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Gan To Kagaku Ryoho 2003 Jan;30(1):105-9
Weekly administration of paclitaxel and pirarubicine for recurrent breast cancer
The therapeutic efficacy of weekly coadministration of paclitaxel (TXL) and pirarubicin (THP) on docetaxel (TXT)- and epirubicin-resistant recurrent breast cancer, adverse reactions caused by this therapy, and the possibility of ambulatory treatment using it were evaluated. The present study was conducted in 11 patients with recurrent breast cancer with pretreatment with CEF and TXT. The site of recurrence was the lung in 9 patients, lymphnodes in 2, bones in 1, liver in 1 and local foci in 1. One cycle consisted of 20 mg/m2 of THP followed by 80 mg/m2 of TXL 4 h later, repeated three times every other week. Three to six cycles were conducted in each patient. An anti-emetic drug was administered before administration of THP as short premedication. Dexamethasone (16 mg; i.v.) and d-chlorpheniramine maleate (12 mg; p.o.) were administered 1 h before administration of TXL and ranitidine (100 mg; i.v.) was administered 30 min before administration of TXL. Ubidecarenone (30 mg/day; p.o.) was administered for 3 days. The response rate was 27.3% with a rating of PR in 3 patients, NC in 6, and PD in 2. Adverse reactions observed included transient facial hot flushes, alopecia grade 1 or milder grade 1 symptoms, and peripheral nerve damage. No adverse reactions such as myocardial disorders or congestive heart failure were noted. Grade 3 and grade 2 neutropenia occurred in 1 and 6 patients, respectively, and 4 patients were admitted for treatment of this. In conclusion, the short premedication was useful, and this was thought to make it possible to conduct ambulatory treatment with TXL + THP in some patients. The response rate of 27.3%, however, was not satisfactory. It will be necessary to clarify the characteristics of this therapy by administering it to a wider spectrum of patients.
J Am Acad Dermatol 2002 Nov;47(5):795
Female pattern hair loss.
In this issue of the Journal (pages 733-9), Shum et al1 describe 4 female patients with increased androgens whose central scalp hair loss responded to finasteride. This is an important observation and one that highlights why the term androgenetic or androgenic alopecia, as used to describe the hereditary pattern balding of men, should be replaced with the term female pattern hair loss when applied to women.2 It is clear that only a small but distinct subset of women with central scalp pattern hair loss, such as the patients presented in the report by Shum et al, has signs of hyperandrogenism such as acne, hirsutism, and irregular periods with or without elevation of serum androgens. Therefore these women may have hair loss resulting from a different mechanism and may respond differently to treatments targeted at androgen blockade than women with a similar type of hair loss but without evidence of hyperandrogenism. Certainly these women with hyperandrogenemia may develop, in contradistinction to those without hyperandrogenemia, a Hamilton pattern of hair loss (male pattern baldness). Many of these women may, on more careful evaluation, have polycystic ovarian syndrome.
It is not surprising that a 5-reductase inhibitor such as finasteride, which has documented efficacy in men with androgenetic alopecia3,4 and has been shown to advantageously affect hirsutism,5,6 may cause hair growth in women with female pattern hair loss and hyperandrogenism. The fact that finasteride has not previously been shown to induce hair growth in postmenopausal women with “androgenetic alopecia”7 speaks for (1) adoption of different terminology for this type of hair loss in women and (2) separate evaluation of the different subgroups of women with female pattern hair loss as recently described,2 that is, early onset with and without hyperandrogenemia and late onset/postmenopausal with and without hyperandrogenemia. We should not be too quick to rule out efficacy of a potential therapeutic agent in all women with female pattern hair loss without first testing it in all the various subsets of women.
Clearly, finasteride may be an effective treatment for women with early-onset female pattern hair loss and hyperandrogenemia, but definitive results would require a large, well-controlled trial. Such a trial would likely necessitate inclusion of a “placebo” run-in phase with an oral contraceptive, both to protect these women of child-bearing potential from getting pregnant while taking a drug known to cause genital abnormalities in male fetuses and to rule out any effect from the oral contraceptive alone on female pattern hair loss (a study that needs to be conducted in any case). Anecdotal reports, such as that presented by Shum et al,1 should ignite interest in evaluating finasteride and other 5-reductase inhibitors, either type II or combination type I/II, in women with female pattern hair loss, a group of patients whose current treatment options are extremely limited.
J Invest Dermatol. 2003 May;120(5):771-5.
Major locus on mouse chromosome 17 and minor locus on chromosome 9 are linked with alopecia areata in C3H/HeJ mice.
Alopecia areata is an autoimmune disease that targets actively growing (anagen) hair follicles in humans, mice, rats, dogs, horses, and cattle. C3H/HeJ mice spontaneously develop alopecia areata from 5 mo of age and older in females and later in males. Frequency of disease approached 20% in a colony by 18 mo of age. C57BL/6J mice do not develop alopecia areata. A segregating F2 population of female mice (n=1096) was generated from crossing these two strains. Alopecia areata (n=138) and clinically normal (n=214) mice were genotyped at 12 mo of age using 211 microsatellite probes. The peak logarithm of odds ratio score on mouse chromosome 17 (10.9) was around marker D17Mit134 at 16.9 cM from the centromere. The mouse histocompatibility locus, H2, the mouse equivalent of human leukocyte antigen in humans, was a likely candidate. Twelve-month-old C3H.SW-H2b/SnJ mice (C3H/HeJ congenic mice in which the H2k purported susceptibility locus was replaced with the H2b purported resistance locus) did not develop alopecia areata, supporting this locus as being important in alopecia areata. A suggestive linkage was also found on mouse Chromosome 9 (logarithm of odds ratio score 2.0) around D9Mit206, 20 cM from the centromere. The interval on mouse Chromosome 17 contains several orthologous genes potentially associated with human alopecia areata.
Hum Genet. 2003 Apr;112(4):400-3. Epub 2003 Feb 14.
Notch4, a non-HLA gene in the MHC is strongly associated with the most severe form of alopecia areata.
Alopecia areata (AA) is a disorder primarily affecting the hair and nails in which associated autoimmune or atopic disease is common. Genetically, it is a complex trait with evidence of a role for genes of the major histocompatibility complex (MHC), the interleukin-1 cluster and chromosome 21 in the pathogenesis. The strongest association is with HLA class II alleles, although whether this indicates a direct contribution to the pathogenesis or results merely from linkage disequilibrium with nearby disease genes is unknown. Notch4 is a recently defined gene in the HLA class III region. Notch signalling is a direct determinant of keratinocyte growth arrest and entry into differentiation. A possible role for Notch in hair growth has been indicated by transgenic mouse findings that activation of the Notch pathway in the hair cortex leads to aberrant differentiation of adjacent hair-shaft layers. Notch4 is therefore a plausible candidate gene for AA. We have examined two polymorphisms in the coding sequence of the Notch4 gene at positions +1297 and +3063 in a case-control study of 116 AA patients and 142 ethnically matched, healthy control subjects. The initial analysis showed a significant association of AA in the overall data set with the Notch4(T+1297C) polymorphism (P<0.001) but not with Notch4(A+3063G). To confirm this association, we genotyped an additional 62 patients and found that the risk for disease was higher in Notch4(+1297C) homozygotes [odds ratio (OR) 3.43 (1.63, 7.19)] than in heterozygotes [OR 2.58 (1.57, 4.24)]. On classifying the patients by severity of disease, the association appeared to be confined to the severest form (alopecia universalis) [OR 4.02 (1.64, 9.88), P=0.0014]. These results support previous findings showing that different HLA susceptibility alleles are associated with mild and severe AA.
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