Some issues related to the stress of winter: “Winter sickness” occurs when there isn't enough daylight to allow us to recover from nocturnal stress. The stress related hormones rise at night, and winter nights are long. The inadequate light produces thyroid and progesterone deficiencies. A progesterone or thyroid deficiency, or estrogen and polyunsaturated fat excess, cause serotonin to increase. Cold, dark, and even minor stresses cause increased serotonin. The amino acid tryptophan can be metabolized into serotonin, which can be converted into melatonin. More than twenty years ago, tryptophan was being promoted as a sedative, even though it was known to be the only amino acid that is carcinogenic. In excess, it suppresses the function of the thyroid gland. A protein deficiency releases tryptophan from muscles. A “serotonin deficiency” was often said to cause depression. Hydroxy tryptophan (5-HTP) is sold as a serotonin precursor that is supposed to improve mood. Many kinds of stress cause serotonin's activity to increase. Melatonin has been sold as a sleeping pill, longevity pill, and anticancer agent. Its production in the body is stimulated by stress and darkness. Light, especially red light, penetrates into the body, and suppresses free radical activity and activates the crucial respiratory enzyme, cytochrome oxidase, which is activated by thyroid, and which is inactivated by polyunsaturated fats. Serotonin released from platelets causes blood clotting and vascular spasms, and stimulates cell division. It and histamine are mediators of inflammation that cause blood vessels to leak. Serotonin ,triggers the release of the stress hormones, ACTH, cortisol, and prolactin. People often gain weight during the winter; in the far north, blood tryptophan is elevated in the winter; depressed women have' increased melatonin, alcohol lowers melatonin; alcohol consumption is increased by darkness. The use of anti-serotonin drugs in alleviating stroke, hypertension, heart failure, diabetes, depression, obesity, rheumatoid arthritis, lupus (SLE), fibrosis, wheezing, and migraine suggests the importance of hyperserotonemia in causing disease.
与冬季压力相关的一些问题： “冬季病”发生在没有足够的阳光让我们从夜间压力中恢复过来的时候。与压力相关的激素在夜间升高，冬夜很长。 光线不足会导致甲状腺和孕酮缺乏。 孕酮或甲状腺缺乏，或雌激素和多不饱和脂肪过多，会导致血清素增加。寒冷、黑暗，甚至轻微的压力都会导致血清素升高。 氨基酸色氨酸可以代谢成血清素，血清素可以转化为褪黑素。 二十多年前，色氨酸作为一种镇静剂被推广使用，尽管它是已知的唯一致癌氨基酸。过量的话，它会抑制甲状腺的功能。蛋白质缺乏会从肌肉中释放色氨酸。 人们常说“血清素缺乏症”会导致抑郁症。羟基色氨酸（5-HTP）是一种5-羟色胺前体，被认为可以改善情绪。许多种压力都会导致血清素的活性增加。 褪黑素作为安眠药、长寿药和抗癌剂销售。它在体内的产生受到压力和黑暗的刺激。 光，特别是红光，穿透人体，抑制自由基活性，激活关键的呼吸酶细胞色素氧化酶，该酶被甲状腺激活，被多不饱和脂肪灭活。 血小板释放的5-羟色胺会导致血液凝结和血管痉挛，并刺激细胞分裂。它和组胺是导致血管渗漏的炎症介质。 血清素，触发应激激素ACTH、皮质醇和催乳素的释放。人们在冬天经常发胖；在遥远的北方，血液色氨酸在冬季升高；抑郁的女性“褪黑激素增加，酒精降低褪黑激素；黑暗增加了酒精的消耗量。 抗5-羟色胺药物在缓解中风、高血压、心力衰竭、糖尿病、抑郁症、肥胖、类风湿性关节炎、狼疮（SLE）、纤维化、喘息和偏头痛方面的应用表明，高睾酮血症在致病中具有重要作用。
When I read, in the early 1950s, about the cyclical peaks of mortality in the early morning hours and winter months, that had been evident in actuarial tables for a long time, it wasn't hard to accept that light was good for us, and that darkness was harmful. “Chronobiology,” the awareness that biological responses are dependent on the time of day, was firmly established by the 1950s.
