健康看守的新聞與觀點

多發性硬化症，蛋白質，脂肪，和孕酮

雷泥炭博士在13/02/10 1:39 PM

雷蒙德泥炭，博士

我們總是受到抗原的負擔。 重要的問題，跟我們這些負擔限制炎症反應的能力。

在MS多發性硬化症，它是明確的，炎症過程本身是破壞性的，雌激素是一個重要的誘發因素。 不飽和脂肪酸，膳食不平衡氨基酸相互作用與hyperestrogenism和甲狀腺功能減退，產生自身免疫性退行性疾病密切。

減少炎症介質的比擴大單一抗炎劑如皮質醇。 雖然免疫抑制藥物，包括“必需脂肪酸”，不減輕炎症症狀暫時的，他們可能有助於病理基礎。

與MS的人有長期增加皮質醇的生產。 蛋白同化失真，這將創建一個類似的營養蛋白質缺乏。 過多的血清素和雌激素引起的皮質醇生產相對不受控制。 一個惡性循環，可能會導致炎症介質和氨基酸不平衡。

抑鬱症，紅斑狼瘡，偏頭痛，更年期，糖尿病和老化有幾個重要的共同點與MS的代謝功能。

流行的療法是不合邏輯的，有可能導致病情惡化。

優質蛋白，甲狀腺，孕烯醇酮和孕激素往往從根本上糾正病理。 這些都是抗炎，但他們沒有免疫或代謝。

高海拔和陽光明媚的氣候相關的MS的發病率較低。

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像其他自身免疫性疾病，多發性硬化症（MS），對婦女的影響往往比男性（約2比1），其在生育年齡發病（尤其是後30時，雌激素是非常高的年齡），往往加劇premenstrually ，有時緩解懷孕（Drew和查韋斯，2000年）時，孕酮是非常高的。 已發現的雌激素，孕激素的比例高的婦女，有最活躍的腦部病變（Bansil，等，1999）。 大部分的MS-肥大細胞，一氧化氮（NO），血清素，催乳素，脂質過氧化，游離脂肪酸，前列腺素和異前列，各種細胞因子參與炎症調解（白細胞介素，腫瘤壞死因子）是密切相關雌激素的行動，並在動物，自身免疫性疾病，可帶來與雌激素治療（艾哈邁德·塔拉勒）。

與雌激素的MS很強的關聯，導致不合邏輯，但流行和廣為宣傳的醫療結論：雌激素對多發性硬化的保護，一些人聲稱，雌激素有利於治療效果。 這種思維奇怪的方式其等值的想法，因為婦女是更容易比男性要開發阿爾茨海默氏症，雌激素是保護反對;或者說，因為女性有更脆弱的骨頭比男人，和他們的進步骨損失發生在他們的最大暴露於雌激素的時代，雌激素預防骨質疏鬆。

在這個醫療環境，是公認的雌激素和退化性疾病之間的密切關聯，但他們說，協會的出現是因為沒有足夠的雌激素的意義有悖常理。 爐灶燃燒，因為它是不夠熱。

正如戴維·巴里說，我不是做這個。 最近廣為人知的文章已經表明，雌激素可以保護大腦（甚至預防中風！），因為它增加血清素和NO [一氧化氮]。 也有一些是幾乎美觀順眼這麼多的重大錯誤時，集中到一個單一的文章。 一氧化氮和羥色胺的神經毒性（Joseph，等，1991; Skaper，等，1996;帕金森等，1997;，聖地亞哥等人，1998年。巴傑爾，等，2000），抑制線粒體呼吸的結果。 NO發揮了重要作用脂質過氧化和脫髓鞘。 有趣的是看到羥色胺和沒有公開相關的雌激素，其已仔細從公眾視線中隱藏的線粒體毒性。

關於MS的舊理論，有關的基因和病毒，細菌，維生素缺乏，石油不足，毒藥，要接種疫苗的反應（尤其是B型肝炎及流感）的新理論的原因有以下幾種學說。 已放棄唯一的理論是19世紀的有關精神論“歇斯底里癱瘓，”雖然偶爾有人還在談論情緒多發性硬化症的原因，“女性歇斯底里”一詞已演變為“轉化症。”

