Hair Loss and Hair Regrowth

Hair Loss Treatment, hair regrowth.

Hair Loss Treatment at the Proctor Clinic

A history of Redox signaling.

Redox cell signaling is important in hair loss, hair regrowth, and in hair loss treatment.

Nat Prod Res. 2009 Sep 16:1-12

Effect of Citrullus colocynthis Schrad fruits on testosterone-induced hair loss.
Dhanotia R,.

Hair loss is a psychologically distressing phenomenon. Androgenetic alopecia (AGA) is the most common form of Hair loss, which affects millions of men and women worldwide, and is an androgen driven disorder. Here, the Citrullus colocynthis Schrad fruit is evaluated for hair regrowth activity in androgen-induced alopecia. Petroleum ether extract of C. colocynthis was applied topically for its hair regrowth-promoting activity. Alopecia was induced in albino mice by testosterone administration intramuscularly for 21 days. Its inhibition by simultaneous administration of extract was evaluated using follicular density, anagen/telogen (A/T) ratio and microscopic observation of skin sections. Finasteride (5alpha-reductase inhibitor) solution was applied topically and served as positive control. Petroleum ether extract of C. colocynthis exhibited promising hair growth-promoting activity, as reflected from follicular density, A/T ratio and skin sections. The treatment was also successful in bringing a greater number of hair follicles in anagenic phase than the standard finasteride. The result of treatment with 2 and 5% petroleum ether extracts were comparable to the positive control finasteride. The petroleum ether extract of C. colocynthis and its isolate is useful in the treatment of androgen-induced alopecia.

Hair loss treatment blog

Arch Dermatol.1984;120:457.

Alopecia areata treated with topical minoxidil.

Weiss VC, et al

edited for hair loss blog

A minoxidil topical solution was used to treat 48 patients with hair loss due to alopecia areata, ie, 24 patients with patchy disease and 24 patients with total hair loss or alopecia universalis. Twenty-five patients had terminal hair regrowth"; in 11 of the 25 patients, it was cosmetically acceptable. No clinical features of the disease seemed to indicate the likelihood of hair regrowth. Hair regrowth began two months after start of treatment and was not uniformly well maintained after the treatment was terminated. One patient had an allergic contact dermatitis reaction to the minoxidil solution; no systemic side effects were seen. No notable systemic absorption was found in 18 adult patients. Effects on cutaneous blood flow or the immune system or some direct effect on hair follicles are possible mechanisms by which minoxidil therapy might stimulate hair regrowth.

...Studies demonstrate that loss of hair follicles involves distinct patterns of expression of active caspases. Active caspase 8, an initiator of the death receptor pathway, was predominately found in the isthmic and upper lower portion of the shaft. This pattern of expression suggests that the death receptor pathway is activated during hair regrowth and is initiated by toxic substances that bind to death receptors, i.e., TNF-alpha. Interestingly, activated caspase 3, a downstream effector caspase, was higher in catagen hair then in other phases of the hair cycle, indicating a role in the terminal stage of the apoptotic pathway. Activated caspase 1 was also found in the hair bulb and hair shaft. This study suggests an important role of the infundibular area of the hair shaft where inner and outer root sheath are abruptly changing and that this area may play a role in the regulation of normal hair apoptosis. Caspase 3 seems to be playing the key role in the apoptotic pathway during the catagen phase of the hair cycle in these areas. Finasteride may exhibit its influence by selectively inhibiting DHT, which affects a multitude of "androgen responsive genes", such as the caspase pathway, which affects programmed cell death in the hair regrwothcycle

Uric acid and Stroke

This is Dr Proctor's paper on the relationship between uric acid and stroke. The same processes modulating hair loss also likely figure in stroke. Similarly, many agents that are effective in hair loss treatment are also effective in experimental models of stroke.

Singh G.Indian J Dermatol Venereol Leprol 2002;68:40

Androgenic alopecia ( hair loss ) genetically-determined., The exact mode of inheritance is unknown. The shortening of the anagen phase of the hair cycle leads to the consequent increase in the proportion of telogen hairs. Autosomal dominant inheritance with increased penetrance in males had been suggested, but there are reports of multifactorial inheritance as well. The role of androgen along with their interaction with genetic factors is demonstrated in men, but in women baldness is often associated with elevated levels of circulating androgens, the factor determining Pattern hair loss is how the follicles of the scalp react to the circulating androgens.

Dr Proctor treats hair loss

Dermatologica. 1987;175 Suppl 2:36-41.

Topical minoxidil in extensive alopecia areata, including 3-year follow-up.
Price VH.

Kaiser Permanente Medical Center, San Francisco, Calif.

