Injury to the thyroid apparently precedes the development of “autoimmune thyroiditis.” There is evidence that tissue injury precedes the appearance of “autoantibodies” in other conditions, too.

甲状腺损伤明显先于“自身免疫性甲状腺炎”的发展。有证据表明，在其他情况下，组织损伤先于“自身抗体”的出现。

Many people with metabolic problems, including hypothyroidism, are being told that they have “a genetic disease.” This belief encourages both physicians and their customers to commit themselves to inappropriate treatments, and to misinterpret the results of tests.

许多患有代谢问题（包括甲状腺功能减退症）的人被告知患有“遗传病”。这种信念鼓励医生和他们的顾客进行不适当的治疗，并误解检测结果。

Eating seaweed or other foods or supplements containing iodine can cause both hypothyroidism and thyroiditis. The iodate sometimes used as an oxidizing agent in breads have probably contributed to thyroid disease in the industrialized countries.

食用海藻或其他含有碘的食物或补充剂会导致甲状腺功能减退和甲状腺炎。在工业化国家，碘酸盐有时用作面包中的氧化剂，可能导致甲状腺疾病。

Dental x-rays, which can cause cancer of the thyroid, brain, and eye, certainly have increased the incidence of thyroiditis and hypothyroidism. The radioactive isotopes that are often foolishly used for supposedly 'diagnostic purposes probably contribute to the incidence and severity of hypothyroidism and thyroiditis.

牙科x光可以导致甲状腺癌、脑癌和眼癌，这无疑增加了甲状腺炎和甲状腺功能减退症的发病率。通常被愚蠢地用于所谓的“诊断”目的的放射性同位素可能会导致甲状腺功能减退和甲状腺炎的发生率和严重程度。

Besides iodine, radioactive isotopes, and x-rays, other environmental toxins, including mercury and dioxins can cause thyroiditis, but diet and estrogens are probably the causes of most thyroid problems.

除了碘、放射性同位素和x射线之外，其他环境毒素，包括汞和二恶英，也会引起甲状腺炎，但饮食和雌激素可能是大多数甲状腺问题的原因。

A generalized inflammatory state, rather than specific “autoimmunity,” is responsible for thyroiditis and other “autoimmune degenerative” diseases.

甲状腺炎和其他“自身免疫性退行性”疾病是由全身炎症状态而非特异性“自身免疫性”引起的。

A “respiratory defect” is behind the inflammatory condition.

炎症状态的背后是“呼吸缺陷”。

Correcting a thyroid deficiency tends to gradually normalize the antibodies.

纠正甲状腺缺陷倾向于逐渐使抗体正常化。

Girls' thyroid glands usually enlarge during puberty, and in pregnancy it's entirely normal for the gland to enlarge and to become more active. Eighty years ago, when iodine deficiency was more common in the US and Europe, the idea of a “colloid goiter” was common. In certain regions, many people had enlarged thyroids that contained a large amount of colloid–colloid is the viscous protein (thyroglobulin) solution formed m tiny compartments in the thyroid gland, which can be broken down by “digestive” (proteolytic) enzymes of the cells that have secreted it, forming the thyroid hormones, and allowing them to be released into the blood stream. The hormones are formed as the accumulated protein is broken down; the hormone itself isn't stored in the gland.

女孩的甲状腺通常在青春期增大，怀孕期间甲状腺增大并变得更活跃是完全正常的。80年前，当缺碘在美国和欧洲更为普遍时，“胶体甲状腺肿”的想法很普遍。在某些地区，许多人的甲状腺增大，含有大量胶体——胶体是在甲状腺中形成的粘性蛋白质（甲状腺球蛋白）溶液，可被分泌它的细胞的“消化”（蛋白水解）酶分解，形成甲状腺激素，让它们被释放到血液中。当积累的蛋白质被分解时，激素就形成了；激素本身并不储存在腺体中。

The reason for the enlargement of the gland during puberty and in pregnancy, and during some kinds of stress, is that the colloid is formed faster than it is digested by the thyroid gland and secreted into the blood. If something, such as an excess of estrogen, is blocking the production of the thyroid hormone, the gland is likely to enlarge, because the pituitary secretes more thyroid stimulating hormone (TSH) when there is a deficiency of thyroid hormone.

