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.
I’ve done the bread today, I used ultra fine almond flour and didn’t read the warning on the packet that the amounts you shall use are less than fo normal normal almond flour. So the bread came out really dense and a little wet. I did slice it on a food slicer in very thin slices and dried them in the oven which gave great cracker-like bread which is amazing with cheese.
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A stack of pancakes might sound like the opposite of a keto-friendly breakfast, but where there's a will, there's a way. These ones from A Big Man's World are made with the perfect combination of almond flour, coconut flour, and eggs for a result so fluffy, you'll hardly be able to tell they're low in carbs. The blueberries add a touch of sweetness (but they contain sugar, so be careful about the portions).
Consistent with the mechanisms described above, changes in AMPK in response to a ketogenic or low-carbohydrate diet have been reported in several studies. In rodents, a ketogenic diet (Bio-Serv F3666) has increased AMPK activity in skeletal muscle [150] and AMPK phosphorylation in the liver [230], and a low-carbohydrate diet (18.5% of energy) supplemented with ketone esters (6% w/v) increased AMPK content in brown adipose [149]. In humans, a nonketogenic low-carbohydrate diet (% energy: 50 fat, 30 carbohydrate, and 20 protein) has increased AMPK phosphorylation in skeletal muscle [231].
People who have metabolic syndrome typically have apple-shaped bodies, meaning they have larger waists and carry a lot of weight around their abdomens. It's thought that having a pear-shaped body — that is, carrying more of your weight around your hips and having a narrower waist — doesn't increase your risk of diabetes, heart disease and other complications of metabolic syndrome.
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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.
Humans have always relied on ketones for energy when glucose sources were scarce (i.e. no fruits available during winter). It is a normal state of metabolism. In fact, most babies are born in a state of ketosis. However, with abundant sources of carbohydrate, people rarely access ketosis and it becomes a dormant metabolic pathway.Our ancestors likely had frequent periods of time when high carbohydrate food wasn’t immediately available. For this reason, our bodies are amazing at adapting to burning of ketones for fuel.
I made this yesterday and had 3 pieces. Had another 2 for breakfast today and after a few minutes I started feeling nauseated. The nausea got worse and worse, and I ended up projectile vomiting in the bathroom. I looked it up and it’s a symptom of psyllium husk overdose. I read that the max dosage per day is around 2tsp. I had around 10 times the daily dosage in my breakfast alone… I love all of Maria’s recipes but this is just a warning to watch out with the husk powder in this recipe! I did not grind mine to decrease the density of it. I am semi comatose in bed now while my husband takes care of our kids. 😁😁😁
Nutritional ketosis may initiate bioenergetic and mitohormetic signaling through an increase in catecholamines or adiponectin, a decrease in insulin or glycogen, or an increase in β-oxidation that leads to an increase in mitochondrial reactive oxygen species (mtROS) or NAD+. This leads to further signaling involving AMP-activated protein kinase (AMPK), silent mating type information regulation 2 homologue 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), forkhead box O 3a (FOXO3a), and nuclear factor erythroid-derived 2-like 2 (NFE2L2), ultimately leading to transcription of genes related to oxidative capacity, mitochondrial uncoupling, and antioxidant defense. These adaptations collectively contribute to resistance against oxidative stress. Other proteins involved include liver kinase B1 (LKB1), which activates AMPK; nicotinamide phosphoribosyltransferase (NAMPT), which facilitates SIRT1 activation through NAD+ synthesis; and nuclear respiratory factors 1 and 2 (NRF-1 and NRF-2) and mitochondrial transcription factor A (TFAM), which promote mitochondrial biogenesis.
In a separate post, I explained the difference between nutritional ketosis (NK) and diabetic ketoacidosis (DKA). If this distinction is not clear, I’d suggest giving this separate post a quick skim for a refresher.  DKA is a pathologic (i.e., harmful) state that results from the complete or near absence of insulin.  This occurs in the setting of type 1 diabetes or very end-stage type 2 diabetes, and often as the result of a physiologic insult (e.g., an infection) where the patient is not receiving sufficient insulin to bring glucose into his cells.  A person with a normal pancreas, regardless of how long he fasts (including the fellow I reference above who fasted for 382 days!) or how much he restricts carbohydrates, can not enter DKA because even a trace amount of insulin will keep B-OHB levels below about 7 or 8 mM, well below the threshold to develop the pathologic acid-base abnormalities associated with DKA. Let me reiterate, it is physiologically impossible to induce DKA in anyone that does not have T1D or very, very, very late-stage T2D with pancreatic “burnout.”

That said, the nutrition facts that I get after entering the recipe into my app came up with almost twice the calories. My Tillamook Mild Cheddar cheese is 110 calories per ounce—so that alone gets me to 385 calories. Overall I end up with 51.5 grams of fat, 34.5 grams protein, 4.5 grams of carbs, and 632 calories. I am hoping to try it again with half the cheese to see if I can still get the great flavor and wonderful crispy taco shell.
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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.
In our keto bread recipe, we use a combination of coconut and almond flours so neither is overpowering. We also use a touch of psyllium husk powder to help achieve the right texture. A little bit of beef gelatin acts as a binder and adds bread-like “chew” to the final result. Our recipe only contains egg whites, which add structure and act as a natural leavening agent, but without the eggy flavor that the yolks would add.
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