The gut microbiome has been implicated in a variety of neuropathologies with recent data suggesting direct effects of the microbiome on host metabolism, hormonal regulation, and pathophysiology. Studies have shown that gut bacteria impact host growth, partially mediated through the growth hormone (GH)/insulin-like growth factor 1 (IGF-1) axis. However, no study to date has examined the specific role of GH on the fecal microbiome (FMB) or the changes in this relationship following a traumatic brain injury (TBI). Current literature has demonstrated that TBI can lead to either temporary or sustained abnormal GH secretion (aGHS). More recent literature has suggested that gut dysbiosis may contribute to aGHS leading to long-term sequelae now known as brain injury associated fatigue and cognition (BIAFAC). The aGHS observed in some TBI patients presents with a symptom complex including profound fatigue and cognitive dysfunction that improves significantly with exogenous recombinant human GH treatment. Notably, GH treatment is not curative as fatigue and cognitive decline typically recur upon treatment cessation, indicating the need for additional studies to address the underlying mechanistic cause.

肠道微生物组与多种神经病理学有关，最近的数据表明微生物组对宿主代谢、激素调节和病理生理学有直接影响。研究表明，肠道细菌影响宿主生长，部分通过生长激素 (GH)/胰岛素样生长因子 1 (IGF-1) 轴介导。然而，迄今为止还没有研究探讨 GH 对粪便微生物组 (FMB) 的具体作用或创伤性脑损伤 (TBI) 后这种关系的变化。目前的文献表明，TBI 可导致暂时或持续的 GH 分泌异常(aGHS)。最近的文献表明，肠道菌群失调可能会导致 aGHS，从而导致长期后遗症，现在被称为脑损伤相关疲劳和认知 (BIAFAC)。在一些 TBI 患者中观察到的 aGHS 表现出复杂的症状，包括严重疲劳和认知功能障碍，通过外源性重组人 GH治疗可显着改善这些症状。值得注意的是，生长激素治疗并不能治愈，因为疲劳和认知能力下降通常在治疗停止后复发，这表明需要进行更多研究来解决潜在的机制原因。