Every time you turn around, there's a new diet plan based on a hormone. While there's some merit to all this madness, most of the plans fail to completely understand their respective physiological underpinnings. The body isn't a simple, linear, straightforward machine – it's complex and redundant at almost every turn.
This article will reveal some new research on the hormone leptin to provide some simple actions for you to take to help you get leaner. Just because the physiology is messy doesn't mean your actions need to be complicated!
First, here's a short crash course on this important hormone.
Leptin 101
Leptin was discovered by Ingalls and friends in the early 1950's (Ingalls, AM, et al 1950). Fast forward to the early 90's when it was "rediscovered", and many were predicting it would be the biggest weight loss breakthrough ever.
It's a hormone that is released primarily by fat cells (adipocytes) and works to regulate appetite, body fat mass, and basal metabolic rate.
Until just a few years ago, researchers thought that fat cells sat on their collective butts all day and were only a storage place for unsightly body fat.
We know now that those pesky fat cells are very metabolically active, releasing and receiving a myriad of messenger hormones, one of which is leptin.
How Does Leptin Work?
Leptin travels up to the brain where it acts on receptors in the hypothalamus toinhibit appetite.
More leptin in your brain = less food intake.
This is great news for anyone looking to get leaner, since more leptin means you'll be less likely to prowl your kitchen at 3 AM in search of leftover birthday cake. Leptin is your body's way of putting the brakes on fat gain by decreasing appetite.
The chronic level of leptin you have is also a rough measure of the amount of fat you have on your body. Many things can affect leptin as shown in the table below:
Factors promoting leptin secretion
• Excess energy stored as fat (obesity)
• Overfeeding
• Glucose
• Insulin
• Glucocorticoids
• Estrogens
• Inflammatory cytokines, including tumor necrosis factor and Interleukin-6 (acute effect)
• Overfeeding
• Glucose
• Insulin
• Glucocorticoids
• Estrogens
• Inflammatory cytokines, including tumor necrosis factor and Interleukin-6 (acute effect)
Factors inhibiting leptin secretion
• Low energy states with decreased fat stores (leanness)
• Fasting
• Catecholamines and adrenergic agonists
• Thyroid hormones
• Androgens
• Peroxisome proliferator–activated receptor-agonists
• Inflammatory cytokines, including tumor necrosis factor (prolonged effect)
• Fasting
• Catecholamines and adrenergic agonists
• Thyroid hormones
• Androgens
• Peroxisome proliferator–activated receptor-agonists
• Inflammatory cytokines, including tumor necrosis factor (prolonged effect)
Leptin Super Mouse to the Rescue!
Researchers lead by Zhang,Y in the mid-1990s did a series of mouse experiments to show that mice with messed up leptin (ob/ob mouse) became fat little fury bastards (Zhang, Y et al. 1994).
Their metabolic rate was lower, they didn't move as much, and they ate tons of mouse chow.
The catch was that this mouse ob/ob (think double obese) didn't make any leptin at all.
To make the mouse lean, they injected it with leptin, and voila – a thin mouse again!
The researchers all joined hands, sang Kumbaya, and went out for tasty adult beverages while taking turns patting each other on the back for single-handedly solving the obesity problems. We just need to inject humans with leptin and poof, thin humans, and more visually appealing shopping experiences at Walmart.
The problem was it didn't work.
Researchers measured blood levels of leptin in obese humans and found that leptin levels were sky high!
That wasn't supposed to happen. Leptin levels were expected to be low since the humans were fat. As leptin increases, it signals that the body has enough fat, so we would expect low leptin levels in obese populations.
As you recall, when injected with leptin (thus increasing the level), the mice in the studies got thinner.
But these obese humans already had high levels of leptin. Injecting more leptin was like pissing in the ocean to try to raise the water level.
Leptin 201: The Receptor
It appeared that the receptor for leptin is out of joint. The receptor isn't telling the brain that leptin is high. Tons of leptin, but the silly brain can't tell since the receptor is as broke as Terrell Owens.
Why it Matters
We already know that sprint training is a great way to burn fat, but it may have another benefit.
A study done by Guerra et al. in 2011 looked at sprints as a leptin signaling mimetic.
Unlike most research, this study used a group of T Nation style humans who were pretty lean (about 15% body fat) and young (23 years old). They split them into two groups: a fasting group, and a glucose group where they ingested 75 grams of glucose one hour before sprints.
Both groups did one Wingate bike sprint for only 30 seconds.
If you're not familiar with this set up, in short, it's hop on a bike set to a high workload (10% of body weight used here) and pedal like a rabid grizzly bear is chasing you.
What They Found
Subjects had a series of muscle biopsies done over the course of the study and researchers found that a single session of sprint training showed alterations in leptin signaling. The sprints were jacking up leptin that, in theory, should get the waddling Walmart shoppers to start dropping fat.
However, this was not seen in the group that ingested glucose before their sprint.Only the fasted group saw leptin alterations.
