It is very interesting to read about the keto/low card diet.I love to change my lifestyle as I an TYPE 2 Diabetic.I subscribed for a free printable low carb meal .The initial email stated that that I will receive an email for instructions to access the members area .Your free download will be there.However it is very deceiving ,I never got the 2nd email with instructions which is frustrating and not good .Hopefully this is not a way to get us to pay to get the printable version.
What a great post. I thought i would add about the selection of food you eat on keto and that everyone is different. Some food gives you energy and some doesnt, this varies person to person. I started and quit keto 3 times before i managed to find my balance. The first few times it made be poorly, from the shock of diet change. However, you can wean yourself into the diet which i did the last time when i had the most success.
Hello, I’m Abbey! I'm a Registered Dietitian (RD), an avid food and recipe writer, a TV nutrition expert and spokesperson, a YouTube host and the founder of Abbey’s Kitchen Inc. Abbey's Kitchen is a multi- faceted food and nutrition media brand developed with the goal of celebrating the pleasurable eating experience. For more information about me, check out my bio here.
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).

Following the ketogenic diet and achieving ketosis may be beneficial if you’re living with type 2 diabetes and need to manage your symptoms. Limiting carbohydrate intake is crucial with type 2 diabetes because too many carbs can increase blood glucose levels, which can damage blood vessels and lead to vision problems, kidney problems, and nerve problems.

It is very interesting to read about the keto/low card diet.I love to change my lifestyle as I an TYPE 2 Diabetic.I subscribed for a free printable low carb meal .The initial email stated that that I will receive an email for instructions to access the members area .Your free download will be there.However it is very deceiving ,I never got the 2nd email with instructions which is frustrating and not good .Hopefully this is not a way to get us to pay to get the printable version.
We can say that no species, including humans, could have survived for millions of years without the ability to withstand brief periods of hunger or starvation (Amen-Ra, 2006). These periods of fasting are themselves ketogenic (McCue, 2010) during which the concentrations of insulin and glucose decrease while that of glucagon increases in the attempt to maintain normal blood glucose levels. When the body passes from a condition of food abundance to one of deprivation (or else via VLCKD simulated deprivation), there is, with a slight delay, an increase in the concentration of free FAs as well as KB in the blood. Thus, from this point of view KD could be compared to caloric restriction for fasting. These manipulations of nutrients, both in quantity and quality, seem to not only act on blood glucose/KB level but also to promote changes in metabolic pathways and cellular signaling. How this kind of metabolic condition (ketosis) can affect satiety and hunger mechanisms is still a matter of debate.
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.

Sometimes we all have leftover chicken on hand that needs to be used up. Maybe you roasted a couple of chickens on the weekend to prep for the week ahead, maybe you had company over and grilled up too many chicken breasts, or maybe rotisserie chicken was on sale at your local grocery store and it was too good a bargain to pass up. Whatever the reason, we all can use a few ideas on how to use up leftover chicken.
Scheme of orexigenic and anorexigenic effects of ketosis. The picture is highly schematic. For more details please see the text. AMPK, AMP-activated protein kinase; CCK, cholecystokinin; GABA, gamma-aminobutyric acid; BHB, β-hydroxybutyric acid; FFA, free fatty acids; ROS, reactive oxygen species; NPY, neuropeptide Y; AgRP, agouti gene-related protein.
The second type of cellular fuel comes from fat and fat metabolism products called ketone bodies.   The average sized human body can store hundreds of thousands of calories in the form of fat, so we could say that this system of energy is almost unlimited, depending on how long one goes without food.  Eventually, it would get used up, but people have been known to fast for months and live through it.
No matter what your diet has been before now, keto will be a big change. If you're coming from a standard American diet (SAD), your carbs will go way down, your protein may either go up or down, and your fat will go way up. If you're coming from a bodybuilding-style diet, your fat intake will jump to alarming levels, and your protein will likely drop significantly.
Ready to head out the door and start buying groceries? Slow down there, chief. Go through the pantry, fridge, freezer, and secret stashes under the bed, and get rid of foods with any significant carb content. In the first few days, you could end up craving them—badly. This means fruit, too. Even carrots and onions are too high-glycemic to work with keto, Wittrock says.
Huge win y’all!! I made this for my family tonight, my first EVER Indian dish, (eating or cooking), and it was so good!!! Granted, it certainly took me longer than an hour, but it was well worth it! I also made the “naan” and oh my goodness, a game changer. My husband has stars in his eyes for all the things we’re going to use those tortillas for. Impressed!! Thank you for sharing this!!!

