" "

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.

"Muscle loss on the ketogenic diet is an ongoing area of research," Clark told Everyday Health. "Small studies suggest that people on the ketogenic diet lose muscle even when they continue resistance training. This may be related to the fact that protein alone is less effective for muscle building than protein and carbohydrates together after exercise."
Because the ketogenic diet alters the body's metabolism, it is a first-line therapy in children with certain congenital metabolic diseases such as pyruvate dehydrogenase (E1) deficiency and glucose transporter 1 deficiency syndrome,[35] which prevent the body from using carbohydrates as fuel, leading to a dependency on ketone bodies. The ketogenic diet is beneficial in treating the seizures and some other symptoms in these diseases and is an absolute indication.[36] However, it is absolutely contraindicated in the treatment of other diseases such as pyruvate carboxylase deficiency, porphyria, and other rare genetic disorders of fat metabolism.[9] Persons with a disorder of fatty acid oxidation are unable to metabolise fatty acids, which replace carbohydrates as the major energy source on the diet. On the ketogenic diet, their bodies would consume their own protein stores for fuel, leading to ketoacidosis, and eventually coma and death.[37]
First reported in 2003, the idea of using a form of the Atkins diet to treat epilepsy came about after parents and patients discovered that the induction phase of the Atkins diet controlled seizures. The ketogenic diet team at Johns Hopkins Hospital modified the Atkins diet by removing the aim of achieving weight loss, extending the induction phase indefinitely, and specifically encouraging fat consumption. Compared with the ketogenic diet, the modified Atkins diet (MAD) places no limit on calories or protein, and the lower overall ketogenic ratio (about 1:1) does not need to be consistently maintained by all meals of the day. The MAD does not begin with a fast or with a stay in hospital and requires less dietitian support than the ketogenic diet. Carbohydrates are initially limited to 10 g per day in children or 20 g per day in adults, and are increased to 20–30 g per day after a month or so, depending on the effect on seizure control or tolerance of the restrictions. Like the ketogenic diet, the MAD requires vitamin and mineral supplements and children are carefully and periodically monitored at outpatient clinics.[48]
I talk about that quite a bit here :https://bengreenfieldfitness.com/2015/09/things-your-pee-can-tell-you-about-your-body/
Moreover, recent studies show that the Inuit have evolved a number of rare genetic adaptations that make them especially well suited to eat large amounts of omega-3 fat.[57][58][59] And earlier studies showed that the Inuit have a very high frequency—68% to 81% in certain arctic coastal populations—of an extremely rare autosomal recessive mutation of the CPT1A gene—a key regulator of mitochondrial long-chain fatty-acid oxidation[60][61]—which results in a rare metabolic disorder known as carnitine palmitoyltransferase 1A (CPT1A) deficiency and promotes hypoketotic hypoglycemia—low levels of ketones and low blood sugar.[62] The condition presents symptoms of a fatty acid and ketogenesis disorder.[62] However, it appears highly beneficial to the Inuit[60] as it shunts free fatty acids away from liver cells to brown fat, for thermogenesis.[63][64] Thus the mutation may help the Inuit stay warm by preferentially burning fatty acids for heat in brown fat cells.[64] In addition to promoting low ketone levels, this disorder also typically results in hepatic encephalopathy (altered mental state due to improper liver function), enlarged liver and high infant mortality.[65] Inuit have been observed to have enlarged livers with an increased capacity for gluconeogenesis, and have greater capacity for excreting urea to remove ammonia, a toxic byproduct of protein breakdown.[57][66][67][68] Ethnographic texts have documented the Inuit's customary habit of snacking frequently [69] and this may well be a direct consequence of their high prevalence of the CPT1A mutation[70] as fasting, even for several hours, can be deleterious for individuals with that allele, particularly during strenuous exercise.[57][70] The high frequency of the CPT1A mutation in the Inuit therefore suggests that it is an important adaptation to their low carbohydrate diet and their extreme environment.[57][60][70]
Awesome… I am a newbie to this i took the keto os for 2 months for weight loss and did well. It a bit pricey. I try hard to conform to lchf diet daily but see no change other than I crave sweets. In 5’7 270 and stuck! My highest weight was 390 had gastric band put in 10 years ago but its just keep me from consumption of large amounts at on time. Is there a more economical way to stay in ketosis? I wAnt more energy… In not an exercise person usually have no energy. In willing to try other ideas.
What about fruits and vegetables? All fruits are rich in carbs, but you can have certain fruits (usually berries) in small portions. Vegetables (also rich in carbs) are restricted to leafy greens (such as kale, Swiss chard, spinach), cauliflower, broccoli, Brussels sprouts, asparagus, bell peppers, onions, garlic, mushrooms, cucumber, celery, and summer squashes. A cup of chopped broccoli has about six carbs.
For patients who benefit, half achieve a seizure reduction within five days (if the diet starts with an initial fast of one to two days), three-quarters achieve a reduction within two weeks, and 90% achieve a reduction within 23 days. If the diet does not begin with a fast, the time for half of the patients to achieve an improvement is longer (two weeks), but the long-term seizure reduction rates are unaffected.[44] Parents are encouraged to persist with the diet for at least three months before any final consideration is made regarding efficacy.[9]

