Obesity has become a global health epidemic, affecting millions of people around the world. While genetics, lifestyle, and diet are recognized as major contributors to obesity, the role of hormones, particularly insulin, in the development of this condition has gained significant attention.
The underlying cause of obesity turns out to be a hormonal, rather than a caloric, imbalance. Insulin is a fat-storage hormone. If excessive insulin is causing obesity, then clearly the answer lies in reducing insulin. Both the ketogenic diet (a low-carb, moderate-protein, high-fat diet) and intermittent fasting are excellent methods of reducing high insulin levels. Insulin inhibits lipolysis—it stops the body from burning fat. High insulin levels, which are normal after meals, signal our body to store some of the incoming energy.
Insulin has two major functions. First, it allows the body to immediately start using food energy. Carbohydrates are absorbed and rapidly turned into glucose, raising blood sugar levels. Insulin allows glucose to enter directly into most cells of the body, which use it for energy. Proteins are broken down into amino acids and absorbed, and excess amino acids may also be turned into glucose. Protein does not raise blood glucose, but it can raise insulin levels. The effect is variable, and it surprises many people to learn that some proteins can stimulate insulin as much as some carbohydrate-containing foods. Fats are directly absorbed as fat and have minimal effect on insulin.
Insulin helps store the excess energy. There are two ways to store the energy. Glucose molecules can be linked into long chains called glycogen and then stored in the liver. There is, however, a limit to the amount of glycogen that can be stored away. Once this limit is reached, the body starts to turn glucose into fat. This process is called de novo lipogenesis.
Make more and work less by growing a profitable aesthetics practice.
Learn the clinical and business skills you need to transform your work/life balance in just 4-days!
October 27-30 (only 3 spots left!)
in sunny Scottsdale, AZ
One of the key ways in which excessive insulin contributes to obesity is by promoting the storage of excess calories as fat. When we consume carbohydrates, they are broken down into glucose, causing a rise in blood sugar levels. In response to this increase, the pancreas releases insulin to help move glucose into cells. However, frequent consumption of high-carbohydrate and high-sugar foods can lead to repeated and excessive insulin spikes.
These frequent insulin surges signal the body to store more fat. The excess glucose that cannot be immediately used for energy is converted into triglycerides, a form of fat, and stored in adipose tissue. Over time, this continuous cycle of high insulin levels and fat storage can contribute to weight gain and, if left unchecked, obesity.
Insulin is normally released when we eat. It directs some of the incoming glucose to be used as energy and some to be stored for later use. In the short term, glucose is stored as glycogen in the liver, but the liver’s storage space for glycogen is limited. Once it’s full, excess glucose is stored as fat: that is, the liver begins manufacturing fat from glucose through de novo lipogenesis. After the meal, as insulin levels fall, this process reverses. With no food energy coming in, stored food energy must be retrieved. Glycogen and fat stores in the liver are turned back into glucose and distributed to the rest of the body for energy. The liver acts like a balloon. As energy comes in, it fills up. As energy is needed, it deflates.
Balancing feeding and fasting periods over a day ensures that no net fat is gained or lost. But what happens if the liver is already crammed full of fat? Insulin then tries to force more fat and sugar into the liver, even though it’s already full of fat and sugar. Just as it is more difficult to inflate a fully inflated balloon, insulin has more difficulty trying to shove more fat into a fatty liver. It takes higher and higher levels of insulin to move the same amount of food energy into a fatty liver.
The body is now resistant to the efforts of insulin, since normal levels will not be enough to push sugar into the liver. Voilà—insulin resistance in the liver. The liver, like an overinflated balloon, will try to expel the sugar back into circulation, so continuously high insulin levels are also required to keep it bottled up in the liver. If insulin levels start to drop, the stored fat and sugar comes whooshing out. To compensate, the body keeps raising its insulin levels. Thus, insulin resistance leads to higher insulin levels.
High insulin levels encourage more storage of sugar and fat in the liver, which causes even more over-cramming of fat in the already fatty liver, causing more insulin resistance—a classic vicious cycle.
Sign up today and expand your knowledge & skills in Botox®, Fillers, Lasers,
Chemical Peels, Microdermabrasion and PRP for Aesthetics!
Excessive insulin secretion is closely linked to obesity through multiple mechanisms. It promotes the storage of excess calories as fat, contributes to insulin resistance, and disrupts appetite regulation. However, it’s crucial to recognize that obesity is a complex condition influenced by various factors, including genetics, lifestyle, and diet.
Understanding the role of insulin in obesity highlights the importance of maintaining balanced blood sugar levels. A diet that includes a balance of carbohydrates, proteins, and healthy fats, combined with regular physical activity, can help regulate insulin secretion and mitigate the risk of obesity. For individuals concerned about their weight and insulin levels, seeking guidance from healthcare professionals is essential to develop a personalized plan for managing and preventing obesity.