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.[27] Ketone bodies are also produced in mitochondria, and usually occur in response to low blood glucose levels.[28] 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.
So our brains do require some glucose, and this is the main reason that registered dietitians (RDs) will tell you that carbohydrates are essential nutrients (meaning we have to eat them or we will die). But a biochemical fact check shows that this is not true. RDs neglect the research which shows that the brain can use ketones for over half of its fuel requirements once carbohydrate intake is lowered and ketone levels ramp up to full production. When ketones are available as a secondary fuel source, the brain requirement for glucose is lower, and the process of gluconeogenesis can make all the glucose the brain needs (about 50 grams/day). So although glucose is essential for the brain, eating carbohydrates to make glucose for the brain is NOT required. If you are have blood ketone levels above 1-3 mmol, the brain can use the ketones as an alternative fuel source.
Drink lots of water. This is especially crucial on a low carb or keto diet. Why? When you eat carbohydrates, your body stores the extra as glycogen in the liver, where they are bound to water molecules. Eating low carb depletes this glycogen, which allows you to burn fat – but it also means you are storing less water, making it easier to get dehydrated. Instead of the traditional recommendation of 8 cups of water per day, aim for 16 cups when following a low carb lifestyle.
“When the body is in ketosis, it lowers the blood pH level, causing the blood to become acidic. To counter this, the body takes calcium away from the bones,” she says. “The increased acidity in the body also increases uric acid, which can lead to the formation of kidney stones.” Therefore, it goes without saying that due to the stress an extremely low-carb diet can have on the body, those with kidney damage shouldn’t try to achieve ketosis or attempt the ketogenic diet. (10)

While it is believed that carbohydrate intake after exercise is the most effective way of replacing depleted glycogen stores,[72][73] studies have shown that, after a period of 2–4 weeks of adaptation, physical endurance (as opposed to physical intensity) is unaffected by ketosis, as long as the diet contains high amounts of fat, relative to carbohydrates.[74] Some clinicians refer to this period of keto-adaptation as the "Schwatka imperative" after Frederick Schwatka, the explorer who first identified the transition period from glucose-adaptation to keto-adaptation.[75]


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.
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.
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.

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.
Drink lots of water. This is especially crucial on a low carb or keto diet. Why? When you eat carbohydrates, your body stores the extra as glycogen in the liver, where they are bound to water molecules. Eating low carb depletes this glycogen, which allows you to burn fat – but it also means you are storing less water, making it easier to get dehydrated. Instead of the traditional recommendation of 8 cups of water per day, aim for 16 cups when following a low carb lifestyle.
The SS providing information to the brain mainly send information to the nucleus of the solitary tract (NTS). These signals are generated in the GIT and abdominal viscera, as well as in the oral cavity and provide information about mechanical and chemical properties of food. The information is transmitted via vagal and spinal nerve to the NTS. The ASs arrive to the median eminence through ARC or through the blood-brain barrier (BBB). All these afferents are integrated in a complex and not fully understood network.
If you’re not sure after your initial test, explore other healthy diets such as clean eating and always have in mind that your number 1 goal should be to avoid overly processed foods (keeping this definition fairly broad of course, as we live in the 21st century and have to adapt to modern age as well, where hardly any of us have time to spend 12 hours a day evolving around food production, gathering and cooking).
Whether ketosis is taking place can be checked by using special urine test strips such as Ketostix. The strips have a small pad on the end, which the user dips in a fresh urine specimen. Within seconds, the strip changes color to indicate the level of acetoacetate ketone bodies, which reflects the degree of ketonuria, which, in turn, gives a rough estimate of the level of hyperketonemia in the body (see table below). Alternatively, some products targeted to diabetics such as the Abbott Precision Xtra or the Nova Max can be used to take a blood sample and measure the β-hydroxybutyrate ketone levels directly. Normal serum reference ranges for ketone bodies are 0.5–3.0 mg/dL, equivalent to 0.05–0.29 mmol/L.[29]
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.
Wow Gloria, you really do love this – way to to go! We just need to work on portion control now 😉 The recipe states serves 6. All that info is right at the top of each recipe. Don’t worry, many scroll past it eagerly wanting to get to the recipe itself. It is the beginning of summer there, but I will continue to make this throughout summer as my youngest absolutely loves it.
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.
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