Perhaps the most intriguing aspect of topical minoxidil is the fact that this drug can promote hair regrowth in two unrelated conditions: alopecia areata (AA) and androgenetic alopecia (male pattern hairloss ). snip... In androgenetic alopecia, genetically marked hair follicles undergo progressive, androgen-mediated miniaturization; antiandrogens have been conventionally sought to intercept this process. It is not known how minoxidil promotes hair regrowth except that living follicles capable of stimulation and hypertrophy are required. It may be that minoxidil influences some fundamental signal for regrowth to the follicular apparatus, ...snip... While topical minoxidil is not very effective for those with 100% scalp hair loss, it is an effective, easy and safe treatment for those with AA affecting 25-99% of the scalp.

Dermatologica. 1987;175 Suppl 2:29-35.

Immunohistochemical characterization of the cellular infiltrate in severe alopecia areata before and after minoxidil treatment.

Fiedler VC,

The mechanism of minoxidil-induced hair regrowth in the treatmen of alopecia areata hair loss (AA) is unknown. In vitro studies suggest that pharmacologic tissue levels of minoxidil may have both epithelial and T cell effects.snip...Nonresponders (that is peoe with no hair regrowth) showed none of these changes. Biopsies from 34 patients subsequently treated with oral minoxidil 5 mg q. 12 h showed no further changes in perifollicular total T, helper-inducer T or suppressor-cytotoxic T cell counts; they did, however, demonstrate significant decreases in perifollicular Langerhans cell and activated T cell counts, and nearly significant decreases in perifollicular monocyte counts. It is possible that minoxidil may be altering a presumed follicular chemoattractive stimulus to a variety of cell types. Decreases in activated T cell counts suggest the possibility of direct immunomodulatory effects of minoxidil on T cells which might contribute to a hair regrowth response in AA.

Geburtshilfe Frauenheilkd.1988;48:203

Hormonal diagnosis in so-called androgenetic alopecia (pattern hair loss) in the female

Moltz L.

Androgenetic alopecia or pattern hair loss occurs quite frequently. Up to 79% of women suffer at least temporarily from varying degrees of intermittent diffuse hair loss in the centro-parietal and/or fronto-temporal regions. A.A. is caused by an androgen excess acting on the hair follicle for prolonged periods of time in the presence of a genetic predisposition. However, often hyperandrogenemia cannot be demonstrated in such patients. 125 women with clinically typical a.A. were investigated prospectively under standardized conditions. Patient age ranged from 18 to 68 years. Atypical uterine bleeding such as menorrhagia, hypermenorrhea and polymenorrhea were found in 69 women. The hair loss varied between 50 and 400 hairs per day. Additional signs of hyperandrogenism, i.e. seborrhea, acne and hirsutism, were often observed. snip.. Treatment was directed at normalizing the disturbed estrogen-androgen-balance. Using low-dose antiandrogens, estrogens, prolactin suppressants, corticoids, iron-II-preparations as well as estrogen-containing hair lotions hair loss was arrested in 74 of 104 treated women, while regrowth of hair was accomplished in 16 patients. 14 women did not respond to therapy.

edited for use in hairloss blog

Dermatology. 1992;185:82

Psoriatic alopecia: acute and chronic hair loss in 47 patients with scalp psoriasis.Runne U, Kroneisen-Wiersma P.

Hair loss and alopecia were seen in psoriatic lesions of the scalp in 47 patients. snip.. Hair loss varied in intensity from protracted to moderate and massive (36% in tufts)..... Thirteen patients (28%) became aware of the hair loss with the beginning of therapy. Hair loss was found to be circumscribed in 75% of the cases and diffuse in 25%. In 2 cases psoriatic alopecia also manifested itself at sites other than the scalp. The telogen count was found to be increased up to 25-86% in the florid stage. ...snip.. This infiltrate can alter the follicle epithelium and may lead to a granulomatous foreign-body reaction with destruction of the hair follicle. After topical antipsoriatic treatment, most of the reexamined patients showed complete hair regrowth, while 5 developed a residual scarring. Therefore, in the patient with circumscribed or diffuse symptomatic hair loss, with or without scarring, psoriatic alopecia should be considered.

J Clin Endocrinol Metab. 1987;65(1):188

The effects of N,N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane-17 beta-carboxamide, a 5 alpha-reductase inhibitor and antiandrogen, on the treatment of baldness in the stumptail macaque.