青春期和怀孕期间，以及在某些压力下，甲状腺肿大的原因是胶体形成的速度快于甲状腺消化和分泌到血液中的速度。如果某种东西，比如雌激素过量，阻碍了甲状腺激素的产生，那么腺体很可能会扩大，因为当甲状腺激素缺乏时，垂体会分泌更多的促甲状腺激素（TSH）。

In vitro experiments show that estrogen activates the formation of the colloid, but inhibits its breakdown into the hormones. Progesterone, on the other hand, activates the process of proteolytic digestion and so increases the release of hormones from the gland, decreasing the accumulation of the colloid.

体外实验表明，雌激素激活胶体的形成，但抑制其分解为激素。另一方面，孕酮激活蛋白水解消化过程，从而增加腺体激素的释放，减少胶体的积累。

Therefore, when progesterone is deficient or estrogen is present in excess, the colloid tends to accumulate (even to the point of causing a visible enlargement of the gland, a “colloid goiter”), at the same time that the person may be hypothyroid, because the hormone isn't being released from the stored colloid, into the blood stream. But, largely because no one wants to suggest that estrogen can be pathogenic, an enlarged thyroid gland is now likely to be diagnosed as “Hashimoto's thyroiditis” (or Hashimoto's struma, or goiter, or disease).

因此，当孕酮缺乏或雌激素过量时，胶质往往会积聚（甚至导致腺体明显增大，称为“胶质性甲状腺肿”），同时患者可能出现甲状腺功能减退，因为激素不会从储存的胶质释放到血液中。但是，很大程度上因为没有人想表明雌激素可能是致病性的，甲状腺肿大现在很可能被诊断为“桥本甲状腺炎”（或桥本甲状腺肿，或甲状腺肿，或疾病）。

Hashimoto's disease is clearly defined as the infiltration of the gland with lymphocytes, “causing destruction” of the gland's active tissue and leading to hypothyroidism. The only way to know that the gland is being invaded by large numbers of lymphocytes is by biopsy, but the condition is normally diagnosed by pure guesswork, without any biopsy. Sometimes “antithyroid antibodies” found in the blood are used to diagnose Hashimoto's disease, but the presence of those antibodies in the blood doesn't mean that they originated in the thyroid gland, and even though they have very specific names (e.g., “antithyroglobulin,” “antithyroperoxidase”) related to the thyroid gland, they aren't even specific for the thyroid gland. It has been suggested that similarities in molecular structure between thyroglobulin and connective tissue proteins could account for the finding of “antithyroid antibodies” more frequently in rheumatoid arthritis and Sjogren's syndrome than in Hashimoto's disease and Graves' disease (Ruggeri, et aI, 2002).

桥本病被明确定义为淋巴细胞浸润腺体，“破坏”腺体的活动组织并导致甲状腺功能减退。知道腺体被大量淋巴细胞侵袭的唯一方法是活组织检查，但这种情况通常是通过纯粹的猜测，没有任何活组织检查来诊断的。有时，血液中发现的“抗甲状腺抗体”被用于诊断桥本氏病，但血液中存在这些抗体并不意味着它们起源于甲状腺，尽管它们有与甲状腺相关的非常特殊的名称（例如，“抗甲状腺球蛋白”、“抗甲状腺过氧化物酶”），它们甚至对甲状腺没有特异性。有人提出，甲状腺球蛋白和结缔组织蛋白分子结构的相似性可以解释类风湿性关节炎和干燥综合征中“抗甲状腺抗体”的发现比桥本病和Graves病更频繁（Ruggeri，et aI，2002）。

In the last 60 years, most of estrogen's toxic effects have been hushed up by the drug industry, and estrogen's central antirespiratory and antithyroid actions are unknown to most contemporary endocrinologists. But endocrinologists often do know that estrogen causes the thymus gland to atrophy, and that the thymus gland is intimately involved in maintaining normal immune functions.

