I see a lot of people say that ketosis is great for insulin sensitivity. BUT, in my experience ketosis causes physiological insulin resistance whereby the muscles and liver are sparing glucose for the brain. Hence, glucose tolerance actually goes down during ketosis. As such, is it possible that post workout carbs could do a lot more damage than they would on a non-ketogenic diet? Or maybe, as Kiefer suggests, glucose uptake post workout is not moderated by insulin at all i.e. muscles soak up glucose regardless of their insulin sensitivity? Or maybe cyclical ketosis doesn’t allow liver glycogen to get low enough to trigger physiological insulin resistance?

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Jalali says people following the diet have the best chance of keeping the weight off if they stay on it long term. And that’s not always easy to accomplish. The weight may come back if you go back to your regular eating habits. And regaining weight may lead to other negative effects. “Chronic yo-yo dieting appears to increase abdominal fat accumulation and diabetes risk,” notes Clark.
Normal body cells metabolize food nutrients and oxygen during cellular “respiration”,  a set of metabolic pathways in which ATP (adenosine triphosphate), our main cellular energy source is created. Most of this energy production happens in the mitochondria, tiny cell parts which act as powerhouses or fueling stations. There are two primary types of food-based fuel that our cells can use to produce energy:
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?
This is an absolutely necessary function for basic survival. As the body can only store carbs for a day or two, the brain would quickly shut down after a couple of days without food. Alternatively it would quickly have to convert our muscle protein into glucose – a very inefficient process – just to keep the brain going. That would make us waste away quickly. It would also ensure that the human race could hardly have survived all those millennia before we had 24-7 food availability.
Alison Moodie is a health reporter based in Los Angeles. She has written for numerous outlets including Newsweek, Agence France-Presse, The Daily Mail and HuffPost. For years she covered sustainable business for The Guardian. She holds a master’s degree from Columbia University’s Graduate School of Journalism, where she majored in TV news. When she's not working she's doting on her two kids and whipping up Bulletproof-inspired dishes in her kitchen.
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.[28]
When you order here, you get 1560g unflavored Glycofuse – 3.4 pound with zero nasty additives or artificial sweeteners, at only 100 calories per serving. Just pure, clean-burning highly branched cluster dextrin for that slow bleed of carbohydrates you need to support energy for a long workout or race, or for the glycogen replenishment you need after a tough day at the gym, without getting massive fluctuations in blood sugar. 
Anticonvulsants suppress epileptic seizures, but they neither cure nor prevent the development of seizure susceptibility. The development of epilepsy (epileptogenesis) is a process that is poorly understood. A few anticonvulsants (valproate, levetiracetam and benzodiazepines) have shown antiepileptogenic properties in animal models of epileptogenesis. However, no anticonvulsant has ever achieved this in a clinical trial in humans. The ketogenic diet has been found to have antiepileptogenic properties in rats.[56]
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.
The Inuit are often cited as an example of a culture that has lived for hundreds of years on a low-carbohydrate diet.[42] However, in multiple studies the traditional Inuit diet has not been shown to be a ketogenic diet.[43][44][45][46] Not only have multiple researchers been unable to detect any evidence of ketosis resulting from the traditional Inuit diet, but the ratios of fatty-acid to glucose were observed at well below the generally accepted level of ketogenesis.[44][47][45][46] Furthermore, studies investigating the fat yields from fully dressed wild ungulates, and the dietary habits of the cultures who rely on them, suggest that they are too lean to support a ketogenic diet.[48][49] With limited access to fat and carbohydrates, cultures such as the Nunamiut Eskimos—who relied heavily on caribou for subsistence—annually traded for fat and seaweed with coastal-dwelling Taremiut.[48]
Around this time, Bernarr Macfadden, an American exponent of physical culture, popularised the use of fasting to restore health. His disciple, the osteopathic physician Dr. Hugh William Conklin of Battle Creek, Michigan, began to treat his epilepsy patients by recommending fasting. Conklin conjectured that epileptic seizures were caused when a toxin, secreted from the Peyer's patches in the intestines, was discharged into the bloodstream. He recommended a fast lasting 18 to 25 days to allow this toxin to dissipate. Conklin probably treated hundreds of epilepsy patients with his "water diet" and boasted of a 90% cure rate in children, falling to 50% in adults. Later analysis of Conklin's case records showed 20% of his patients achieved freedom from seizures and 50% had some improvement.[10]
If I see a TSH above 2.0 or a trend towards higher values in someone who is testing repeatedly, I get worried – and prefer to see TSH at 0.5-2.0. Of course, this doesn’t mean that you begin to shove carbohydrates indiscriminately down the hatch. However, it means that your high-fat, low-carb diet should include thyroid supporting foods rich in iodine and selenium, such as sea vegetables and brazil nuts, and should also include carbohydrates timed properly, such as before, during or after workouts, when the carbohydrate is more likely to be utilized for energy and less likely to spike blood glucose levels.
