We hear a lot about leptin in the weight loss industry, mainly because of its effects in animal research.
In 1994, it was discovered that a protein hormone called leptin, which is released from fat cells and monitored by the brain, was deficient in a certain strain of genetically mutated obese mice.
Normal mice had a gene which caused fat cells to secrete leptin, but the mutated obese mice lacked that gene. When the leptin-deficient mice were injected with leptin, their weight eventually returned to non-obese levels. Soon it was discovered that leptin could increase metabolic rate, or energy expenditure, in mice.
Those in the weight loss industry soon learned about this research, and began claiming that leptin was the cure for obesity.
What works for mice, however, doesn’t always work for humans. Researchers quickly learned that even an 80% increase in leptin levels in humans doesn’t change the body’s resting metabolic rate [Chan JL, 2007]. Changes in leptin levels, in fact, don’t seem to have any effect on resting metabolic rates in humans [Rosenbaum M, 1997; 2002].
Leptin, in humans, seems to be correlated to the amount of food we eat. The more we eat, the more leptin we can find in our bloodstream.
Leptin levels can be increased when an individual overeats for several days, but those levels return to normal within hours [Kolacznyski JW, 1996].
Leptin appears to be a marker of both fat mass and caloric intake. Leptin levels are highly correlated with body fat levels even in cases of severe calorie restriction (as in those found in anorexic women). The lower the body fat, the lower the leptin levels [Bossu C, 2007].
Research shows there are substantial differences in the physiological actions of leptin in mice and humans [Ahima RS, 2000], which could explain why there are so many confusing theories about leptin in the diet industry.
Leptin is complicated. In different situations, its levels rise and fall, and explanations for the changes aren’t always logical. Long term endurance exercise and resistance exercise can reduce leptin levels. So can fasting, increased testosterone levels, and increased catecholamine levels. Injected anabolic steroids can also decrease leptin levels.
In all of these situations, an increase in fat burning occurs in spite of decreases in leptin levels.
While leptin is an important hormone, it is not all that it is made out to be by the fitness industry.
While short term fasting usually involves an acute decrease in leptin levels, the consistent increase in growth hormone ensures that fat loss remains elevated during that time. Even when leptin is injected into fasting individuals, more fat isn’t burned and growth hormone levels aren’t decreased [Chan JL, 2008].
Short term, flexible intermittent fasting combined with resistance training remains one of the most effective and simple ways to reduce body fat.