I’m following the ketogenic diet and I find it very easy, pleasant and varied. I can even say that my diet today is more varied than the previous one. I do not intend to leave this diet and I cannot really see why. My initial focus was not to lose weight, I’ve always been lean, but to feel better, well disposed. And I got it! I am very pleased, I have read a lot about it (including scientific literature) and I have influenced other people who need to lose weight or improve some aspects of their health. But from the beginning I went on my own way, without the help of a nutritionist because I did not want to suffer the influence of others’ ideas.
Most people who have metabolic syndrome already have a closely related condition called insulin resistance, which is when the body stops responding to insulin (a hormone produced in the pancreas). After the food we eat is converted into a type of sugar called glucose, insulin is what enables the glucose to enter the body’s cells and be used as energy. For someone who is insulin resistant, however, the glucose builds up in the blood, setting the stage for damage.
Keep in mind that the ketogenic diet takes into account net grams of carbohydrates, not simply total grams. Net carbohydrates are the amount of carbohydrates left over after you subtract grams of fiber from total grams of carbohydrates. For example, if vegetables you’re eating have 5 grams of carbohydrates total, but 3 grams come from fiber, the total number of net carbohydrates is only 2 grams, which is the number you add to your daily total.
Menopause is the time in a woman's life when menstrual periods permanently stop, also called the "change of life." Menopause symptoms include hot flashes, night sweats, irregular vaginal bleeding, vaginal dryness, painful intercourse, urinary incontinence, weight gain, and emotional symptoms such as mood swings. Treatment of menopausal symptoms varies, and should be discussed with your physician.
Now, back to the real question at hand.  Why would our body make these substances? To understand why or when the body would do this requires some understanding of how the body converts stored energy (the food we eat or the energy we store in our body, i.e., fat or glycogen) into phosphate donors.  For a refresher on this process, please refer to the video in this post, specifically the section from 2:15 to 13:30.
Why is the keto diet good for you? A keto diet is one that prioritizes fats and proteins over carbohydrates. It can help reduce body weight, acne, and the risk of cancer. Find out about the mechanisms through which it achieves these benefits and the research that supports it. This MNT Knowledge Center article also discusses the risks of the diet. Read now
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!
Keep in mind that the ketogenic diet takes into account net grams of carbohydrates, not simply total grams. Net carbohydrates are the amount of carbohydrates left over after you subtract grams of fiber from total grams of carbohydrates. For example, if vegetables you’re eating have 5 grams of carbohydrates total, but 3 grams come from fiber, the total number of net carbohydrates is only 2 grams, which is the number you add to your daily total.

Oh Maria! Your bread recipe is fabulous! I have been playing around with it a little because the psyllium was a little too much for my gut! Went to 8 TBS of psyllium and added 2 TBS of Jay Robb Protein Isolate powder and a little sweetener (trying to make a yeasty flavor) I also turned it into buns which are easier for my household. I must say they turned out great! I even added caraway seeds to one batch for a rye flavor! I cannot thank you enough for making it so much easier to eat right when you have BREAD, ROLLS and DESSERTS that are fabulous!
Mohanraj, R., & Sivasankar, S. (2014, June). Sweet Potato (Ipomoea batatas [L.] Lam) – a valuable medicinal food: A review.  Journal of Medicinal Food, 17(7), 733–741. Retrieved from https://www.researchgate.net/profile/Remya_Mohanraj2/publication/263096030_Sweet_Potato_Ipomoea_batatas_L_Lam_-_A_Valuable_Medicinal_Food_A_Review/links/54ee2b8b0cf2e55866f22c1a.pdf
If your blood sugar gets too high, then you may have Ketoacidosis. What happens is that the body does not have enough insulin to use the glucose cells, so it starts to break down fat and muscle for fuel. This causes ketones to enter the bloodstream and causes a pretty bad chemical imbalance. Ketones can also be found in your urine, which is an easy way to test. Signs of Diabetic Ketoacidosis are:
Abundant data suggest that patients meeting these diagnostic criteria have a greater risk of significant clinical consequences, the 2 most prominent of which are the development of diabetes mellitus [6] and of coronary heart disease. Pooled data from 37 studies involving more than 170,000 patients have shown that metabolic syndrome doubles the risk of coronary artery disease. [7] It also increases risk of stroke, fatty liver disease, and cancer. [8] (See Prognosis.)