在过去的60年中，大多数雌激素的毒性作用被制药行业掩盖了，而雌激素的中枢抗呼吸道和抗甲状腺功能对大多数当代内分泌学家来说都是未知的。但内分泌学家通常知道雌激素会导致胸腺萎缩，胸腺与维持正常免疫功能密切相关。

The degenerating thymus gland undergoes invasion by lymphocytes and the replacement of active tissue by fibrous tissue, under the influence of estrogen or stress. The process of cellular invasion in the thyroid gland probably develops more slowly than that in the thymus, because estrogen's effect on the thymus is very rapid.

在雌激素或应激的影响下，退化的胸腺受到淋巴细胞的侵袭，活性组织被纤维组织取代。甲状腺中的细胞浸润过程可能比胸腺中的细胞浸润过程慢，因为雌激素对胸腺的作用非常迅速。

The cells that make up the thymus are extremely varied, but a large portion of them are able to phagocytize other cells. This self-phagocytosis probably contributes to the gland's ability to shrink with such great rapidity. When other organs are damaged, the removal of debris can be delayed for days, as phagocytic cells gradually enter the tissues from the blood stream.

构成胸腺的细胞种类繁多，但其中很大一部分能够吞噬其他细胞。这种自我吞噬作用可能有助于腺体迅速收缩。当其他器官受损时，由于吞噬细胞逐渐从血流进入组织，碎屑的清除可能会延迟数天。

Hypothyroidism is an important cause of thymic atrophy, and a thyroid supplement can stimulate regeneration of the thymus.

甲状腺功能减退是胸腺萎缩的一个重要原因，补充甲状腺可以刺激胸腺的再生。

This correction of the thymic portion of the “immune system” by the thyroid hormone is probably involved in the observation that the “antithyroid” autoantibodies decrease under the influence of supplemental thyroid hormone, but the supplement also affects the thyroid gland, by decreasing the thyroid stimulating hormone, TSH. Excess production of TSH causes an inflammation-like stress, that contributes to the production of the colloid goiter and eventually to disordered structural changes in the thyroid gland. A more efficient production and use of thyroglobulin will decrease the tendency of the overstimulated gland to produce a defective globulin that is antigenic.

甲状腺激素对“免疫系统”胸腺部分的纠正可能与观察到的“抗甲状腺”自身抗体在补充甲状腺激素的影响下减少有关，但补充甲状腺激素也会通过减少促甲状腺激素TSH影响甲状腺。TSH的过度产生会导致类似炎症的压力，从而导致胶质甲状腺肿的产生，最终导致甲状腺结构紊乱。更有效地生产和使用甲状腺球蛋白将减少过度刺激腺体产生抗原性缺陷球蛋白的趋势。

So, rather than ignoring the frequency of the simple colloid goiter and calling everything “Hashimoto's autoimmune thyroiditis,” if we look at the mechanisms involved in the production of autoantibodies, we will tend to see “thyroiditis” as, usually, the last stage in the development of a simple colloid goiter. The autoantibodies, in a healthy person, are probably part of a corrective repair process, rather than a simply pathogenic factor.

因此，如果我们观察自身抗体产生的机制，我们将倾向于将“甲状腺炎”视为单纯性胶体甲状腺肿发展的最后一个阶段，而不是忽视单纯性胶体甲状腺肿的发生频率，并称之为“桥本自身免疫性甲状腺炎”。健康人的自身抗体可能是修复过程的一部分，而不仅仅是致病因素。

There is an almost obligatory medical genuflection toward “genetic causation” of disease, and especially of thyroid disease, autoimmune disease, and other chronic or degenerative diseases. The fact that thyroid disease and autoimmune diseases are from five to ten times more frequent in women than in men somehow hasn't increased medical interest in the pathogenic role of estrogen, and it doesn't prevent platoons of medical researchers from making claims to have discovered “which chromosome carries the disease.”

