Cortisol and belly fat part 1
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This document discusses how the stress hormone cortisol contributes to belly fat accumulation. It notes that cortisol inhibits the release of growth hormone, which normally breaks down fat for energy. Cortisol also increases the activity of the enzyme HSD-1 in belly fat cells. This causes more inactive cortisone to be converted to active cortisol locally in belly fat. Overall, higher cortisol levels lead to less fat breakdown and more cortisol production in belly fat tissues, promoting belly fat storage. Part 2 will discuss common causes of overactive stress responses and ways to control cortisol levels.
![Hormones and Body Composition: Cortisol and Belly Fat, Part 1
Hormones are one of the bodys main internal messaging systems. We have many of
them, and each one effects the body is different ways.
Most of us have witnessed the effects of massive amounts of anabolic steroids, the
change into menopause, or the beginning of puberty, what most of us dont realize is
how hormones effect the way we express the storage of body fat.
The most obviously example is the characteristic body fat distribution pattern
women start to express at the beginning of puberty due to the effects of the estrogen
hormones and the storage of body fat around the hips and thighs.
The following is a discussion on the hormone most associated with belly fat,
Cortisol!
The stress hormone Cortisol stimulates the synthesis of abdominal fat by inhibiting
growth hormone (GH). [1][2]
Cortisol is a potent stimulus to both the subcutaneous fat stored around the belly
and also visceral fat stored internally around the internal organs, causing the belly
to protrude. [1][3]
Cortisols inhibition of GH works to counter act GHs fatty acid liberating effects
from fat cells, so less fat is being released from fat cells being converted to energy,
and it works locally in the belly region because of the reduction of GH increases the
activity of 11 beta-hydroxysteriod dehydrogenase-1, or HSD-1, which is the enzyme
responsible for converting in-active cortisol, cortisone, back into cortisol[6]. This
effect is localized because there are more HSD-1 enzymes located in the fat cells of
the belly region then fat cells elsewhere in the body [4][5].
To summarize, more cortisol production(stress!) leads to less GH, which in turn
leads to increased local cortisol production from overactive HSD-1 in the fat tissue
surrounding the belly, leading to increased belly fat.
Now what are some ways to prevent this besides living on another planet where we
arent constantly bombarded with stress?
Look at for Part 2 where I discuss the most common reason people are over-reactive
to stress and help get the belly producing cortisol hormone under control!
References:
1. Sher et al. Type D personality:the heart, stress, and cortisol. QJM205; 98:323-
329
2. Erfurth EM, Bulow B, Eskilsson J, Hagmar L. High incidence of cardiovascular
disease and increased prevalence of cardiovascular risk factors in women with](https://image.slidesharecdn.com/cortisolandbellyfatpart1-121022033158-phpapp01/85/Cortisol-and-belly-fat-part-1-1-320.jpg)
Cortisol and belly fat part 1
- 1. Hormones and Body Composition: Cortisol and Belly Fat, Part 1 Hormones are one of the bodys main internal messaging systems. We have many of them, and each one effects the body is different ways. Most of us have witnessed the effects of massive amounts of anabolic steroids, the change into menopause, or the beginning of puberty, what most of us dont realize is how hormones effect the way we express the storage of body fat. The most obviously example is the characteristic body fat distribution pattern women start to express at the beginning of puberty due to the effects of the estrogen hormones and the storage of body fat around the hips and thighs. The following is a discussion on the hormone most associated with belly fat, Cortisol! The stress hormone Cortisol stimulates the synthesis of abdominal fat by inhibiting growth hormone (GH). [1][2] Cortisol is a potent stimulus to both the subcutaneous fat stored around the belly and also visceral fat stored internally around the internal organs, causing the belly to protrude. [1][3] Cortisols inhibition of GH works to counter act GHs fatty acid liberating effects from fat cells, so less fat is being released from fat cells being converted to energy, and it works locally in the belly region because of the reduction of GH increases the activity of 11 beta-hydroxysteriod dehydrogenase-1, or HSD-1, which is the enzyme responsible for converting in-active cortisol, cortisone, back into cortisol[6]. This effect is localized because there are more HSD-1 enzymes located in the fat cells of the belly region then fat cells elsewhere in the body [4][5]. To summarize, more cortisol production(stress!) leads to less GH, which in turn leads to increased local cortisol production from overactive HSD-1 in the fat tissue surrounding the belly, leading to increased belly fat. Now what are some ways to prevent this besides living on another planet where we arent constantly bombarded with stress? Look at for Part 2 where I discuss the most common reason people are over-reactive to stress and help get the belly producing cortisol hormone under control! References: 1. Sher et al. Type D personality:the heart, stress, and cortisol. QJM205; 98:323- 329 2. Erfurth EM, Bulow B, Eskilsson J, Hagmar L. High incidence of cardiovascular disease and increased prevalence of cardiovascular risk factors in women with
- 2. 3. hypopituitarism not receiving growth hormone treatment: Preliminary results. Growth Horm IGF Res 1999; 9(Suppl. A):214. 4. Gold PW, Chrousos GP. Organization of the stress system and its dysregulation in melancholic and atypical depression: high vs. low CRH/NE states. Mol Psychiatry 2002; 7:25475 5. Bujalsak, I. J., Quinkler, J.W. Tomlinson, C.T. Montague, D.M. Smith, and P. M. Stewart. Expression Profiling of 11-Beta-Hydroxysteriod Dehydrogenase Type- 1 and Glucocorticoid Target Genes in Subcutaneous and Omental Human Preadipocytes. Journal of Molecular Endocrinology, October 2006, 37(2): 327-40 6. Desbriere, R., V. Vuaroqueaux, V. Archard, S. Boullu-Ciocca, M. Labuhn, A. Dutour, and M. Grino. 11 Beta-HydroxysteriodDehydrogenase Type 1 mRNA Is Increased in Both Visceral and Subcutaneous Adipose Tissue of Obese Patients. Obesity, May 2006, 14(5): 794-8. 7. Paulsen, S. K., S.B. Pedersen, J.O. Jorgensen, S. Fisker, J.S. Christiansen, A. Flyvbjerg, and B. Richelsen. Growth Hormone (GH) Substitution in GH-Deficient Patients Inhibits 11 Beta-HydroxysteroidDehydrogenase Type 1 Messanger Ribonucleic Acid Expression in Adipose Tissue. Journal of Clinical Endocrinology and Metabolism, March 2006, 91(3): 1093-8, E-pub 20 December 2005