忧郁症的根本原因可能是免疫系统产生的炎症
纽约—-免疫系统努力维持我们的体格健康，但它是否有可能是一些精神疾病的罪魁祸首呢？
"The immune system may play a significant role in the development of depression," Andrew Miller, a professor of psychiatry and behavioral sciences at Emory University School of Medicine, said Tuesday at a symposium on neuroscience and immunology at the New York Academy of Sciences. Evidence for this link has been mounting in recent years, and he described this research, which falls in the jauntily named field of psychoneuroimmunology, one of the most exciting recent developments in psychiatry.
“免疫系统对忧郁症的产生起重要作用，”在周二纽约科学院开展的有关神经系统科学与系统学的研讨会上，埃默里大学医学院的精神与行为学教授安德鲁.米勒是这么说的。近年来证实这一联系的证据正在增加，这一领域的研究得意地被命名为精神神经免疫学，他称为是近来精神学上最激动人心的发展。
Research has shown that depressed or stressed-out people tend to be more susceptible to medical ailments, such as infectious diseases and perhaps even cancer. But the correlation might also work in the opposite direction, Miller explained. People who are critically ill have about five to 10 times higher rates of depression, and that might not just be due to battling their illness, he noted. It could be stemming from underlying inflammation—a common bodily response to illness or injury.
研究表面患抑郁症或者是承受巨大压力的人脉特别容易得医学疾病，例如是传染性疾病，甚至是癌症。但是，米勒解释道，两者的相互关系有可能向相反的一面作用的。他说，换上急病的人得抑郁症的概率要高出大约5到10倍，这可能不是疾病引起的。可能是潜在的炎症引发的，这是身体里对疾病和损伤的正常反应。
Studies have shown that people with depression or bipolar disorder, both those who had a physical illness and those who were medically healthy, had higher levels of inflammation. And as the depression faded, so, too, did the evidence of inflammation. Similarly, a 2009 study showed that mice that with chronic inflammation showed depressive symptoms, but blocking a key inflammatory enzyme alleviated the downer behavior in the mice.
研究表明患抑郁症或躁郁症的人，不管是有身体疾病还是医学上认为健康的，均更容易得炎症。抑郁症痊愈后，炎症的症状也会消失。同样地，2009年一项研究指出患慢性炎症的老鼠表现出抑郁症的病征，然而，限制一种主要的炎性酶能减缓老鼠的沮丧行为。
The big discovery has been that depressed patients who have proven most resistant to traditional treatments (such as therapy or selective serotonin re-uptake inhibitor drugs) seem to have particularly high rates of inflammation. And in studies from the last few years, inhibiting inflammatory cytokines (signaling cells found in both the immune and nervous systems) seems to help alleviate depressive symptoms. Miller said that these results suggest that "cytokines might have an effect on fundamental dopamine synthesis," an important chemical process that, if thrown out of whack, can have big impacts on mood, energy and motivation.
对传统的治疗，诸如对治疗或选择性血清素再吸收抑制物，最为排斥的抑郁症病患者似乎尤其容易得炎症，这个发现是重大的。在过去几年的研究中，抑制炎症因子（在免疫系统和神经系统都可找到的信号细胞）似乎能够减缓抑郁症的症状。米勒表示，这些结果表明“细胞因子对基本的多巴胺合成有影响”，这是一个重要的化学反应过程，如果失衡，就会对情绪，精力和积极性产生重大影响。
If this association holds, keeping inflammatory cytokines in check could also help treat conditions beyond classic depression, such as cancer-related fatigue or even chronic fatigue syndrome, Miller noted. And because much of the inflammation in question seems to be coming from outside of the brain—the periphery, as the neuroscientists like to call it—new depression-targeting drugs might not even have to cross the blood-brain barrier to have palliative effects.
米勒说，如果这种联系是真的话，抑制炎性因子可以有助于治疗除了典型的抑郁症外的病，如癌因性疲倦甚至是慢性疲劳综合症。因为尚存在疑问的炎症好像都源于大脑之外——神经学家喜欢称之为神经末梢——那么新的治疗抑郁症的药物或许不用经过血脑障碍就能产生姑息性治疗作用。
抑郁症有时只是炎症“反应”
加州大学洛杉矶分校临床心理学家George Slavich研究抑郁症多年，他认为，抑郁症不仅与心理有关，也与生理和身体健康有关。首先，许多炎症相关疾病都会表现抑郁样行为。生病时几乎每个人都会觉得疼痛、疲倦、无聊和不爱动。这是生物进化中获得的保护性反应，疾病后的这些表现能让我们减少活动，保存体力，应对其他可能的伤害。这种表现和抑郁症患者的表现并没有差别。这种相似性表现是否来自共同的原因，或许真的存在共同的基础，科学家首先考虑到的共同原因是炎症。炎症反应是免疫系统为清除有害刺激或病源体，促进组织修复的保护措施，各种促炎性因子会引发人体组织发炎。抑郁症发病期间炎性细胞因子释放和炎症反应都显著活跃。炎症因子在外周的效应是产生炎症反应，在中枢的作用是启动抑郁样行为。抑郁症患者不仅有炎症因子增加，也有炎症反应增强，健康人会因为接种疫苗后炎症反应出现暂时抑郁或焦虑状态。大脑成象研究发现患者注射伤寒疫苗后大脑奖赏惩罚中枢发生改变。各种炎症相关疾病如生产后、糖尿病、中风等患者都容易发生抑郁症，类风湿患者发生抑郁症的几率也明显超过健康人。为促进炎症反应对抗癌细胞，有时候会给癌症患者注射干扰素，这种情况下，患者经常表现出抑郁样副作用。一些科学家开始寻找抑郁症患者是否存在原发炎症性疾病，纽约州立大学石溪分校Turhan Canli教授认为，感染是最有可能的炎症诱因（这个判断似乎过于武断，尤其是当前代谢性或无菌性炎症研究热潮下），他甚至认为抑郁症就是一种感染性疾病。
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