We now know why you can lose weight with reduced hunger and desire
Article published by Virta Health in the US, written by Doctors: Brooke Bailey, Jeff Volek and Stephen Feeney and published on July 25, 2018. You can find the original article by clicking here. Translation provided by Virta Health for and by EatFat2BeFit.com.
The challenge of losing weight and keeping it off can be discouraging, especially if you have traveled on diet trains in the past. Diet, physical activity, and repeated wills of will usually cause temporary weight loss, followed by weight gain and increased frustration. If you think that every time you count and / or limit your calories, the more your appetite starts to increase gradually, the more deliberately you count or limit your calorie intake, you are probably on the right track to identify the problem. Our body has an innate survival mode that comes into play to maintain energy balance when our energy stores (ie body fat) are threatened. Obesity and metabolic diseases, such as type 2 diabetes, can disrupt those natural signals that the body uses to regulate appetite and energy balance, which makes weight loss even more difficult. Here we examine the scientific basis of appetite, the various factors that govern how we suffer from hunger and the subsequent effects of these signals on weight loss. We also look at the effects of a well-formulated ketogenic diet (WFKD) on appetite and the many mechanisms through which this diet can help you lose weight and maintain this weight loss while improving your health.
Over the last few decades, randomized studies of obese people comparing very low carbohydrate and high carbohydrate diets have consistently demonstrated initial weight loss and body fat more significant with low carb diets cause nutritional ketosisBut in almost all such studies, lasting one year or more, after 6 months, weight loss is stopped and weight gain begins, which diminishes some of the benefits of a low-carb diet. This observation of what appears to be a temporary benefit of the ketogenic diet is more common in patients with type 2 diabetes (T2D) who are prescribed a food or ketogenic diet plan overall, for 3 to 5 months, followed by a return to increased carbohydrate consumption   ,
Table 1. Dietary characteristics of these 4 studies, including the duration of the ketogenic diet phase
* 12 weeks VLCD (very low calorie content), 12 weeks LCD (low carb), then 12 weeks back in VLCD
** 21-24 months – kcal per day
VLCD = a very low calorie diet
We have observed that most people who are asked to follow a well-formulated ketogenic diet to satiety can lose significant weight while experiencing reduced hunger and desire. In other words, nutritional ketosis promotes weight loss by reducing appetite and / or facilitating access to body fat stores as fuel, This effect of nutritional ketosis has been attributed to others for various reasons ranging from increased energy costs (metabolic benefit) to aversion or boredom caused by limited food options with a high lipid diet. But there may be more nuanced factors here.
Weight loss with a ketogenic diet
In our recently published survey results Virta / IUH for reversing diabetes, we reported an average weight loss of 12 months greater than 12% in patients with type 2 diabetes, continuous weight loss over 8 months, then prolonged to 12 months, without even a tendency to gain weight ( Figure 1). In addition, in the 10e week from this study, patients reported less appetite than at baselineBut what is particularly interesting is the way this is achieved – from day 1 to day 365, these patients are instructed to eat a well-formulated ketogenic diet to satiety. As a result, thanks to Virta Health’s long-term long-term treatment, our patients maintain blood ketone levels averaging 0.6 mM after 10 weeks and 0.4 mM after 12 months. This means that these remarkable and lasting weight loss results are achieved without deliberate calorie restriction or the need to resist persistent hunger and are associated with long-term adherence to the ketogenic diet.
By definition, most diets limit total calories and advise patients to explore behavioral methods to control hunger and craving. For example, we are told when we are hungry to drink a full glass of water, go for a walk, or eat a high fiber breakfast. But this does not take into account that appetite, hunger and desire are innate symptoms of the body to restore energy balance. Severe calorie restriction or a noticeable increase in body energy expenditure during exercise leads, as you might expect, to this compensatory reactionTherefore, the longer a person maintains calorie restriction and greater weight loss, the more appetizing signals are unbearable.,
Hormones and hunger
Twenty-five years ago, the only known appetite control hormone was insulin. When blood levels of insulin are high, glucose is stored as glycogen and fat is stored in adipose tissue. The resulting reduction in circulating fuels, such as glucose and free fatty acids, stimulates appetite. This leads to the common attempt to be hungry 2 to 3 hours after a meal rich in carbohydrates and low in fat. In fact, many people continue to argue that an increase in insulin is the dominant signal that makes us obese. But in the meantime, we have found many other circulating signals that report the energy status of the body and regulate energy intake (appetite) as well as metabolism. Leptin (produced mainly in adipose tissue) and ghrelin (produced in the upper digestive tract) are among these regulatory hormones. Both have specific receptors in the brain that disseminate their biochemical message in behavior: for leptin, it eats less and for ghrelin, it eats more.
The way these signaling hormones interact with insulin turns out to be complex. Add to this the increased underlying inflammation characteristic of obesity and diabetes, and the picture becomes even more complex and continues to promote obesity. Fortunately, we now know that when you add a well-formulated and followed ketogenic diet to this chart, it changes dramatically in a positive way, but in a pattern that is difficult to explain. Yes, insulin levels in the blood drop, but leptin, the satiety hormone, also decreases. In fact, people on a low-carbohydrate diet who lose weight have a significantly greater reduction in leptin levels than those on a low-fat diet.This is usually a signal to eat more, but here’s one important fact: the sensitivity of the brain to the signal for leptin increases dramatically with a well-formulated ketogenic diet.