20世纪50年代初，当我读到关于早起时间和冬季月份的周期性死亡高峰，这在精算表中已经很明显很长一段时间了，我不难接受光对我们是好的，而黑暗是有害的。“时间生物学”，即生物反应依赖于一天中的时间的意识，在20世纪50年代已经牢固确立。
“…Tryptophan transport was increased in the major depressions and in the dysthymic disorders.” D. Pringuey,' et al., 1986. “…色氨酸转运在主要抑郁症和恶劣心境障碍中增加。”D.Pringuey等人，1986年。
“ …We propose that there is a hyperserotonergic state in the hippocampal formation of some subjects with schizophrenia….” E. Scarr, D.L. Copolov, B. Dean, L. Rebecca. > “……我们认为，一些精神分裂症受试者的海马结构中存在一种超促性欲状态……”E.Scarr, D.L.Copolov，B.Dean，L.Rebecca > > “ …a hyperserotonemic condition has been documented in preeclampsia.” Carrasco, et al., 2000. > “先兆子痫患者存在高性激素血症。”Carrasco等人，2000年。 > > “Both melatonin and serotonin were potent inhibitors of progesterone release.” Schaeffer and Sirotkin, 1997. > “褪黑素和5-羟色胺都是孕酮释放的有效抑制剂。”Schaeffer和Sirotkin，1997年
Beginning in the 1950s, when I would spend the summers working in the woods, I noticed effects of sunlight that I didn't understand, such as the worsening of acne in proportion to the amount of sun exposure, as well as during times of stress. In 1965, I noticed that even incandescent light exposure during the night could immediately provoke my acne, so I realized that ultraviolet irritation wasn't the essential factor. First I thought the eyes' consumption of vitamin A might be responsible, since taking additional vitamin A would control my acne, but then I realized that an extended photoperiod stimulated the sex hormones, and that this increased demands for vitamin A.
从20世纪50年代开始，当我夏天在树林里工作的时候，我注意到阳光的影响，我不理解，例如，痤疮的恶化与阳光照射量成比例，以及在压力时期。1965年，我注意到即使在夜间暴露在白炽灯下也会立即引发我的痤疮，因此我意识到紫外线刺激不是根本因素。首先我认为眼睛对维生素A的消耗可能是原因，因为补充维生素A可以控制我的粉刺，但后来我意识到延长光周期刺激性激素，这增加了对维生素A的需求。
When I moved to the northern US from Mexico in 1965, I began noticing other interesting hormonal and nutritional effects relating to the seasons. In the winter of 1966-67 I began referring to “winter sickness” as the consequence of the hormonal changes produced by a lack of light exposure. Women who moved from a sunny climate to cloudy Eugene, and who often lived in gloomy basement apartments while they were at the university, described premenstrual depression and other symptoms that they had never experienced before. Many serious diseases had their onset during these times of light deprivation and hormonal upset.
1965年我从墨西哥搬到美国北部时，我开始注意到与季节有关的其他有趣的荷尔蒙和营养作用。1966年至1967年的冬天，我开始提到“冬季病”，这是由于缺乏光照而引起的荷尔蒙变化的结果。从阳光明媚的气候搬到多云的尤金的女性，她们在大学期间经常住在阴暗的地下室公寓，她们描述了她们从未经历过的经前抑郁症和其他症状。许多严重的疾病都是在光线缺乏和激素紊乱的时期发病的。
I submitted some of my observations on winter sickness to various journals, and didn't get any responses from most of the editors, except for occasional sarcastic remarks about how ridiculous it is to suggest that *light *would have biological or psychological effects on humans.
我向各种杂志提交了一些关于冬季疾病的观察结果，大多数编辑都没有回应，只是偶尔讽刺地说，光会对人类产生生物或心理影响是多么荒谬。
Since 1966 I had been including a discussion of light's effects in my classes on nutrition and hormones and aging, and in the early seventies I began travelling around to talk to health-food, alternative medicine, and church groups, and to talk on occasional radio and television programs, where I would emphasize the importance of good light along with good nutrition. I found that the general public, and especially so-called “conservative” people, were remarkably receptive to ideas of interactions between organism and environment, and between mood and chemistry. I think their receptiveness had to do with the attitude called “paranoia,” an attitude that has its positive features, as Salvador Dali observed.
从1966年开始，我就在课堂上讨论光对营养、激素和衰老的影响。70年代初，我开始四处旅行，与健康食品、替代医学和教会团体交谈，偶尔在广播和电视节目中交谈，在这里，我要强调良好的光照和良好的营养的重要性。我发现，公众，尤其是所谓的“保守派”人士，对于生物体与环境、情绪与化学之间的相互作用的观点非常容易接受。我认为他们的接受能力与被称为“偏执狂”的态度有关，正如萨尔瓦多·达利所观察到的，这种态度有其积极的特点。
Professional people, especially journal editors, on the other hand, seemed to suffer from a mental rigidity that was the polar opposite of paranoia, a belief that nothing was happening outside of the set of beliefs residing in their own minds. This is a psychiatric condition that can be called “editorness,” or simply “professionalism.”
另一方面，专业人士，尤其是期刊编辑，似乎患有一种与偏执症截然相反的精神僵硬症，一种认为在他们自己头脑中的一套信念之外什么都没有发生的信念。这是一种精神疾病，可以称为“编辑性”或简单的“专业性”
Although no journal or magazine had responded favorably to my articles on winter sickness and light therapy, some of those editors later began publishing similar observations by themselves or others, and by 1985 “Seasonal Affective Disorder” was becoming something like a “movement,” with people arguing about the proper use of “light panels” and phase-shifting of melatonin, and even direct supplementation of melatonin. When its factors are reduced to a minimum, usually two, a new thought can sometimes penetrate into the professional mentality, though they are likely' to get one or both of those factors wrong, as often as not. The use of bright light to treat depression should have made people realize that a melatonin excess contributed to depression, but that simple idea has been generally evaded.
