Department of Chemistry, University of New England, Armidale, NSW 2351, Australia.
J Ethnopharmacol. 2018 Dec 5;227:206-236. doi: 10.1016/j.jep.2018.09.009. Epub 2018 Sep 6.
Research in the past half a century has gradually sketched the biological mechanism leading to androgenetic alopecia (AGA). Until recently the aetiological paradigm has been too limited to enable intelligent commentary on the use of folk remedies to treat or reduce the expression of this condition. However, our understanding is now at a point where we can describe how some folk remedies work, predict how effective they will be or why they fail.
The new paradigm of AGA is that inheritance and androgens (dihydrotestosterone) are the primary contributors and a secondary pathology, microinflammation, reinforces the process at more advanced stages of follicular miniaturisation. The main protagonist to microinflammation is believed to be microbial or Demodex over-colonisation of the infundibulum of the pilosebaceous unit, which can be ameliorated by antimicrobial/acaricidal or anti-inflammatory therapies that are used as adjuvants to androgen dependent treatments (either synthetic or natural). Furthermore, studies reveal that suboptimal androgen metabolism occurs in both AGA and insulin resistance (low SHBG or high DHT), suggesting comorbidity. Both can be ameliorated by dietary phytochemicals, such as specific classes of phenols (isoflavones, phenolic methoxy abietanes, hydroxylated anthraquinones) or polycyclic triterpenes (sterols, lupanes), by dual inhibition of key enzymes in AGA (5α-reductase) and insulin resistance (ie., DPP-4 or PTP1B) or agonism of nuclear receptors (PPARγ). Evidence strongly indicates that some plant-based folk remedies can ameliorate both primary and secondary aetiological factors in AGA and improve insulin resistance, or act merely as successful adjuvants to mainstream androgen dependent therapies.
Thus, if AGA is viewed as an outcome of primary and secondary factors, then it is better that a 'multimodal' or 'umbrella' approach, to achieve cessation and/or reversal, is put into practice, using complementation of chemical species (isoflavones, anthraquinones, procyanidins, triterpenes, saponins and hydrogen sulphide prodrugs), thereby targeting multiple 'factors'.
在过去半个世纪的研究中，逐渐勾勒出导致雄激素性脱发（AGA）的生物学机制。直到最近，病因学范例还过于局限，无法对民间疗法治疗或减轻这种情况的表达进行明智的评论。然而，我们的理解现在已经到了可以描述一些民间疗法如何发挥作用、预测它们的有效性或为什么它们会失败的地步。
AGA 的新范例是遗传和雄激素（二氢睾酮）是主要贡献者，而二级病理学，微炎症，在毛囊微型化的更高级阶段加强了这个过程。微炎症的主要主角被认为是微生物或 Demodex 在毛囊单位的漏斗部过度定植，这可以通过抗菌/杀螨或抗炎疗法来改善，这些疗法被用作雄激素依赖性治疗（无论是合成的还是天然的）的辅助剂。此外，研究表明，AGA 和胰岛素抵抗（低 SHBG 或高 DHT）中都存在雄激素代谢不佳，表明存在合并症。这两者都可以通过饮食中的植物化学物质来改善，例如特定类别的酚类（异黄酮、酚甲氧基松香烷、羟基蒽醌）或多环三萜（甾醇、羽扇豆烷），通过对 AGA（5α-还原酶）和胰岛素抵抗（即 DPP-4 或 PTP1B）的关键酶的双重抑制，或对核受体（PPARγ）的激动作用。有证据强烈表明，一些基于植物的民间疗法可以改善 AGA 中的主要和次要病因因素，并改善胰岛素抵抗，或者仅仅作为主流雄激素依赖疗法的成功辅助剂。
因此，如果将 AGA 视为主要和次要因素的结果，那么最好采用“多模式”或“伞状”方法，通过补充化学物质（异黄酮、蒽醌、原花青素、三萜、皂苷和硫化氢前药）来实现停止和/或逆转，从而针对多个“因素”。