A combination of baking soda, lemon juice, and baking powder eliminates the need for yeast in this bubbly keto bread recipe. With tons of Italian seasonings, olive oil, and flaky salt sprinkled on top, you’ll want to include this loaf with every meal. Each generous slice is 3 net carbs — and to stay more Bulletproof, simply avoid eating garlic and xanthan gum too often.
82. Schwarz J. M., Neese R. A., Turner S., Dare D., Hellerstein M. K. Short-term alterations in carbohydrate energy intake in humans. Striking effects on hepatic glucose production, de novo lipogenesis, lipolysis, and whole-body fuel selection. Journal of Clinical Investigation. 1995;96(6):2735–2743. doi: 10.1172/jci118342. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Formation of O2•− at complexes I and III primarily occurs in the mitochondrial matrix, but some of the O2•− produced at complex III is produced in the intermembrane space [63]. Within the matrix, O2•− is rapidly dismutated into hydrogen peroxide (H2O2) by manganese superoxide dismutase (SOD2) [41, 53]. Some O2•− may escape into the mitochondrial intermembrane space [64] and cytosol [65], where copper/zinc superoxide dismutase (SOD1) can dismutate it into H2O2 [41]. The large majority of mitochondrial H2O2 is removed by peroxiredoxin (Prx) 3, followed by much smaller contributions from Prx5 and glutathione peroxidases (GPx) 1 and 4 [66]. GPx also removes other peroxides, including lipid hydroperoxides [41]. Catalase is another antioxidant enzyme capable of removing H2O2 but is primarily located in peroxisomes and is therefore unlikely to directly remove mitochondrial H2O2 [41, 66]. However, H2O2 can be transported out of mitochondria [67], and it is possible that the majority of mitochondrial H2O2 is removed in the cytosol. Since Prxs and GPxs rely on NADPH for recycling of their cofactors (thioredoxins and glutathione, resp.) [41], and since NADH is required for recycling of NADPH [68], activity of these enzymes would decrease availability of NADH for oxidative phosphorylation. Therefore, transport of H2O2 out of mitochondria for removal in the cytosol may be a more likely defense mechanism [67], implying a more important role of catalase and other antioxidant enzymes outside of mitochondria. Despite the lower reactivity of H2O2, it is still reactive and can oxidize metal ions, particularly iron, to form the hydroxyl radical (•OH), which readily damages DNA, lipids, and proteins [41]. •OH is scavenged by metallothioneins I and II [69, 70] and glutatathione [71], indicating that these antioxidant proteins may be important defenses against byproducts of unaddressed mtROS. Other important antioxidant enzymes include glutamate-cysteine ligase (GCL), which is the rate-limiting step in glutathione synthesis, and glutathione reductase (GSR) and thioredoxin reductase (TRXR), which recycle glutathione and thioredoxin, respectively, to their reduced forms [41].
If your blood sugar gets too high, then you may have Ketoacidosis. What happens is that the body does not have enough insulin to use the glucose cells, so it starts to break down fat and muscle for fuel. This causes ketones to enter the bloodstream and causes a pretty bad chemical imbalance. Ketones can also be found in your urine, which is an easy way to test. Signs of Diabetic Ketoacidosis are:
Adiponectin increases AMPK activity in skeletal muscle [188, 189] and the liver [189] by promoting Thr172 phosphorylation, likely in response to an increase in the AMP to ATP ratio [189]. Similarly, α-adrenergic signaling increases AMPK activity in skeletal [190] and cardiac muscle [191], and β-adrenergic signaling increases AMPK activity in adipose [192, 193], all through promotion of Thr172 phosphorylation. While activation through β-adrenergic signaling appears to involve the AMP to ATP ratio [192], α-adrenergic signaling appears to work independently of AMP and ATP [190]. Increases in adiponectin have been observed during ketogenic or low-carbohydrate diets, although primarily in obese individuals [194–196]. BHB induces adiponectin secretion in adipocytes [197], indicating that the level of nutritional ketosis may be an important determinant of the extent to which ketogenic diets influence AMPK activity through adiponectin. In regard to catecholamines, epinephrine increases during fasting, and this appears to be dependent on carbohydrate restriction [198], implying that epinephrine is likely to be elevated during nutritional ketosis. Consistent with this, dietary carbohydrate restriction increases catecholamines at rest [155, 199] and in response to exercise [155, 199–202]. This may be, at least in part, a result of glycogen depletion [200, 203], suggesting both direct and indirect effects of glycogen on AMPK activity. The potential for nutritional ketosis to increase catecholamines is further supported by the dependency of the antiseizure effects of ketogenic diets on norepinephrine [204].
