[Lotus]

Cortisol and Stress: How to Stay Healthy

Higher and more prolonged levels of cortisol in the bloodstream (like those associated with chronic stress) have been shown to have negative effects, such as:

Impaired cognitive performance
Suppressed thyroid function
Blood sugar imbalances such as hyperglycemia
Decreased bone density
Decrease in muscle tissue
Higher blood pressure

Lowered immunity and inflammatory responses in the body, slowed wound healing, and other health consequences.

Increased abdominal fat, which is associated with a greater amount of health problems than fat deposited in other areas of the body. Some of the health problems associated with increased stomach fat are heart attacks, strokes, the development of metabolic syndrome, higher levels of “bad” cholesterol (LDL) and lower levels of “good” cholesterol (HDL), which can lead to other health problems!

http://stress.about.com/od/stresshealth/a/cortisol.htm

[Lotus]

Neuroendocrinology of stress

It is obvious that the higher cortical functions must exercise some effect on the mediation of stress. The best example of this is Wolff's description of unconditional (direct stressors)and conditional (indirect stressors/ie symbols). In both situations the GAS is activated. To understand this activation we must understand the hypothalamic-pituitary system.

Hypothalamic-pituitary-adrenal system
As you recall the pitiutary has two parts, the anterior and posterior hypophysis. It is connected to the hypothalamus via a portal vessel system. Releasing factors corticotrophin releasing hormone, (CRH) and thyrotropin releasing hormone, (TRH) and inhibitory factors such as prolactin inhibiting factor (PIF) from the hypothalamus enter this portal system and arrive in the adenohypophysis (anterior pituitary) and cause the release of pituitary hormones. In stress there is a vigorous release of CRH (CRF is the same molecule) centrally by the hypothalamus. CRH causes a release of ACTH by the pituitary. ACTH which enters the venous blood and on arrival at the adrenal cortex causes a stimulation of the synthesis and release of cortisol. The released cortisol goes "everywhere" including the ptiuitary where it inhibits further release of ACTH. In addition there are cortisol receptors in the central nervous system on which the cortisol acts. Some of these receptors inhibit hypothalamic release of CRH. CRH also causes a vigorous medullary secretion of epinephrine and norepinephrine when given intraventricullarly. This suggest a common pathway for the central transduction of stress onto the adrenal cortex and adrenal medulla.
A significant aspect of the release of ACTH involves its synthesis. ACTH is part of a prohormone, proopiomelanocortin (POMC). In addition to ACTH this hormone is split into MSH (melanocyte stimulating hormone) and beta-endorphin.

Neurotransmitters and HPA
The neural systems which influence the HPA has been studied by various groups. The neurotransmitters acetylcholine and serotonin appear to stimulate ACTH release. Serotonin is produced from tryptophan. In fact the availablitlity of tryptophan is the rate limiting factor for serotonin synthesis. Tryptophan is of interest in stress. This amino acid is carried in the blood stream primarily bound to albumen at the fatty acid site. The uptake into the brain is the result of a facilatated transport system. The free concentration of tryptophan is increased by increased concentration of free fatty acids in the blood. As we mentioned earlier epinephrine and cortisol increase free fatty acids. This increase in availability of tryptophan acts to increase serotonin synthesis. This increase could act as a feed-forward regulatory system because ACTH increases cortisol synthesis. Continued stress would exhaust the tryptophan supply and result in a relative serotonin depletion. The symptoms of serotonin depletion are essentially indistinguishable from clinical depression and include effects on appetite, sleep, concetration, and irritability.

Norepinephrine inhibits ACTH release.
The effects of norepinephrine is complicated by evidence for a norepinephrine alpha receptor stimulatory pathway. It is known is that stress is a strong stimulus for the activation of the locus ceruleus. It is possible that the norepinephrine released acts as a govenor or restraint for the feedforward effects of the serotonin system mentioned above.

GABA causes an inhibition of CRF release.
The antianxiety drugs known as benzodiazepines are GABA agonist. In some models GABA agonist may reduce the chronic stress response. The cost of such treatment is the potential for addiction. In addition it is likely that the anti-stress effect of the benzodiazepines is short-lived and the animal becomes tolerant to the medication.

Neuropeptides such as beta-endorphin and met-enkephalin have been associated with the stress response since their discovery. These neuropeptides have opiate receptor binding ability. Of interest is that beta-endorphin is part of the same pro-hormone which contains the ACTH sequence, POMC. Beta-endorphin and met-enkephalin inhibits ACTH release.


   
http://www.uams.edu/m2004/Behavioral%20S...20text.htm

[Lotus]

Role of cortisol in mammary gland development. The role of cortisol is shown for the different post-embryonic developmental stages of the mammary gland. Other hormones involved in the different developmental stages are also listed. Estrogen and progesterone promote ductal system proliferation during puberty. However, the DNA binding function of the glucocorticoid receptor also appears to be required. During pregnancy, cortisol contributes to lobuloalveolar development of the mammary gland, in conjunction with estrogen and progesterone. Prolactin and cortisol prepare the mammary cells for lactation and stimulate milk protein production following parturition. In addition, cortisol contributes to the maintenance of lactation by suppressing involution. ER, endoplasmic reticulum.
Stress and breast cancer: from epidemiology to molecular biology

http://www.ncbi.nlm.nih.gov/pmc/articles...po=1.00000





   

[Happyme]

Thanks Lotus,
Its scary.. I think I'm beginning to understand some of this stuff.
Bobbi
Are you going to continue expanding this thread?

