The Inuit are often cited as an example of a culture that has lived for hundreds of years on a low-carbohydrate diet. However, in multiple studies the traditional Inuit diet has not been shown to be a ketogenic diet. 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. 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. 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.
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. 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—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. The condition presents symptoms of a fatty acid and ketogenesis disorder. However, it appears highly beneficial to the Inuit as it shunts free fatty acids away from liver cells to brown fat, for thermogenesis. Thus the mutation may help the Inuit stay warm by preferentially burning fatty acids for heat in brown fat cells. In addition to promoting low ketone levels, this disorder also typically results in hepatic encephalopathy (enlarged liver) and high infant mortality. 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. Ethnographic texts have documented the Inuit's customary habit of snacking frequently  and this may well be a direct consequence of their high prevalence of the CPT1A mutation as fasting, even for several hours, can be deleterious for individuals with that allele, particularly during strenuous exercise. 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.
The keto diet changes the way your body converts food into energy. Eating a lot of fat and very few carbs puts you in ketosis, a metabolic state where your body burns fat instead of carbs for fuel. When your body is unable to get glucose from carbs, your liver converts fatty acids from your diet into ketones, an alternative source of energy. Burning ketones in place of glucose reduces inflammation and spurs weight loss.
In the 1920s, doctors began to realize that when fed a high fat and extremely low carbohydrate diet their patients began to notice a remarkable reduction in frequency and severity of seizures. They found that the breakdown of dietary fat caused the body to produce ketones which have GABAergic and glutamatergic effects causing a reduction in nerve impulses thus having an anticonvulsant effect. The ketogenic diet was used as the mainstream therapy until the development of new anticonvulsant medications in the late 1930s.
How often you eat is also up to your personal preference. "For most people, I recommend three to four meals per day with a few healthy keto snacks in between," says Dr. Axe. "This ensures that you're getting a good mix of protein and fat all day long to keep you feeling energized and satisfied." That being said, he encourages people to listen to their bodies and tune in to when they're truly hungry. "If you find that you feel better eating five to six smaller meals spread throughout the day, do what works best for you."
Many questions about the role of such an important intermediate of lipid metabolism remains unanswered, e.g., the role of BHB in food control. For example, whether or not BHB could act as a satiety signal in the brain, considering its role in energy supply to CNS. We have to consider that the effects of KBs on hunger reduction can only be seen after many days following fasting or KD initiation (Paoli et al., 2010); this is consistent with the abovementioned threshold of brain utilization of KB as an energy source, i.e., 4 mmol/L (Veech, 2004), which is close to the Km for the monocarboxylate transporter (Leino et al., 2001). During the first days of fasting or KD there is a rise of BHB and adiponectin concentrations (Halberg et al., 2005). One of the putative causes of hunger in starved humans may be due—together with other causes—to adiponectin. When adiponectin binds to its receptor AdipoR1, AMP-activated protein kinase (AMPK) is phosphorylated in the ARC of the hypothalamus (Valassi et al., 2008). The increase of AMPK activity in the hypothalamus may increase food intake and hepatic glucose output in mice while the decrease seems to reduce food intake (Zhang et al., 2009). KDs can also act similarly to a caloric restriction on AMPK (Newman and Verdin, 2014). Interestingly, AMPK seems to have opposing actions on the liver, muscle tissues and the brain: in liver and muscle AMPK activation increases FA oxidation by decreasing malonyl-CoA concentrations (Malonyl-CoA is the first intermediate in the lipogenic pathway and is also an inhibitor of carnitine palmitoyltransferase-1 (CPT-1). CPT-1 activity can be limiting for FA oxidation), through the inactivation of the acetyl-CoA carboxylase 1 (ACC1). AMPK can also increase the activity of malonyl-CoA decarboxylase (MCD), which enhances the decrease of malonyl-CoA levels.
If you give your body any more than the absolute minimum amount of protein that it needs, it will immediately break it down into carbs. This is why keto sites often give a guideline for not eating too much protein. The problem is that there’s no one guideline that works for everyone, and without specifically tailoring keto to your body it’d be easy to accidentally ingest too much protein.
Its simple, eat this; lose weight. I feel like I’ve finally amassed enough recipes to create several simple keto meal plans. AKA you print out a couple of recipes, hit the store, and you can know you’ll be doing keto right. If you’re not familiar with keto, its a low carb, high fat, medium protein diet designed to put your body into ketosis. Once in ketosis, your body burns fat instead of sugar and you’ll see accelerated weight loss as a result. The ideal ratio of fat to protein to carbs is 65% / 30% / 5% and you also want to keep your maximum net carbs at less than 20g a day. Net carbs = carbs – fiber.
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.
Wondering what fits into a keto diet — and what doesn’t? “It’s so important to know what foods you’ll be eating before you start, and how to incorporate more fats into your diet,” says Kristen Mancinelli, RD, author of The Ketogenic Diet: A Scientifically Proven Approach to Fast, Healthy Weight Loss, who is based in New York City. We asked her for some guidelines.