All cells of the human body require ATP as the fundamental energy source to support life. Because mitochondria produce the majority of ATP, impaired mitochondrial function is implicated in the majority of today's most concerning chronic and degenerative health conditions including obesity, cardiovascular disease, cancer, diabetes, sarcopenia, and neurodegenerative diseases [1]. Much of this association between mitochondrial function and disease can be attributed to excessive mitochondrial production of reactive oxygen species (ROS) [2].
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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Hunger and satiety are two important mechanisms involved in body weight regulation. Even though humans can regulate food intake by will, there are systems within the central nervous system (CNS) that regulate food intake and energy expenditure. This complex network, whose control center is spread over different brain areas, receives information from adipose tissue, the gastrointestinal tract (GIT), and from blood and peripheral sensory receptors. The actions of the brain's hunger/satiety centers are influenced by nutrients, hormones and other signaling molecules. Ketone bodies are the major source of energy in the periods of fasting and/or carbohydrate shortage and might play a role in food intake control.
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Hi, I’ve made this recipe twice and LOVE the taste. However, both times the bread would rise so high in the oven, but as soon as I take it out to cool it deflated and middle sink down. What could’ve gone wrong? Over mixing? I did switch coconut flour to all almond flour instead. Could that be a problem? Please help as I’m anxious to make another batch. Thank you.
Hey there… I’m new to keto, so I’m hoping my questions don’t come across as really stupid. Your bread looks great, and if I can get bread again, then that’s simply awesome. The pictures remind me of banana bread. Is there a way of adding this flavor without going insanely overboard on the carbs? And without that artificial banana taste? Also, would this recipe work as muffins? Thanks, Kelly
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).
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]
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.

Hey Maya!! This is the 2nd recipe I’ve tried off your website and again I love it!! Turned out really well. I can have sandwiches again or a quick piece Of toast when I’m in a hurry to get out the door. I was skeptical about the xanthan gum since I tried a recipe using psyllium husk powder. I did not like it. I can’t taste the xanthan gum so I have no problem using it going forward. Thanks again for the recipe!!!

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.


So I made my own coconut-flour from flaked coconut(according to a recipe I found on line). Psyllium Husk i managed to find only in whole husks form so I grind it up to a powder in a blender. I understand now it sounds like a recipe for disaster but I don’t have another choice (getting the ingredients from the internet will take about 2 weeks and until then it is all I have).
For a diagnosis of metabolic syndrome, a child must have at least three of the four risk factors. The most common risk factors in teens are hypertension and abnormal cholesterol. Even when just one risk factor is present, a doctor will likely check for the others. This is especially true if a child is overweight, has a family member with type 2 diabetes, or has acanthosis nigricans.
Moreover, recent studies show that the Inuit have evolved a number of rare genetic adaptations that make them especially well suited to eat large amounts of omega-3 fat.[57][58][59] And earlier studies showed that the Inuit have a very high frequency—68% to 81% in certain arctic coastal populations—of an extremely rare autosomal recessive mutation of the CPT1A gene—a key regulator of mitochondrial long-chain fatty-acid oxidation[60][61]—which results in a rare metabolic disorder known as carnitine palmitoyltransferase 1A (CPT1A) deficiency and promotes hypoketotic hypoglycemia—low levels of ketones and low blood sugar.[62] The condition presents symptoms of a fatty acid and ketogenesis disorder.[62] However, it appears highly beneficial to the Inuit[60] as it shunts free fatty acids away from liver cells to brown fat, for thermogenesis.[63][64] Thus the mutation may help the Inuit stay warm by preferentially burning fatty acids for heat in brown fat cells.[64] In addition to promoting low ketone levels, this disorder also typically results in hepatic encephalopathy (altered mental state due to improper liver function), enlarged liver and high infant mortality.