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When starting a diet, have you ever wondered why exactly hunger and cravings suddenly sky rocket? Obviously a reduced food intake leads to these sensations, but the actual root cause can be attributed to two key hunger hormones…

People often cite insulin as the major hormone behind body composition, and while this has some truth, insulin is only one of many key hormones playing a role in: regulation, weight loss, obesity, and weight management (Considine, Sinha, & Heiman, 1996; Allison & Myers, 2014).

Instead, the culprits are in fact, ‘leptin’, and its partner in crime, ‘ghrelin’.

Leptin will be the topic of today’s article – ghrelin will be discussed in a follow-up article.

Leptin

Leptin plays a direct role with regard to energy (calorie, or food) consumption – researchers have even dubbed it the ‘master regulator of food intake’.

Quite simply, if your leptin health is good, you will find it much easier to eat less and stick to your diet.  In contrast, if your leptin health is poor (termed “leptin resistance’), you will have constant cravings and likely find yourself continually overeating.

If you, or someone you know, is particularly overweight, this scenario will probably sounds familiar…

If you’ve competed, or know someone that has, perhaps you’re aware of the all too common (and dreaded) ‘rebound’ post-show?

Leptin’s key role as it relates to obesity and weight management, comes down to its direct effect on the hypothalamus, a region of the brain known as the ‘Central Governor’.

The hypothalamus controls many processes and emotions such as hunger, thirst, sleep, mood etc.

Initial research in mice has demonstrated that those lacking leptin tend to become obese and diabetic in a short period of time (Allison & Myers, 2014).

On the opposite end of the spectrum, research on obese humans with chronically elevated levels of leptin suggests that those individuals fail when it comes to controlling their calorie intake, despite the fact they have an abundance of stored energy – this is has been deemed to be leptin resistance (Allison & Myers, 2014).

Leptin functions as a feedback mechanism signalling key regulatory centers in the brain to inhibit food intake, regulate body weight and energy balance.  This means that in healthy individuals, where leptin is functioning as it should be, leptin will help to regulate food intake telling you to stop eating when you’ve eaten enough at each meal.

However, if an individual is leptin resistant, or if the leptin pathway is dysfunctional, that individual will tend to overeat due (at least in part) to an unconsciously diminished control over energy intake – they will often feel hungry / unsatisfied no matter how much they eat.

As you gain body fat, leptin levels go up in an attempt offset the rate at which that’s occurring.  In contrast, as you diet, leptin levels decrease, causing hunger cravings, overeating and increased fat storage!

As we’ve touched on, one exception to this is leptin resistance – much like insulin resistance, this is when cells stop responding to the signal they are receiving, often leading to a viscous cycle of fat gain.

Leptin Resistance – The Vicious Cycle

1. A person gains body fat – this increases the number of fat cells, and therefore leptin levels go up.

2. Their increase in fat, along with the increased inflammation that is likely to accompany it, increases their march towards leptin resistance.

3. Despite the fact that the individual now has an abundance of stored energy in their fat cells, leptin resistance can ‘trick’ their brain into making them feel hungry and low in energy.

4. The above results in further cravings and an increased likelihood of overeating.

5. The individual continues to gain fat, increases leptin resistance, and continually feels hungry.

Optimizing Leptin Health

One of the most obvious ways to reduce leptin levels is to lose body fat.  Some other basic lifestyle alterations may also help:

• Reduce cellular inflammation – failure to do so may negatively effect the leptin signalling on the hypothalamus.  This can be achieved by exercise and eating a diet low / free of unprocessed foods, high in fruits & vegetables, and the inclusion of supplements such as omega 3 and antioxidants.

• ‘Regular’ exercise has a myriad of benefits of course which includes improving leptin resistance and decreasing inflammation (Reseland (2001).

• Eat more protein!  Along with the integrative role of protein on satiety, it may also improve leptin sensitivity (Weigle 2005).

• Sleep of course has an array of positive benefits for the bodybuilder or fitness enthusiast.  Along with the all of the obvious benefits a good night’s sleep has, it may also help to improve leptin sensitivity (Spiegel 2004).

• Avoid chronic and regular yo-yo dieting.  Taking dieting breaks or ‘refeed’ periods during a long diet or contest prep may help to protect your hormones from the negative adaptations discussed.

In Summary

While leptin may not be the next designer supplement, it’s an extremely important hormone with regard to health and body composition.  Leptin alteration is just one of the many negative effects in which yo-yo dieting can play havoc on your hormones.  Being aware of this, and doing your best to optimize leptin, and your hormone health in general is vital – this is especially the case if you wish to enhance your physique and performance over the long term!

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Check back soon to read about leptin’s counterpart, ‘ghrelin’, a hunger hormone with an even larger effect when it comes to hunger and overeating and while dieting.

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References

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Weigle, D. S., Breen, P. A., Matthys, C. C., Callahan, H. S., Meeuws, K. E., Burden, V. R., & Purnell, J. Q. (2005). A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations. The American journal of clinical nutrition, 82(1), 41-48.

Spiegel, K., Leproult, R., L’Hermite-Balériaux, M., Copinschi, G., Penev, P. D., & Van Cauter, E. (2004). Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. The Journal of clinical endocrinology & metabolism, 89(11), 5762-5771.

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