Rittmaster RS, et al

We used a primate model of male-pattern baldness to test the efficacy of a topically applied 5 alpha-reductase inhibitor and antiandrogen (4-MA) in the treatment of hair loss. Six periadolescent stumptail macaques were given daily topical applications of either 4-MA in dimethylsulfoxide or dimethylsulfoxide alone for 27 months. The three control monkeys developed varying degrees of baldness, while the three 4-MA-treated monkeys retained their juvenile pattern of hair regrowth. The percentage of actively growing hair follicles in the frontal scalp did not change in the 4-MA-treated group [46 +/- 6 (+/- SE) vs. 48 +/- 4], while a significant decrease occurred in the control group (63 +/- 6 vs. 25 +/- 12; P less than 0.025). Skin 5 alpha-reductase activity was reduced in the scalp of the 4-MA-treated monkeys. We conclude that topical 4-MA can prevent the development of baldness in the stumptail macaque, a primate model of androgen-dependent baldness.

Toxicol Pathol. 1987;15(2):149

Histologic changes in nude mouse skin and human skin xenografts following exposure to sulfhydryl reagents:
\
arsenicals. et al

This report documents the histological changes in nude mouse skin and in human skin xenografts on nude mice following exposure to phenyldichloroarsine (PDA), a vesicant arsenical. Under light microscopy, we observed in PDA-treated human skin grafts: 1) degeneration of epidermal cell nuclei (apparent by 2 hr after exposure with increasing severity through 48 hr); 2) loss of epidermal cytoplasmic basophilia (apparent by 4 hr, maximal within 12 hr); 3) epidermal cytoplasmic vacuolization (vacuoles appeared within 4 hr and increased in size through 24 hr); 4) cleft formation within the basement membrane zone (apparent by 12 hr, increasing in severity through 24 hr); 5) inflammation evidenced by polymorphonuclear leukocyte (PMN) infiltration (apparent by 4 hr and increasing through 48 hr). The PMNs frequently formed a wall around the lesion, but did not infiltrate the treated area. Nude mouse skin reacted faster to PDA than did the grafts, but the histological changes were similar. Nude mouse hair follicles and sebaceous glands showed similar cellular changes at approximately the same time as did epidermal cells. Transmission electron microscopy of mouse skin exposed to PDA revealed a widening of intercellular spaces with attenuation of desmosomes. The subepidermal clefts resulted from separation within the lamina lucida with the lamina densa forming the base of the cleft. Diphenylchloroarsine caused lesions histologically indistinguishable from those of PDA. Lesions resulting from exposure to other sulfhydryl-binding compounds were very different from arsenical lesions. The arsenical-sensitive cellular constituents were not identified.

hair loss and hair loss treatment

Tohoku J Exp Med. 1977;121(1):1

Histochemical quantification of glucose-6-phosphate dehydrogenase activity in human hair follicles.

Sasai Y, et al

Glucose-6-phosphate dehydrogenase activity was studied in hair follicles from both the bald and hairy regions of the scalp of 5 patients with male pattern alopecia by the application of the method of Lineweaver-Burk to the histochemistry and by the fluorometric method of Lowry. In vitro experiment showed that the incubation time necessary for yielding a certain amount of formazan is related to the amount of enzyme present. In the case of section experiment, the time required for the first appearance of formazan deposition in the tissue at various substrate concentrations was plotted against the reciprocal of the substrate concentration. The data obtained by this method seem to be consistent with the data by the fluorometric method.

Br J Dermatol. 1997 Oct;137(4):491-7.

Topical FK506: a potent immunotherapy for alopecia areata?

McElwee KJ, et al

We elected to examine the efficacy of the topically applied immunosuppressive agent FK506 (Prograf) in the treatment of alopecia areata (AA) using the Dundee experimental bald rat (DEBR) model. Thirty lesional DEBR rats were allocated to five groups of six. Group 1 rats received 0.1 mL of a 0.25% solution of FK506 within a 2 x 2 cm marked area on one bald flank twice a week (125 micrograms FK506/cm2 per week) for 8 weeks, while the contralateral flank was left untreated. In group II, 0.05 mL of a 0.1% solution of FK 506 was applied 5 days per week on one flank (62.5 micrograms FK506/ cm2 per week) and control vehicle to the opposite flank for 8 weeks. Group III rats were treated as in group II except that drug and vehicle were applied twice a week (25 micrograms FK506/cm2 per week) for 4 weeks. A positive control group received orally administered cyclosporin A (CsA) (10 mg/kg daily) for 8 weeks and a further group was left untreated. Rats were regularly examined and photographed with skin biopsies taken from groups II and III. All FK 506-treated rats regrew hair at the site of drug application within 14-21 days. Growth continued for 3 weeks beyond termination of hair loss treatment after which gradual hair loss was observed. No hair growth was seen as a result of vehicle application and hair loss continued on untreated areas and in the untreated control group. Immunohistology revealed a drastic reduction in the follicular inflammatory infiltrate at the site of the FK506 application. The oral CsA group responded by simultaneous regrowth of hair over the whole body. Our findings suggest that FK506 may have considerable potential as a topical treatment for AA.