尽管没有一家杂志或杂志对我关于冬季疾病和光疗法的文章做出了积极的回应，但这些编辑中的一些人后来开始发表自己或他人的类似观察结果，到1985年，“季节性情感障碍”变得有点像一场“运动”，人们在争论如何正确使用“光面板”以及褪黑素的相移，甚至直接补充褪黑素。当它的因素减少到最低限度（通常是两个）时，一个新的想法有时会渗透到职业心理中，尽管他们很可能“把这些因素中的一个或两个都弄错了，但往往不会。使用强光治疗抑郁症应该让人们意识到褪黑激素过量会导致抑郁症，但这个简单的想法通常被回避了。
The reluctance to see any connection between mood and hormones, or between light and health, probably resulted from an education in which there was already an explanation for everything. Now that medicine accepts a role for light and hormones in mood and behavior, it is within a culture dominated by Estrogen Replacement Therapy and Selective Serotonin Reuptake Inhibitors, such as Prozac. When there is a product for everything, explanations are degraded, and professionalism reaches a new low. The use of Prozac and similar drugs to treat PMS is an example of how product-professionalism works. (Its action in PMS is probably the result of increasing a brain steroid, compensating for a progesterone deficiency, exactly contrary to the doctrine that it acts by increasing serotonin availability.)
人们不愿意看到情绪和荷尔蒙之间，或者光线和健康之间的任何联系，这可能是因为教育中已经有了对一切的解释。现在，医学接受了光和激素在情绪和行为中的作用，它处于一种以雌激素替代疗法和选择性5-羟色胺再摄取抑制剂（如百忧解）为主的文化中。当每件事都有一个产品时，解释力就会降低，专业性就会达到新低。使用百忧解和类似药物治疗经前综合症就是产品专业化运作的一个例子。（它在经前综合症中的作用可能是由于增加了脑类固醇，以补偿孕酮缺乏，这与它通过增加血清素可用性而起作用的学说完全相反。）
People who believe that there is a “biological clock” in the brain· think that light signals entering through the eye provide the cues that set the clock, and that the brain then organizes the behavior that's appropriate for the season and time of day. But pigeons wearing opaque hoods can sense environmental light if the rest of their body is uncovered. The same sort of bodily sensitivity to light was demonstrated by shining light onto the back of a person's knee.
相信大脑中有一个“生物钟”的人认为，通过眼睛进入的光信号提供了设定生物钟的线索，然后大脑组织适合一天中季节和时间的行为。但是，如果身体其他部位没有遮盖，戴着不透明头巾的鸽子可以感觉到环境光。同样的身体对光线的敏感性也通过将光线照射到人的膝盖后部来证明。
Instead of a “clock” that consists of some procedure for counting enzyme reactions or DNA oscillations or something of the sort, for which there is not even a clear theory, I think the evidence supports the idea that physiological states reflect the organism's relation to the environment, and that, in the absence of the necessary amount of light and heat from the environment, energy stores in the form of glycogen become depleted, creating hunger and a variety of stress reactions. It takes some time to deplete glycogen stores, and it takes time to assimilate food, and so hunger and satiation tend to be cyclic, but it isn't productive to call these processes “a biological clock.”
我认为证据支持生理状态反映生物体与环境的关系这一观点，而不是一个由计算酶反应、DNA振荡或诸如此类的过程组成的“时钟”，甚至没有明确的理论，在缺乏来自环境的必要数量的光和热的情况下，以糖原形式储存的能量会耗尽，造成饥饿和各种应激反应。消耗糖原储存需要一段时间，消化食物也需要一段时间，因此饥饿和饱腹往往是周期性的，但将这些过程称为“生物钟”是没有成效的
Mitochondria change their shape and function during the night, becoming radically less effective at producing energy. Light regenerates the crucial cytochrome oxidase enzyme, creating the energy needed to repair mitochondria. During darkness, glycogen stores in the liver, brain and other tissues are used rapidly, because of the mitochondrial respiratory inefficiency. Fats are mobilized from storage under the influence of adrenalin that rises when glucose is scarce. Rapid eye movement sleep, the phase of active dreaming, increases with hunger, and the arousal subsides cyclically as adrenalin is suppressed by other adjustments, including increased cortisol, melatonin, GABA, and many other regulatory substances and processes.
线粒体在夜间改变其形状和功能，从根本上降低了产生能量的效率。光再生关键的细胞色素氧化酶，产生修复线粒体所需的能量。在黑暗中，储存在肝脏、大脑和其他组织中的糖原被迅速利用，因为线粒体呼吸效率低下。脂肪是在葡萄糖缺乏时肾上腺素升高的影响下从储存中动员出来的。快速眼动睡眠是积极做梦的阶段，随着饥饿而增加，随着肾上腺素受到其他调节（包括皮质醇、褪黑激素、GABA和许多其他调节物质和过程的增加）的抑制，觉醒周期性消退。
Light suppresses melatonin and serotonin, but its action is biological and biochemical, not just informational–it's a component of our metabolism, not just a “cue.” Our biological rhythms, of approximately 24 hours, do have a learned component, but Frank A. Brown's experiments in the 1960s made it clear that there are important rhythmic environmental influences other than the cycle of light and dark. Brown's biological experiments were complemented by Alexandre Rothen's physical experiments which made it clear that the diurnal cycles aren't just light cues. In the university's hamster house where I worked, the cycles of light and dark were automatically controlled, air temperature was kept constant, and there were no windows, but in the winter the hamsters' thymus glands practically disappeared, and then in the summer they were restored. The infrared and microwave radiation of the environment, that can penetrate walls, must be constant to avoid biological stress.
