You could certainly use butter, but I’m not sure how that would be more appealing to him if he thinks fat is the enemy. It’s tough to get heart patients to go against the “conventional wisdom” we’ve been fed for so many decades. They have a right to be fearful, but I would suggest offering him research that shows fat isn’t the enemy at all. For what it’s worth, after 6 months of heavy keto (my testing period, though I’ve been keto longer than that) with lots of fats, including butter, bacon, and avocados, my cholesterol and triglycerides dropped! And I’m not the only person to have those same results. Best of luck!
Be sure to use full-fat canned coconut milk, not lite or coconutmilk beverage. If desired, you can use the seeds from a vanilla bean instead of the extract. To make the keto ice cream: Stir together the milk, sweetener, salt, and vanilla extract. If you have an ice cream machine, simply churn according to manufacturer’s directions. Or to make it without an ice cream machine, freeze the mixture in ice cube trays, then blend the frozen cubes in a high-speed blender such as a Vitamix OR thaw them enough to then blend in a food processor or regular blender. Eat as-is, or freeze an hour or so for a firmer texture. Due to not having any preservatives or stabilizers, the keto ice cream is best the day it’s made, but you can technically freeze leftovers up to a month and thaw before serving.
Unfortunately, this particular meal plan has dairy interwoven in it, it would be difficult to substitute those ingredients. I have plans to create a dairy-free keto plan. If you’re not subscribed to our newsletter, you can go ahead and do that (scroll up to see the form on this page above the comments) and you’ll be notified when the dairy-free plan is available.
This is the first time I heard about Keto diet I need to lose weight because I am a diabetic 2 and high cholesterol and high blood pressure the doctor want me to do but bypass lot of people told me not to everybody was telling me about this new diet keep Keto I want to try it and I made it my goal my weight is 257 on 5 for messaging and I think this is going to be good for me I need a lot of help thank you
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.
Because every person's metabolism is different, the sticks turn different shades of purple or pink for different people. And, yes, results vary depending upon the time of the day, whether or not you exercise and what you last ate. It doesn't matter whether your strips turn a dark or light color. Some people never even get into ketosis, but still lose weight easily. So don't worry about the exact level of ketosis shown on your test strips; what is more important is how your clothes are fitting, what the scale says and how you feel.
The keto lifestyle can sometimes cause me to get dizzy and have brain fog. It can be really hard to focus. Each night before bed I like to drink bone broth. Kettle and Fire is my favorite brand. They have beef and chicken flavors. I add a little liquid aminos and hot sauce for flavor. You can sip it from a mug or eat it like a miso soup in a bowl. 
No and yes. The liver can make ketones out of alcohol, so technically, when you drink you'll continue to produce ketones and so will remain in ketosis. The problem is ... alcohol converts more easily to ketones than fatty acids, so your liver will use the alcohol first, in preference to fat. Thus, when you drink, basically your FAT burning is put on hold until all the alcohol is out of your system.
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.
I wanted to put it out there that I made this meal plan specifically with women in mind. I took an average of about 150 women and what their macros were. The end result was 1600 calories – broken down into 136g of fat, 74g of protein, and 20g net carbs a day. This is all built around a sedentary lifestyle, like most of us live. If you need to increase or decrease calories, you will need to do that on your own terms.
Hi Cyn, The numbers are general guidelines but will vary depending on many factors, such as activity level, insulin resistance, weight and more. There is no single magic number, just conventional recommendations that are a good starting point. I will have a macro calculator coming soon that will help determine what is best for each person, but even then it’s an approximation. The only way to know for sure is to test. If keto is your goal, it’s usually best to start lower and then see if you can stay in ketosis when increasing.
You’ll need to focus on titrating your insulin. Given the low amount of carbs in the Keto diet, I suggest you take detailed notes on how your blood sugar reacts to protein and fats. That way you can determine how much insulin to take with food. As for your basal, if you consistently go high/low without any bolus on board it might be a good idea to revisit your basal rates

