Dr Leon Massage

The Hunger Hormone: Leptin and Leptin Resistance

The Hunger Hormone: Leptin and Leptin Resistance

There are two hormones that are intimately involved in weight gain and obesity. One of these is insulin, which is relatively well known, and I have covered in past articles on carbohydrates and the metabolic syndrome. The other, and much lesser known of the two hormones, is leptin.

Recent obesity research points the finger at leptin as a major cause of obesity. And some researchers believe that being resistant to the effects of leptin – a condition called leptin resistance – is the leading cause of excessive fat gain in humans.

Leptin hormone
Leptin is a hormone that controls body weight in humans by regulating the body’s fat stores. It is produced by fat cells, and is released after a meal to signal to the satiety centre in the brain that it is time to stop eating. That is why leptin is often referred to as the satiety hormone.

Leptin levels are influenced by the amount of fat the body has stored. When there is an excess of fat in our fat stores, leptin levels are increased. The higher levels of leptin are supposed to notify our brain that we have enough fat stored and we don’t need extra food. In other words, it is time to stop eating.

Leptin and energy balance

Leptin also has an impact on the regulation of energy balance. It influences the amount of calories we burn.

When our body fat levels get too low, leptin levels go down, and as a result we eat more. At the same time, the body is instructed to burn less calories.

When our body fat levels get too high, the opposite happens. Leptin levels go up and, as a result, we eat less food and burn more calories.

In the obese population, leptin levels are high because their higher fat content causes more leptin to be produced. So, in theory, these people should be eating less. Their brain should be telling them to cut back.

However, many people in the obese population are not eating less in respose tp their excess fat stores and rising leptin levels. And in many cases, they are even eating more.

So where does the problem lie?
The problem is that the satiety centre in their brain is not responding to leptin in the way that it should. The higher leptin levels are not being recognised by the brain because these people are leptin resistant.

So, instead of eating less, these people are eating more because the brain is led to think that they are fat deficient.

In a similar way, instead of the higher leptin levels causing their body to increase their energy expenditure and burn more fat, they decrease energy expenditure in an effort to conserve energy and gain weight.

Simply trying to use willpower to overcome the hunger signal created by this phenomenon is very difficult, if not impossible.

Diets and leptin

The reason that most diets don’t produce good results in the long-term is that losing weight reduces the body’s fat levels. As a result leptin levels drop; and this signals the brain that there is a need to increase food intake and decrease energy expenditure, in an effort to regain the lost fat.

The body doesn’t like weight loss and always tries to regain the lost fat mass. The lower leptin levels lead to hunger and an increase in appetite, and a simultaneous drop in metabolic rate.

This creates a perfect storm of increasing hunger and food cravings, as well as a decrease in the motivation to exercise. Left unchecked, these mechanisms lead to a regain of the lost weight.

The causes of leptin resistance are unclear. However, it seems that having chronically high levels of leptin could be one of the culprits, and results in the hypothalamus becoming desensitised to the higher leptin levels.

Some of the factors that may decrease leptin resistance are similar to the factors that decrease insulin resistance. Factors such as exercise and a higher intake of protein.

To learn more about how to combat this hormone…

Checkout the metabolic syndrome and insulin resistance information in Dr Leon’s Book: I can’t believe it’s a diet, available through Amazon.