每一個主要的理論有幾個事實似乎支持，但忽略了許多其他事實。 大家都同意，在MS以某種方式參與免疫系統，但是這確實問題出在哪裡開始，因為這個想法，炎症是一種內在的免疫力。 炎症如果“是必要的和好”，那麼它成為一個問題準確定義之間的邊界是一個適當的反應和退化過程。 在良好的光線，可以看到水腫，降低細胞呼吸，喪失正常功能，其不同程度的纖維化，炎症的每個組件的一部分作為“防禦性免疫反應。”當組織損傷導致修復，“必須”被看作是有益的，即使它會導致在功能組織的地方形成疤痕，因為比較是一個想像的最壞的結果，一個不完美的恢復，而不是比較的可能性，潛在的有害炎症過程劑可能有做沒有壞處。

炎症如何與生物體的資源最簡單的例證是血糖變化，而變化從輕度刺激性潛在致命的化學物質，動物暴露實驗。 當動物有非常低血糖，溫和的刺激可能是致命的，但是當其血糖保持非常高的，甚至是致命的抗原只有輕度刺激性。 不同的血液中鈉離子濃度相似，但較弱，影響。

有一種傾向，不僅看到了作為一個正常的免疫炎症，但要看到它作為抗原的性質成正比，除時，免疫系統已被引為它以前接觸，在這種情況下，機體所有（要么沒有反應，因為它已成為免疫），或反應會更猛烈，比它的第一次接觸，因為它已成為過敏。 但是，在現實中，只是血液中的葡萄糖和鈉濃度（甲狀腺，和許多其他物質不被認為是免疫系統的一部分），可以在“免疫”反應程度的巨大差異。

在過於敏感的條件下產生的低血糖，幾件事情發生有助於不適應誇張的炎症反應的。

腎上腺素增加，低血糖，如果腎上腺素失敗糖原轉化為葡萄糖，它會提供從脂肪細胞中解放出來的自由脂肪酸替代燃料。

如果解放的不飽和脂肪酸，它們會導致血清素分泌，血清素和不飽和脂肪酸會抑制線粒體呼吸，加劇了低血糖。 它們會刺激細胞因子的釋放，激活多種免疫和炎症過程，他們會導致血管滲漏，創造水腫和纖維化的第一階段開始。 腎上腺素和血清素會刺激釋放皮質醇，從大骨骼肌等組織動員的氨基酸。 這些肌肉中含有大量的半胱氨酸和色氨酸，其中，除其他作用，抑制甲狀腺。 色氨酸的增加，尤其是在游離脂肪酸的存在，是有可能被轉換成額外的羥色胺，脂肪酸釋放白蛋白色氨酸進入大腦，提高其入境。 游離脂肪酸和增加血清素，減少代謝效率（例如，導致胰島素抵抗）和促進炎症狀態。

脂肪在血液流很容易進入到大腦，和不飽和游離脂肪酸產生腦水腫（陳等人，1983年，1988年）。 當血管滲漏引起的腦水腫，通常被排除的蛋白質可以進入。 刺激，興奮和疲憊的大腦交流谷氨酰胺色氨酸，加速其從血液中攝取。

當組織受傷或強調，應對該組織的改變組件形成抗體。 因此，我們可以調用挫傷或扭傷是一種自身免疫性條件，但有沒有商業撞傷，脛抗體測試。 的特異性抗體測試的情況下，似乎是在歸類為自身免疫性條件，如要素“自身免疫性甲狀腺炎。”不幸的是，這種方式使用的語言是嵌套在一個文化，是因果關係的不切實際的想法，還有數千人上搜索“突變基因是負責疾病”，並為糾正缺陷的藥物，將建立自己的職業生涯。

早在免疫學的研究，重點是抗體。 甚至更早，炎症已經概念化的“幽默”，和其他前科學思想。 盡快多發性硬化症/歇斯底里麻痺被列為一種自身免疫性疾病，免疫系統的性質有關的原始想法相互作用有關的性質和大腦細胞的結構與原始的想法，什麼病的各種理論混合是。

而非看到免疫神經損傷多發性硬化症的所有其他功能的原因，我認為，重要的是看上下文中解釋神經的事件，在一些條件的一般特徵。

它一直被稱為MS的發病率增加與赤道的距離往往很長一段時間。 在陽光明媚的氣候乾燥，並在高海拔地區低發病率。 兩個清晰的膳食影響已發現：吃豬肉，馬肉。

與MS的人不很好調節自己的體溫。 他們的神經傳導速度很慢，在正常的人，傳導是在較高溫度下更快，但在人與MS傳導速度比正常溫度在98.6度的F在較低溫度下。 低於正常溫度也與老年，更年期的潮熱。

