Use fat as a lever.  We’ve been taught to fear fat, but don’t! Both keto and low carb are high fat diets. Fat is our source of energy as well as satiety. The key to understand, though, is that fat is a lever on a low carb or keto diet. Carbs and protein stay constant, and fat is the one you increase or decrease (push the lever up or down) to gain or lose weight, respectively. So if your goal is weight loss, eat enough fat to be satisfied, but there’s no need to “get your fats in” once you’re satisfied.

How often you eat is also up to your personal preference. "For most people, I recommend three to four meals per day with a few healthy keto snacks in between," says Dr. Axe. "This ensures that you're getting a good mix of protein and fat all day long to keep you feeling energized and satisfied." That being said, he encourages people to listen to their bodies and tune in to when they're truly hungry. "If you find that you feel better eating five to six smaller meals spread throughout the day, do what works best for you."

The gastrointestinal tract (GIT) plays a central role in the control of energy balance. Many molecules produced by the GIT exert hunger or satiety effects on the brain. Ghrelin is a peptide produced mainly by the stomach's oxyntic cells that stimulates ghrelin secretion in the hypophysis and has some neuroendocrine activities. However, its orexigenic properties are the most relevant to us and ghrelin is the only known peripheral orexigenic hormone (Date, 2012). Cholecystokinin (CCK) is a peptide produced mainly in the duodenum and jejunum that acts on the vagus nerve and directly on the hypothalamic nuclei. CCK is an anorexigenic factor and it reduces food intake, meal size and duration (Murphy et al., 2006). Three other related hormones are pancreatic polypeptide (PP), amylin, and peptide YY (PYY). PP is a peptide produced by the endocrine pancreas in relation to the caloric content of meals, and it reduces food intake both in rodents and humans. Amylin is a peptide co-secreted with insulin; its main effect on food control is a reduction of meal sizes and food intake (Murphy et al., 2006). Peptide YY (PYY) is produced in the gut and is similar to PP. PYY is stored in intestinal cells and released into the circulation as PYY3−36, a truncated form of PYY. The release of PYY3−36 is dependent on a meal's caloric and fat content (Veldhorst et al., 2008). The glucagon-like peptide 1 (GLP-1) is produced by the cleavage of pro-glucagon gene in the intestine. It acts as incretin at a pancreatic level, promoting insulin secretion and as neuro hormone on hypothalamic nuclei, inducing satiety (Valassi et al., 2008).
In the 1920s, doctors began to realize that when fed a high fat and extremely low carbohydrate diet their patients began to notice a remarkable reduction in frequency and severity of seizures. They found that the breakdown of dietary fat caused the body to produce ketones which have GABAergic and glutamatergic effects causing a reduction in nerve impulses thus having an anticonvulsant effect. The ketogenic diet was used as the mainstream therapy until the development of new anticonvulsant medications in the late 1930s.
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).
Brandi currently lives in Kansas City, Missouri and is a self-taught cook and fitness enthusiast. She has focused on healthy recipe development and exercise for 5+ years after reaching a fitness plateau and struggling to lose weight and maintain body goals. Brandi’s goal is to share recipes and workouts that support a consistently healthy lifestyle.

Thank you Mira for your quick reply. I didn’t make it that same day but I just made a batch now and they are excellent! I really enjoyed them. I made the recipe times 10 for 12 large muffin slots in the muffin tin. I’m thinking of shaping a larger round of batter on a parchment lined pan next time and after baking, carefully cutting in half to make 2 rounds to make a pizza crust. Thank you so much!!!