After initiation, the child regularly visits the hospital outpatient clinic where they are seen by the dietitian and neurologist, and various tests and examinations are performed. These are held every three months for the first year and then every six months thereafter. Infants under one year old are seen more frequently, with the initial visit held after just two to four weeks.[9] A period of minor adjustments is necessary to ensure consistent ketosis is maintained and to better adapt the meal plans to the patient. This fine-tuning is typically done over the telephone with the hospital dietitian[19] and includes changing the number of calories, altering the ketogenic ratio, or adding some MCT or coconut oils to a classic diet.[18] Urinary ketone levels are checked daily to detect whether ketosis has been achieved and to confirm that the patient is following the diet, though the level of ketones does not correlate with an anticonvulsant effect.[19] This is performed using ketone test strips containing nitroprusside, which change colour from buff-pink to maroon in the presence of acetoacetate (one of the three ketone bodies).[45]
Sleep enough – for most people at least seven hours per night on average – and keep stress under control. Sleep deprivation and stress hormones raise blood sugar levels, slowing ketosis and weight loss a bit. Plus they might make it harder to stick to a keto diet, and resist temptations. So while handling sleep and stress will not get you into ketosis on it’s own, it’s still worth thinking about.
Con: Results can vary depending on how much fluid you drink. By drinking more water, you dilute the concentration of ketones in the urine and thus a lower level of ketones will be detected on the strips. The strips don’t show a precise ketone level. Finally, and most importantly, as you become increasingly keto-adapted and your body reabsorbs ketones from the urine, urine strips may become unreliable, even if you’re in ketosis.
This article really bothers me in that if you do a few incorrect things with this diet, it will actually do more harm than a full carb diet. I have been in ketosis for a month or so but to what detriment? Based on the “ketosis darkside” list you highlighted, i could be doing any or all of these without realising. Could i share with you my meal plans and see if in your opinion they are beneficial and healthy or if im digging myself an early grave?