腦葡萄糖代謝的多發性硬化症是非常低的，在我自己的觀察，一般代謝率低於正常。 然而，有些人的原因造成的代謝低下的病灶，而不是反之亦然。

缺乏的不飽和脂肪酸的動物，有較高的代謝率和利用葡萄糖的能力，將其轉換為二氧化碳更容易，有一個更大的抗毒素（哈里斯等人，1990年甚至是眼鏡蛇毒液。Morganroth，等， 1989年），包括內毒素（李等人，1990年），防止過度的血管滲漏和免疫損傷（高橋等人，1992年），和創傷，他們的肌肉反應速度加快而快速抽搐肌肉少容易疲倦（艾雅和Hulber，1996）。

在與MS的人，血液更粘稠，血小板易於聚集在一起更容易。 他們的皮質醇水平高於正常，和他們 - 垂體 - 腎上腺皮質激素是難以抑制。 這是一個條件，也看到在抑鬱症和老年。 儘管皮質醇的長期升高，與MS的人通常有低血糖。 他們偶爾發現有低鈉血症，低血鈉，但這是難以確定時，血液中的水分含量是可變的。 他們的催乳激素可能會很高，這可能會導致高雌激素，血清素高，低鈉鹽，或低甲狀腺。 喝太多水可以增加催乳素，並能損害神經的髓鞘外殼過多的血清素，往往造成過量飲酒。 血糖，鈉和水含量的干擾可以破壞大腦的髓鞘結構。 高雌激素會干擾血液滲透，使得它保留溶質的水太多，並與許多雌激素的影響的關係，因為簡單的滲透壓變化可以破壞的髓鞘結構，它似乎，這個機制應該被調查的深入之前，它是假定免疫活動是主要的。

肥大細胞，促進炎症釋放物質如組胺和5 - 羥色胺（使血管滲漏），比正常的大腦更在許多多發性硬化症腦。 由於血小板凝結釋放血清素，而且還因為建議 - 羥色胺過剩是由許多其他功能的MS，血清素拮抗劑（昂丹司瓊和酮色林，例如）已成功地用於治療。

雌激素會導致肥大細胞釋放炎症介質，它會導致血小板聚集，釋放他們的血清素。 由於雌激素的優勢是存在活躍的腦部病變密切相關，抗雌激素治療，似乎是顯而易見的，在MS。 孕激素對抗雌激素對肥大細胞和血小板的影響。

阿司匹林防止各種炎症過程，但它是最著名的抑制前列腺素的。 而阿司匹林常被用來減輕疼痛在MS，另一種前列腺素合成酶抑製劑，消炎痛，已被用於在MS治療，它似乎是適當的，更仔細地探討阿司匹林在防止或減輕MS的可能發揮的作用。

一個簡單的蛋白質缺乏症有許多令人驚訝的效果。 它降低體溫，並抑制甲狀腺，但它增加了炎症和血液凝塊的趨勢。 由於大腦和心臟和肺需要連續供應的必需氨基酸，如果他們繼續運作，膳食蛋白質的情況下，產生皮質醇，必須不斷的消耗性組織，主要是骨骼肌氨基酸動員。 這些肌肉有高濃度的色氨酸和半胱氨酸，從而抑制甲狀腺。 半胱氨酸是excitoxic的，和色氨酸是羥色胺的前體。 據推測，他們的存在，誘導應力釋放，肌肉是在某些類型的壓力，減少代謝活性的機制之一。

當懷孕的動物蛋白質被剝奪，新生動物有異常高的水平，血清素，負責，過量的酶傾向於保持多餘的，即使他們都已經長大，有足夠的蛋白質 - 羥色胺。 這是類似於過剩的雌激素的影響早在生活中，創建一個趨勢，以發展在成年後乳腺癌或前列腺癌。 妊娠期的經驗，例如，懷孕和出生體重長的人誰後開發的MS，這將是有趣的研究。