It appears insulin may interfere with the leptin signaling to some degree. To quote the researchers directly:
"Altogether, these results indicate that sprint exercise performed under fasting conditions elicits signaling events similar to those described in the rodent skeletal muscle after leptin injections, i.e. sprint exercise under fasting conditions acts as a leptin signaling mimetic in human muscle. However, glucose ingestion before the sprint training exercise blunts this effect." (Guerra et al. 2011)
So it appears that fasted sprint training can pinch hit for leptin.
Do This! A Training Template
Hop on a bike and work up to one maximum, all out, pedal-as-hard-as-you-can sprint for 30 seconds.
The tension should be relatively high, but the goal is to keep your pedaling at a fast pace for the entire 30 seconds. If you slowed to a snail pace 20 seconds in, go to a lighter workload.
Make sure this is done in a fasted condition, such as first thing in the morning.
Don't have a bike? While the study didn't look at running, it may elicit the same response as the pathways are very similar.
It sounds ridiculously simple, but my purely anecdotal experience with my athletes shows that this does seem to help speed fat loss.
Summary
• More leptin is associated with less food intake.
• Some may have a leptin receptor issue where it's not responding to the amount of leptin floating around. Unfortunately, science isn't at the point yet where we can easily tell who has a receptor issue, but the more overweight you are, the more prone you are to having broken leptin receptors.
• Doing just one sprint in a fasted state works to pinch hit for leptin, putting you on the road to leanness. However, non-fasted training does not have the same effect. So add some sprint training in, but it has to be done in a fasted state.
• Fasted sprints can be done any time on a fasting day (where you're not consuming any calories), or done before breakfast. This way it's unlikely to interfere with your normal training session.
While we don't have a long-term study to show how much this will help your body composition, it's simple to add in and there's some very strong data to show it will help.
Heck, it only takes literally 30 seconds to do the sprint. Try it out, and let me know what you find.
Questions or comments? Post them in the LiveSpill below.
Selected References
Everard, A., Lazarevic, V., Derrien, M., Girard, M., Muccioli, G. G., Neyrinck, A. M., Cani, P. D. (2011). Responses of gut microbiota and glucose and lipid metabolism to prebiotics in genetic obese and diet-induced leptin-resistant mice. Diabetes, 60(11), 2775-2786. doi:10.2337/db11-0227
Finocchietto PV, Holod S, Barreyro F, Peralta JG, Alippe Y, Giovambattista A, Carreras MC, Poderoso JJ. Defective leptin-AMP-dependent kinase pathway induces nitric oxide release and contributes to mitochondrial dysfunction and obesity in ob/ob mice. Antioxid Redox Signal. 2011 Nov 1;15(9):2395-406. Epub 2011 Jun 28.
Galgani, J. E., Greenway, F. L., Caglayan, S., Wong, M. L., Licinio, J., & Ravussin, E. (2010). Leptin replacement prevents weight loss-induced metabolic adaptation in congenital leptin-deficient patients. The Journal of Clinical Endocrinology and Metabolism, 95(2), 851-855. doi:10.1210/jc.2009-1739
Guerra, B., Olmedillas, H., Guadalupe-Grau, A., Ponce-Gonzalez, J. G., Morales-Alamo, D., Fuentes, T., . . . Calbet, J. A. (2011). Is sprint exercise a leptin signaling mimetic in human skeletal muscle? Journal of Applied Physiology (Bethesda, Md.: 1985), 111(3), 715-725. doi:10.1152/japplphysiol.00805.2010
Ho, J. N., Jang, J. Y., Yoon, H. G., Kim, Y., Kim, S., Jun, W., & Lee, J. (2012). Anti-obesity effect of a standardised ethanol extract from curcuma longa L. fermented with aspergillus oryzae in ob/ob mice and primary mouse adipocytes. Journal of the Science of Food and Agriculture, doi:10.1002/jsfa.5592; 10.1002/jsfa.5592
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Kelesidis, T., Kelesidis, I., Chou, S., & Mantzoros, C. S. (2010). Narrative review: The role of leptin in human physiology: Emerging clinical applications. Annals of Internal Medicine, 152(2), 93-100. doi:10.1059/0003-4819-152-2-201001190-00008
Kowalik, S., & Kedzierski, W. (2011). The effect of interval versus continuous exercise on plasma leptin and ghrelin concentration in young trotters. Polish Journal of Veterinary Sciences, 14(3), 373-378.
Plinta, R., Olszanecka-Glinianowicz, M., Drosdzol-Cop, A., Chudek, J., & Skrzypulec-Plinta, V. (2011). The effect of three-month pre-season preparatory period and short-term exercise on plasma leptin, adiponectin, visfatin and ghrelin levels in young female handball and basketball players. Journal of Endocrinological Investigation, doi:10.3275/8014
Wolsk, E., Mygind, H., Grondahl, T. S., Pedersen, B. K., & van Hall, G. (2011). The role of leptin in human lipid and glucose metabolism: The effects of acute recombinant human leptin infusion in young healthy males. The American Journal of Clinical Nutrition, 94(6), 1533-1544. doi:10.3945/ajcn.111.012260
Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994). Positional cloning of the mouse obese gene and its human homologue. Nature, 372(6505), 425-432. doi:10.1038/372425a0