光抑制褪黑素和血清素，但它的作用是生物和生化的，而不仅仅是信息——它是我们新陈代谢的一个组成部分，而不仅仅是一个“线索”。我们大约24小时的生物节律确实有一个习得的组成部分，但是Frank A.Brown在20世纪60年代的实验清楚地表明，除了光与暗的循环之外，还有重要的节奏性环境影响。布朗的生物学实验得到了亚历山大·罗森物理实验的补充，该实验清楚地表明，昼夜循环不仅仅是光的信号。在我工作的大学仓鼠房里，光线和黑暗的循环被自动控制，空气温度保持恒定，没有窗户，但在冬天仓鼠的胸腺几乎消失了，到了夏天它们又恢复了。可以穿透墙壁的环境红外和微波辐射必须保持恒定，以避免生物压力。
Winter, at least in some species, causes serotonin to increase. (Philo and Reiter, 1980) In the winter, and in the morning, intraocular pressure (lOP) increases (Qureshi, et al., 1999), and drugs that antagonize serotonin reduce lOP. Women, on average, have higher lOP than men, and estrogen increases lOP (and serotonin).
冬天，至少在某些物种中，会导致血清素增加。（Philo和Reiter，1980）在冬季和早晨，眼压（lOP）升高（Qureshi等人，1999年），对抗血清素的药物降低lOP。平均而言，女性的lOP高于男性，雌激素会增加lOP（和血清素）。
Serotonin is a mediator of inflammation that suppresses metabolism, disturbs blood pressure, and promotes clotting, 'so it would be a Manichean-seeming misfortune if it was also essential to have lots of it to experience eupohoria. But in reality a state of “serotonergia” is a state of torpor, discomfort; and depression, rather than a state of alert pleasure. Its levels are above normal in autism, attention deficit disorder, and some forms of mental retardation, as well as in various types of depression.
血清素是一种炎症介质，抑制新陈代谢，扰乱血压，促进凝血。因此，如果大量使用血清素也能让人经历优波霍症，那将是摩尼教的不幸。但实际上，“血清素能”状态是一种迟钝、不适的状态；抑郁，而不是一种警觉愉悦的状态。在自闭症、注意力缺陷障碍、某些形式的智力迟钝以及各种类型的抑郁症中，其水平高于正常水平。
A mediator of stress transduces an infinite range of harmful influences into a stereotyped response, mobilizing the adaptive anti-stress systems. A relatively harmless stress, such as overheating, chilling, oxygen deficiency or exertion, can leave the organism stronger as a result of its adaptation, but other 'kinds of challenge, such as prolonged darkness, leave the organism more vulnerable despite its mobilization of its anti-stress systems. The difference seems to be that passivity allows a generalized catabolism, while an active response strengthens the functional system that is being challenged. Winter stress is a prolonged passive stress. The passive responses of hibernation, over-eating, lethargy or depression probably represent the best biological response under the circumstances, which have impaired the capacity for energetic response.
压力的调停者将无限范围的有害影响转化为刻板的反应，调动适应性抗压力系统。相对无害的压力，如过热、寒冷、缺氧或劳累，会使机体因适应而变得更强壮，但其他类型的挑战，如长时间的黑暗，会使机体更脆弱，尽管机体的抗压力系统已动员起来。不同之处似乎在于被动性允许广义分解代谢，而主动反应则加强了受到挑战的功能系统。冬季压力是一种长期的被动压力。冬眠、过度进食、嗜睡或抑郁等消极反应可能是在这种情况下最好的生物反应，它们削弱了能量反应的能力。
Depression, like inflammation, is a costly reaction for an organism that can't achieve a better adaptation. Serotonin is a mediator of both depression and inflammation. On the cellular level, serotonin depresses respiration, and on the organismic level it depresses body temperature which depresses biochemical reactions generally. For mood and mental function, it's probably significant that serotonin depresses blood circulation in the brain (Mendelow, et al., 1977; Eidelman, et al., 1978). There is no question about serotonin's being a mediator of depression, except for the stereotype that got its start in the 1960s that wants to see it as a sedative euphoriant, a deficiency of which produces many psychological problems. The tryptophan and melatonin industries were built up around this serotonin myth.