[65] Inuit have been observed to have enlarged livers with an increased capacity for gluconeogenesis, and have greater capacity for excreting urea to remove ammonia, a toxic byproduct of protein breakdown.[57][66][67][68] Ethnographic texts have documented the Inuit's customary habit of snacking frequently [69] and this may well be a direct consequence of their high prevalence of the CPT1A mutation[70] as fasting, even for several hours, can be deleterious for individuals with that allele, particularly during strenuous exercise.[57][70] The high frequency of the CPT1A mutation in the Inuit therefore suggests that it is an important adaptation to their low carbohydrate diet and their extreme environment.[57][60][70]
Ketones may also be important, or even necessary, for the bioenergetic signaling associated with mitohormesis. As will be discussed later, peroxisome proliferator-activated receptor α (PPARα) is a nuclear receptor that is responsible for many of the bioenergetic adaptations associated with nutritional ketosis and mitohormesis [120]. In mice, a ketogenic diet (% energy: 90 fat, 0 carbohydrate, and 10 protein) increased blood BHB concentration to 1-2 mM and upregulated expression of numerous PPARα targets in the liver [37]. However, in mice fed a nonketogenic low-carbohydrate diet (% energy: 75 fat, 15 carbohydrate, and 10 protein), which did not raise blood concentration of BHB, the increased expression of PPARα targets did not occur [37], implying that induction of PPARα signaling by a ketogenic diet is dependent on ketones. This response may be, at least in part, a result of the epigenetic effects of BHB. In addition to HDAC inhibition, BHB also influences gene expression through β-hydroxybutyrylation of histone lysine residues [121]. In the livers of mice subjected to prolonged fasting, this β-hydroxybutyrylation has been associated with upregulation of PPAR signaling, oxidative phosphorylation, fatty acid metabolism, the proteasome, and amino acid metabolism related to redox balance [121]. Upregulation of these pathways is largely influenced by β-hydroxybutyrylation of the histone residue H3K9 [121], which is also involved in the upregulation of antioxidant defense through BHB-induced HDAC inhibition [103]. This potential for BHB to influence expression of both mitochondrial and antioxidant genes through a common histone residue is further indication of the overlap between bioenergetics and antioxidant defense and suggests that if mitohormesis is indeed induced during nutritional ketosis, induction may be dependent on ketones and may therefore not occur during a low-carbohydrate diet that is not ketogenic.

The trick here is not only to avoid all obvious sourced of carbohydrate (sweets, bread, spaghetti, rice, potatoes), but also to be careful with your protein intake. If you eat large amounts of meat, eggs and the like, the excess protein will converted into glucose in the body. Large amounts of protein can also raise your insulin levels somewhat. This compromises optimal ketosis.

The coordinated effects of AMPK, SIRT1, and SIRT3 are primarily mediated through PGC-1α, which is activated through phosphorylation by AMPK [242, 265] and deacetylation by SIRT1 [77, 242, 266–269]. SIRT3 also increases PGC-1α activity [270], possibly through cAMP response element binding protein (CREB) [271, 272], but the exact mechanism has not been elucidated. In addition to phosphorylating PGC-1α, activated AMPK also increases PGC-1α expression [260, 273–276]. Activation of β2-adrenergic receptors [277–280] and the adiponectin AdipoR1 receptor [281] also increase PGC-1α expression, independently of AMPK activation [278, 281]. PGC-1α activity is increased by oxidative stress [76, 77, 282–284], possibly through activation of AMPK [259, 260] or p38 mitogen-activated protein kinase (MAPK) [283, 284], or inhibition of glycogen synthase kinase 3β, which inhibits PGC-1α through phosphorylation [77, 283]. In contrast, insulin decreases PGC-1α activity through phosphorylation by PKB [285]. Once activated, PGC-1α interacts with the PPAR family of nuclear receptors [286] and the FOXO family of transcription factors [287] to influence expression of a variety of bioenergetic and antioxidant proteins. PGC-1α most notably increases transcription of proteins involved in mitochondrial biogenesis and respiration [76, 242, 265, 267, 269, 274, 279, 282, 285, 288–293] but also increases transcription of antioxidant proteins including SOD1 [76], SOD2 [76, 282, 289, 292–294], catalase [282], GPx [76, 294], thioredoxins [282, 283, 292], TRXR [282, 292], Prx3 [282, 292], and Prx5 [282, 292], as well as the mitochondrial uncoupling proteins UCP2 [76, 265, 282, 288, 294], UCP3 [76, 265, 294], and ANT [76, 295].
