“I never knew there would be so much freedom in eating this way!” These are the exact words from one of our Well-Being Tribe members. So many of us are plagued with feelings of chronic, gnawing hunger. We simply can’t stop ruminating about that next meal. We may as well have a ball and chain attached to our stomachs. Welcome, hope. There is a way to feel freedom from not just hunger, but even some of the more unrelenting food cravings and addictions. Be assured, this plan does not require a drug with a laundry list of side effects.
Let’s first understand that hunger and cravings are NORMAL and are meant to serve as a messenger for survival. Unfortunately, our hyper-palatable, sugar-filled, ultra-processed, micronutrient-depleted westernized eating lifestyle is typically lacking the thing we need most- nourishment. Therefore, the message is being delivered ad nauseam, but never received. Why does this happen? While there are several contributing factors, we largely have leptin resistance to thank. So, what the heck is leptin? Leptin is a hormone produced by our fat cells, which then communicates with our brain’s hypothalamus to say, “I am full. Stop eating!”. Sadly, the receptors within our hypothalamus have downregulated, which ultimately means they are no longer responding. There is a direct correlation between obesity and leptin resistance. We see a similar process with insulin resistance, which leads to the development of Type 2 Diabetes, Metabolic Syndrome, and a plethora of other disease processes. Often, insulin resistance and leptin resistance work in an insidious partnership. Here is the silver lining- when we combat one, we simultaneously heal the other.
Welcome a Mediterranean low carbohydrate/ketogenic eating plan. As we reduce carbohydrates within our diet and increase the number of plant-based food sources, coupled with healthy fats and adequate protein, we see a shift in our metabolic climate. Lowering carbohydrates in all forms reduces our blood glucose response. As a result, our need for insulin is diminished. When we reduce the need for insulin, we upregulate the cells’ sensitivity to insulin thereby resolving insulin resistance. This is when we unlock the door to permit our fat cells to break down fat through a hormone called Lipase. This metabolic shift improves the lines of communication from our fat cells to our hypothalamus. Now, when leptin talks, the hypothalamus listens. As our tribe members transition through these changes, we hear the same testimonials. “I no longer need the donut”. “I thought you were crazy, but I do crave salads”. “Food is no longer the primary driving force to get me through the day”.
Let the good news continue. There are far more hunger hormones affected by low carbohydrate/ketogenic nutrition. Let’s talk ghrelin. This is the hormone produced largely from the stomach and small intestine. This guy is responsible for the ‘hunger pangs’ you feel and the grumbling you hear when you get ‘hangry’. Ghrelin not only screams at us to get some food but also instructs our cells to store fat. Unfortunately, typical caloric restrictive dieting results in an uptick of ghrelin, which is one of the many reasons why many people gain weight once they discontinue the ‘diet’. We see a different response, however, when we are in ketosis. The ghrelin response dampens. The dramatic yoyo effect seen with typical caloric restrictive dieting is also stimulated by ghrelin’s unique contribution to our ‘reward pathways’. Ghrelin stimulates food cravings and addictions given its communication with the brain’s amygdala through dopamine. In a nutshell, as ghrelin increases with caloric restriction, so do our obsessive food cravings.
While there are many more hunger hormones I can touch on, for the sake of your time, I will end on GLP-1 (Glucagon-like peptide). GLP-1 is produced within our small intestine, controls insulin function, reduces gastric emptying and gastric acid secretion collectively working together to lessen our hunger. Once again, we see this common theme. Low carbohydrate/ketogenic nutrition has been shown to favorably mitigate hunger by increasing GLP-1 activity. This hormone has been so well researched we now have a pharmaceutical drug class used to increase GLP-1. Welcome GLP-1 agonists and include medications such as Trulicity, Ozempic, and Vytorin. I much prefer for my patients to create this affect through their diet when possible. Synergy develops when we eat a whole-food-based diet low in carbohydrates. Fiber-rich foods packed with phytonutrients, create a catalyst to ignite the favorable insulin and hunger hormone affects.
While there is current research to support these findings, Well-Being has partnered with USF’s Dom D’Agostino, PhD and Levels Health so we can continue to better understand the science of metabolic health and its impact on hunger. In our current study, we are investigating these hunger hormones and other biometric markers with Eve Technologies Human Metabolic Hormone Array 9-Plex. This research is currently underway and will be continuing. At Well-Being our mission is to improve the health and lifespan of as many people as possible. It is imperative we use sound science to guide us on how to best lead both our members and our public to a place of better health and longevity.
I will end with this. The ultimate place of freedom is felt when you are eating nutritious foods simply because you are innately drawn to do so. Knowing the science and strategy to accomplish this will yield great success. It can be done. You, too, can be screaming from the rooftops, “I never knew there would be so much freedom in eating this way!”
-Allison Hull, DO
Diplomate of Internal Medicine and Pediatrics Associate Professor of USF Co-Creator of Well-Being: A Tribe Planted with Purpose
References:
- Sumithran P, Prendergast LA, Delbridge E, Pucell K, Shulkes A, Kriketosis A, Proietto J. Ketosis and appetite- mediating nutrients and hormones after weight loss. Eur J Clin Nutr. 2013, July(7):759-64.
- Gutzwiller JP, Drewe J, Goke B, Schmidt H, Rohrer B, Lareida J, Belinger C. Glucagon-like peptide-1 promotes satiety and reduces food intake in patients with diabetes mellitus type 2. Am J Physiol. 1999 May; 276(5):R1541-4.
- Flint A, Raben A, Ersboll AK, Holst JJ, Astrup A. The effect of physiological levels of glucagon-like-peptide-1 on appetite, gastric emptying, energy and substrate metabolish in obesity. Int J Obes Relat Metab Disord. 2001 Jun; 25(6):781-92.