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AutonomousOne1980

emotional stress cause of acne???

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Exp Dermatol. 2004

Neuroendocrine regulation of sebocytes -- a pathogenetic link between stress and acne

A causative link between emotional stress and acne has long been postulated. There is mounting evidence that the molecular mechanism underlying this observation is related to the expression of receptors for several neuroendocrine mediators by the sebaceous gland. Recent and ongoing studies have indicated that human sebocytes express functional receptors for corticotropin-releasing hormone, melanocortins, beta-endorphin, vasoactive intestinal polypeptide, neuropeptide Y and calcitonin gene-related peptide. After ligand binding, these receptors modulate the production of inflammatory cytokines, proliferation, differentiation, lipogenesis and androgen metabolism in sebocytes. By means of their autocrine, paracrine and endocrine actions, these neuroendocrine factors appear to mediate centrally and topically induced stress towards the sebaceous gland, ultimately affecting the clinical course of acne.

Proc Natl Acad Sci U S A. 2002 May 14;99(10):7148-53. Links

Corticotropin-releasing hormone: an autocrine hormone that promotes lipogenesis in human sebocytes

Sebaceous glands may be involved in a pathway conceptually similar to that of the hypothalamic-pituitary-adrenal (HPA) axis. Such a pathway has been described and may occur in human skin and lately in the sebaceous glands because they express neuropeptide receptors. Corticotropin-releasing hormone (CRH) is the most proximal element of the HPA axis, and it acts as central coordinator for neuroendocrine and behavioral responses to stress. To further examine the probability of an HPA equivalent pathway, we investigated the expression of CRH, CRH-binding protein (CRH-BP), and CRH receptors (CRH-R) in SZ95 sebocytes in vitro and their regulation by CRH and several other hormones. CRH, CRH-BP, CRH-R1, and CRH-R2 were detectable in SZ95 sebocytes at the mRNA and protein levels: CRH-R1 was the predominant type (CRH-R1/CRH-R2 = 2). CRH was biologically active on human sebocytes: it induced biphasic increase in synthesis of sebaceous lipids with a maximum stimulation at 10(-7) M and up-regulated mRNA levels of 3 beta- hydroxysteroid dehydrogenase/Delta(5-4) isomerase, although it did not affect cell viability, cell proliferation, or IL-1 beta-induced IL-8 release. CRH, dehydroepiandrosterone, and 17 beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10(-7) M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h. Based on these findings, CRH may be an autocrine hormone for human sebocytes that exerts homeostatic lipogenic activity, whereas testosterone and growth hormone induce CRH negative feedback. The findings implicate CRH in the clinical development of acne, seborrhea, androgenetic alopecia, skin aging, xerosis, and other skin disorders associated with alterations in lipid formation of sebaceous origin.

Horm Res. 2000;54(5-6):281-6. Links

Neuroimmunoregulation of androgens in the adrenal gland and the skin

Human adrenals produce large quantities of androgens, especially DHEA which is the most abundant circulating hormone in the human body. Adrenal androgens are regulated by several factors, including pituitary ACTH and an intricate intraadrenal network involving immune cells, cytokines and neuroendocrine factors. The skin is a major target of androgens and androgen receptors are expressed in the epidermis, dermis, sebaceous glands and hair. In addition, the skin has the capacity to metabolize androgens into more powerful compounds. Similar to the adrenal gland, there is an intradermal neuro-immune network involving the local expression of cytokines and neuropeptides. Dysregulation of androgens in the adrenals and/or the skin is associated with acne, hirsutism and androgenic alopecia. Therefore, understanding the mechanisms of these intricate networks is of both basic and clinical relevance and may help to develop new strategies for the treatment of androgen-dependent skin disorders. Copyright 2001 S. Karger AG, Basel

Horm Metab Res. 2007 Feb;39(2):166-70. Links

Corticotropin-releasing hormone skin signaling is receptor-mediated and is predominant in the sebaceous glands

There is increasing evidence that the sebaceous gland expresses receptors for several neuropeptides and is involved in responses to stress. Among them, corticotropin-releasing hormone (CRH) was currently found to be produced also in the skin. In this study, the distribution of CRH, CRH receptors 1 and 2 (CRH-R1 and CRH-R2), and CRH binding protein (CRH-BP) in cultured human (SZ95) sebocytes was further characterized. Moreover, the effects of CRH and CRH-like peptides on proliferation and inflammatory signaling of CRH receptor-expressing SZ95 sebocytes IN VITRO were investigated. Urocortin (Uct), urotensin and sauvagine are recently described members of the family of structurally related CRH-like peptides, whereas Uct shares a 45% homology with CRH. CRH and Uct inhibited SZ95 sebocyte proliferation with CRH also stimulating interleukin-6 (IL-6) and interleukin-8 (IL-8) release from SZ95 sebocytes. However, CRH had no effect on interleukin-1alpha and interleukin-1beta production in these cells. alpha-Helical-CRF, a CRH antagonistic peptide, annulled the CRH effect on SZ95 sebocyte proliferation and interleukin secretion, while the non-peptidic CRH-R1 selective antagonist antalarmin inhibited the increased production of neutral lipids caused by CRH. In conclusion, CRH, and to a lesser extent Uct, may be involved in signaling of stress pathophysiology in the skin. However, further investigations into the downstream effects of CRH and Uct are required to elucidate the mechanism by which these neuropeptides could establish a stress-related pathophysiological condition in the skin.

also read this

http://www.pubmedcentral.nih.gov/articlere...p;artid=2232898

over the past few months if been considering this a real possibility. my first experiance was with with meditation and practicing relaxation, then my recent friendship that was going really well which helped ease my stress, and my acne has improved drastically, or its just coincidence but i can tell you that i dont ever think ive been able to deal with my emotions effectively, also my famly is in shambles but we deny it, and i also noticed that when i was clear it was when i was most satisfied with my life, but when trouble came acne usually returned.