抑郁症和炎症一样，对于一个无法实现更好适应的机体来说是一种代价高昂的反应。血清素是抑郁症和炎症的介质。在细胞水平上，血清素抑制呼吸，在机体水平上，血清素抑制体温，这通常会抑制生化反应。对于情绪和精神功能而言，5-羟色胺抑制大脑血液循环可能很重要（Mendelow等人，1977年；Eidelman等人，1978年）。毫无疑问，5-羟色胺是抑郁症的调停者，除了20世纪60年代开始的一种刻板印象，认为5-羟色胺是一种镇静愉悦剂，这种缺乏会产生许多心理问题。色氨酸和褪黑素产业就是围绕着这个血清素神话建立起来的。
Aging and the degenerative diseases involve combinations of metabolic depression and inflammation. Anti-serotonin agents are coming to be recognized as treatments for a wide variety of degenerative diseases.
衰老和退行性疾病包括代谢抑制和炎症。抗5-羟色胺药物逐渐被认为是治疗各种退行性疾病的药物。
Minks that have mated in the winter don't implant the fertilized ovum in the uterus until the spring equinox, when progesterone rises suddenly, and allows both the uterus ai1d the embryo to begin the process of pregnancy and gestation. Progesterone provides the oxygen needed for the successful implantation of the embryo, while estrogen and serotonin lower the intrauterine oxygen.
冬季交配的水貂在春分前不会将受精卵植入子宫，此时黄体酮突然升高，子宫和胚胎都开始怀孕和妊娠过程。孕酮提供胚胎成功植入所需的氧气，而雌激素和5-羟色胺降低宫内氧气。
Under good conditions, the (premenstrual) luteal phase of the monthly cycle resembles pregnancy, as a period of progesterone dominance, in which the abundance of progesterone causes cells to decrease their estrogen content. The luteal phase is actually the first stage of pregnancy, and if there is implantation of an embryo all of the processes that begin at ovulation progress continuously until childbirth occurs. When there is no implantation, the luteal phase progesterone dominance is terminated, allowing estrogen to enter tissues and producing menstruation. The sudden decrease of progesterone production before menstruation is similar to decrease of hormone production just before childbirth. The same conditions that produce the premenstrual syndrome, if they aren't corrected by the placenta's massive production of progesterone, will produce preeclampsia, toxemia of pregnancy, eclampsia, and postpartum depression. They are also related to the problems that become so common at menopause. Whenever the production of progesterone falls, tissues are susceptible to estrogen.
在良好的条件下，每个月周期的（经前）黄体期类似于怀孕，是孕酮占优势的时期，孕酮的丰富导致细胞雌激素含量降低。黄体期实际上是怀孕的第一阶段，如果有胚胎植入，从排卵开始的所有过程都会持续进行，直到分娩。当没有着床时，黄体期孕酮的优势被终止，允许雌激素进入组织并产生月经。月经前孕酮分泌的突然减少与分娩前激素分泌的减少相似。产生经前综合征的同样条件，如果不能通过胎盘大量产生孕酮来纠正，将产生子痫前期、妊娠毒血症、子痫和产后抑郁症。它们也与更年期常见的问题有关。每当孕酮产量下降时，组织就容易受到雌激素的影响。
There are several common causes of a progesterone deficiency. Deficiencies of thyroid, vitamin A, and cholesterol are often responsible for a progesterone deficiency. Inadequate light exposure can cause it. Excess polyunsaturated fats, interfering with gonads and thyroid, can cause it. And excess serotonin can cause it.
*黄体酮缺乏症有几个常见的原因。甲状腺、维生素A和胆固醇的缺乏通常是孕酮缺乏的原因。*光照不足会导致这种情况。过多的多不饱和脂肪会干扰性腺和甲状腺，从而导致肥胖。过量的5-羟色胺会导致这种情况。
'Serotonin is a precursor of melatonin, which tends to be produced at night. Because of the books published during the intensive marketing campaign for melatonin, many people are familiar with the work of Maestroni and Pierpaoli, who reported that treatment with melatonin, or with the transplantation of pineal' glands from young animals, would extend the life span of mice and prevent cancer. Melatonin is often called the “pineal hormone,” though there are other hormones in the pineal, and many other tissues can produce melatonin.
5-羟色胺是褪黑素的前体，通常在夜间产生。由于褪黑素密集营销活动期间出版的书籍，许多人都熟悉迈斯特罗尼和皮尔保利的工作，他们报告说，用褪黑素治疗，或用年轻动物的松果腺移植，可以延长小鼠的寿命并预防癌症。褪黑素通常被称为“松果体激素”，尽管松果体中还有其他激素，许多其他组织可以产生褪黑素。
Mice and rats are nocturnal animals, so they are notoriously inappropriate for evaluating the nocturnal hormones as they might relate to humans and other animals that are active in the daytime. Although melatonin sometimes antagonizes serotonin in a protective way, in itself it can lower body temperature and alertness, suppressing thyroid and progesterone. (Sirotkin, 1997) Women who are depressed have been found to have higher daytime melatonin levels. (Danilenko, et aI., 1994) While the popular books have given the impression that there is no question about the protective nature of melatonin, it turns out that in only five out of 36 strains of inbred mice can melatonin be demonstrated in the pineal glands. The famous cancer prone strain, in which mammary cancer kills practically all the females, is one of these. When they are given melatonin the development of tumors is accelerated. When their pineal gland is removed, their life span is extended.
