After 2 years in ketosis suddenly I find my blood glucose has risen to high levels even while in ketosis. I thought it was the dawn phenomenon, stress hormones like cortisol but now I am beginning to think I am eating too many exongenous keytones like too much MCT oil? I am not taking exogenous keytone supplements but wondering if too much oil/ fat in the diet generates exogenous keytones which inhibits the livers production of endogenous keytones. I have read if the liver is producing endogenous keytones it is not at the same time producing glucose through gluconeogenisis?
-Cancer: Numerous studies have found that the risk for cancer increases with high blood sugar, which makes sense, since cancer cells feed primarily on glucose. This includes cancers of the endometrium, pancreas, and colon and colorectal tumors. Tim Ferriss recently hosted a fantastic article by Peter Attia about this very issue, and how ketosis may indeed be a potential cancer cure.
The ketogenic diet is not a benign, holistic, or natural treatment for epilepsy; as with any serious medical therapy, complications may result. These are generally less severe and less frequent than with anticonvulsant medication or surgery. Common but easily treatable short-term side effects include constipation, low-grade acidosis, and hypoglycaemia if an initial fast is undertaken. Raised levels of lipids in the blood affect up to 60% of children and cholesterol levels may increase by around 30%. This can be treated by changes to the fat content of the diet, such as from saturated fats towards polyunsaturated fats, and if persistent, by lowering the ketogenic ratio. Supplements are necessary to counter the dietary deficiency of many micronutrients.
I'd recommend starting with glucose and hemoglobin A1C, along with a good multi like https://bengreenfieldfitness.com/multi and a fish oil like the one at greenfieldfitnesssystems.com – Anyways, I'd be happy to help you via a personal one-on-one consult. Just go to https://bengreenfieldfitness.com/coaching. and then choose a 20 or 60 minute consult, whichever you'd prefer. I can schedule ASAP after you get that.
People on the diet report being significantly more full and satisfied. Even though you may be ingesting LESS calories on the diet, your hunger doesn't increased. One possible explanation is greater consumption of satiating foods, primarily protein and fat. However, multiple studies indicate that the state of ketosis itself (apart from effects from food) plays a role as well.10
I'm constantly on the lookout for low-carb diet and ketosis friendly option that allow hard charging athletes, especially athletes who have glycolytic, high-intensity demands during sport, to get a “slow bleed” of carbohydrate into their body. For example, “UCAN Superstarch” is one such option, but, unfortunately, I've found that many athletes and exercise enthusiasts tend to get gastric distress or excessive fermentation from that slow-release starch.
The DNA test does not necessarily take into account your goals (e.g. breathholding, Ironman, cognition, etc.) and if your goals would benefit from ketosis, then you may want to choose it as a dietary strategy even though it could indeed be true that for FAT LOSS a higher carb intake may suit you. So it all depends on your goals. Or you could just us the supplements like ketones AND eat more carbs and get "best of both worlds".
When you’re eating the foods that get you there (more on that in a minute), your body can enter a state of ketosis in one to three days, she adds. During the diet, the majority of calories you consume come from fat, with a little protein and very little carbohydrates. Ketosis also happens if you eat a very low-calorie diet — think doctor-supervised, only when medically recommended diets of 600 to 800 total calories.
In ketogenesis, two acetyl-CoA molecules instead condense to form acetoacetyl-CoA via thiolase. Acetoacetyl-CoA momentarily combines with another acetyl-CoA via HMG-CoA synthase to form hydroxy-β-methylglutaryl-CoA. Hydroxy-β-methylglutaryl-CoA form the ketone body acetoacetate via HMG-CoA lyase. Acetoacetate can then reversibly convert to another ketone body—D-β-hydroxybutyrate—via D-β-hydroxybutyrate dehydrogenase. Alternatively, acetoacetate can spontaneously degrade to a third ketone body (acetone) and carbon dioxide, although the process generates much greater concentrations of acetoacetate and D-β-hydroxybutyrate. When blood glucose levels are low, ketone bodies can be exported from the liver to supply crucial energy to the brain.
Shifting your metabolism and achieving ketosis may speed up weight loss and result in other health benefits, like more energy and a lower blood pressure. But while ketosis is a preferred nutritional state for some people, it isn’t recommended for everyone — and it’s not a good long-term eating approach due to its restrictive nature, which may lead to potentially dangerous nutritional deficiencies.