雖然在北部國家的人是不正常蛋白質匱乏，他們往往得到了他們的蛋白質的肌肉的很大一部分。 在傳統文化中，所有食品動物部分食用雞的腳，頭，脖子，動物的耳朵和眼球等，使氨基酸平衡良好，保持了較高的代謝率，防止壓力。

多發性硬化症是豬肉和馬肉的消費，而不是牛肉，羊肉，或山羊，觀察是非常有趣的，因為這些動物的脂肪基本上是一樣的，他們吃的植物材料的脂肪，這意味著它亞油酸和亞麻酸是非常高的。 牛，綿羊和山羊瘤胃中包含細菌，轉換成更多的飽和脂肪多不飽和脂肪。 不飽和脂肪抑制酶消化蛋白質，MS患者已報告有肉的消化不好古普塔等人（1977）。

多不飽和脂肪本身是線粒體毒性，抑制葡萄糖氧化，抑制甲狀腺功能，氧化葡萄糖的能力上具有相同的抑製作用，但他們也已經打開，enzymically，到前列腺和非-enzymically的，自發性脂質過氧化，變成有毒的異前列。 異前列，一些前列腺素，升高與MS的人的大腦和其他組織。

多發性硬化症是非常高的脂質過氧化。 一氧化氮（其合成的雌激素在大腦的大部分地區推廣）是激活過氧化自由基。

脂質過氧化選擇性破壞，自然不穩定的多不飽和脂肪。 在動脈粥樣硬化，血管斑塊中含有不飽和脂肪很少。 這是因為它們過氧化如此迅速，但其飽和不飽和脂肪的比例高，已被用來論證，多不飽和油“保護心臟。”類似的論點往往在MS，雖然一些研究不支持這一想法是有任何的不飽和脂肪的缺乏。 由於脂質過氧化是非常高的，這將是合理的假設，有豐富的多不飽和脂肪過氧化反應，通過催化劑，如鐵（SM萊文，1997年）和一氧化氮和peroxynitrile。

我相信，所以往往在與MS的人熱不容忍現象的一個重要方面可能相對熱療釋放到血液中的游離脂肪酸增加的趨勢。 婦女，由於雌激素的影響，通常比男人血液中的游離脂肪酸的水平要高得多。 雌激素增加釋放游離脂肪酸從脂肪儲存，不飽和脂肪與雌激素和催乳素增效，提高他們的影響。

溫度調節顯然涉及一些感溫度非常準確的神經細胞，並相應地改變他們的活動。 水有非常高的熱容量，這意味著它需要相對大量的熱量，以改變其溫度。 “消失的熱量被消耗在水的結構性變化。 蛋白質有同類型結構複雜，水和他們一起可以做出有效的溫度傳感器，“溫度計”。（其他物質往往發生重大的結構性變化，只因為他們熔化或汽化。著名的“液態晶體”，有幾個不同的結構階段，但細胞質就像是一個非常微妙的液晶）。“調溫細胞”實際上是回應到一定程度的內部結構，而不是抽象的溫度。 這樣的事情，改變其內部結構，將修改其溫度設定點。“

增加雌激素會導致動物，以降低其溫度，它可能增加“結構溫度”恆溫細胞，“融化”，其內部結構。 孕激素引起的動物，以提高其溫度，它顯然沒有結構，增加/減少溫度的恆溫細胞結構。 如果你把冰溫控器，房間變熱。

一個細胞的內部結構，相當於其準備工作。 疲勞稍微“融化”的細胞的狀態，在這種結構似乎已消耗化學能源儲備。 實驗表明這種影響是非常明確的，但他們被忽略，因為它們不符合人的細胞的刻板想法。 有了一個非常敏感的溫度計，它可以測量由神經所產生的熱量，當它受到刺激。 這並不奇怪。 但它是令人驚訝，神經刺激復甦時，它從它的環境中吸收熱量，降低局部溫度。 ，甚至侵犯了一些人的概念“熵”，但它可以很容易地被證明，改變某些材料的形式改變了它們的熱容量，當橡皮筋被拉長，它也變熱，或合同，它變得涼爽。