Another important point is that inflammation inhibits the brain’s response to leptinleading to leptin resistance. As we now know that inflammation is significantly reduced with prolonged nutritional ketosis , it appears that the decrease in leptin resistance is due to a decrease in inflammation more than offset by low leptin levels. In other words, with a well-formulated ketogenic diet, the brain experiences a greater response to satiety with less leptin. This decrease in inflammation and increased sensitivity to leptin, combined with a decrease in blood insulin levels characteristic of nutritional ketosis, may explain the paradox of decreased appetite associated with ketosis nutrition.
It seems difficult to understand and so it is. But in simple terms, nutritional ketosis reduces high levels of insulin as well as inflammation, allowing normal signals from excess body fat to tell the brain “Eat less!” “Therefore, when overweight people eat a well-formulated ketogenic diet to their fullest, they tend to lose quite a bit of weight, while the balance of these signals naturally directs them to a lower and more stable weight.”
For many of our readers, this is probably more than enough in terms of science. For the rest, here are the details and additional references that support this very complex but important story.
The appetite science: what we can learn from many low-calorie diets
As anyone who has tried to lose weight can testify, appetite often becomes an important factor in the weight loss process. A well-documented example of the link between weight loss and appetite can be seen in studies using many low-calorie diets (VLCDs) under medical supervision in obese patients. These diets, often in the range of 400 to 800 kcal per day, usually cause ketosis shortly after starting them. Ketosis, which is the result of this extreme caloric restriction, probably contributes to reducing reported hungerAs you would expect, in the weeks or months after these diets, patients typically experience significant weight loss, often ranging from 10 to 20% 2 3  However, naturally, this level of calorie restriction is not sustainable in the long run and people need to return to the level of maintaining food intake. This is where the problems begin.
During the transition from a low-calorie (VLCD) diet after weight loss, there is often a change in appetite-regulating hormones in the sense of a greater desire to eat 15 16. And, well, ketosis reduces hunger, return to normal diet, or the addition of carbohydrates and then quitting ketosis have the opposite effect, leading to an increase in ghrelin and hunger. higher levels before losing weight 15. What does this mean specifically? For many (if not most) people, this means that if they start to eat again, as before losing weight, they will have a good chance of regaining the weight they have lost or even more.
To further exacerbate the difficulty of maintaining weight loss after several months of VLCD treatment, patients often undergo a moderate (30 to 50%) or high (> 50%) carbohydrate diet that appears to be the one contributing for their metabolic dysfunction. As mentioned earlier, insulin resistance can be thought of as a functional intolerance to carbohydratesPeople with metabolic diseases, such as prediabetes and type 2 diabetes, often do not fully resolve their major insulin resistance despite significant weight loss and therefore do not respond well when restarting a diet. rich in carbohydrates. From this point of view, these people should take advantage of the continued limitation of carbohydrate intake in order to maintain weight loss. Glycemic improvements observed on a low-calorie diet (VLCD) can also return to the levels observed before the introduction of the diet, when the patient reintroduces high carbohydrates. Would these patients perform better if they switched from a low-calorie diet (VLCD) to a sustainable ketogenic diet that allows them to maintain nutritional ketosis? Perhaps. This is certainly a study we would like to see since our Virta / IUH diabetes reversal study showed progressive weight loss up to 8 months and then weight stabilization up to 12 months6.
Mechanisms for regulating appetite and leptin resistance
Many researchers believe that the decreased hunger attack and changes in certain appetite-regulating hormones seen with ketogenic diets and low-calorie interventions (VLCDs) are due to ketosis. Mechanically, this may be due to the effect of ketosis on the activity of the hormones regulating appetite, ketones acting directly on the brain, or the connection with the gut microbiota. It’s more likely a combination of all thatStudies in patients who are prescribed a low-calorie diet (VLCD) and who are fasting show that subjects who maintain beta-hydroxybutyrate levels of 0.3 mM or more have inhibited ghrelin levels, ie. while those who were not in ketosis had ghrelin levels higher than baseline15. Thus, the power of nutritional ketosis in weight loss efforts can not only contribute to weight loss, but can also play an important role in stabilizing that weight.
We mentioned the hormones that regulate appetite and their effect on eating behavior, especially in diets and weight loss. They are important because they seem to play an important role in how our bodies try to regulate the amount of food we eat. Ghrelin and leptin are two of the most commonly studied hormones for appetite stimulants in the neuroendocrine aspect. Ghrelin, often referred to as the “hunger hormone”, is a multifaceted orexigenic hormone produced by the stomach that, among other things, affects eating closer to eating, Leptin is a satiety hormone secreted mainly by adipocytes. It regulates energy intake as well as costsis largely due to leptin-sensitive signaling cascades in the hypothalamusTogether, they both affect our appetite and how we respond to changes in food intake and our body fat levels.
