My husband is trying to eat more Keto meals and this recipe is made up of his FAVORITE things! I sent him the link to it and he was inspired! Last night, he made himself a big hearty batch of this recipe and thoroughly loved it. He even shared photos of his meal on Facebook and our friends were in awe of his creation and the recipe you provided. I don’t enjoy mushrooms, so I’m reviewing this on my husband’s behalf. It was EXCELLENT!

As a bonus, I’m making this amazing meal plan – and other keto meal plans – available in my MealPrepPro app!  So, if you’ve been wondering what the hype is all about and you want me to some of the heavy work for you by providing a fresh, customizable keto meal plan each week, then make sure you test drive my MealPrepPro app. The app is FREE to try and available right now to download on iPhone and iPad.


Fasting is another way to achieve ketosis. This doesn’t suggest going days without food, but rather intermittent fasting. You can eat for eight hours and then fast for 16 hours, or eat a low-calorie diet for a few days (about 1,200 daily calories if you’re a woman and 1,500 daily calories if you’re a man). As you take in less food, your body uses more of its fat stores for fuel.
Ally, We haven’t tried this recipe with another cooking method, but it should actually be pretty easy! The objective is to cook the chicken (any way you like, poached, baked, grilled, or even rotisserie) until it can be shredded, and then mix the shredded chicken with the creamy sauce. To cook the creamy sauce on the stovetop, we recommend crisping the bacon in a saucepan and then removing it and adding the water and spices. Once the water is simmering, add the cream cheese a bit at a time (slightly softened would probably work best), whisking until it’s incorporated. Cooked this way, you may need to add a splash more liquid (water or broth, if you prefer) to the sauce, because some of the liquid will evaporate off as the cream cheese melts down. Finally, stir in the cooked shredded chicken and shredded cheddar, and serve! If you try it this way, please let us know how it goes!
Lastly, if you're active, you might need to make some adjustments to take that into account. "For the first one to two weeks, temporarily reducing your exercise load can be helpful as your body adjusts to being in ketosis," he says. "Additionally, for those who have an intense workout schedule, carb cycling may be a good option." Carb cycling essentially means you'll increase your carb intake on the days you're doing exercise, ideally just two to three days per week. "While low-carb days may be around 20 to 30 grams of net carbs daily, high-carb days can range all the way up to 100 grams, although it can vary based on your size and activity level," says Dr. Axe. (Related: 8 Things You Need to Know About Exercising on the Keto Diet.) 
Even though intracellular metabolism and activation of the ATP-sensitive K+ channels appear to be necessary for some signaling effects of FAs, a great amount of the FA responses in the ventromedial hypothalamic neurons are mediated by interactions with fatty acid translocase (FAT)/CD36. Translocase is a FA transporter/receptor that activates downstream signaling even in the absence of intracellular metabolism (Moulle et al., 2014).

Ketosis is an option for many people with type 2 diabetes because they still produce insulin, which helps their body maintain a safe level of ketones in the blood. If you’re considering trying ketosis or the ketogenic diet with type 2 diabetes, be sure to consult your healthcare provider first to ensure it’s safe for you. This eating approach may interfere with some types of diabetes medication or be inappropriate for you if you have certain diabetes complications, such as kidney damage.
Ketone bodies are acidic, but acid-base homeostasis in the blood is normally maintained through bicarbonate buffering, respiratory compensation to vary the amount of CO2 in the bloodstream, hydrogen ion absorption by tissue proteins and bone, and renal compensation through increased excretion of dihydrogen phosphate and ammonium ions.[9] Prolonged excess of ketone bodies can overwhelm normal compensatory mechanisms, defined as acidosis if blood pH falls below 7.35.
Jump up ^ Fumagalli M, Moltke I, Grarup N, Racimo F, Bjerregaard P, Jørgensen ME, Korneliussen TS, Gerbault P, Skotte L, Linneberg A, Christensen C, Brandslund I, Jørgensen T, Huerta-Sánchez E, Schmidt EB, Pedersen O, Hansen T, Albrechtsen A, Nielsen R (September 2015). "Greenlandic Inuit show genetic signatures of diet and climate adaptation". Science. 349 (6254): 1343–7. Bibcode:2015Sci...349.1343F. doi:10.1126/science.aab2319. hdl:10044/1/43212. PMID 26383953.
This is the only way my kids will eat Brussels sprouts! It’s actually great for me because this dish is fast, easy and healthy, and it makes a lovely side. Quick-cooking Brussels sprout halves are available in the prepackaged salad aisle at the grocery store. They’re a timesaver if you can find them, but you can always just buy whole ones and slice them in half. —Teri Rasey, Cadillac, Michigan

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.
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.

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.
Articles and information on this website may only be copied, reprinted, or redistributed with written permission (but please ask, we like to give written permission!) The purpose of this Blog is to encourage the free exchange of ideas. The entire contents of this website is based upon the opinions of Dave Asprey, unless otherwise noted. Individual articles are based upon the opinions of the respective authors, who may retain copyright as marked. The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the personal research and experience of Dave Asprey and the community. We will attempt to keep all objectionable messages off this site; however, it is impossible to review all messages immediately. All messages expressed on The Bulletproof Forum or the Blog, including comments posted to Blog entries, represent the views of the author exclusively and we are not responsible for the content of any message.

Articles and information on this website may only be copied, reprinted, or redistributed with written permission (but please ask, we like to give written permission!) The purpose of this Blog is to encourage the free exchange of ideas. The entire contents of this website is based upon the opinions of Dave Asprey, unless otherwise noted. Individual articles are based upon the opinions of the respective authors, who may retain copyright as marked. The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the personal research and experience of Dave Asprey and the community. We will attempt to keep all objectionable messages off this site; however, it is impossible to review all messages immediately. All messages expressed on The Bulletproof Forum or the Blog, including comments posted to Blog entries, represent the views of the author exclusively and we are not responsible for the content of any message.
The keto diet changes the way your body converts food into energy. Eating a lot of fat and very few carbs puts you in ketosis, a metabolic state where your body burns fat instead of carbs for fuel. When your body is unable to get glucose from carbs, your liver converts fatty acids from your diet into ketones, an alternative source of energy. Burning ketones in place of glucose reduces inflammation and spurs weight loss.[1] 
Take a multivitamin. “Because you are removing grains, the majority of fruit, some vegetables, and a significant amount of dairy from your menu, a multivitamin is good insurance against any micronutrient deficiencies,” says Jadin. Depending on what your individual overall diet looks like, Jadin says you might also need to add a calcium, vitamin D, and potassium supplement.
The findings of a stable (Chearskul et al., 2008) or slightly increased response (Sumithran et al., 2013) of post-prandial FFA after KD can be viewed in the nutrient-static context. Elevated circulating FFA may actually reduce food intake and glucose production through actions on specific hypothalamic neurons (Obici et al., 2003). It has been suggested that this effect could be mediated by the increase of cellular concentration of long-chain FAs-CoA in the arcuate nuclei of the hypothalamus (Obici et al., 2003).
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