A study with an intent-to-treat prospective design was published in 1998 by a team from the Johns Hopkins Hospital and followed-up by a report published in 2001. As with most studies of the ketogenic diet, no control group (patients who did not receive the treatment) was used. The study enrolled 150 children. After three months, 83% of them were still on the diet, 26% had experienced a good reduction in seizures, 31% had had an excellent reduction, and 3% were seizure-free.[Note 7] At 12 months, 55% were still on the diet, 23% had a good response, 20% had an excellent response, and 7% were seizure-free. Those who had discontinued the diet by this stage did so because it was ineffective, too restrictive, or due to illness, and most of those who remained were benefiting from it. The percentage of those still on the diet at two, three, and four years was 39%, 20%, and 12%, respectively. During this period, the most common reason for discontinuing the diet was because the children had become seizure-free or significantly better. At four years, 16% of the original 150 children had a good reduction in seizure frequency, 14% had an excellent reduction, and 13% were seizure-free, though these figures include many who were no longer on the diet. Those remaining on the diet after this duration were typically not seizure-free, but had had an excellent response.
It’s also important to note there have been no long-term studies on the ketogenic diet, nor has there been research that details what may happen to the body if it’s in a constant state of ketosis itself. But given how the body needs carbs to function properly, diets that are based on fat burning may lead to nutritional deficiencies, and supplements and multivitamins are recommended because you’re cutting out entire food groups, warns Alyssa Rothschild, RDN, who is in private practice in New York City.
In sheep, ketosis, evidenced by hyperketonemia with beta-hydroxybutyrate in blood over 0.7 mmol/L, occurs in pregnancy toxemia. This may develop in late pregnancy in ewes bearing multiple fetuses, and is associated with the considerable glucose demands of the conceptuses. In ruminants, because most glucose in the digestive tract is metabolized by rumen organisms, glucose must be supplied by gluconeogenesis, for which propionate (produced by rumen bacteria and absorbed across the rumen wall) is normally the principal substrate in sheep, with other gluconeogenic substrates increasing in importance when glucose demand is high or propionate is limited. Pregnancy toxemia is most likely to occur in late pregnancy because most fetal growth (and hence most glucose demand) occurs in the final weeks of gestation; it may be triggered by insufficient feed energy intake (anorexia due to weather conditions, stress or other causes), necessitating reliance on hydrolysis of stored triglyceride, with the glycerol moiety being used in gluconeogenesis and the fatty acid moieties being subject to oxidation, producing ketone bodies. Among ewes with pregnancy toxemia, beta-hydroxybutyrate in blood tends to be higher in those that die than in survivors. Prompt recovery may occur with natural parturition, Caesarean section or induced abortion. Prevention (through appropriate feeding and other management) is more effective than treatment of advanced stages of ovine ketosis.
I don’t know about you, but I find these risks pretty damn concerning. The fact is that I want to be around to play with my grandkids, and considering that my genetic testing with 23andMe has revealed that I have a higher-than-normal risk for type 2 diabetes, I doubt that shoving more gooey gels and sugary sports drinks into my pie hole is going to do my health any favors. So if I can achieve similar levels of performance and body composition with carbohydrate restriction, I’m all in.
Endogenous ketone production denotes ketones produced naturally by the body. It's the body’s natural adjustment to the absence or restriction of carbohydrate in the diet. Without enough glucose from carbs to fuel its cells, the body turns to fat to replace glucose as its primary source of energy. In the liver, fat that is not burned for energy directly is converted to ketones. This means that you are in a ketogenic state. Ketone levels increase in the bloodstream and provide an alternate and efficient fuel source for the body and brain. As a result, muscle protein is spared from being converted to glucose for energy.
And what I’m writing has nothing to do with taking supplements to induce ketosis or whatever. I believe these things are covered in Volek & Phoney’s book The Art and Science of Low Carb Living, which I would have thought you to be very familiar with. The iodine stuff you can read about in Iodine, Why We Need, Why We Can’t Live Without It by Brownstein.
If you are already in ketosis and accustomed to high-fat, low-carb diets, you can take one heaping scoop in about eight ounces of water fifteen minutes prior to working out. It stays in your system and will provide your body with elevated ketone levels for about three hours. When taken as a pre-workout, KetoCaNa has also been shown to decrease the amount of oxygen consumed at a given power output.
A survey in 2005 of 88 paediatric neurologists in the US found that 36% regularly prescribed the diet after three or more drugs had failed, 24% occasionally prescribed the diet as a last resort, 24% had only prescribed the diet in a few rare cases, and 16% had never prescribed the diet. Several possible explanations exist for this gap between evidence and clinical practice. One major factor may be the lack of adequately trained dietitians, who are needed to administer a ketogenic diet programme.