If you feel like whenever you count and/or restrict calories your appetite begins a progressive climb the longer you count or restrict your calorie intake, you may be right.
Our bodies have an innate survival mode that kicks in to maintain energy balance when our stored energy reserves (i.e., body fat) are threatened. Obesity and metabolic diseases, like type 2 diabetes (T2D), can upset these natural signals the body uses to regulate appetite and energy balance, making weight loss even more difficult.
In this Post, we will explore the scientific basis behind appetite, the various factors that regulate how we experience hunger and the subsequent effect those signals have to counteract weight loss. We also look at the ways in which a well-formulated ketogenic diet (WFKD) affects appetite and the mechanisms through which this manner of eating can help you lose weight and maintain the weight loss while simultaneously improving your health.
For more information the Ketogenic diet, please see my Blog Post, How Do I Do the Ketogenic Diet? https://2healthyhabits.wordpress.com/2018/04/13/how-do-i-do-the-ketogenic-diet/
Most individuals who are instructed to eat healthy fats till satisfied on a WFKD can lose substantial amounts of weight by a combination of reduced hunger and cravings and/or better access to body fat stores for fuel.
Weight Loss on a Ketogenic Diet
In Virta’s recently published results they reported an average 12-month weight loss of greater than 12% in patients with T2D, and weight loss continued out to 8 months and was then sustained out to 12 months without weight regain.
Additionally, at week 10, the patients reported less hunger than at the beginning. This was because from day 1 through day 365 these patients were instructed to eat a WFKD to satiety. As a result our patients maintained average blood ketones of 0.6 mM after 10 weeks and 0.4 mM after 12 months. What this means is that these lasting weight loss results were achieved with long-term adherence to a WFKD and without purposeful calorie restriction or the need to resist persistent hunger.
Severely restricting calories or significantly increasing the volume exercise predictably brings on appetite, hunger, and cravings. Therefore, the longer an individual maintains the caloric restriction and the greater the amount of weight loss, the stronger the appetite signals.
Hormones and Hunger
When blood insulin levels are high, glucose (carbs) gets stored as glycogen and fats get stored in adipose tissue, the resulting reduction in glucose and free fatty acids, then stimulates appetite. This leads to the common experience of being hungry 2-3 hours after a high carbohydrate, low fat meal. Other hormones are leptin and ghrelin. Both have specific receptors in the brain that transmit their message – for leptin it is “eat less” and for ghrelin it is “eat more”.
The brain’s response to leptin is inhibited by inflammation, resulting in leptin resistance. Inflammation is dramatically reduced by sustained nutritional ketosis, it appears that the reduction in leptin resistance due to reduced inflammation more than compensates for the lower leptin levels.
On a WFKD the brain perceives a greater satiety response to less leptin.
Simply put, nutritional ketosis reduces elevated insulin levels and inflammation, which allows the normal signals from excess body fat stores to tell the brain “Eat less!” Therefore, when heavy people eat a WFKD to satiety, they tend to lose quite a bit of weight until the balance of these signals naturally guides them to a stable lower weight.
For many this is probably more than enough science. For the rest of you, what follows are the details and additional references that back up this very complex but important story.
The Science of Appetite: What We Can Learn From Very Low Calorie Diets
A Very Low Calorie Diet (800 per day) is not sustainable for the long-term and individuals often return to a carbohydrate-rich diet that resembles the one that contributed to their metabolic dysfunction. There is often a significant increase in hunger signals. For most individuals there is a good chance they will regain the weight they lost and possibly more.
Individuals with metabolic diseases, such as pre-diabetes and T2D, frequently have not fully resolved their underlying insulin resistance and the glycemic (glucose/sugar blood levels) improvements can also rebound to pre-WFKD levels. These patients would have fared better had they been transitioned from the Very Low Calorie Diet (VLCD) onto a sustainable ketogenic diet that allowed them to sustain nutritional ketosis for metabolic health as seen in the Virta diabetes reversal study which showed progressive weight loss out to 8 months and then weight stability to month 12.
Mechanisms of Appetite Regulation and Leptin Resistance
The reduction in perceived hunger may be due to combination of an effect of ketosis on the activity of appetite-regulating hormones, or ketones acting on the brain directly, or a relationship with the gut microbiota. Studies looking at patients prescribed a VLCD maintained beta-hydroxybutyrate levels of 0.3mM or greater had suppressed ghrelin levels, while those who were not in ketosis had higher ghrelin levels. Thus, nutritional ketosis in a weight loss effort may not only contribute to initial weight loss but may also play an important role in sustainability and weight maintenance.
A pro-inflammatory diet rich in a combination of sugar and saturated fat has been shown to effect chronic energy imbalance and changes in fat mass. Because leptin acts within the hypothalamus, the over-activation of immune cells can impair leptin signaling. For example, C-reactive protein has been shown to actively inhibit leptin’s satiety signal. This multi-dimensional inflammatory response likely begins before obesity and contributes to the development of metabolic dysfunction.
Another proposed mechanism to explain leptin resistance is that elevated blood triglycerides cross the blood brain barrier (BBB) and impair both the transport of leptin across the BBB as well as inhibit receptor function in the brain, thereby promoting leptin resistance. Because it has been repeatedly demonstrated that carbohydrate restriction reduces triglyceride levels, this is an additional explanation for the significantly lower leptin levels observed with ketogenic diets, adding to the anti-inflammatory effects of the diet, which increase leptin sensitivity.
If functioning optimally, leptin also indirectly effects our responses to feeding; which helps us avoid over-eating simply because something tastes good instead of eating for true hunger. Leptin, therefore, may end up being more of a factor in the maintenance of weight loss than in losing weight itself.
Nutritional Ketosis and Appetite
The anti-inflammatory properties of nutritional ketosis can be directly linked to improved satiety giving us both successful weight loss and maintenance.
Consistently following a WFKD promotes improvements in metabolic health that go beyond weight loss and contribute to long-term well-being. Nutritional ketosis can enhance appetite control signals, reduce inflammation and facilitate diet adherence and sustainability. These advantages can go a long way towards supporting your health while not requiring you to suffer through constant hunger and the frustration of roller-coaster weight fluctuations.
This Post has been condensed from the source: The Science of Nutritional Ketosis and Appetite by Brooke Bailey, Ph.D Stephen Phinney, MD, PhD, Jeff Volek, PhD, RD. Please see the original for the Footnotes and Citations for the scientific studies.
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