as well, so your body keeps making more and more of it to cope with the rising level of glucose. Eventually, this can lead to diabetes. Insulin resistance is closely connected to having excess weight in the belly.
The brain is a particularly greedy organ when it comes to energy requirement. To put this comment in perspective consider the following: though our brain represents only about 2% of our body mass, it accounts for about 20% of our energy expenditure.  (In children, by the way, this may be closer to 40-50% of basal metabolic demand.) So, beyond the ATP issue, above, there is a substrate issue with the brain as neurons derive most of their energy from glucose.  While there is emerging evidence that neurons can also oxidize fatty acids directly in small amounts and may even prefer lactate (over glucose), these two substrates do not approach the levels of consumption by neurons that glucose does.  So, for the purpose of this discussion, let’s just focus on the need of the body to provide glucose to the brain.
Schele E., Grahnemo L., Anesten F., Hallen A., Backhed F., Jansson J. O. (2013). The gut microbiota reduces leptin sensitivity and the expression of the obesity-suppressing neuropeptides proglucagon (Gcg) and brain-derived neurotrophic factor (Bdnf) in the central nervous system. Endocrinology 154, 3643–3651. 10.1210/en.2012-2151 [PubMed] [CrossRef] [Google Scholar]
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.
Metabolic syndrome (metabolic syndrome X, insulin resistance syndrome, dysmetabolic syndrome, hypertriglyceridaemic waist, obesity syndrome, Reaven syndrome) is the name for a group of risk factors that increase the risk for ischaemic heart disease (IHD), diabetes and stroke (Fig. 23.1). The metabolic syndrome is diagnosed when at least three of the IHD risk factors listed in Table 23.1 are present. Whether the syndrome, which affects possibly 25% of the US population, is a specific syndrome, and nothing more than the sum of its parts, is controversial.

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In low carb and keto baking, we’re concerned with two things: 1) keeping carbs low, and 2) still achieving a baked good that has great flavor and texture (because if we can’t gag it down there’s just no point, right? Lol). Low carb bread recipes are usually gluten free and grain free (although we’ve seen a couple that use oat fiber), but then the challenge is to get creative to get the right combination of ingredients to yield something that rises properly and tastes good.
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