When you’ve eaten all of the crustless spinach quiche and keto frittata recipes that you can, these keto everything bagels are another great breakfast staple. With their help, you don’t have to cut out your favorite breakfast sandwiches. You can also try a bread-less keto breakfast sandwich with chicken sausage patties as the “buns” when you’re craving a keto-approved breakfast option.
To encourage ketone production, the amount of insulin in your bloodstream must be low. The lower your insulin, the higher your ketone production. And when you have a well-controlled, sufficiently large amount of ketones in your blood, it’s basically proof that your insulin is very low – and therefore, that you’re enjoying the maximum effect of your low-carbohydrate diet. That’s what’s called optimal ketosis.

Forget the heavy casserole recipes and try this low-carb pot pie tonight! Nothing says comfort food like a chicken pot pie. This low-carb pot pie recipe skips the traditional gluten-filled dough of chicken pot pies and replaces it with cauliflower for a more low-carb option. I simply suggest switching out the cornstarch with arrowroot or tapioca starch.

Alcoholic ketoacidosis (AKA) presents infrequently, but can occur with acute alcohol intoxication, most often following a binge in alcoholics with acute or chronic liver or pancreatic disorders. Alcoholic ketoacidosis occurs more frequently following methanol or ethylene glycol intoxication than following intoxication with uncontaminated ethanol.[11]
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.
Have you heard all the buzz about the keto diet and want to know more? Did a friend tell you they’re “in ketosis” and you got interested? Here’s everything you need to know about ketogenic diets and being in ketosis for fat loss, brain function, satiety, and performance. Editor’s Note: This article is being updated … Continue reading The Keto Diet: Next Big Thing or Dangerous Fad?
Ariel Warren is a Registered Dietitian, Diabetes Educator, graduate from Brigham Young, and was diagnosed with Type 1 at the age of 4 years old. Ariel understands diabetes and enjoys working with clients to improve their blood sugar management, healthy eating, weight loss, fitness, and pregnancy. For coaching from a T1D Dietitian, you can contact Ariel directly, through her website: arielwarren.com.
Ketoacidosis is a dangerous condition for diabetics, and the main element is ACID not ketones. The blood pH becomes dangerously acidic because of an extremely high blood SUGAR level (the diabetic has no insulin, or doesn't respond to insulin .... so blood sugar rises ... ketones are produced by the body to provide the fuel necessary for life, since the cells can't use the sugar). It's the high blood sugar, and the acid condition that is so dangerous. Ketones just happen to be a part of the picture, and are a RESULT of the condition, not the CAUSE. Diabetics can safely follow a ketogenic diet to lose fat weight ... but they must be closely monitored by their health care provider, and blood sugars need to be kept low, and stable.
Another mechanism that could be involved in food-regulation during KD is the gamma aminobutyric acid (GABA) and glutamate regulation. Wu et al. demonstrated that GABAergic signaling from the NPY/AgRP neurons to the parabrachial nucleus (located in the dorsolateral part of the pons) is involved in many regulatory sensory stimuli including taste and gastric distension, regulate feeding behavior. GABA signaling seems to prevent animals from anorexia when AgRP neurons were destroyed (Wu et al., 2009). These findings are yet another contradictory aspect of KDs and food behavior; ketosis should increase the availability of glutamate (via diminution of transamination of glutamate to aspartate) and therefore increase GABA and glutamine levels; moreover, in ketosis, the brain imports a huge amount of acetate and converts it through glia into glutamine (an important precursor of GABA) (Yudkoff et al., 2008). The result of these mechanisms, together with the increased mitochondrial metabolism and flux through the TCA cycle, is an increased synthesis of glutamine and a “buffering” of glutamate. These results are not consistent with the well-documented anorexigenic effect of KDs, and therefore the GABA hypothesis cannot be taken into account despite the mild euphoria often reported during a KD that is probably due to the action of BHB (Brown, 2007) and can help to reduce appetite.
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).
When you eat a ketogenic diet, you switch your body’s fuel source to fat rather than the body’s usual source, glucose (1). From this fuel source switch, the hunger hormone, Ghrelin, is reduced which causes your appetite to decrease (1). Because of the reduction in appetite, it is easier to adopt an intermittent fasting approach or an approach that lessons unwanted eating behavior outside your desired hours (AKA curbs the late night munchies). Therefore, I recommend eating 4 bigger meals rather than 6 small meals on a Ketogenic Meal Plan.
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