Fitoestrogeni alla riscossa:
http://www.ncbi.nlm.nih.gov/pubmed/21738079
ma quello veramente interessante è il brevetto:
http://patents.com/us-20110091435.html
Alcuni passi, a mio avviso, importanti:
The female sex hormone, estrogen, is generally recognized as a promoter of scalp hair growth and an inhibitor of hair growth elsewhere on the body. In that respect, estrogen has the opposite effects of the male sex hormone, testosterone, which can be converted to dihydrotestosterone (DHT). Prior to menopause, while estrogen levels are high, the level of DHT being produced in the skin and follicle region is kept low. When women enter menopause, their levels of estrogen decline with the result that testosterone becomes more bioactive and more of it is converted to DHT in hair follicles. This results in a shorter hair growth cycle, finer hair and eventually, general hair loss.
An increase in estrogen levels is proven to be beneficial for alleviating or stopping hair loss. Indeed, estrogen has been prescribed by physicians to treat hair loss in women. However, the excess of estrogen can promote various diseases such as breast cancers, which prevents the use of such a therapy in Xxxxxx.
[0010] Androgenic alopecia or male pattern baldness (MPB) accounts for more than 95% of hair loss in men. By the age of 35, two-thirds of American men will experience some degree of appreciable hair loss. By the age of 50, approximately 85% of men have significantly thinning hair. Approximately 25% of men who suffer with MPB begin the painful process before they reach the age of 21.
[0012] It has been suggested that estrogen may also offer some benefits in treating MPB. However, due to the feminizing effects of estrogen, use of estrogen in men has been very limited.
[0013] Two nuclear receptors for estrogen (ERs), ER.alpha. and ER.beta., have been identified. In the central nervous system, both ER.alpha. and ER.beta. are expressed in the hippocampus and cortex of rodent and human brains. Previous studies have demonstrated that both ER.alpha. and ER.beta. can equivalently promote neuronal survival by activating estrogen mechanisms of action in rat hippocampal neurons. Increasing evidence indicates that ER.beta. is a key requirement for activation of mechanisms that underlie estrogen-inducible neuronal morphological plasticity, brain development, and cognition. ER.alpha., on the other hand, is more predominant in mediating the sexual characteristics of estrogen effects in the reproductive organs such as breast and uterus. Taken together, these data establish a potential therapeutic application for ER.beta. as a pharmacological target to promote memory function and neuronal defense mechanisms against age-related neurodegeneration such as Alzheimer's disease (AD), while avoiding activating untoward estrogenic proliferative effects in the breast and uterus, although this might be at the cost of lower efficacy due to the lack of activation of ER.beta. in the brain. Other potential therapeutic advantages associated with ER.beta. include regulation of estrogen vasculoprotective action and development of interventions targeting diseases such as depression, colon cancer, prostate cancer, obesity, leukemia, and infertility. However, a potential disadvantage of an ER.beta.-selective ligand is the lack of activation of ER.alpha. in bone, as ER.alpha. has been demonstrated to mediate estrogen regulation of bone density.
[0014] In searching for an effective ER.beta.-selective estrogen alternative replacement therapy for preventing hair loss, promoting neurological function and preventing age-related neurodegeneration, such as AD, in postmenopausal women, it is of particular interest to identify and develop naturally occurring molecules or analogues that potentially have a less toxic profile for long-term administration. It is known that several plant-derived estrogenic molecules (referred to as phytoestrogens) bind to ER.alpha. and to ER.beta. subtypes, and some of these molecules possess moderate binding selectivity for ER.beta. and exert estrogenic effects in multiple tissues.
Soy extracts or soy protein supplements generally contain multiple phytoestrogenic molecules, some of which may be ER.alpha.-selective agonists, while others may be ER.beta.-selective agonists, and others may be ineffective in activating either ER.alpha. or ER.beta. but may function as inhibitors of ER binding of those ER.alpha. and/or ER.beta. phytoestrogenic agonists.
It is therefore an object of the present invention to provide an ER.beta.-selective phytoestrogen formulation maximizing the therapeutic benefits associated with activation of ER.beta. while minimizing the adverse effects associated with the activation of ER.alpha. in reproductive tissues.
Compositions containing one or more phytoestrogens are described herein. A number of phytoestrogens have been isolated and identified and additional analogs created, all of which have estrogen receptor binding selectivity. In one embodiment, the composition contains two or more plant-derived estrogenic molecules and/or structural analogues, which possess ER.beta.-binding selectivity and exhibit neuroprotective activity when administered individually. These compositions are useful for preventing estrogen-deficiency associated symptoms and disorders, particularly age-related cognitive decline and neurodegenerative diseases, such as Alzheimer's disease (AD). The compositions are also useful for minimizing or preventing one or more symptoms of menopause including, but not limited to, hot flashes, hair loss/thinning, mood changes, insomnia, fatigue, memory problems, and combinations thereof. Some studies have suggested that ER.beta. is the predominant ER and the main mediator of estrogen action in human skin and hair follicles. With respect to hair growth, ER.beta. is believed to play a regulatory role on androgen receptor expression in hair follicles leading to a promoting effect on hair growth. Since estrogen's feminizing effects are mainly mediated by ER.alpha., where ER.beta. is less involved, ER.beta. should represent a safer therapeutic target for promoting estrogenic actions, for example, hair growth, without exerting feminizing activities.
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