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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]

Question: I have recently done my 23&me DNA test and have also put my info into AthletiGen. I’m curious about your thoughts about high fat/low carb diet in context of this info. My test says I am ‘2x more likely to loose weight on a low fat diet’, and that I have ‘normal sensitivity to weight gain due to saturated fat intake/and unsaturated fat intake’, & ‘likely to eat normal amounts of carbs’! All interesting but in the ketosis context, I took this to mean that eating high fat/low carb would not be of greatest benefit to me?! (I have tried getting into ketosis prior to all the new supps, for about 3 months, and I couldn’t get in to it (tested w/ blood finger prick) and didn’t feel great). Which leads me to wonder what Macro ratio would be best, as I’m also a endo-meso)!
Before you consume a BHB salt, these individual components are held together by ionic bonds. However, when you consume a supplement containing a BHB salt, it is absorbed into the blood where it dissociates into free sodium (Na+), potassium (K+), and finally, the actual ketone. This means that consuming a product containing a BHB directly and immediately puts ketones into your blood, without the need for you to eat tons of fats or engage in carbohydrate restriction or fasting to generate the ketones.
And it all culminated with me stepping into Dr. Jeff Volek’s world famous laboratory at University of Connecitut to subject myself to extensive blood testing, chunks of muscle removed from my legs, fat sucked out of my butt-cheeks, urine, stool and gut microbiome testing, oxygen and carbon dioxide testing and countless hours of treadmill running to discover what a full twelve months of eating a ketotic diet had actually done to my body.
The ketone bodies are possibly anticonvulsant; in animal models, acetoacetate and acetone protect against seizures. The ketogenic diet results in adaptive changes to brain energy metabolism that increase the energy reserves; ketone bodies are a more efficient fuel than glucose, and the number of mitochondria is increased. This may help the neurons to remain stable in the face of increased energy demand during a seizure, and may confer a neuroprotective effect.[56]
Meat products make up a big part of the keto diet, but experts stress the importance of choosing quality. "Since the keto diet is based a lot on animal proteins, it's important to buy organic poultry and grass-fed, organic beef," says Aimee Aristotelous, RD. "Not only do organic selections help with limiting environmental toxins, but grass-fed options of red meats even change the composition of fats." The result, she explains, is that your body is able to better absorb those healthy fats.
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]
Short-term results for the LGIT indicate that at one month approximately half of the patients experience a greater than 50% reduction in seizure frequency, with overall figures approaching that of the ketogenic diet. The data (coming from one centre's experience with 76 children up to the year 2009) also indicate fewer side effects than the ketogenic diet and that it is better tolerated, with more palatable meals.[18][50]

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.
Lots of apps and websites offer keto diet challenges—basically, a blueprint for the keto diet with a fixed starting and ending point (they typically last for a week to a month, though some may be longer). Speaking of apps, plenty of keto-centric ones are right at your fingertips (a.k.a., your smartphone), like the KetoDiet app, which can help you calculate your macros and track your keto diet effectively.
As I learned in a University of Connecticut lab experiment I mentioned earlier in this article (gory details here), a high-fat, low-carb diet can teach and allow the muscles to tap into more fat for fuel, making your body crave less use of oxygen in the large muscles of the legs, arms or other areas that you’ve learned oxygen gets shunted away from when deep underwater.
Peak fat oxidation was 2.3-fold higher in the LC group (1.54 ± 0.18 vs 0.67 ± 0.14 g/min; P = 0.000) and it occurred at a higher percentage of VO2max (70.3 ± 6.3 vs 54.9 ± 7.8%; P = 0.000). Mean fat oxidation during submaximal exercise was 59% higher in the LC group (1.21 ± 0.02 vs 0.76 ± 0.11 g/min; P = 0.000) corresponding to a greater relative contribution of fat (88 ± 2 vs 56 ± 8%; P = 0.000). Despite these marked differences in fuel use between LC and HC athletes, there were no significant differences in resting muscle glycogen and the level of depletion after 180 min of running (−64% from pre-exercise) and 120 min of recovery (−36% from pre-exercise).
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.
Insulin is a hormone that lets your body use or store sugar as fuel. Ketogenic diets make you burn through this fuel quickly, so you don’t need to store it. This means your body needs -- and makes -- less insulin. Those lower levels may help protect you against some kinds of cancer or even slow the growth of cancer cells. More research is needed on this, though.

^ Jump up to: a b c d e f g h i j k l m n o p q r s Kossoff EH, Zupec-Kania BA, Amark PE, Ballaban-Gil KR, Bergqvist AG, Blackford R, et al. Optimal clinical management of children receiving the ketogenic diet: recommendations of the International Ketogenic Diet Study Group. Epilepsia. 2009 Feb;50(2):304–17. doi:10.1111/j.1528-1167.2008.01765.x. PMID 18823325
Those issues can be part of what's known as the “keto flu,” Warren says. Other side effects of the keto diet, all of which are tied to carb withdrawal, can include lightheadedness, nausea, mental fog, cramps, and headaches, in addition to tiredness. Luckily, the keto flu doesn't usually last more than a week—which is coincidentally about when people start to see the number on the scale go down, says Warren.

The popular low-carb diets (such as Atkins or Paleo) modify a true keto diet. But they come with the same risks if you overdo it on fats and proteins and lay off the carbs. So why do people follow the diets? "They're everywhere, and people hear anecdotally that they work," McManus says. Theories about short-term low-carb diet success include lower appetite because fat burns slower than carbs. "But again, we don't know about the long term," she says. "And eating a restrictive diet, no matter what the plan, is difficult to sustain. Once you resume a normal diet, the weight will likely return."
The original therapeutic diet for paediatric epilepsy provides just enough protein for body growth and repair, and sufficient calories[Note 1] to maintain the correct weight for age and height. The classic therapeutic ketogenic diet was developed for treatment of paediatric epilepsy in the 1920s and was widely used into the next decade, but its popularity waned with the introduction of effective anticonvulsant medications. This classic ketogenic diet contains a 4:1 ratio by weight of fat to combined protein and carbohydrate. This is achieved by excluding high-carbohydrate foods such as starchy fruits and vegetables, bread, pasta, grains, and sugar, while increasing the consumption of foods high in fat such as nuts, cream, and butter.[1] Most dietary fat is made of molecules called long-chain triglycerides (LCTs). However, medium-chain triglycerides (MCTs)—made from fatty acids with shorter carbon chains than LCTs—are more ketogenic. A variant of the classic diet known as the MCT ketogenic diet uses a form of coconut oil, which is rich in MCTs, to provide around half the calories. As less overall fat is needed in this variant of the diet, a greater proportion of carbohydrate and protein can be consumed, allowing a greater variety of food choices.[4][5]
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