老鼠和老鼠是夜间活动的动物，因此它们不适合评估夜间活动的激素，因为它们可能与人类和其他白天活动的动物有关。虽然褪黑素有时以保护性的方式对抗血清素，但其本身可以降低体温和警觉性，抑制甲状腺和孕酮。（Sirotkin，1997）研究发现，患有抑郁症的女性白天褪黑激素水平较高。（Danilenko，et al.，1994）虽然流行书籍给人的印象是褪黑素的保护性质是毫无疑问的，但事实证明，36种近交系小鼠中只有5种能够在松果腺中显示褪黑素。著名的易患癌症的菌株就是其中之一，乳腺癌几乎杀死了所有的女性。当他们被给予褪黑素时，肿瘤的发展会加快。当松果体被切除时，它们的寿命延长了。
Estrogen and stress increase free fatty acids, and unsaturated free fatty acids cause serotonin release; serotonin, at least under some circumstances, can be lipolytic, increasing the free circulating fatty acids.
雌激素和压力增加游离脂肪酸，不饱和游离脂肪酸导致5-羟色胺释放；血清素，至少在某些情况下，可以分解脂肪，增加自由循环脂肪酸。
Darkness creates stress, by free radical inactivation of the respiratory enzyme, cytochrome oxidase, and light restores the activity of that enzyme, and probably also has a variety of anti-free-radical actions. Free fatty acids rise in the darkness, intensifying free radical production and suppressing respiration. Progesterone synthesis is suppressed by darkness. The serotonin liberated by the fatty acids suppresses progesterone by inhibiting the secretion of luteinizing hormone (LH) which stimulates progesterone synthesis, and also seems to act directly on the ovary to suppress progesterone secretion (Wilson, et aI., 1975). While estrogen increases serotonin's actions, progesterone antagonizes them.
黑暗通过呼吸酶、细胞色素氧化酶的自由基失活产生压力，而光则恢复该酶的活性，可能还具有多种抗自由基作用。游离脂肪酸在黑暗中上升，加强自由基的产生并抑制呼吸。黄体酮的合成被黑暗所抑制。脂肪酸释放的5-羟色胺通过抑制促黄体生成素（LH）的分泌抑制孕酮，促黄体生成素（LH）刺激孕酮合成，并且似乎直接作用于卵巢抑制孕酮分泌（Wilson，et al.，1975）。当雌激素增加血清素的作用时，黄体酮对抗它们。
Serotonin depletes glycogen stores, much the way estrogen and histamine do. This can cause hyperglycemia. Thyroid, carbon dioxide, and caffeine, which inhibit serotonin release, all tend to protect glycogen stores. Under the influence of carbon dioxide, noradrenaline can still liberate glucose from glycogen, but serotonin's effect is inhibited by carbon dioxide.
血清素会消耗糖原储备，就像雌激素和组胺一样。这会导致高血糖。甲状腺、二氧化碳和咖啡因都会抑制血清素的释放，它们都会保护糖原的储存。在二氧化碳的影响下，去甲肾上腺素仍然可以从糖原中释放葡萄糖，但5-羟色胺的作用受到二氧化碳的抑制。
Serotonin interferes with slow-wave sleep, creating a situation resembling that of depression or old age. Brain glycogen is depleted in old age, and this depletion contributes to inefficient brain metabolism. Serotonin's stimulation of ACTH, which stimulates the adrenal cortex, and its direct stimulation of cortisone production by the adrenals, is probably involved in the chronic excess of cortisone seen in depression and old age, which contributes to insulin resistance and diabetes, and to the atrophy of all tissues including the brain. (People who are studying chronic inflammatory processes are gathering data that will be meaningful for understanding depression and aging, but it seems that psychiatrists don't know about their work.)
血清素干扰慢波睡眠，造成类似抑郁或老年的情况。脑糖原在老年时耗尽，这种耗尽导致大脑代谢效率低下。5-羟色胺对促肾上腺皮质激素（ACTH）的刺激，以及对肾上腺产生可的松的直接刺激，可能与抑郁症和老年期可的松的慢性过量有关，这导致胰岛素抵抗和糖尿病，以及包括大脑在内的所有组织的萎缩。（研究慢性炎症过程的人正在收集对理解抑郁症和衰老有意义的数据，但精神科医生似乎不知道他们的工作。）
Anti-serotonin drugs such as bromocriptine have been found to correct diabetes, apparently because serotonin interferes with the use of sugar, acting on cells' metabolism to decrease its use, and preventing the secretion of insulin. Bromocriptine's correction of obesity also seems to be the result of its correction of glucose metabolism.
