White v. Black Bulbs

[taserbrod]

Okay...so 7 months on finasteride. I am actually taking a week long break from finasteride so that I can hump w/o worries. I think I may be going through a shed. Feeling very bad about my hair.

The hairs that I am seeing fall out have white little bulbs at the end. Does this mean anything?

 

[powersam]

this is one of those questions that appears with sickening regularity. why won't people use the search function?

whatever is on the end of a shed hair has absolutely nothing to say to you. it doesnt matter at all, wont tell you anything.

i will say that going on and off finasteride can cause you problems as your body's hormones never get a chance to settle down. could cause you more libido problems than simply taking finasteride regularly

 

[pleasegodno]

shedding hairs with white bulbs is normal. shedding hairs with black bulbs is not. a hair with a short sheathed region and a black bulb is in the anagen stage--you should not be shedding these hairs.

 

[powersam]

and where do you get that info from pleasegodno?

 

[pleasegodno]

here's something relevant (not my original source):

http://www.electrology.com/rmpart3.htm

it is not normal to lose anagen hairs, obviously, but one can suffer from anagen effluvium or loose anagen syndrome.

you stated, authoritatively, in another thread that increased insulin resistance is the only way that stress can possibly contribute to hair loss--where'd you get that info from?

 

[powersam]

its the only connection between the two that i can see, the effects stress will have on your body are caused by raised cortisol levels for the most part. cortisol levels effect insulin levels. though my point was more that i don't really think stress has a huge effect on your hair. but you're right, it was just a semi educated guess on my part and i probably should have qualified it as such. can you tell me any other way in which stress would cause baldness? disregarding telogen effluvium of course because that happens too rapidly to be confused with male pattern baldness you'd think

 

[pleasegodno]

i believe that there are degrees of telogen effluvium. it's my contention that stress/anxiety can contribute significantly to the rate of progression of male pattern baldness through the induction of a telogen effluvium, be it mild or severe, acute or chronic, depending on the intensity and duration of psychological distress. there have been no specific studies (that i know of) that address that exact issue, but i think it's highly likely that such scenarios could hasten follicle miniaturization (accelerating the appearance of the male pattern baldness pattern), given that follice/ECM remodeling would be taking place in an inflamed environment, which would be pro-apoptotic/fibrotic.

you're right, though, about the cortisol/insulin resistance connection--that's definitely a potential factor as well.

anyway, here are some studies on stress and hair:


Exp Dermatol. 2006 Jan;15(1):1-13. Related Articles, Links


Hair growth inhibition by psychoemotional stress: a mouse model for neural mechanisms in hair growth control.

Peters EM, Arck PC, Paus R.

Biomedical Research Center, Psychoneuroimmunology Research Group, Internal Medicine, Psychosomatics, University Medicine Berlin, Charite Virchow Campus, Germany. eva.peters@charite.de

Stress has long been discussed controversially as a cause of hair loss. However, solid proof of stress-induced hair growth inhibition had long been missing. If psychoemotional stress can affect hair growth, this must be mediated via definable neurorendocrine and/or neuroimmunological signaling pathways. Revisiting and up-dating relevant background data on neural mechanisms of hair growth control, we sketch essentials of hair follicle (HF) neurobiology and discuss the modulation of murine hair growth by neuropeptides, neurotransmitters, neurotrophins, and mast cells. Exploiting an established mouse model for stress, we summarize recent evidence that sonic stress triggers a cascade of molecular events including plasticity of the peptidergic peri- and interfollicular innervation and neuroimmune crosstalk. Substance P (SP) and NGF (nerve growth factor) are recruited as key mediators of stress-induced hair growth-inhibitory effects. These effects include perifollicular neurogenic inflammation, HF keratinocyte apoptosis, inhibition of proliferation within the HF epithelium, and premature HF regression (catagen induction). Intriguingly, most of these effects can be abrogated by treatment of stressed mice with SP-receptor neurokinin-1 receptor (NK-1) antagonists or NGF-neutralizing antibodies - as well as, surprisingly, by topical minoxidil. Thus there is now solid in vivo-evidence for the existence of a defined brain- HF axis. This axis can be utilized by psychoemotional and other stressors to prematurely terminate hair growth. Stress-induced hair growth inhibition can therefore serve as a highly instructive model for exploring the brain-skin connection and provides a unique experimental model for dissecting general principles of skin neuroendocrinology and neuroimmunology well beyond the HF.




Trends Immunol. 2006 Jan;27(1):32-9. Epub 2005 Nov 2. Related Articles, Links


Neuroimmunoendocrine circuitry of the 'brain-skin connection'.

Paus R, Theoharides TC, Arck PC.