I suspect that life satisfaction as defined by experiancing joy and pleasure on a consistent basis could be the cure for most. Learning to stomp out negative stressful feelings by either altering your life our altering your perception of life, im sure a combination of the two, and also good healthy relationships that make you feel so good and not sick to your stomach.

There is an new area of psychology that is called emotional intelligence and it studies peoples ability and skill in dealing with emotions, such as learning to sense the subtle emotions and discomforting feelings and finding healthy solutions to dealing with them as opposed to denying that you feel them, becoming emotionally numb or dealing with them the wrong way like indulging in your anger towards someone or taking drugs but you get the jist of it.

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I must say I stress many times due to study/family/ girlfriend.. is hard man, to control your anger...I don't know what to do when I feel that way, I wish I could inject some sort of tranquilizer ..

I like your approach on healing your acne through meditation, maybe I will give it a try

but the beast inside me is stronger.

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I must say I stress many times due to study/family/ girlfriend.. is hard man, to control your anger...I don't know what to do when I feel that way, I wish I could inject some sort of tranquilizer ..

I like your approach on healing your acne through meditation, maybe I will give it a try

but the beast inside me is stronger.

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is it anger related with genes? my grandfather is a person of short temper, all his life he would get angry at almost everything! it was insane back then, now he is getting older, I don't live with him anymore so I don't know if he still the same..

I wonder if I got my short temper from him.

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is it anger related with genes? my grandfather is a person of short temper, all his life he would get angry at almost everything! it was insane back then, now he is getting older, I don't live with him anymore so I don't know if he still the same..

I wonder if I got my short temper from him.

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Influence of substance-P on cultured sebocytes.Lee WJ, Jung HD, Lee HJ, Kim BS, Lee SJ, Kim do W.

Department of Dermatology, Kyungpook National University School of Medicine, 700-721 Sam-duck 2 Ga 50, Jung-gu, Daegu, Republic of Korea, [email protected]

Acne is a complex, chronic and common skin disorder of pilosebaceous units. Although it is known that exacerbation of acne results from emotional stress, the nature of the association between stress and acne remains unclear. This is due in part to the lack of substantial evidence regarding the participation of cutaneous neurogenic factors in the pathogenesis of acne. Culture of sebocytes provides a new insight into the participation of neuropeptides, notably substance P (SP), in the pathophysiology of acne. To examine the possible involvement of neurogenic factors in the pathogenesis of acne, we used immunohistochemistry and RT-PCR to compare the expression of interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), peroxisome proliferators activated receptors-gamma (PPAR-gamma) on the cultured sebocytes stimulated by SP. IL-1 is primarily proinflammatory cytokines to stimulate the expression of genes associated with inflammation. IL-6 is a pleiotropic cytokine with a wide range of biological activities and regulates inflammation. TNF-alpha is a pleiotropic pro-inflammatory cytokine that exerts multiple biologic effects. PPAR-gamma is a nuclear hormone receptor and plays a unique role in stimulating sebocyte lipogenesis. More numerous immunoreactivity to IL-1, IL-6, TNF-alpha and PPAR-gamma and increased RNA amplification for IL-1, IL-6, TNF-alpha and PPAR-gamma were observed after addition of SP compared with the control. This study reveals that SP is involved in the pathogenesis of acne.

PMID: 18427822 [PubMed - in process]

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I lack the expertise to understand these studies fully. I suffer from major anxiety and depression. my parents tell me that that is the cause of my acne and excess sebum production. over the years, it seems to make sense..in the past 3 years I've steadily increased my levels of anxiety - i've had more and more fits and panic attacks and now my skin is more oily than a teenage boy.

the problem of course being that now one of my niggest stressors is my skin.

I wonder if there are any studies (which would most likely be unethical if even possible) where individuals were put under long term anxiety (months) and compared to "normal" vs. individuals put into some type of coma like state where they body is monitored with the intent of ...i dont know where im going with this.

i guess what really worries me is that no matter how hard i try to free my mind of anxiety and depression - living as stress free as possible - that the sebum still flows and the acne still comes - I wonder sometimes if the years of severe stress and anxiety have casued permanent changes in the body and mind...and hormones

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Long story short, I went through a bad break up 6 months ago and have been breaking out ever since. I'm convinced stress is the main cause of my inflamed acne. It's really hard because I'm suffering from panic attacks and depression also which I believe is leading to more acne which is in turn leading more stress, leading to more acne etc. etc. It's a never ending cycle. I was thinking that if I artificially relaxed myself (Xanax), that I would stop breaking out as much. I will soon find out.

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I was thinking that if I artificially relaxed myself (Xanax), that I would stop breaking out as much. I will soon find out.

Probably the precise biochemical aspect of "stress" that matters to acne is a lack of a normal melatonin cycle. Since Xanax may depress melatonin levels, I'll predict it will not improve your acne, and may make it worse.

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