A question we frequently get asked is whether you have to defrost boneless, skinless chicken breasts before making this recipe, or if you can just use them frozen. If you forgot to pull the chicken out of the freezer in the morning, we have good news for you! Crack Chicken can easily be made with frozen chicken. If using an Instant Pot, just add 5 minutes on to the cooking time (for a total of 20 minutes on Manual High Pressure).
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.
Acetyl-CoA can be metabolized through the TCA in any cell, but it can also undergo a different process in liver cells: ketogenesis, which produces ketone bodies. Ketone bodies are also produced in mitochondria, and usually occur in response to low blood glucose levels. When glucose levels are low, oxaloacetate is diverted away from the TCA cycle and is instead used to produce glucose de novo (gluconeogenesis). But when oxaloacetate is unavailable to condense with acetyl-CoA, acetyl-CoA cannot enter the cycle, and so the body has evolved an alternative way to harvest energy from it.
On the contrary, in the brain, as mentioned above, the increase of AMPK activity leads to higher food intakes. But the effect of AMPK in the brain is more complicated; mice lacking AMPKa2 in pro-opiomelanocortin neurons develop obesity, while the deficiency of AMPKa2 in agouti-related protein neurons results in an age-dependent phenotype. Thus, the conclusion is that even while AMPK is a regulator of hypothalamic functions, it does not act as a signal for energy deficit or excess (Claret et al., 2007). However, the picture is more complex than this (Figure (Figure3);3); BHB induces AgRP expression while increasing ATP and inhibiting AMPK phosphorylation (Cheng et al., 2008). Moreover, Laeger and colleagues have recently demonstrated that under physiological conditions BHB decreases AMPK phosphorylation and AgRP mRNA expression in GT1-7 hypothalamic cells (Laeger et al., 2012).
If you remain under your optimal net carbs limit, then you should enter ketosis within 2 to 3 days. But it can take up to 7 days. The fastest way to get into ketosis is to exercise on an empty stomach, in order to accelerate the depletion of glycogen in your body. You can also do a Fat Fast for a few days (eating more fat) to speed up the rate at which you enter ketosis AND start to cut out refined carbs (like sugar) before you go for full ketosis. Another option is to do a water fast, (only drinking water) which also speeds up getting into ketosis.
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).
As a matter of fact, in animal models intracerebroventricular injections of long-chain FA reduced hypothalamic expression of NPY. NPY is an important orexogenic neuropeptide that is a downstream target of leptin and insulin in the hypothalamus. In some forms of hyperphagic obesity, characterized by elevated plasma leptin and insulin levels, the lack of action of insulin on NPY expression could explain the pathological condition. Central administration of oleic acid, fatty-acid synthase, or CPT-1 inhibitors prevents the rise in hypothalamic NPY mRNA induced by fasting (Obici et al., 2003). But glucose level is also involved in KD's food control mechanisms. According to glucostatic theory (Mayer, 1955) data indicates that ketosis did not influence FA glucose but instead stimulated the elevation of post-prandial glucose (Sumithran and Proietto, 2013) in non-diabetic subjects, while in diabetics there was a reduction of fasting glucose (Westman et al., 2008). It is important to note that carbohydrate availability may increase cellular levels of long-chain FA-CoA through an increase of malonyl-CoA, which inhibits oxidation of FAs.
Everyone has to find their nutritional sweet spot for producing enough ketones and staying in ketosis, but “the core principle of the diet is to keep carbohydrate intake low enough, so your body continues producing ketones at elevated levels,” says Volek. “Your body adapts to this alternative fuel and becomes very efficient at breaking down and burning fat.”
Initially you may be surprised that on keto diets you eat less frequently. That’s because the fats are pretty satisfying. But as you normalize and adjust into a ketogenic state, that may change and your appetite may increase. That’s fine and completely normal. Use whatever diet you decide to follow as a starting point – it should be “written in pencil” so that you can make changes along the way. Consider adding an extra meal, marginally increasing the size of the meals or just adding a shake between meals. It’s up to you – just listen to your body. For example for me, I added a low-carb “green powder” shake supplement to my regimen along with either flax seed oil or some nuts in order to satisfy my hunger.
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.
For breakfast, we are going to change it up a bit. Here’s where we introduce ketoproof coffee. Now, don’t get me wrong – I know some of you won’t like it. If you’re not a fan of coffee, then try it with tea. If you’re not a fan of the taste (which is very rare), then try making a mixture of the ingredients by themselves and eating it like that. So, why ketoproof coffee?
There are three instances where there’s research to back up a ketogenic diet, including to help control type 2 diabetes, as part of epilepsy treatment, or for weight loss, says Mattinson. “In terms of diabetes, there is some promising research showing that the ketogenic diet may improve glycemic control. It may cause a reduction in A1C — a key test for diabetes that measures a person’s average blood sugar control over two to three months — something that may help you reduce medication use,” she says.