Probiotics are an obvious supplement for digestive health, but they may play an important role in lowering blood sugar, too. One small study found that people who were following a heart-health DASH diet and also consumed probiotics experienced a decrease in fasting blood sugar and hemoglobin A1C levels (a marker for testing long-term blood sugar levels). Start by adding healthy, probiotic-rich foods to your diet such as kefir, plain yogurt, sauerkraut, kimchi, or even a little low-sugar kombucha. And, to help probiotic bacteria to thrive, eat plenty of prebiotic foods such as fiber-rich leafy greens and vegetables.
Because it lacks carbohydrates, a ketogenic diet is rich in proteins and fats. It typically includes plenty of meats, eggs, processed meats, sausages, cheeses, fish, nuts, butter, oils, seeds, and fibrous vegetables. Because it is so restrictive, it is really hard to follow over the long run. Carbohydrates normally account for at least 50% of the typical American diet. One of the main criticisms of this diet is that many people tend to eat too much protein and poor-quality fats from processed foods, with very few fruits and vegetables. Patients with kidney disease need to be cautious because this diet could worsen their condition. Additionally, some patients may feel a little tired in the beginning, while some may have bad breath, nausea, vomiting, constipation, and sleep problems.
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In a subsequent series of experiments, glucose metabolism in C. elegans was inhibited by knockdown of the insulin receptor, insulin-like growth factor 1 (IGF-1) receptor, and insulin receptor substrate 1 (IRS-1) [73]. Consistent with the previous study [72], inhibition of glucose metabolism increased mitochondrial respiration concomitant with ROS-dependent increases in lifespan, stress resistance, and antioxidant enzyme activity. However, in this case, detection of ROS was mitochondria-specific, and repeated measures allowed for changes in antioxidant enzyme activities to be evaluated more closely in relation to the timing of changes in mtROS. Compared to controls, inhibition of glucose metabolism resulted in higher mitochondrial O2 consumption at 12 h, higher mtROS production at 24 h, and higher activities of SOD and catalase at 48 h, suggesting a dependence of antioxidant activity on mtROS and a dependence of mtROS on mitochondrial respiration. The most striking result is the lower mtROS at 120 h, indicating that the initial increase in mtROS and subsequent increase in antioxidant enzyme activity ultimately lowered net mtROS production to a level lower than controls, which is the proposed explanation for the more than twofold increase in lifespan. As with the previous study, this demonstration of mitohormesis is further supported by the changes in ROS production, antioxidant enzyme activity, and lifespan having been prevented with antioxidant treatment.
I halved this recipe and added 1 tsp cocoa powder and 1 tsp ajwain seeds (I was out of caraway) to the dry ingredients, and 1 tsp black strap molasses to the hot water, and baked for 1 hr (cooled slowly with the oven door ajar and allowed to cool completely before removing from the pan. It turned out wonderfully – very much like a dark european style bread.
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.
184. Davies S. P., Helps N. R., Cohen P. T., Hardie D. G. 5′-AMP inhibits dephosphorylation, as well as promoting phosphorylation, of the AMP-activated protein kinase. Studies using bacterially expressed human protein phosphatase-2C alpha and native bovine protein phosphatase-2AC. FEBS Letters. 1995;377(3):421–425. doi: 10.1016/0014-5793(95)01368-7. [PubMed] [CrossRef] [Google Scholar]

Apart from administering insulin, the fastest way to lower your blood glucose is to engage in physical activity. Exercise results in an increased sensitivity to insulin. It causes your muscle cells to take up more glucose, leaving less of it to circulate in your bloodstream during and after the physical activity (which means a lower blood glucose when you test). Frequent, regular exercise is very important to good blood glucose control no matter what type of diabetes you have. Research has shown that it is vital in warding off long-term complications like neuropathy, retinopathy, and heart and kidney diseases. Don't forget to check with a doctor, though, before making any major changes to your exercise routine. And, if you have type 1 diabetes and your glucose is 250 mg/dl or higher, check for urine ketones. You should not exercise if ketones are present.


^ Bechtel PJ (2 December 2012). Muscle as Food. Elsevier Science. pp. 171–. ISBN 978-0-323-13953-3. Retrieved 19 May 2014. Freezing does stop the postmortem metabolism but only at about −18ºC and lower temperatures. Above −18ºC increasing temperatures of storage cause an increasing rate of ATP breakdown and glycolysis that is higher in the comminuted meat than in the intact tissue (Fisher et al., 1980b). If the ATP concentration in the frozen tissue falls below ~ 1 µmol/g no contraction or rigor can occur because they are prevented by the rigid matrix of ice.
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.
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