I have never been able to fix the electrolyte loss symptoms I get on the ketogenic diet (heart palpitations, dry mouth, air hunger) by supplementing with electrolytes. Blogosphere says that is just the transition, but mine seem to only get worse over time. I’ve tried about 2 grams of extra potassium, 800 mg extra magnesium, and 3 grams extra salt (in addition to my already liberally salted foods) spread throughout the day. This did not help. Also does eating salt alone cause you to retain water and therefore retain the rest of the electrolytes without supplementing them?
^ Bechtel PJ (2 December 2012). Muscle as Food. Elsevier Science. pp. 171–. ISBN 978-0-323-13953-3. Retrieved 19 May 2014. Freezing does stop the postmortem metabolism but only at about −18ºC and lower temperatures. Above −18ºC increasing temperatures of storage cause an increasing rate of ATP breakdown and glycolysis that is higher in the comminuted meat than in the intact tissue (Fisher et al., 1980b). If the ATP concentration in the frozen tissue falls below ~ 1 µmol/g no contraction or rigor can occur because they are prevented by the rigid matrix of ice.
The first modern study of fasting as a treatment for epilepsy was in France in 1911.[12] Twenty epilepsy patients of all ages were "detoxified" by consuming a low-calorie vegetarian diet, combined with periods of fasting and purging. Two benefited enormously, but most failed to maintain compliance with the imposed restrictions. The diet improved the patients' mental capabilities, in contrast to their medication, potassium bromide, which dulled the mind.[13]
Other research further supports the potential benefits of this diet. For example, preliminary studies link following the keto diet to reduced symptoms of Alzheimer’s disease. (4) Previous research suggests it may also help reverse metabolic syndrome, manage Parkinson’s disease, has been proven to help control seizures in children with epilepsy, and, according to the results of a small pilot study, may potentially even improve symptoms of polycystic ovary syndrome (PCOS). (5, 6, 7)
There are many ways in which epilepsy occurs. Examples of pathological physiology include: unusual excitatory connections within the neuronal network of the brain; abnormal neuron structure leading to altered current flow; decreased inhibitory neurotransmitter synthesis; ineffective receptors for inhibitory neurotransmitters; insufficient breakdown of excitatory neurotransmitters leading to excess; immature synapse development; and impaired function of ionic channels.[7]
A keto diet has shown to improve triglyceride levels and cholesterol levels most associated with arterial buildup. More specifically low-carb, high-fat diets show a dramatic increase in HDL and decrease in LDL particle concentration compared to low-fat diets.3A study in the long-term effects of a ketogenic diet shows a significant reduction in cholesterol levels, body weight, and blood glucose. Read more on keto and cholesterol >

“Loss of muscle mass as we age has a number of serious consequences,” notes Clark. “Muscle is metabolically active and helps boost daily energy expenditure and mitigate age-related weight gain.” Losing muscle mass can also decrease functional strength and heighten the risk of falls, notes Clark. Falls are the top cause of death from injury in older populations, according to the Institute of Medicine Division of Health Promotion and Disease Prevention.
^ Lawrie 2014, pp. 92-. "A much delayed onset of rigor mortis has been observed in the muscle of the whale (Marsh, 1952b). The ATP level and the pH may remain at their high in vivo values for as much as 24h at 37ºC. No adequate explanation of this phenomenon has yet been given; but the low basal metabolic rate of whale muscle (Benedict, 1958), in combination with the high content of oxymyoglobin in vivo (cf 4.3.1), may permit aerobic metabolism to continue slowly for some time after the death of the animal, whereby ATP levels can be maintained sufficiently to delay the union of actin and myosin in rigor mortis."
“Adequate dietary carbohydrate is critical to raise muscle glycogen to high levels in preparation for the next day’s endurance competition or hard training session. Accordingly, during the 24 h prior to a hard training session or endurance competition, athletes should consume 7-12 g of carbohydrate per kilogram of body weight. However, during the 24 h prior to a moderate or easy day of training, athletes need to consume only 5-7 g of carbohydrate per kilogram of body weight.”
Advocates for the diet recommend that it be seriously considered after two medications have failed, as the chance of other drugs succeeding is only 10%.[9][31][32] The diet can be considered earlier for some epilepsy and genetic syndromes where it has shown particular usefulness. These include Dravet syndrome, infantile spasms, myoclonic-astatic epilepsy, and tuberous sclerosis complex.[9][33]
Another possible nutrient deficiency: potassium, a mineral important for both electrolyte balance and blood pressure control, notes MedlinePlus. “Inadequate intake of potassium is likely when consumption of fruits and starchy vegetables are decreased,” says Asche. She recommends adding lower-carb sources of potassium to the diet, including avocado and spinach — as well as lower-carb sources of fiber, such as chia seeds and flaxseed (be sure to enjoy ground for the best health benefits).
A systematic review in 2018 looked at 16 studies on the ketogenic diet in adults. It concluded that the treatment was becoming more popular for that group of patients, that the efficacy in adults was similar to children, the side effects relatively mild. However, many patients gave up with the diet, for various reasons, and the quality of evidence inferior to studies on children. Health issues include high levels of low-density lipoprotein, high total cholesterol, and weight loss.[24]
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