对于疾病的“遗传原因”，尤其是甲状腺疾病、自身免疫性疾病和其他慢性或退行性疾病，医学界几乎有义务做出让步。女性甲状腺疾病和自身免疫性疾病的发病率是男性的五到十倍，这一事实并没有增加医学界对雌激素致病作用的兴趣，也没有阻止医学研究人员宣称已经发现“哪条染色体携带疾病”

This medical bias means that even the physicians who recognize that hypothyroidism is a condition that should be corrected are not likely to believe that it is important to modify the treatment according to changes in the patient's condition. Many doctors assume that a person never recovers from thyroiditis, but the evidence is clear that simply giving supplementary thyroid usually gradually corrects the problem. If other protective measures are taken, recovery will be quicker and more complete. When the diet is optimal, the TSH is likely to be “abnormally low,” below 1.0 on the standard scale, even without use of a thyroid supplement. Keeping the level of TSH low contributes to the reduction of the generalized inflammatory state that characterizes hypothyroidism andautoimmunity. TSH should be considered to be one of the stress-related pro-inflammatory antirespiratory hormones, along with serotonin, histamine, estrogen, parathyroid hormone, and prolactin.

这种医学偏见意味着，即使认识到甲状腺功能减退是一种需要纠正的疾病的医生也不太可能认为根据患者病情的变化改变治疗方法很重要。许多医生认为一个人从未从甲状腺炎中康复，但有证据表明，简单地补充甲状腺通常会逐渐纠正这个问题。如果采取其他保护措施，恢复将更快、更彻底。当饮食达到最佳状态时，即使不使用甲状腺补充剂，TSH也可能“异常低”，低于标准量表上的1.0。保持TSH水平较低有助于减轻甲状腺功能减退和自身免疫的全身炎症状态。TSH应与5-羟色胺、组胺、雌激素、甲状旁腺激素和催乳素一起被视为应激相关的促炎性抗呼吸激素之一。

Part of the problem, Lewontin points out, is the casual way in which geneticists· speak. “This is seen even in the naming of genes,” he notes. “Geneticists speak casually of the 'gene for white eyes', but of course, there is no such gene. There is a variety of genes whose reading by the cell is proximally involved in the production of eye pigment and its deposition in the eye cells.” He points out that genes are said to be “self-replicating, ”. engaged in “gene action ”, “make” proteins and are “turned on ” or “off” by regulatory DNA. “But none of this is true… DNA is among the most inert and non-reactive of organic molecules,” he writes. S. W. Samuels, in Genes, Ethics & Environment!, an internet public policy journal. Vol. I, No. I October, 2000 Lewontin指出，部分问题在于遗传学家说话的随意性。“这甚至可以在基因命名中看到，”他指出。“遗传学家漫不经心地谈论‘白眼睛基因’，但当然，没有这样的基因。有多种基因的细胞阅读与眼睛色素的产生及其在眼睛细胞中的沉积密切相关。”他指出，基因被称为“自我复制”。参与“基因作用”、“制造”蛋白质，并被调控DNA“开启”或“关闭”。“但这一切都不是真的……DNA是最惰性和最无反应的有机分子之一，”他写道。S.W.Samuels，基因、伦理与环境！，互联网公共政策杂志。第一卷第一期2000年10月

The diet should be relatively free of antithyroid foods, especially legumes and polyunsaturated fats, and the foods of the cabbage family, such as broccoli, should be well cooked, and used no more often than once a week. The polyunsaturated fats interfere with the thyroid hormone, disturb the thymus and other immune functions, and increase the antigenicity of tissues.

饮食应相对不含抗甲状腺食物，尤其是豆类和多不饱和脂肪，卷心菜类食物，如花椰菜，应烹调良好，每周使用不超过一次。多不饱和脂肪干扰甲状腺激素，干扰胸腺和其他免疫功能，并增加组织的抗原性。

A high protein diet, of about 100 grams of good protein daily, is protective, and protein deficiency is a common cause of hypothyroidism. But too much emphasis on the muscle meats, including fish fillets, chicken breast or legs, and the usual steaks and chops, can be antithyroid by providing too much tryptophan. That can be offset by using gelatin liberally (chicken soup and ox-tail soup contain lots of gelatin from the bones and connective tissues), because gelatin contains no tryptophan. Whey, which is sold as a protein supplement, and egg whites contain too much tryptophan, and can be antithyroid if used excessively.

