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The bottom line? If you’re thinking about trying the ketogenic diet, run it by your doctor first — regardless of any preexisting health conditions. And consult a registered dietitian nutritionist (find one at EatRight.org) to find a nutrition professional who can work with you to create a meal plan you can stick to. People with kidney disease or a history of disordered eating should avoid the diet, and people with type 1 diabetes may want to avoid it, as well. If you have risk factors for heart disease, you’ll want to speak with your doctor before considering the diet.
For example, a key component of safe and lasting fat loss is your capability to tap into your body’s own storage fat for energy. This access to fat cannot happen if your body is constantly drawing on carbohydrate reserves and blood glucose for energy. In the type of moderate- to high-carbohydrate diets you’ve learned are widely recommended by prevailing nutrition science, not only does the utilization of fat for energy become far less crucial (since you’re constantly dumping readily available sugar sources into your body), but your metabolism never becomes efficient at using fat. There is a growing body of evidence proving that a high-fat, low-carbohydrate diet results in faster and more permanent weight loss than a low-fat diet. Furthermore, appetite satiety and dietary satisfaction significantly improve with a high-fat, low-carbohydrate diet that includes moderate protein.
-Pancreatic Dysfunction: The beta cells in the pancreas that produce the insulin to help control blood sugar become dysfunctional with high blood glucose, raising the risk for type 2 diabetes. Researchers have discovered that beta cell issues are detectable in people whose glucose levels spike two hours after eating, despite those levels staying within the range considered normal and safe by the medical establishment.
When you eat foods high in carbohydrates and fat, your body naturally produces glucose. Carbohydrates are the easiest thing for the body to process, and therefore it will use them first – resulting in the excess fats to be stored immediately. In turn, this causes weight gain and health problems that are associated with high fat, high carbohydrate diets (NOT keto).
I would do breath ketone measurements. That's exactly what I do and this is what I use :https://greenfieldfitnesssystems.com/product/ketonix-breath-ketone-monitor/
"Many of the richest sources of fiber, like beans, fruit, and whole grains are restricted on the ketogenic diet," registered dietician Edwina Clark told Everyday Health. "As a result, ketogenic eaters miss out on the benefits of fiber-rich diet such as regular laxation and microbiome support. The microbiome has been implicated in everything from immune function to mental health."
During the 1920s and 1930s, when the only anticonvulsant drugs were the sedative bromides (discovered 1857) and phenobarbital (1912), the ketogenic diet was widely used and studied. This changed in 1938 when H. Houston Merritt, Jr. and Tracy Putnam discovered phenytoin (Dilantin), and the focus of research shifted to discovering new drugs. With the introduction of sodium valproate in the 1970s, drugs were available to neurologists that were effective across a broad range of epileptic syndromes and seizure types. The use of the ketogenic diet, by this time restricted to difficult cases such as Lennox–Gastaut syndrome, declined further.
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.
There are theoretically no restrictions on where the ketogenic diet might be used, and it can cost less than modern anticonvulsants. However, fasting and dietary changes are affected by religious and cultural issues. A culture where food is often prepared by grandparents or hired help means more people must be educated about the diet. When families dine together, sharing the same meal, it can be difficult to separate the child's meal. In many countries, food labelling is not mandatory so calculating the proportions of fat, protein and carbohydrate is difficult. In some countries, it may be hard to find sugar-free forms of medicines and supplements, to purchase an accurate electronic scale, or to afford MCT oils.
On the keto diet, your body begins to shed fat, water and glycogen, and as this happens you lose key electrolytes, such as sodium, potassium and magnesium. When you're running low on these electrolytes, you might experience headaches or extreme fatigue. These losses are most pronounced during the first few weeks after you enter ketosis, so if you're going to start the keto diet it's best to plan ahead to make sure you get healthy amounts of these electrolytes — and other vitamins and minerals — either through supplements or a thoughtfully-designed meal plan.
Children who discontinue the diet after achieving seizure freedom have about a 20% risk of seizures returning. The length of time until recurrence is highly variable, but averages two years. This risk of recurrence compares with 10% for resective surgery (where part of the brain is removed) and 30–50% for anticonvulsant therapy. Of those who have a recurrence, just over half can regain freedom from seizures either with anticonvulsants or by returning to the ketogenic diet. Recurrence is more likely if, despite seizure freedom, an electroencephalogram shows epileptiform spikes, which indicate epileptic activity in the brain but are below the level that will cause a seizure. Recurrence is also likely if an MRI scan shows focal abnormalities (for example, as in children with tuberous sclerosis). Such children may remain on the diet longer than average, and children with tuberous sclerosis who achieve seizure freedom could remain on the ketogenic diet indefinitely.
Apparently, Dominic’s research seems to be suggesting the fact that diet-induced ketosis from a high-fat, low-carb intake, especially when combined with the use of nutrition supplements such as powdered ketones or MCT oil, can vastly reduce the need for the brain to use oxygen to burn glucose. This is because the brain can use up to around 75% of its fuel from ketones. So a ketone-fed or a fat-adapted brain can be better equipped to withstand low oxygen availability and potentially support longer breath-hold times. Dominic’s research also shows that in the presence of ketosis, the brain and body are able to resist the potential cell damage of long periods of time with low oxygen, also known as “hypoperfusion”.
