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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 in the Journal of Applied Physiology showed that people who do twice-a-day workouts, but defy standard nutrition recommendations by not eating for two hours after the first session (thus depleting carbohydrate stores with the first session) experienced a better ability to burn fat (with no loss in performance) compared with a group that trained only once a day and ate carbohydrates afterward.
In other words, I personally found that while following “strict ketosis”, things became eerily similar to the days in college when I was a competitive bodybuilder pursuing sub-3% body fat percentages. I simply wasn’t the most fun guy to hang out with in social situations due to my extreme dietary restrictions, the intense self-control became nearly exhausting, and when I traveled, I missed out on many culinary experiences, such as homemade ravioli in Rome, freshly baked crostinis in the Basque regions of Spain, and Korean rice bowls in Seoul.
In addition to the seaweed and glycogen carbohydrates mentioned above, the Inuit can access many plant sources. The stomach contents of caribou contain a large quantity of partially digested lichens and plants, which the Inuit once considered a delicacy. They also harvested reindeer moss and other lichens directly. The extended daylight of the arctic summer led to a profusion of plant life, and they harvested plant parts including berries, roots and stems, as well as mushrooms. They preserved some gathered plant life to eat during winter, often by dipping it in seal fat.[71]
Alcoholic ketoacidosis (AKA) presents infrequently, but can occur with acute alcohol intoxication, most often following a binge in alcoholics with acute or chronic liver or pancreatic disorders. Alcoholic ketoacidosis occurs more frequently following methanol or ethylene glycol intoxication than following intoxication with uncontaminated ethanol.[11]
In sheep, ketosis, evidenced by hyperketonemia with beta-hydroxybutyrate in blood over 0.7 mmol/L, occurs in pregnancy toxemia.[78][79] This may develop in late pregnancy in ewes bearing multiple fetuses,[78][79] and is associated with the considerable glucose demands of the conceptuses.[80][81] In ruminants, because most glucose in the digestive tract is metabolized by rumen organisms, glucose must be supplied by gluconeogenesis,[82] 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.[83][84] 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),[79] 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.[78] Among ewes with pregnancy toxemia, beta-hydroxybutyrate in blood tends to be higher in those that die than in survivors.[85] 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.[86]
A study with an intent-to-treat prospective design was published in 1998 by a team from the Johns Hopkins Hospital[20] and followed-up by a report published in 2001.[21] 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.[21][22]
The concentration of ketone bodies may vary depending on diet, exercise, degree of metabolic adaptation and genetic factors. Ketosis can be induced when a ketogenic diet is followed for more than 3 days.[34] This induced ketosis is sometimes called nutritional ketosis.[35] This table shows the concentrations typically seen under different conditions[1]
Awesome info. I’ve been LCHF moderate protein (about 1 g per lean lbs/mass) and 50-100g of carbs for about a year. I’d consume around 2500 cals. I’m active 4-5 days a week (60-90 min cycling sessions) I started using MCT/Butter coffee. It surpressd my appetite and I would only eat whole food at lunch/dinner…still LCHF, but since my appetite was lower I was only takin in about 1800 cals. After about 2 weeks I started to gain body fat. Do you think the reduced caloric intake is the culprit? Should I “force” myself to eat…maybe up the MCT intake to make up the difference?
Twenty elite ultra-marathoners and ironman distance triathletes performed a maximal graded exercise test and a 180 min submaximal run at 64% VO2max on a treadmill to determine metabolic responses. One group habitually consumed a traditional high-carbohydrate (HC: n = 10, %carbohydrate:protein:fat = 59:14:25) diet, and the other a low-carbohydrate (LC; n = 10, 10:19:70) diet for an average of 20 months (range 9 to 36 months).
Twenty elite ultra-marathoners and ironman distance triathletes performed a maximal graded exercise test and a 180 min submaximal run at 64% VO2max on a treadmill to determine metabolic responses. One group habitually consumed a traditional high-carbohydrate (HC: n = 10, %carbohydrate:protein:fat = 59:14:25) diet, and the other a low-carbohydrate (LC; n = 10, 10:19:70) diet for an average of 20 months (range 9 to 36 months).
Keeping a food diary can help you identify foods that don't agree with you. Every day, list the foods you eat and any symptoms that occur. Once you pinpoint a food that seems to trigger your symptoms, cut it out of your diet for a couple weeks and see what happens. Then add it back in. If the symptoms went away with its subtraction but return with its addition, you've found your culprit.
Hi Ben great science & sound advice. May I share with the group? I’m 42, in australia, have been an alcoholic for 10 yrs. In April 2016 I gave up drinking & started living strictly ketogenic. In 3 months I dropped 25 kilos. I have cheated on weekends but I go through a fast of sorts on Mondays to get back into ketosis by Tues. I work afternoon / evenings so I wake at 10.30am take a pre workout drink with raspberry ketones & a splash of mct oil & all my vitamins as well. I then do weights for an hr then get ready to go to work. I take 2 800ml protein shakes consisting of 20 ml mct & 30grm amino enhanced protein. I work in warehousing so I walk anywhere between 10 km & 5 km a nite. I feel great all the time, thanks largely to your research & advice. If have any thoughts or opinions I’d love hear them.
The difference between ketosis and ketoacidosis is the level of ketones in the blood. Ketosis is a physiological adaptation to a low carbohydrate environment like fasting or a ketogenic diet. There are situations (such as treatment-resistant epilepsy) where ketosis can be beneficial to health. Ketoacidosis is an acute life-threatening state requiring prompt medical intervention; its most common form is diabetic ketoacidosis where both glucose and ketone levels are significantly elevated.
3) Cholesterol levels usually go up with inflammation, because inflammation causes damage to the tissues, and cholesterol is manufactured and released in circulation to patch things up. So, again, eating high fat is the best way to drop inflammation; not increase it. My hsCRP are always below 0.1, and most of the time, below detection level. Oxidation of cholesterol causes inflammation; not the other way around. So, your point about inflammation is a non-issue.
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