Leptin has been a buzzword in the weight loss world for a while now. It’s a hormone secreted by fat cells and has proven to have major effects on body weight. Leptin signals to our brains that we are full or have had enough to eat and therefore we stop eating. Since it is produced by our fat cells, logically as we gain weight we should create more Leptin and therefore eat less. However, this is not always the case. Our bodies can get overwhelmed by the Leptin and begin ignoring it as a signal of fullness. This is called Leptin resistance, and it’s often marked by not being hungry in the morning contrasted with excessive hunger at night.
Of course this resistance creates a problem that readily leads to obesity and constant hunger. Speaking of hunger, another hormone called Ghrelin is largely to blame for those hunger pains we all get while dieting. This hormone signals to the brain that our stomachs are empty; it’s considered the counterpart of Leptin. In cases of obesity, the normal hormone responses are disrupted and Leptin and Ghrelin work irregularly, that is, the body does not respond like it should.
Clearly Leptin resistance presents a major barrier to weight loss, making resistant people unaware when they’re full and overly hungry despite sufficient consumption. Research suggests that certain diet factors can greatly increase the incidence of Leptin resistance; the main cause being overconsumption of fructose. Fructose is what’s known as fruit sugar because it gives fruit and root vegetables their sweet flavor. The problem with this monosaccharide is it doesn’t cause an insulin spike. Because insulin spikes serve as signals to produce Leptin, consuming fructose leaves the body void of this response. The result? Overconsumption and increased fat tissue.
In a 2008 study, researchers showed that rats previously fed a fructose-heavy diet were much more likely to develop Leptin resistance. Additionally, these rats had higher average body weights than the control group when put on a calorie-rich diet. The researchers concluded, “Thus, a high-fructose diet predisposes to obesity, and deleterious effects of chronic fructose consumption develop long before any visible signs of elevated leptin or the metabolic syndrome. The significance is that this mechanism might well explain why fructose ingestion is associated with obesity.” (Shapiro A, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ)
Given this research and similar studies, it seems that Leptin and Ghrelin have a very complicated relationship and contribute to obesity in non-linear ways. However, we are learning more about contributing factors of high Ghrelin, Leptin resistance, and the weight gain associated with diets high in fast-acting sugars.