Department of Dermatology, University Hospital Schleswig-Holstein, Campus Lubeck, University of Lubeck, D-23538 Lubeck, Germany. ralf.paus@uk-sh.de

The skin offers an ideally suited, clinically relevant model for studying the crossroads between peripheral and systemic responses to stress. A 'brain-skin connection' with local neuroimmunoendocrine circuitry underlies the pathogenesis of allergic and inflammatory skin diseases, triggered or aggravated by stress. In stressed mice, corticotropin-releasing hormone, nerve growth factor, neurotensin, substance P and mast cells are recruited hierarchically to induce neurogenic skin inflammation, which inhibits hair growth. The hair follicle is both a target and a source for immunomodulatory stress mediators, and has an equivalent of the hypothalamus-pituitary-adrenal axis. Thus, the skin and its appendages enable the study of complex neuroimmunoendocrine responses that peripheral tissues launch upon stress exposure, as a basis for identifying new targets for therapeutic stress intervention.



Brain Behav Immun. 2005 May;19(3):252-62. Related Articles, Links


Stress exposure modulates peptidergic innervation and degranulates mast cells in murine skin.

Peters EM, Kuhlmei A, Tobin DJ, Muller-Rover S, Klapp BF, Arck PC.

Department of Internal Medicine, Charite-University Medicine, Berlin, Germany. eva.peters@charite.de

Stress is said to induce itchiness of the skin, exacerbate inflammatory skin diseases, and inhibit wound healing. Neuropeptides such as substance P (SP) may play a role in these processes. Recently, we were able to show that both stress or SP are associated with neurogenic inflammation and increased apoptosis in the murine hair follicle. Moreover, peptidergic cutaneous innervation is subject to lifelong plasticity due to its association with the cyclic growth of hair follicles. However, peripheral neuronal plasticity has never been reported in altered interactions between the nervous and immune systems under perceived stress. Here, we show for the first time plasticity of the cutaneous peptidergic innervation in response to stress. After exposure to sonic stress, the number of SP+ nerve fibers in the back skin of C57BL/6 mice with their hair follicles in the resting phase of the hair cycle (telogen-low numbers of nerve fibers) increased significantly. Such nerve fibers contacted mast cells more frequently. At the same time, the percentage of degranulated mast cells increased significantly associated with a rise in apoptotic cells in the skin. Increased numbers of peptidergic nerve fibers correlated with increased numbers of growth-associated protein 43 (Gap-43)+ nerve fibers, which is a marker for growing nerves. Thus, neuronal plasticity and increased neuro-immune interaction occur under stress and may alter inflammatory skin diseases and trophic functions in the skin where neurogenic inflammation plays a part.





J Mol Med. 2005 May;83(5):386-96. Epub 2005 Mar 10. Related Articles, Links


Mast cell deficient and neurokinin-1 receptor knockout mice are protected from stress-induced hair growth inhibition.

Arck PC, Handjiski B, Kuhlmei A, Peters EM, Knackstedt M, Peter A, Hunt SP, Klapp BF, Paus R.

Biomedizinisches Forschungszentrum, Campus Virchow Klinikum, Charite University Medicine, Augustenburger Platz 1, 13353 Berlin, Germany. petra.arck@charite.de

Despite the lack of insight on distinct mediators in the skin orchestrating the pathophysiological response to stress, hair loss has often been reported to be caused by stress. Recently we revealed the existence of a "brain-hair follicle axis" by characterizing the neurokinin (NK) substance P (SP) as a central element in the stress-induced threat to the hair follicle, resulting in premature onset of catagen accompanied by mast cell activation in the skin. However, our understanding of possible SP-mast cell interactions in the skin in response to stress was limited since the receptor by which SP activates skin mast cells and the extent of mast cell mediated aggravation of SP remained to be elucidated. We now employed NK-1 receptor knockout mice (NK-1R(-/-)) and mast cell deficient W/W(v) mice and observed that stress-triggered premature induction of catagen and hair follicle apoptosis does not occur in NK1(-/-) and W/W(v) mice. Furthermore, the activation status of mast cells was less in stressed NK1(-/-) mice than in wild-type control. Additionally, stress-induced upregulation of SP positive nerve fibers was absent in both NK-1R and W/W(v) mice. These results indicate that the cross-talk between SP and mast cell activation via NK-1R appears to be the most important pathway in the regulation of hair follicle cycling upon stress response.


Int J Dermatol. 2003 Sep;42(9):691-3. Related Articles, Links


The presence of trichodynia in patients with telogen effluvium and androgenetic alopecia.

Kivanc-Altunay I, Savas C, Gokdemir G, Koslu A, Ayaydin EB.