抗血清素药物如溴隐亭已被发现可以纠正糖尿病，显然是因为血清素干扰糖的使用，作用于细胞的代谢以减少糖的使用，并阻止胰岛素的分泌。溴隐亭对肥胖的纠正似乎也是其对葡萄糖代谢的纠正。
In the 1970s, it was established that darkness increases the appetite for alcohol. More recently (Lin and Hubbard, 1995) it has been found that the anti-serotonin drugs prevent the dark-induced appetite for alcohol. Alcohol is probably a self-medication to alleviate serotonin-related depression. Alcohol, like progesterone, is neuroprotective in brain trauma Alcohol increases formation of the sedative neurosteroid (“THP”) derived from progesterone (VanDoren, et aI., 2000), and alcohol increases brain circulation, countering serotonin's effect.
在20世纪70年代，人们确定黑暗会增加对酒精的食欲。最近（Lin和Hubbard，1995）发现抗5-羟色胺药物可以防止黑暗诱导的酒精食欲。酒精可能是缓解血清素相关抑郁症的自我药物。酒精和黄体酮一样，在脑外伤中具有神经保护作用。酒精增加黄体酮衍生的镇静神经甾体（“THP”）的形成（VanDoren等人，2000年），酒精增加脑循环，对抗血清素的作用。
Progesterone withdrawal and alcohol withdrawal are so closely related that one can alleviate the symptoms of the other.
黄体酮戒断和酒精戒断密切相关，一方可以缓解另一方的症状。
Isolation might be another factor contributing to depression and alcoholism, since it decreases the formation of the protective neurosteroid.
隔离可能是导致抑郁和酗酒的另一个因素，因为它减少了保护性神经甾体的形成。
The “brain fog” that is often described in depressed people (and people with other serotonin syndromes, such as the fibromyalgia syndrome) is probably produced by a combination of factors, including hypothyroidism, low body temperature, and hyperserotonemia. The amnesia produced by shock was found to be prevented by anti-serotonin drugs (Montanaro, et al., 1979). The same researchers suggested that the drugs had an “anti-punishment” effect, in effect making the animals less fearful.
抑郁症患者（以及患有其他5-羟色胺综合征的患者，如纤维肌痛综合征）经常出现的“脑雾”可能是由多种因素共同造成的，包括甲状腺功能减退、体温过低和高尿酸血症。休克引起的健忘症被发现可以通过抗血清素药物预防（Montanaro等人，1979年）。同样的研究人员认为，这些药物具有“抗惩罚”的效果，实际上可以使动物不那么害怕。
There is more confusion in the medical literature regarding the actions of serotonin than there is about practically any other subject.
在医学文献中，关于血清素的作用比任何其他学科都要混乱。
For example, there is clear evidence from both animal and human studies that serotonin, like estrogen, is associated with aggression, but the dominating stereotype is that serotonin is the agent of serenity and peace. In an epidemiological study (Moffitt, et al., 1998), a record of violence was clearly associated with above-average blood serotonin levels. Animal studies show that darkness stimulates both aggression and eating (Russell and Singer, 1983), and that serotonin increases, while anti-serotonin drugs decrease, aggression (Carlini and Lindsey, 1983).
例如，动物和人类研究都有明确的证据表明，血清素和雌激素一样，与攻击性有关，但主要的刻板印象是血清素是一致性与和平的媒介。在一项流行病学研究（Moffitt等人，1998年）中，暴力记录显然与高于平均水平的血液血清素水平有关。动物研究表明，黑暗刺激攻击性和进食（Russell和Singer，1983），5-羟色胺增加，而抗5-羟色胺药物减少攻击性（Carlini和Lindsey，1983）。
When lysergic acid derivatives came onto the pharmaceutical market, the spirit of the times caused them to be described as dopamine agonists, rather than as serotonin antagonists, but the latter would be at least as descriptive of their effects. Bromocriptine fulfills many of the requirements of being a serotonin antagonist, for example by suppressing prolactin. As a class, the serotonin antagonists have a very interesting place in pharmaceutical medicine, because the broad spectrum of their therapeutic activity suggests the great variety of problems caused by excess serotonin.
当麦角酸衍生物进入医药市场时，时代精神使它们被描述为多巴胺激动剂，而不是血清素拮抗剂，但血清素拮抗剂至少可以描述它们的作用。溴隐亭满足作为5-羟色胺拮抗剂的许多要求，例如通过抑制催乳素。作为一个类别，5-羟色胺拮抗剂在药学中有一个非常有趣的位置，因为其广泛的治疗活性表明，过量的5-羟色胺会引起各种各样的问题。
The documentation of extensive government supported fraud in research on LSD and marihuana should make us question subsequent research that plows the same or similar furrows. My inclination is to believe that incompetence can't account for the glaring errors in research on serotonin-related questions. Commercial commitments to particular theories of drug action have undoubtedly contributed to the crazy quality of the psychiatric serotonin literature.