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.
High blood sugar levels coupled with high blood ketones, on the other hand, will mean that you have a pathologically low level of insulin – something non-diabetics do not suffer from. This can lead to ketoacidosis – a potentially life-threatening condition. If this happens, you’ll need to inject more insulin; if you’re at all unsure of what to do, contact a medical professional. Coveting really high blood ketones for weight control is not worth the risk for type 1 diabetics.
The discovery of many appetite-related hormones provided molecular basis for appetite control, decreasing the relevance of the metabolites hypothesis (Karatsoreos et al., 2013). Recently, Sumithran et al. demonstrated that there is a long-term persistence of changes in some peripheral hormones involved in food control (Sumithran et al., 2011). In this study, they found a significant difference in mean levels of many food intake-related hormones 1 year after the cessation of weight loss via the hypocaloric diet. There was a long lasting decrease of anorexigenic compounds: leptin, PYY, cholecystokinin, insulin, and pancreatic peptide and an increase of the orexigenic molecule ghrelin. Moreover, they found that hunger remained elevated 1 year after diet cessation. In a successive study the same group investigated hunger-related hormones after 8 weeks of KD, demonstrating that during ketosis the increase of ghrelin (a strong stimulator of appetite) was suppressed (Sumithran et al., 2013). These results are consistent with those of Ratliff et al (Ratliff et al., 2009), who found no significant change in fasting plasma ghrelin after 12 weeks of VLCD.
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.
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.

KBs can cross the BBB but not in a homogenous manner. For example, past experiments have demonstrated that BHB utilization is different in various brain areas (Hawkins and Biebuyck, 1979). Areas without BBB, hypothalamic regions and the lower cortical layers have a higher BHB metabolism compared to the lower one of the basal ganglia (Hawkins and Biebuyck, 1979). Also the metabolic meaning of the three KBs is different: while the main KB produced in the liver is AcAc, the primary circulating ketone is BHB. The third one, acetone, is produced by spontaneous decarboxylation of AcAc, and it is the cause of the classic “fruity breath.” Acetone does not have any metabolic functions, but it can be used as a clinical diagnostic marker. BHB acid is not, strictly speaking, a KB because the ketone moiety has been reduced to a hydroxyl group. Under normal conditions the production of free AcAc is negligible and this compound, transported via the blood stream, is easily metabolized by various tissues including skeletal muscles and the heart. In conditions of overproduction, AcAc accumulates above normal levels and a part is converted to the other two KBs. The presence of KBs in the blood and their elimination via urine causes ketonemia and ketonuria. Apart from being the fundamental energy supply for CNS, glucose is necessary for the replenishment of the quota of oxaloacetate, since this intermediate of the tricarboxylic acid cycle (TCA) is labile at body temperature and cannot be accumulated in the mitochondrial matrix. Hence it is necessary to refurnish the TCA with oxaloacetate via the anaplerotic cycle that derives it from glucose through ATP dependent carboxylation of pyruvic acid by pyruvate carboxylase (Jitrapakdee et al., 2006). This pathway is the only way to create oxaloacetate in mammals. Once produced by the liver, KBs are used by tissues as a source of energy (Fukao et al., 2004; Veech, 2004; McCue, 2010): initially BHB is converted back to AcAc that is subsequently transformed into Acetoacetyl-CoA that undergoes a reaction producing two molecules of Acetyl-CoA to be used in the Krebs cycle (Figure ​(Figure22).


Hey there! Welcome to my site! I am Kyndra Holley - International Best Selling Cookbook Author, and the face behind this blog. I am an avid lover of all things low carb and gluten free. I focus on real, whole food ingredients that you can find at your local grocer. I am a lifter of heavy things, world traveler, obsessed dog mom, hiker, essential oiler, nature lover, just to name a few. I believe that kindness is king! Read more...
Ive bern on ompresole proton prohibiter..which I went off because 1. Caused me to have sibo ane 2. Caused me to have pneumonia seversl times a year. The sibo, intestinal distress was hideous, I got told by my last primary I would pretty much have to live with this, my homeopathic Doctor said no, the antibiotics from pneumonia treatment plus my multiple contrasts test (ive lost count) messed everything up. Eating clean is amazing..goes against everything ive bern taught snd convinced it wouldn’t work…till I tried it. So any doubters, educate yourselves.
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You’ll need to focus on titrating your insulin. Given the low amount of carbs in the Keto diet, I suggest you take detailed notes on how your blood sugar reacts to protein and fats. That way you can determine how much insulin to take with food. As for your basal, if you consistently go high/low without any bolus on board it might be a good idea to revisit your basal rates
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