“Keto is not easy to maintain, it’s not a palatable diet,” says Andrea Giancoli, a dietician and nutrition consultant in California. Getting 80-90 percent of your calories from fat—which is what’s generally required for keto—is actually difficult. It involves eating a lot of rich, heavy foods with little variety—think fatty meats and gravy on cauliflower. You’re only allowed 10 to 15 grams of carbohydrates per day, and though many dieters stretch that to more like 20 or 30 grams that’s still only about one banana. A single apple could also get you past that limit depending on its size (though the fiber in an apple means that many dieters don't count those carbs towards their daily limit) and a couple slices of bread likely fulfill the requirement as well.
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 easiest macro to calculate in the ketogenic diet is fat. Once you've got your carbs and protein set, simply fill the rest of your daily calorie needs with fat sources. If you find yourself wanting to gain a bit of weight, add approximately 500 calories, or 55 grams. If you want to lose weight, cut down on your fat intake by 200-500 calories, or 22-55 grams.
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.
As is in the case of GABA, the intracellular reactive oxygen species (ROS) hypothesis works against the hunger-suppressive role of KD: it has been demonstrated that the hypothalamic ROS increase through NADPH oxidase is required for the eating-inhibitory effect of insulin (Jaillard et al., 2009); moreover it has been demonstrated that there is a ROS-dependent signaling pathway within the hypothalamus that regulates the energy homeostasis, and that activation of ROS-sensitive mechanisms could be sufficient to promote satiety (Benani et al., 2007). On the other side, KBs decreases mitochondrial production of ROS by increasing NADH oxidation in the mitochondrial respiratory chain (Maalouf et al., 2007).
Hi Barb, That can definitely be it. Losing when you are close to goal can be more difficult. It could also be that your body’s healthy weight is a little higher than what you’d like – which doesn’t mean you can’t lose, but makes it more difficult. If just eating Keto foods isn’t working, double check the macros for your weight and see if the amount you’re eating needs to be adjusted. You’ll find more help and support in our support group here.
^ Jump up to: a b c Taboulet P, Deconinck N, Thurel A, Haas L, Manamani J, Porcher R, Schmit C, Fontaine JP, Gautier JF (April 2007). "Correlation between urine ketones (acetoacetate) and capillary blood ketones (3-beta-hydroxybutyrate) in hyperglycaemic patients". Diabetes & Metabolism. 33 (2): 135–9. doi:10.1016/j.diabet.2006.11.006. PMID 17320448.
Although the hunger-reducing effect of KD is well-documented, its main mechanisms of action are still elusive. The global picture is complicated by the contradictory role of ketosis on anorexigenic and orexigenic signals (summarized in Figure Figure4).4). Ketones (mainly BHB) can act both orexigenically or anorexigenically. In the orexigenic mechanism, it increases the circulating level of adiponectin, increasing brain GABA and AMPK phosphorylation and decreasing brain ROS production. The anorexigenic mechanism triggers a main normal glucose meal response, increasing circulating post-meal FFA (thus reducing cerebral NPY), maintaining CCK meal response and decreasing circulating ghrelin. It can be postulated that the net balance of the contrasting stimuli results in a general reduction of perceived hunger and food intake. More studies are needed to explore the mechanism of potential beneficial effects of KD on food control.
Ariel Warren is a Registered Dietitian, Diabetes Educator, graduate from Brigham Young, and was diagnosed with Type 1 at the age of 4 years old. Ariel understands diabetes and enjoys working with clients to improve their blood sugar management, healthy eating, weight loss, fitness, and pregnancy. For coaching from a T1D Dietitian, you can contact Ariel directly, through her website: arielwarren.com.