高蛋白饮食，每天大约100克优质蛋白质，具有保护作用，而蛋白质缺乏是甲状腺功能减退的常见原因。但是，过分强调肌肉肉，包括鱼片、鸡胸或鸡腿，以及通常的牛排和排骨，会通过提供过多的色氨酸而抗甲状腺。这可以通过大量使用明胶来抵消（鸡汤和牛尾汤含有大量来自骨骼和结缔组织的明胶），因为明胶不含色氨酸。乳清是一种蛋白质补充剂，蛋清中含有过多的色氨酸，如果使用过量，可以抗甲状腺。

Using large amounts of seaweed can cause hypothyroidism and can injure the thyroid cells, contributing to thyroiditis. Seaweed and other iodine-containing food supplements are often sold to improve thyroid function, but they usually have the opposite effect. An iodine deficiency used to cause goiters in some regions, but in the last 50 years most people in the US and Europe have been getting an excessive amount of iodine.

大量使用海藻可导致甲状腺功能减退，并可损伤甲状腺细胞，导致甲状腺炎。海藻和其他含碘食品补充剂通常被出售以改善甲状腺功能，但它们通常具有相反的效果。碘缺乏曾在一些地区引起甲状腺肿，但在过去50年中，美国和欧洲的大多数人摄入了过量的碘。

“We can recall when a TSH of 7.0 or below was considered normal. Years later, the TSH cutoff was 6.4, meaning that anything below that level was considered normal. Still later, the cutoff was moved to 5.5. Now, some labs are reporting a lever of 4.2 as being the cutoff level, above which the patient may be hypothyroid.” “ …at our clinic, a TSH over 3 is considered suspicious….” (p. 75) “Some doctors prefer the lower limit of a corrected TSH to be 1.0. Others are comfortable with a TSH of 0.5. Some thyroid specialists at the University of California Medical Center in San Francisco like to see the corrected level around 0.2 (slightly below the normal range of 0.4-5.0)..That figure is generally considered by many non-university doctors to be too low, suggesting to them that the patient is on too much thyroid medication. “At our clinic, we have patients who do not feel well until they take enough medication to lower their TSH level to 0.1.” (page 79) R.L. Shames and K.H. Shames, Thyroid Power, 2001.

“我们可以回忆起当TSH为7.0或更低时被认为是正常的。几年后，TSH临界值为6.4，这意味着低于该水平的任何东西都被认为是正常的。再后来，临界值被移动到5.5。现在，一些实验室报告临界值为4.2，高于该水平的患者可能患有甲状腺功能减退。”“……在我们的诊所，超过3的TSH被认为是可疑的……”（第75页） “一些医生更喜欢校正TSH的下限为1.0。其他人对0.5的TSH感到满意。旧金山加利福尼亚大学医学中心的一些甲状腺专家喜欢看到大约0.2的校正水平（略低于0.4-5.0的正常范围）。这一数字通常被许多非大学医生认为太低，这表明他们对甲状腺药物太多了。 “在我们的诊所，我们有一些患者在服用足够的药物将TSH水平降至0.1之前感觉不好。”（第79页）R.L.Shames和K.H.Shames，《甲状腺动力》，2001年。

Endotoxin or other material absorbed from intestinal bacteria contributes to a variety of autoimmune problems, including thyroiditis (Penhale and Young, 1988). Combining an indigestible fiber, such as raw carrot, with mild germicides, such as vinegar and coconut oil, can improve the hormonal environment, while reducing the immunological burden.

内毒素或从肠道细菌吸收的其他物质会导致各种自身免疫问题，包括甲状腺炎（Penhale和Young，1988）。将不易消化的纤维（如生胡萝卜）与温和的杀菌剂（如醋和椰子油）相结合，可以改善激素环境，同时降低免疫负担。

Adequate light is another important factor in maintaining a high energy respiratory state and preventing the whole complex of inflammatory, autoimmune, degenerative diseases.

充足的光线是维持高能量呼吸状态和预防炎症、自身免疫、退行性疾病的另一个重要因素。

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