The ARC exerts opposing actions on food intake responding not only to leptin and insulin, but also to gut hormones (the most studied are ghrelin and, recently, PYY). The neurophysiological pathways suggest that feeding is regulated by a feedback loop, where the hypothalamus provides the long-term regulatory input to the NTS, which acts as a setpoint (Williams et al., 2001).
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).
Yvette, Oh no, sorry to hear about the chicken not being cooked! Was the chicken frozen to start with? If so, be sure to add 5 minutes to your Instant Pot cooking time (on manual high pressure). When we tested this, we literally just put everything into the IP (nestled down into the liquid, of course), and let it do its thing. The cream cheese softened, and when it was done cooking we removed the chicken to shred it, and the sauce stirred together nicely.
Many questions about the role of such an important intermediate of lipid metabolism remains unanswered, e.g., the role of BHB in food control. For example, whether or not BHB could act as a satiety signal in the brain, considering its role in energy supply to CNS. We have to consider that the effects of KBs on hunger reduction can only be seen after many days following fasting or KD initiation (Paoli et al., 2010); this is consistent with the abovementioned threshold of brain utilization of KB as an energy source, i.e., 4 mmol/L (Veech, 2004), which is close to the Km for the monocarboxylate transporter (Leino et al., 2001). During the first days of fasting or KD there is a rise of BHB and adiponectin concentrations (Halberg et al., 2005). One of the putative causes of hunger in starved humans may be due—together with other causes—to adiponectin. When adiponectin binds to its receptor AdipoR1, AMP-activated protein kinase (AMPK) is phosphorylated in the ARC of the hypothalamus (Valassi et al., 2008). The increase of AMPK activity in the hypothalamus may increase food intake and hepatic glucose output in mice while the decrease seems to reduce food intake (Zhang et al., 2009). KDs can also act similarly to a caloric restriction on AMPK (Newman and Verdin, 2014). Interestingly, AMPK seems to have opposing actions on the liver, muscle tissues and the brain: in liver and muscle AMPK activation increases FA oxidation by decreasing malonyl-CoA concentrations (Malonyl-CoA is the first intermediate in the lipogenic pathway and is also an inhibitor of carnitine palmitoyltransferase-1 (CPT-1). CPT-1 activity can be limiting for FA oxidation), through the inactivation of the acetyl-CoA carboxylase 1 (ACC1). AMPK can also increase the activity of malonyl-CoA decarboxylase (MCD), which enhances the decrease of malonyl-CoA levels.
If you would like to read more on ketogenic diets and ketosis, Jeff Volek and Steve Phinney discuss the new method of checking blood ketones in their book "The Art and Science of Low Carbohydrate Performance", and they also offer another good book "The Art and Science of Low Carbohydrate Living", which is a good book for those who need an introduction to the science of ketogenic diets. 
This week we’re introducing a slight fast. We’re going to get full on fats in the morning and fast all the way until dinner time. Not only are there a myriad of health benefits to this, it’s also easier on our eating schedule (and cooking schedule). I suggest eating (rather, drinking) your breakfast at 7am and then eating dinner at 7pm. Keeping 12 hours between your 2 meals. This will help put your body into a fasted state.
A review of multiple studies in the journal Nutrients found that ketogenic diets are connected to significant reductions in total cholesterol, increases in “good” HDL cholesterol levels, dips in triglycerides levels and decreases in “bad” LDL cholesterol; there are questions as to whether diets high in saturated fat negate these benefits. The same paper reports that a ketogenic may slightly reduce blood pressure, but science is still very scant on this point.

The easiest macro to calculate in the ketogenic diet is fat. Once you've got your carbs and protein set, simply fill the rest of your daily calorie needs with fat sources. If you find yourself wanting to gain a bit of weight, add approximately 500 calories, or 55 grams. If you want to lose weight, cut down on your fat intake by 200-500 calories, or 22-55 grams.

Moreover, in the above study of Sumithran et al. (2013), ketosis maintains post-prandial secretion of CCK as previously demonstrated by other researchers (Chearskul et al., 2008). Note that the orexigenic effect of BHB is blocked by transection of the common hepatic branch of the vagus nerve (Langhans et al., 1985). The hepatic branch contains fibers from the proximal small intestine, stomach and pancreas, and is sensitive to CCK (Horn and Friedman, 2004); ghrelin signals to brain are also transmitted via vagus nerve (Habara et al., 2014). Thus, the effects of ketosis on these two appetite-related hormones could be one of the many factors related to the effects of such nutritional regimen on food control.
Achieving this state isn’t easy: You’ll need to severely minimize your intake of carbohydrates, eating no more than 20 to 50 grams (g) of carbs per day to get there and stay there. A single medium pear, for example, contains 26 g of carbs, and even foods that aren’t generally considered high in carbs — such as nuts and nonstarchy veggies — contain a small amount of carbohydrates, and so will need to be limited or avoided on this plan.
Positive science on ketosis coupled with personal successes passed by word-of-mouth have driven more people to explore the ketogenic diet, says Volek. More recently, the keto diet hints at having a promising therapeutic role in cancer, Alzheimer’s, Parkinson’s and polycystic ovary syndrome (PCOS). Research is still early in many areas, but Volek suspects there will more definitive answers on the wider scope of the diet’s benefits within the next decade.
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.
Some clinicians[37] regard eliminating carbohydrates as unhealthy and dangerous.[38] However, it is not necessary to eliminate carbohydrates from the diet completely to achieve ketosis. Other clinicians regard ketosis as a safe biochemical process that occurs during the fat-burning state.[35] Ketosis, which is accompanied by gluconeogenesis (the creation of glucose de novo from pyruvate), is the specific state that concerns some clinicians. However, it is unlikely for a normally functioning person to reach life-threatening levels of ketosis, defined as serum beta-hydroxybutyrate (B-OHB) levels above 15 millimolar (mM) compared to ketogenic diets among non diabetics, which "rarely run serum B-OHB levels above 3 mM."[39] This is avoided with proper basal secretion of pancreatic insulin. People who are unable to secrete basal insulin, such as type 1 diabetics and long-term type II diabetics, are liable to enter an unsafe level of ketosis, eventually resulting in a coma that requires emergency medical treatment.[citation needed] The anti-ketosis conclusions have been challenged by a number of doctors and advocates of low-carbohydrate diets, who dispute assertions that the body has a preference for glucose and that there are dangers associated with ketosis.[40][41]
Wow!! This was sooo good! Tried another crack chicken recipe with a ranch packet and had to throw away the leftovers…no one would eat them. This, however is much better!! Didn’t change recipe other than use pre cooked bacon that I cut up. Probably would be better with the grease involved, however, this is AWESOME!! Also, my chicken tenders were still 3/4 frozen and I didn’t adjust time. They were just fine. Thanks for sharing!! A def do over say myself, hubby, and kids!!!
My Husband and I started doing Keto July 2018. We got over weight after we got out of the Marine Corps. It has been hard to workout because I became disabled, but my diet was not good. After our friend Amber recommended your site and support group, we found a lot of helpful information to get us started on a successful journey. So far it’s been one month and we have lost 18 pounds each!
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