Once inside the mitochondrion, the dominant way that the bound fatty acids are used as fuel in cells is through β-oxidation, which cleaves two carbons off of the acyl-CoA molecule in every cycle to form acetyl-CoA. Acetyl-CoA enters the citric acid cycle, where it undergoes an aldol condensation with oxaloacetate to form citric acid; citric acid then enters the tricarboxylic acid cycle (TCA), which harvests a very high energy yield per carbon in the original fatty acid.
Wilder's colleague, paediatrician Mynie Gustav Peterman, later formulated the classic diet, with a ratio of one gram of protein per kilogram of body weight in children, 10–15 g of carbohydrate per day, and the remainder of calories from fat. Peterman's work in the 1920s established the techniques for induction and maintenance of the diet. Peterman documented positive effects (improved alertness, behaviour, and sleep) and adverse effects (nausea and vomiting due to excess ketosis). The diet proved to be very successful in children: Peterman reported in 1925 that 95% of 37 young patients had improved seizure control on the diet and 60% became seizure-free. By 1930, the diet had also been studied in 100 teenagers and adults. Clifford Joseph Barborka, Sr., also from the Mayo Clinic, reported that 56% of those older patients improved on the diet and 12% became seizure-free. Although the adult results are similar to modern studies of children, they did not compare as well to contemporary studies. Barborka concluded that adults were least likely to benefit from the diet, and the use of the ketogenic diet in adults was not studied again until 1999.
For any long 90+ minute workouts or competitions for which glycogen depletion is a potential issue, use Glycofuse, but use half of the recommended serving of it, and add one scoop of Catalyte electrolytes, one scoop of Aminos, and one serving of medium chain triglycerides in the form of Brain Octane, KetoCaNa or KETO//OS (pick your poison, it’s up to you).
First, decide if you need to check ketones. Amy Berger of Tuit Nutrition has a great post here to help you decide. If, after reading that, you still want to check your ketone levels, there are several ways to check them. You can buy Bayer ketone stix, and check the levels of ketones in your urine. Or you can use a blood ketone meter. The Precision Xtra has been the one to use until just recently. The problem is that this meter is hard to find, as the manufacturer Abbott keeps changing the name. The strips are even harder to find and buy.
You need to do a “common man’s” version of a good ketogenic nutrition program or discussion. Great article, and I leaned a few things. Those Ketone Salts and other supplements can get pricey. I eat a very low carb and high fat diet and meander in and out of ketosis during the week. A pure ketogenic diet is so restrictive that meals it can get very repetitive during the week. I’d like to learn more about cooking with oils and how temperature effects their qualities. I can only handle eating so much raw food, and I love to cook my greens and other vegetables in bacon fat and coconut oil. It will be next May before I can get my blood work performed (insurance reasons) so until then I’ll need to be careful and hold back on those after supper dark chocolate excursions! Thanks!!
I talk about that quite a bit here :https://bengreenfieldfitness.com/2015/09/things-your-pee-can-tell-you-about-your-body/
As a matter of fact, from a pure biology perspective, lauric acid should actually be considered a LCT, because unlike C8 and C10 forms of MCT, lauric acid gets processed by your liver. This matters because your body metabolizes MCT’s differently than LCT’s: unlike LCT’s, MCT’s get very quickly converted into ketone energy to fuel your brain and body instead of requiring a pit stop in the liver for processing.
^ 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."
The keto diet isn’t new, and it’s been around for nearly a century. It was originally developed to treat people with epilepsy. In the 1920s, researchers found that raised levels of ketones in the blood led to fewer epileptic seizures in patients. The keto diet is still used today to treat children with epilepsy who don’t respond well to anti-epileptic drugs.
On the ketogenic diet, carbohydrates are restricted and so cannot provide for all the metabolic needs of the body. Instead, fatty acids are used as the major source of fuel. These are used through fatty-acid oxidation in the cell's mitochondria (the energy-producing parts of the cell). Humans can convert some amino acids into glucose by a process called gluconeogenesis, but cannot do this by using fatty acids. Since amino acids are needed to make proteins, which are essential for growth and repair of body tissues, these cannot be used only to produce glucose. This could pose a problem for the brain, since it is normally fuelled solely by glucose, and most fatty acids do not cross the blood–brain barrier. However, the liver can use long-chain fatty acids to synthesise the three ketone bodies β-hydroxybutyrate, acetoacetate and acetone. These ketone bodies enter the brain and partially substitute for blood glucose as a source of energy.
I have been taking Ucan 30 Minutes before run and take UCAN 1 Hour into run and 1 hour later. Also take BCAA powder in 8 ounce liquid during run. I have been doing HFAT and LCARB diet. Problem i slow down after 1 1/2 hour during my long run. I need your advice help fueling my run after 14 miles. This my first Marathon, I have run 7 Half Marathon around 1.58.
Ideally, you combine supplemental ketones with a relatively low carb diet, especially if metabolic efficeincy is important to you. HOWEVER, you can achieve most of the benefits of ketosis aside from the fat burning efficiency by using exogenous ketones. So it all depends on how lean you are, what's important to you from a performance vs. fat loss standpoint, etc.
Fascinating stuff and I am quite curious how we know for certain one is actually in ketosis i.e. using ketones as primary fuel source BECAUSE we do know that glucose has a shorter metabolic pathway to burn and under most conditions, given the presence of glucose, that is what the body will default to which is why high fat and high sugar together in diet is so detrimental. So if we use one or more of the above “boosters” and show high levels of blood ketones but also highish levels of glucose (during initial transition) will be mostly burning ketones or still defaulting to glucose?