Therefore, more people experiencing "keto crotch" need to visit doctors to determine what's really happening. It could be that some of the people claiming "keto crotch" are instead detecting smells that are not related to their diets. Many different smells could emanate from your crotch, some are normal, some are not. Conversely, who knows for sure what a drastic change in your diet may do to different parts of your body? There is still a lot unknown about the links between nutrition and your various bodily functions. You are a complex system with many unknowns. The keto crotch could be a real phenomenon, but more scientific evidence and studies are needed.
You indicate that exogenous ketones do not shut down the ability, of your body, to oxidize fat. Is that to say it does not have an effect on your body at all? My specific question is… does my body oxidize less fat, when supplementing with exogenous ketones? I think you indicate in your article that it could. I would expect it to, in that if I supplement then my body would not “need” to oxidize the fat to provide the energy.
In addition, most studies that compare carbohydrate utilization with fat utilization fail to take into account the fact that full “fat adaptation” that allows you to gain all the benefits of using fat as a fuel actually takes time – often more than four weeks – and up to a couple years. But since most studies that compare fat and carbohydrate burning are short-term, you rarely see the benefits of this kind of fat adaptation actually fleshed out in research. Instead, the average research participant begins the study in a non-fat adapted state, gets either a high fat or high carb diet, then launches into exercise. But in an ideal study, that person would have followed either a high-fat or high-carb diet for many months before getting their fat burning capability investigated.
Frankly, the results of my foray into ketosis and eventually keto-adaptation were astounding. I had the best Ironman triathlon season of my life and shocking levels of mental focus and physical ease, especially for races and workouts that lasted longer than two hours. Without experiencing muscle loss, hunger pangs or brain fog, I found I could go the entire day without eating, which was enormously helpful for business and personal productivity. My gas, bloating, fermentation and GI “issues” disappeared. My blood levels of inflammatory markers like HS-CRP and cytokines dropped to rock-bottom, while my levels of good cholesterol, vitamin D, and anti-inflammatory fatty acids skyrocketed.
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?
“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.”
I've been on the diet for about a month and a half now and I've noticed that my vaginal odors have gotten MUCH stronger... (It smells like a mix between urine and discharge... I'm not exactly sure how vaginas are 'supposed' to smell like. Many say 'musky' but I feel like that's too mild of a word... It's much stronger than 'musk' for me :/ ). My discharge is white in color and it doesn't smell fishy. Sometimes when it dries on my underwear it's a light yellow? Has this happened to anyone before? Is it because of my change in diet (if so, can anybody explain why?), or could it be something else?

This article is excellent and I’ve actually read it a few times just to make sure I’m absorbing as much as possible. With that said can we talk a bit about protein? Why does it seem like protein is taking a back seat? What about the athlete who needs to maintain and/or increase muscle mass. I don’t want to make any assumptions and with all the research I’ve done along with personal testing into Keto it just seems to me that protein and its benefits are not a discussion point in this diet. Why?
One more thing that I noticed is that my HR does not move Beyond a certain point. I can still perform quite at a high level and faster than most people at my box but weirdly enough it’s like there’s a block on my HR which doesn’t allow it to move beyond 160 bpm. I’m not sure if this is good or bad! Could I go even faster if my HR would pass this limit?? It is a physiological barrier created by the glycogen sparing mechanism that doesn’t allow my body to move after a certain point so it won’t have to tap into my glycogen stores or force my body to go into gluconeogenesis?? If I added some more carbs around my workouts would it be easier to get the glycolytic pathway to work more effectively since it’d be faster and easier fuel? I read about the downregulation of PDH enzymes after prolonged keto and I constantly worry that I dont use my glycolytic pathway as effective anymore. I LOVE this lifestyle but at the same time, as athletes; we’re always thinking on how to improve performance. What are your thoughts?! Thank you so much!!
First reported in 2003, the idea of using a form of the Atkins diet to treat epilepsy came about after parents and patients discovered that the induction phase of the Atkins diet controlled seizures. The ketogenic diet team at Johns Hopkins Hospital modified the Atkins diet by removing the aim of achieving weight loss, extending the induction phase indefinitely, and specifically encouraging fat consumption. Compared with the ketogenic diet, the modified Atkins diet (MAD) places no limit on calories or protein, and the lower overall ketogenic ratio (about 1:1) does not need to be consistently maintained by all meals of the day. The MAD does not begin with a fast or with a stay in hospital and requires less dietitian support than the ketogenic diet. Carbohydrates are initially limited to 10 g per day in children or 20 g per day in adults, and are increased to 20–30 g per day after a month or so, depending on the effect on seizure control or tolerance of the restrictions. Like the ketogenic diet, the MAD requires vitamin and mineral supplements and children are carefully and periodically monitored at outpatient clinics.[48]
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