Hair Million, for hair growth




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Fatty acids resources:

Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5







Clin Endocrinol (Oxf). 1979;11(2):235-44.
The influence of bromocriptine on serum levels of growth hormone and other pituitary hormones and its metabolic effects in active acromegaly.

Roelfsema F, Goslings BM, Frolich M, Moolenaar AJ, Seters AP, Van Slooten H.

The effect of treatment with bromocriptine for 12--18 months on serum GH and metabolic responses was studied in sixteen patients with active acromegaly. Of this group ten patients showing a sustained GH reduction of more than 50% during an 8 h bromocriptine test, proved to be responsive to long-term therapy. In the responding patients GH levels decreased to 38% of the pretreatment level after 12 months of therapy. A dose higher than 10 mg did not produce a significantly greater effect. Prolactin and LH levels decreased in all patients, FSH levels showed a significant rise. Testosterone levels in the male patients increased significantly, indicating that the state of hypogonadism can at least be partially reversed. The GH levels became normal in only one patient. We conclude that the role of bromocriptine in acromagaly is limited and selective pituitary operation and/or irradiation is preferred as definitive treatment in most patients.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=114344&dopt=Abstract



Contraception. 1979 Aug;20(2):177-84.
Treatment of rhesus monkeys (Macaca mulatta) with intrauterine devices loaded with levonorgestrel.

Wadsworth PF, Heywood R, Allen DG, Sortwell RJ, Walton RM.

The effects of levonorgestrel-loaded plastic intrauterine devices on endometrial morphology were investigated in 15 rhesus monkeys for 14 weeks. The devices were designed to release 25 microgram of the hormone per day and were inserted in the uterus by hysterotomy. Control animals were sham operated or received inert placebo devices. With the levonorgestrel-releasing devices, widespread changes in endometrial morphology were seen. These changes included atrophy of the endometrial mucosal and glandular epithelium and decidualization of the endometrial stroma. With the inert placebo control devices, only minor changes in endometrial morphology were observed.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=114355&dopt=Abstract



Gut. 1979 Aug;20(8):653-9.
Distribution of the gut hormones in the primate intestinal tract.

Bryant MG, Bloom SR.

Reliable and specific radioimmunoassays have been developed for the gut hormones secretin, gastrin, cholecystokinin, pancreatic glucagon, VIP, GIP, motilin, and enteroglucagon. Using these assays, the relative pattern of distribution of the gut hormones has been determined using the same bowel extracts for all measurements. VIP occurred in high concentration in all regions of the bowel, whereas secretin, GIP, motilin, and CCK were predominantly localised in the proximal small intestine. Pancreatic glucagon was almost exclusively confined to the pancreas. Like VIP, enteroglucagon also exhibited a wide pattern of distribution but was maximal in the ileum. The acid ethanol extraction method that was used was found to be unsuitable for gastrin. On gel chromatography of the extracts, motilin and VIP eluted as single molecular species in identical position to the pure porcine peptides. CCK, pancreatic glucagon, enteroglucagon and GIP were all multiform.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=114457&dopt=Abstract



Horm Res. 1979;11(3):115-27.
Characterization of an in vitro method for demonstrating thyrotropin-releasing hormone-stimulated prolactin secretion.

Turpen C, Knigge KM.

Anterior pituitaries of normal adult male rats were subjected to synthetic thyrotropin-releasing hormone (TRH) treatment in an acute incubation system which employed pretreatment of the glands with plasma obtained from the donor animals. Following a 60-min preincubation period in a 1:1 mixture of Krebs-Ringer bicarbonate buffer (KRB) and plasma, media and hemipituitary prolactin (PRL) concentrations were significantly (p less than 0.01) increased after a 40-min treatment with 500 pg TRH. The TRH effect was absent among hemipituitaries preincubated in KRB alone. Plasma obtained from older donors was more potent than was plasma from younger rats in this effect. TSH secretion was markedly increased by 500 pg TRH, whether or not plasma preincubation was employed. A dose response of PRL release to concentrations of TRH from 100 pg to 6.0 ng was observed. Crude extracts of median eminence also effected enhanced PRL release using the plasma preincubation technique. The results suggest that plasma preincubation of explanted pituitaries increases PRL cell sensitivity to TRH, perhaps by enzymatic inactivation of endogenous TRH bound to cellular membrane receptors.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=114467&dopt=Abstract



Horm Res. 1979;11(3):128-41.
In vitro release of prolactin by thyrotropin-releasing hormone: influence of dopamine, thyroxine, and cycloheximide.

Turpen C, Knigge KM.

An acute incubation procedure, using explanted normal rat hemipituitaries pretreated with fresh plasma obtained from pituitary donor animals, was employed to further investigate the in vitro stimulation of prolactin (PRL release by thyrotropin-releasing hormone (TRH). Pretreatment with dopamine (0.1 microgram/ml) caused a 30-50% decrease in the amount of PRL released into incubation media; the inhibitory effect of dopamine was not reversed by treatment with 0.5-6.0 ng. TRH, although these TRH concentrations consistently stimulated PRL release from pituitaries not exposed to dopamine. Treatment with thyroxine (10(-6) to 10(-5) M) showed a competitive inhibition of thyrotropin release by TRH (0.5 ng), but was without effect on TRH-stimulated PRL release. Cycloheximide (100 microgram/ml) blocked a net increase in PRL levels. TRH, nevertheless, significantly increased PRL release in the presence of cycloheximide. The results indicate that neither dopamine nor thyroxine compete with TRH in causing PRL release, and that the TRH stimulation of PRL release is unrelated to ongoing levels of hormone synthesis.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=114468&dopt=Abstract








Prescription drugs, surgical hair transplantation, topical application of various oils or creams... Also prayer and wishing...
Hair Million is an alternative approach to hair loss problems. Anecdotes and personal experiences testify that it works. Hair Million shows positive results and improvement for age-related hair thinning and hair loss for a large fraction of people who take it. How does it work? Good question. The molecular biological or clinical mechanisms of action as to how Hair Million exactly works to help stop hair loss, and promote hair growth is completely unknown. The only evidences for the effecacy of Hair Million on hair growth are only anedotal and based on personal experiences. There has been no clinical trials or placebo controlled statistical analysis on the efficacy of Hair Million on hair loss and hair growth.
That's enough for many people. Also, there are two merits in the hair restoration herbal formula:
Firstly, HairMillion is comparatively inexpensive, and secondly, it is made only of herbs that are known to be safe when consumed in regular quantities. Herbs in Hair Million are also known for cardiotonic effects, meaning that the herbs will make your heart stronger.














DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells.







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