By Brad Pilon, MS
Leptin is a very interesting hormone. It gets lots of ‘buzz’ in the weight loss industry, mostly because of its effects in animal research.
In 1994, researchers discovered that a certain strain of genetically mutated obese mice had a deficiency of a protein-hormone called leptin, which is released from fat cells and is monitored by the brain.
Whereas normal mice had a gene that causes fat cells to secret leptin, these mutated obese mice lacked this gene.
When these leptin-deficient mice were injected with leptin, their weight slowly returned to non-obese levels.
Shortly after this discovery it was found that leptin could even increase metabolic rate (energy expenditure) in mice.
The weight loss industry quickly jumped on this story, and Leptin was hailed as the cure for obesity.
Unfortunately, what works in mice, doesn’t always work in humans. It has since been found that when leptin levels are reduced by 80% in humans there is no change in resting metabolic rate [Chan JL, 2007].
In fact, changes in leptin levels do not seem to have any influence nor are they influenced by changes in resting metabolic rate in humans [Rosenbaum M, 1997; 2002]
In humans Leptin seems to be correlated to the amount of food we eat.
The more food, the more leptin in our blood stream.
Overeating for several days can increase leptin levels, however these levels return to normal within hours after the overeating is stopped [Kolacznyski JW 1996].
Leptin seems to be a marker of both fat mass and calorie intake. Even in severe conditions of calorie restriction (like those found in anorexic women) Leptin levels are highly correlated with body fat levels. In other words, the lower the body fat, the lower the leptin levels [Bossu C, 2007].
Research has shown consistently that there are substantial differences in the physiological actions of leptin between rodents and humans [Ahima RS, 2000] and this may explain why there is so much leptin-confusion in the diet industry.
Leptin is a complicated hormone.
It rises and falls in different situations, which are not always logical. Both long term endurance exercise and resistance exercise can cause reductions in leptin levels, as can fasting, as well as increased testosterone levels and increased catecholamine levels.
Even injected anabolic steroids can decrease leptin levels.
In all of these situations an increase in fat burning occurs despite decreases in leptin levels.
Leptin is an important hormone, but it is not the ‘master regulator’ of fat burning that it has been made out to be by the fitness industry.
The bottom line is that while short term fasting typically involves an acute decrease in leptin levels , the consistent increase in Growth Hormone ensures that fat loss remains elevated during periods of fasting. In fact even when Leptin is injected into fasting individuals it doesn’t improve fat burning or decrease GH levels [Chan JL, 2008]
Using short-term flexible intermittent fasting combined with resistance training remains one of the most effective and simple ways to lose weight and reduce your body fat.
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Brad Pilon is a nutrition professional with over eight years experience working in the nutritional supplement industry specializing in clinical research management and new product development. Brad has completed graduate studies in nutritional sciences specializing in the use of short term fasting for weight loss.
His trademarked book Eat Stop Eat has been featured on national television and helped thousands of men and women around the world lose fat without sacrificing the foods they love. For more information on Eat Stop Eat, visit www.eatstopeat.com