Department of Dermatology, Sisli Etfal Research and Training Hospital, Istanbul, Turkey. derma14@turk.net

BACKGROUND: Trichodynia refers to pain, discomfort, and/or paresthesia in the skin of the scalp or the hair. There may be an associated psychologic comorbidity. Although androgenetic alopecia (Androgenetic Alopecia) and telogen effluvium (Telogen Effluvium) are different entities in terms of pathogenesis, etiology, and clinical picture, both may be influenced by psychologic stress and may be the cause of secondary stress. AIMS: To investigate the presence of trichodynia in patients with Telogen Effluvium and Androgenetic Alopecia and to evaluate psychologic comorbidity in patients with trichodynia. MATERIALS AND METHODS: A total of 248 patients (153 females, 95 males), presenting with hair loss due to either Telogen Effluvium or Androgenetic Alopecia, were enrolled in this study. The prevalence of trichodynia in these two groups was compared with that in controls (n = 184). In addition, psychiatric evaluation was performed in 25 patients with trichodynia (13 females, 12 males) and in 25 controls (16 females, nine males) without alopecia and trichodynia by a psychiatrist; Diagnostic and Statistical Manual of Mental Disorders (DSM)IV criteria were used for the assessment. RESULTS: Trichodynia was found in 72 patients (29%) with hair loss and in six controls (3.3%; P < 0.0001); 25 of the 72 patients with trichodynia underwent psychiatric evaluation and 19 of the 25 patients were found to have psychopathologic signs (76%). In the control group, only five patients had psychopathologic signs (20%; P = 0.0004). Of those with hair loss, trichodynia was more frequent in the Telogen Effluvium group than in the Androgenetic Alopecia group (P < 0.0071). CONCLUSIONS: Trichodynia is a common symptom in patients with Telogen Effluvium and Androgenetic Alopecia, and often coexists with psychopathologic findings, including depression, obsessive personality disorder, and anxiety.



Scalp Dysesthesia
Diane Hoss, MD; Samantha Segal, MD
Arch Dermatol. 1998;134:327-330.
ABSTRACT

Background

Cutaneous dysesthesia syndrome is a disorder characterized by chronic cutaneous symptoms without objective findings. Patients complain of burning, stinging, or itching, which is often triggered or exacerbated by psychological or physical stress. These symptoms may be manifestations of an underlying psychiatric disorder or may represent a type of chronic pain syndrome.

Observations

Eleven women presented with chronic severe pain and/or pruritus of the scalp only without objective physical findings, a condition we term "scalp dysesthesia." Five women described pain, stinging, or burning only; 4 women complained of pain and pruritus; and 2 women reported pruritus only. The patients ranged in age from 36 to 70 years. The duration of symptoms ranged from 9 months to 7 years. Five women had physician-diagnosed psychiatric disorders, including dysthymic disorder, generalized anxiety, and somatization. Seven women reported that stress triggers or exacerbates their symptoms. Eight women experienced improvement or complete resolution of symptoms with treatment with low-dose doxepin hydrochloride or amitriptyline hydrochloride. One patient responded completely to treatment with sertraline and hydroxyzine hydrochloride but then experienced a relapse.

Conclusions

We describe 11 patients with a new syndrome that we term scalp dysesthesia. Of 11 patients, 9 benefited from treatment with low doses of antidepressants.




Hautarzt. 2000 Dec;51(12):899-905. Related Articles, Links


[Idiopathic chronic telegon effluvium in the woman]

[Article in German]

Trueb RM.

Dermatologische Klinik, Universitatsspital Zurich, 8091 Zurich, Schweiz. ramitru@derm.unizh.ch

In approximately 30% of cases of chronic diffuse loss of scalp hair with a duration of at least 6 months, no underlying abnormality can be found. Typically this occurs in women, starting abruptly without a recognizable initiating factor, and involving the entire scalp area with increased shedding of telogen hair. With the exception of bitemporal recession, hair thinning is usually discrete, and contrasts to the great emotional overtones in this situation. This may initially lead to the differential diagnosis of psychogenic pseudo effluvium. Due to synchronization of the hair cycle, the amount of shed hair is greater than that in androgenetic alopecia, while miniaturized hairs are not a feature of the disorder. Overlap with androgenetic alopecia and/or psychogeneic pseudo effluvium is not uncommon. Scalp dysesthesia or a sensation of "pain in the hair" (trichodynia) is an accompanying symptom in a significant proportion of cases, and correlates better with emotional upset than with actual hair loss. Current therapeutic recommendations are pragmatic, and based on both experimental observations of the sheep wool industry and clinical experience. They include the use of L-cystine-containing oral preparations and of corticosteroids. Further investigation into the molecular controls of the hair cycle are required to find a more specific form of therapy, for which the expense and risk-benefit ratio seem appropriate for the treatment of this benign condition.