How Your Brain and Hormones Impact Your Weight Loss
...and how these hormones may actually be making you FATTER than ever before!
By Kevin DiDonato MS, CES0--Level 1 Certified Precision Nutrition and Certified Personal Trainer
The brain is the control center for most process and functions that happen in the body. Through the use of two different systems, the brain controls most activities, and possibly activities such as weight loss and fat mobilization.
There are some systems in the body that protect us without us even knowing it. The sympathetic system is one that helps to stimulate a response in the body to stay and fight, or to flee.
Researchers are also finding that adipose tissue, or fat, can possibly send a signal to the brain stimulating the body to start the process of fat breakdown.
They have determined that when our bodies break down enough sugar in the body stored as glycogen, then our fat cells send a signal back to the brain that informs the brain if the body needs more fuel.
The brain then returns a signal to the fat cells to start the fat breakdown process in order to utilize energy stored in the fat - pretty amazing stuff, but it does not stop there.
The fat cells then send a message back to the brain telling the brain how much energy has been released; and, the brain determines if there is a need for further fat breakdown, or if the body should slow down the process. There is more research to be done for longer-term weight loss and reduction, as this research showed the effects on short-term utilization of fat breakdown.
Researchers have possibly found another way the body, specifically hormones, can affect weight loss success and weight regaining after losing.
The hormone, Leptin, is a key hormone in regulating energy expenditure and energy intake. Ghrelin works hand-in-hand with Leptin, and increases before a meal, and decreases after a meal. Ghrelin is responsible for satiety or satisfaction after a meal.
With weight loss, there are usually changes in the levels of these two hormones.
Weight loss is associated with a decrease in Leptin levels. Leptin is considered a defense hormone in weight loss, which results in regaining weight, especially body fat, after losing weight.
But Ghrelin and Leptin aren’t the only two hormones that impact your weight loss. Cortisol, which is a stress hormone, may also influence your ability to lose weight.
For starters, increased cortisol levels may cause increased inflammation, c-reactive protein levels, and an increase in food cravings.
Most of the time, people with high cortisol levels, tend to crave sugary and fatty foods—which could easily increase your risk for weight gain.
But that’s not all…
Research has shown that when someone is overweight, there is a suppression of Ghrelin levels which can account for storage of body fat and not having the ability to lose weight. Having higher levels of Leptin and cortisol has been shown to cause an increase in weight regain after losing weight.
Weight loss is mediated by different systems and hormones in the body. Each hormone and system plays in integral part in if a person will maintain weight after weight loss, or regain a portion of all of the weight after weight loss.
But you must be careful...
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Hansen, T. Dall, R. Hosoda, H. Kojima, M. Kangawa, K.Christiansen, J. Jorgensen, J. Weight Loss Increases Circulating Levels of Ghrelin in Human Obesity. Clinc. Endo. Feb. 2002. Vol. 56(2) pp. 203-206
Rosenbaum, M. Sy, M. Pavlovich, K. Leibel, R. Hirsch, J. Leptin Reverses Weight Loss-Induced Changes in Regional Neural Activity Responses to Visual Food Stimuli. J. Clin. Invest. J Clin Invest. 2008 July 1; 118(7): 2583–2591.
Crujeiras, A. Goyenechea, E. Abete, I. Lage, M. Carriera, M. Martinez, J. Casaanueva, F. Weight Regain after a Diet-Induced Loss is Predicted by Higher Baseline Leptin and Lower Ghrelin Levels. J. Clin. Endo. Met. Vol. 95(11). 5037-5044.
Song, C. Schwartz, G. Bartness, T. Anterograde Transneuronal Viral Tract Tracing Reveals Central Sensory Circuits From White Adipose Tissue. Regu. Physiol. Martch 2009. Vol. 296 (3) pp. 501-511.