Keep up electrolytes. The major electrolytes in our bodies are sodium, potassium and magnesium. Because a low carb diet (especially a keto diet!) reduces the amount of water you store, this can flush out electrolytes and make you feel sick (called “keto flu”). This is temporary, but you can avoid or eliminate it by salting your food liberally, drinking broth (especially bone broth), and eating pickled vegetables. Some people also choose to take supplements for electrolytes, but it’s best to first consult a doctor that understands and supports keto/low carb lifestyles.
This is questionable. There ARE a few studies that suggest caffeine may cause blood sugar to rise, with consequent effect on insulin ... The studies involve consuming 50 gm glucose orally, followed by a dose of caffeine. This is quite different from a low carber, who is consuming only 20 gm carbs, in the form of high-fiber vegetables, spread throughout the day.
The hypothalamus is the brain's main center responsible for hunger/satiety (H/S) control. In the theory that Mayer proposed more than 60 years ago, he assigned a central role to glucose levels in the H/S control: the so-called “glucostatic theory” (Mayer, 1955). Mayer suggested that depletion of carbohydrate availability leads to hunger, and the hypothalamic centers with receptors sensitive to glucose levels might be involved in the short-term regulation of energy intake (Mayer, 1955). The “feeding center” in the lateral hypothalamic area (LHA), according to the glucostatic theory, reacts to the between-meal fall of blood glucose and stimulates food intake. The LHA contains glucose-inhibited neurons that are stimulated by hypoglycemia, a process crucial to mediating the hyperphagia normally induced by hypoglycemia. The subsequent post-prandial hyperglycemia activates the “satiety center” in the ventromedial hypothalamus (VMH), which contains glucose-excited neurons and inhibits both “feeding center” and food intake.
People (and even some ill-informed doctors) often confuse ketosis, which is a perfectly normal metabolic process, with ketoacidosis, which is a life-threatening condition. The latter is the consequence of insulin-deficient subjects having out-of-control blood sugar levels, a condition that can occur as well in alcoholics and people in a state of extreme starvation. Ketosis and ketoacidosis may sound vaguely alike, but the two conditions are virtually polar opposites and can always be distinguished from each other by the fact that the diabetic has been consuming excessive carbohydrates and has high blood sugar, in sharp contrast to the fortunate person who is doing Atkins.
I just made this keto bread, and it is amazing! It’s better than most bread I’ve tasted! I made mine with bacon, American cheese, Brie, and Camembert (because I wanted to be extra). If you use bacon, cook it to how you normally like it in a seperate pan, as the bacon doesn’t cook much extra while baking. I think I used a little too much butter, but, oh boy, was it nice and moist!
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]

Its simple, eat this; lose weight.  I feel like I’ve finally amassed enough recipes to create several simple keto meal plans.  AKA you print out a couple of recipes, hit the store, and you can know you’ll be doing keto right. If you’re not familiar with keto, its a low carb, high fat, medium protein diet designed to put your body into ketosis.  Once in ketosis, your body burns fat instead of sugar and you’ll see accelerated weight loss as a result.  The ideal ratio of fat to protein to carbs is 65% / 30% / 5% and you also want to keep your maximum net carbs at less than 20g a day. Net carbs = carbs – fiber.


"It was extremely difficult," he recalls. "You spend your entire life hearing that fat makes you fat and causes heart attacks and strokes. Now, all of a sudden, you're eating 200 grams of fat per day. There is a huge psychological component to conquer before you can become successful with the keto diet. In the beginning, it's like trying to convince people 1,000 years ago that the world is in fact round, not flat."
Longer-term ketosis may result from fasting or staying on a low-carbohydrate diet (ketogenic diet), and deliberately induced ketosis serves as a medical intervention for various conditions, such as intractable epilepsy, and the various types of diabetes.[6] In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed.[5][7] For this reason, ketosis is sometimes referred to as the body's "fat burning" mode.[8]
The gastrointestinal tract (GIT) plays a central role in the control of energy balance. Many molecules produced by the GIT exert hunger or satiety effects on the brain. Ghrelin is a peptide produced mainly by the stomach's oxyntic cells that stimulates ghrelin secretion in the hypophysis and has some neuroendocrine activities. However, its orexigenic properties are the most relevant to us and ghrelin is the only known peripheral orexigenic hormone (Date, 2012). Cholecystokinin (CCK) is a peptide produced mainly in the duodenum and jejunum that acts on the vagus nerve and directly on the hypothalamic nuclei. CCK is an anorexigenic factor and it reduces food intake, meal size and duration (Murphy et al., 2006). Three other related hormones are pancreatic polypeptide (PP), amylin, and peptide YY (PYY). PP is a peptide produced by the endocrine pancreas in relation to the caloric content of meals, and it reduces food intake both in rodents and humans. Amylin is a peptide co-secreted with insulin; its main effect on food control is a reduction of meal sizes and food intake (Murphy et al., 2006). Peptide YY (PYY) is produced in the gut and is similar to PP. PYY is stored in intestinal cells and released into the circulation as PYY3−36, a truncated form of PYY. The release of PYY3−36 is dependent on a meal's caloric and fat content (Veldhorst et al., 2008). The glucagon-like peptide 1 (GLP-1) is produced by the cleavage of pro-glucagon gene in the intestine. It acts as incretin at a pancreatic level, promoting insulin secretion and as neuro hormone on hypothalamic nuclei, inducing satiety (Valassi et al., 2008).
You’ll need to focus on titrating your insulin. Given the low amount of carbs in the Keto diet, I suggest you take detailed notes on how your blood sugar reacts to protein and fats. That way you can determine how much insulin to take with food. As for your basal, if you consistently go high/low without any bolus on board it might be a good idea to revisit your basal rates
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