The interesting thing about leptin is that its influence extends beyond the regulation of appetite and that it can play a complex role in the pathophysiology of obesity. this in immune functionAs with insulin resistance, there is evidence of leptin resistance in obese people. This indicates that although obesity often coincides with elevated levels of circulating leptin, there is resistance to appetite suppression signals that are thought to reduce food intake. So even if a high level of leptin in the blood is supposed to reduce hunger, the body becomes resistant to the signal and no longer receives this message. Therefore, leptin resistance may contribute to obesity and overeating instead of acting to suppress it.,
This paradox of increased appetite and obesity, which despite the high levels of leptin in the blood, may be partly due to inflammation11. You may have heard about obesity as a low-grade chronic inflammatory condition, but in this case leptin resistance may be due to an increased immune and inflammatory response in the brain. The neuro-regulatory aspects of appetite make it clear that the brain and central nervous system (CNS) are involved in energy homeostasis and “foraging behavior.” Thus, as a major regulator of appetite, the hypothalamus integrates the peripheral and central pathways to mediate appetite signals.
In fact, it has been shown that the regulation of the inflammatory pathways in the hypothalamus, caused by an anti-inflammatory diet rich in sugar and saturated fat, causes chronic energy imbalance and changes in fat mass 11. Since leptin acts in the hypothalamus, overactivating cells , may alter leptin signalingFor example, the C-reactive protein has been shown to actively inhibit the leptin saturation signal, This multidimensional inflammatory response probably begins before obesity manifests and contributes to the overall development of metabolic dysfunction25.
Another proposed mechanism for explaining leptin resistance in the brain is hypertriglyceridemia. In this scenario, high levels of triglycerides in the blood pass through the blood-brain barrier (BBB) and interfere with both the transport of leptin through the BBB and the function of receptors in the brain, thereby promoting leptin resistance As carbohydrate restriction has been shown repeatedly to reduce triglyceride levels, this is an additional explanation for the significantly lower leptin levels observed in ketogenic diets that contribute to the anti-inflammatory effects of increasing dietary sensitivity to leptin and maintaining a frequency of leptin anorectic signaling.
Abnormal leptin signaling is one of the ways in which increased appetite-related inflammation affects hunger and feed behavior. When the leptin signal does not tell us to stop eating, we are more likely to overeat and gain weight. Ако работи оптимално, лептинът също влияе косвено на удовлетворението ни от храната, помагайки ни да избягваме преяждането, просто защото нещо има вкус, вместо да ядем в отговор на истински глад., Следователно лептинът може в крайна сметка да играе по-важна роля за поддържане на отслабването, отколкото при самата загуба на тегло, Тази сравнително нова информация за хипоталамичното възпаление като допринасящ фактор за индуцираното от диета затлъстяване може да подобри нашето разбиране за това как диетата и възпалението изострят симптомите на метаболитен синдром и диабет тип 2. 2,
Хранителна кетоза и апетит
В този момент може да мислите, че звучи като безбройна война срещу биологията. За щастие, това, което продължаваме да научаваме за кетогенната диета, показва, че тя е огромен съюзник в нашите усилия да контролираме апетита и възпалението. Драматичните намаления на възпалителните биомаркери, наблюдавани при добре формулирана кетогенна диета (WFKD), включително значително намаляване на общите бели кръвни клетки и реактивен протеин С (CRP), могат да окажат положително въздействие върху хипоталамичното възпаление, което допринася устойчивост на хранителен лептин и произтичащото от това повишаване на теглото12 13. С други думи, противовъзпалителните свойства на хранителната кетоза могат да бъдат пряко свързани с подобряване на ситостта14, което ни дава двойна полза за отслабване и за устойчивото му поддържане.
В допълнение към мощните противовъзпалителни ефекти на хранителната кетоза, наскоро е доказано, че употребата на екзогенни кетони намалява постпрандиалното увеличение на грелина и възприемането на глад., По този начин се оказва, че както хранителната кетоза, така и увеличаването на бета-хидроксибутират в резултат на консумацията на екзогенни кетонови естери могат да модулират хормоните, които сигнализират за апетит и помагат за намаляване на глада. Въпреки че това изследване на екзогенните кетони все още е в начална фаза, то подчертава множеството и разнообразни роли, които кетоните могат да играят в уравнението на енергийния баланс.
Тази нова перспектива за сигнализиране на апетита ни показва, че след добре формулирана кетогенна диета систематично насърчава подобряването на здравето на нашия метаболизъм, които надхвърлят загубата на тегло и допринасят за дългосрочното благополучие. термин. Така че независимо дали просто започвате да изследвате идеята да използвате хранителна кетоза за подобряване на здравето си или се чудите дали това е нещо, което можете да направите в дългосрочен план, става все по-ясно, че Хранителната кетоза може да засили сигналите за контрол на апетита, да намали възпалението и да улесни спазването и спазването на диетата във времето. Тези ползи могат да изминат дълъг път към подобряване на здравето ви, без да ви принуждават да страдате от постоянен глад и неудовлетвореност от влакчетата на промените в теглото.
 Volek, JS., Phinney, SD., Изкуството и науката за живота с ниски въглехидрати. 2011