[Lotus]

Thanks Lotus,
Its scary.. I think I'm beginning to understand some of this stuff.
Bobbi
Are you going to continue expanding this thread?

Haha that is scary cool Boobi, this stuff drives you to new ideas and understanding for sure. For instance, this idea of what free energy does in metabolism makes thermogenesis so interesting, and specifically how we use adipose (fat tissue) to promote the body's own release of E2. The study below suggests we're not too far from pressing play without great difficulty (aka• aromatase to E2). I'll probably fold in the other research threads I have to the program x thread, it makes it easy to reference material in one section.


Non-exercise activity thermogenesis.
Review article
Levine JA. Proc Nutr Soc. 2003.
Show full citation
Abstract
Non-exercise activity thermogenesis (NEAT) is the energy expended that is not from sleeping, eating or sports-like exercise. It ranges from the energy expended walking to work, typing, performing yard work, undertaking agricultural tasks and fidgeting. NEAT can be measured by one of two approaches. The first approach is to measure or estimate total NEAT. Here, total daily energy expenditure is measured and from it is subtracted BMR + thermic effect of food. The second is the factoral approach whereby the components of NEAT are quantified and total NEAT calculated by summing these components. The amount of NEAT that human subjects perform represents the product of the amount and types of physical activities and the thermogenic cost of each activity. The factors that affect the NEAT of a human subject are readily divisible into biological factors, such as weight, gender and body composition, and environmental factors, such as occupation or dwelling within a 'concrete jungle'. The combined impact of these factors explains the substantial variance in human NEAT. The variability in NEAT might be viewed as random but human data contradict this perception. It appears that changes in NEAT subtly accompany experimentally-induced changes in energy balance and are important in the physiology of weight change. NEAT and sedentariness may thus be important in obesity. It then becomes intriguing to dissect mechanistic studies that delineate how NEAT is regulated by neural, peripheral and humoral factors. NEAT may be a carefully-regulated 'tank' of physical activity that is crucial for weight control.

PMID 14692603 [PubMed - indexed for MEDLINE]

[Tanya Marie Squirrel]

Lotus, my dear, you truly are a heavy-weight in the arena of information! its a one-two knock out!

your apt description of findings help make understanding of such technical info palatable to our mental feast!

my mind grows fat and gluttenous on the info you provide

it is my suspicion, that by us all putting our little pieces to the puzzle together, we may find new information and causations in endocrinology that even the endocrinologists didn't see/realize . at the very least, it makes it easier for us non-endocrinologists to understand

[missboobshirt]

Cortisol and Stress: How to Stay Healthy

Higher and more prolonged levels of cortisol in the bloodstream (like those associated with chronic stress) have been shown to have negative effects, such as:

Impaired cognitive performance
Suppressed thyroid function
Blood sugar imbalances such as hyperglycemia
Decreased bone density
Decrease in muscle tissue
Higher blood pressure

Lowered immunity and inflammatory responses in the body, slowed wound healing, and other health consequences.

Increased abdominal fat, which is associated with a greater amount of health problems than fat deposited in other areas of the body. Some of the health problems associated with increased stomach fat are heart attacks, strokes, the development of metabolic syndrome, higher levels of “bad” cholesterol (LDL) and lower levels of “good” cholesterol (HDL), which can lead to other health problems!

http://stress.about.com/od/stresshealth/a/cortisol.htm

Thank you SO much for this, Lotus. I am going to bookmark it-- it is crazy how much stress can effect our bodies.. I really think this was / still could be a main issue for me! Thank you for all of your info, I second a little alle ^

[Lotus]

Cortisol believe it or not has a surprising link to breast growth.

Role of cortisol in mammary gland development. The role of cortisol is shown for the different post-embryonic developmental stages of the mammary gland. Other hormones involved in the different developmental stages are also listed. Estrogen and progesterone promote ductal system proliferation during puberty. However, the DNA binding function of the glucocorticoid receptor also appears to be required. During pregnancy, cortisol contributes to lobuloalveolar development of the mammary gland, in conjunction with estrogen and progesterone. Prolactin and cortisol prepare the mammary cells for lactation and stimulate milk protein production following parturition. In addition, cortisol contributes to the maintenance of lactation by suppressing involution. ER, endoplasmic reticulum.
Stress and breast cancer: from epidemiology to molecular biology

http://www.ncbi.nlm.nih.gov/pmc/articles...po=1.00000