关于LSD和大麻研究中政府支持的大量欺诈行为的文件应该让我们质疑后续的研究，这些研究同样或相似。我倾向于相信无能不能解释血清素相关问题研究中的明显错误。对药物作用的特定理论的商业承诺无疑促成了精神病5-羟色胺文献的疯狂质量。
In the case of some anti-serotonin drugs, there is commercial support for research, so they might come into general use in spite of the mythic stature of tryptophan/serotonin/melatonin. But thyroid, protein, magnesium, thiamine, progesterone and light are natural factors that keep serotonin under control, and that don't. have the side effects of the synthetic anti-serotonergic agents. Knowledge of serotonin's harmful actions can guide our use of the natural protective factors. For example, whey protein contains much more tryptophan than whole milk or cheese does, and would tend to suppress the thyroid and activate the whole serotonin-stress system. Whey might be good food for fattening pigs, but its acceptance in the health food industry as a powdered protein supplement is just another example oft he harmful effects of the serotonin mythology.
在一些抗血清素药物的案例中，研究得到了商业支持，因此尽管色氨酸/血清素/褪黑素的神秘地位，它们可能会被广泛使用。但是甲状腺、蛋白质、镁、硫胺素、黄体酮和光是控制血清素的自然因素，而事实并非如此。具有合成抗5-羟色胺药物的副作用。了解血清素的有害作用可以指导我们使用天然保护因子。例如，乳清蛋白比全脂牛奶或奶酪含有更多的色氨酸，并且会抑制甲状腺并激活整个血清素应激系统。乳清可能是肥育猪的好食物，但它在保健食品行业中作为粉状蛋白质补充剂被接受只是5-羟色胺神话有害影响的另一个例子。
(Some comments on research methods:)
“Serotonin activity” may be judged by the response of prolactin to serotonin or to a drug that is thought to mimic serotonin, or by serotonin metabolites in cerebrospinal fluid, or by the total amount of serotonin in the blood, or by its efflux from platelets, or the ratio of its concentration in the plasma and in the platelets. It isn't very clear whether serotonin's concentration or its turnover rate is most important, and the number and sensitivity of the many “serotonin receptors” varies, and presumably changes the meaning of any given quantity of serotonin. When serotonin's activity is judged indirectly, interpretation and subjectivity are involved.
“5-羟色胺活性”可以通过催乳素对5-羟色胺或被认为是模拟5-羟色胺的药物的反应来判断，或者通过脑脊液中的5-羟色胺代谢物来判断，或者通过血液中5-羟色胺的总量来判断，或者通过它从血小板中的流出，或者它在血浆和血小板中的浓度比来判断。目前还不清楚5-羟色胺的浓度或其周转率是否是最重要的，许多“5-羟色胺受体”的数量和敏感性各不相同，可能会改变任何给定数量的5-羟色胺的含义。当间接判断血清素的活性时，涉及到解释和主观性。
Even the “synaptic reuptake inhibitors,” such as fluoxetine, sometimes relieve symptoms that are believed to be caused by an excess of serotonin (c. Advokat and V. Kutlesic, 1995, Neurosci Biobehav Rev 1995 Spring;19(l):59-66 Pharmacotherapy of the eating disorders: a commentary.)
即使是“突触再摄取抑制剂”，如氟西汀，有时也会缓解被认为是由5-羟色胺过量引起的症状（c.Advokat和V.Kutlesic，1995，Neurosci Biobehav Rev 1995 Spring；19（l）：59-66进食障碍的药物治疗：评论）
But the actual injection of serotonin, or of serotonin antagonists that are known to approximately neutralize serotonin's effects, and the examination of the basal concentrations of the hormones known to be regulated by serotonin, are much Less likely to be distorted by arbitrary interpretations.
但是，实际注射5-羟色胺或已知可大致中和5-羟色胺作用的5-羟色胺拮抗剂，以及检查已知由5-羟色胺调节的激素的基础浓度，不太可能被任意解释所扭曲。
When a “receptor” is first proposed or “discovered, ” it is always “a protein, ” though because of the idea of a barrier (semipermeable) membrane around cells, “membrane lipids” are sometimes invoked. But after a few years of research, the “receptor” becomes a more and more complex system of interacting molecules. The doctrine of the “receptor” is intended to explain why cells have a specific response to a specific substance. Gradually, a receptor becomes a “response element,” but the “element, ” in its complexity, begins to shade off into the system “membrane/cytoplasm/nucleus.” which is to say, the cell. The cell is the response element The “transmitter substance” interacts with various agonists. antagonists. inverse agonists and binding competitors to produce an effect that is a summation of influences. A single protein or protein system can serve as a “receptor” for antagonistic substances.
当一个“受体”被首次提出或“发现”时，它总是“一种蛋白质”，尽管由于细胞周围有一层屏障（半透膜）的概念，“膜脂”有时会被调用。但是经过几年的研究，“受体”变成了一个越来越复杂的相互作用分子系统。“受体”学说旨在解释为什么细胞对特定物质有特定反应。渐渐地，一个受体变成了一个“反应元件”，但这个“元件”，在其复杂性中，开始在系统“膜/细胞质/核”中消失，也就是说，细胞。细胞是“递质物质”与各种激动剂相互作用的反应元件。对手。反向激动剂和约束竞争对手以产生影响总和的效果。单个蛋白质或蛋白质系统可作为拮抗物质的“受体”。
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