的excitants，雌激素和皮質醇，減緩神經的傳導，因為它們會導致其內部結構將消散。 他們創造了“預疲勞”狀態中的細胞。

森特 - Gyorgyi兔心實驗，表明，雌激素減少心臟的準備工作，孕激素增加的準備工作，和他說，它沒有通過這種“建築結構。”他指出，為1給予藥物或其他的刺激，細胞有一個特點，響應，成為或者更多的激活或抑制，但他表明，正常的濃度或強度範圍的刺激外，細胞的反應往往是扭轉。

如果是這樣的情況在MS的神經，它解釋了奇怪的行為，在升溫的神經，降低其功能。 言下之意是，內部結構（能源）必須恢復到的神經。 在我所描述的，在以前的通訊，鈉，ATP，二氧化碳和孕激素增加，增加鎂鈣比，實驗中已經發現，增加細胞的能量和結構。 甲狀腺激素是最終負責維持細胞的能量和結構，並響應，但是，如果它不允許所有其他因素調整的情況下突然增加，這將提高溫度，太突然。 它不需要花費很長時間，但所有的因素都必須在同一時間出席。

血清素，褪黑激素，雌激素，多不飽和脂肪都傾向於降低體溫。 由於雌激素和不飽和脂肪蜂窩excitants，在實際體溫下降有助於抵消他們的興奮作用。

無論是明亮的光線和高海拔傾向於降低血清素的影響。 該組織保留在高海拔地區的二氧化碳減少了許多疾病的發病率，心臟疾病和癌症，多發性硬化症，可能會受到影響。 據了解，二氧化碳在參與髓鞘的調節自身的含水量。 換氣過度，造成損失的二氧化碳，釋放組胺和血清素，使血液更粘稠，同時使血管滲透，並導致他們收縮。

如果用MS的人過多的雌激素，血清素，不飽和脂肪，鐵，水，和缺乏甲狀腺，缺乏孕烯醇酮生產中的髓鞘形成細胞（少突膠質細胞）的相互作用，通過開發，有很多事情可以做停止其進展情況，並有可能扭轉這種局面。

Since a sudden increase in temperature will release increased amounts of the pro-inflammatory fats, things should be changed gradually. Increased salt is thermogenic, but increased magnesium is protective against hyperthermia, so increased magnesium (epsom salts baths, for example, coffee, fruits, some vegetables and meats) would be helpful. Magnesium is rapidly lost from cells in hypothyroidism. Sugar, when accompanied by fats and minerals, as in milk, is needed to lower cortisol, and to maintain thyroid activity. Balanced proteins, such as cheese, potatoes, eggs, and beef- or lamb-broth (for the gelatin and mineral content in particular) will prevent the tryptophan excess that suppresses the thyroid and is potentially a nerve toxin. Saturated fats, used regularly, reduce the immediate toxic antimetabolic effects of the stored unsaturated fats, but it takes a long time to change the balance of stored fats.

Since aspirin lowers temperature, is antiinflammatory, in some situations antiestrogenic, and is a powerful antioxidant, it is likely that it would alleviate symptoms and prevent progression of MS, as it does in other degenerative diseases. Since platelet aggregation is likely to be involved in the focuses of inflammation, aspirin might help to prevent the formation of new areas of damage.

While the glucocorticoids are useful for their antiinflammatory actions, cortisol is known to promote the killing of brain cells by excitotoxicity. Since estrogen decreases GABA, and both estrogen and serotonin activate the excitatory amino acid transmitters, the addition of synthetic glucocorticoids to the pre-existing cortisol excess is likely to damage parts of the brain in addition to the inflamed areas.

The excess cortisol of depression, old age, and hyperestrogenism often comes down with use of a thyroid supplement, but pregnenolone has a very direct action (in opposition to serotonin) that can quiet the pituitary, reducing ACTH and cortisol. Progesterone has some similar effects, and is protective against excess cortisol, and is a major factor in nerve and brain restoration. Thyroid, progesterone, and pregnenolone are all involved in the formation of new myelin, and in the prevention of the edema that damages it.

Since thyroid and progesterone decrease the formation of estrogen in inflamed tissue, while cortisol stimulates its formation, it would seem wise to use thyroid and progesterone for their immediate antiinflammatory effects, which include the inhibition of NO formation (Drew and Chavez, 2000), and their lack of the excitotoxic, estrogen-stimulating effects of the glucocorticoids. While the glucocorticoids are catabolic and liberate cysteine and tryptophan from muscles, thyroid and progesterone are not catabolic, and protect against the toxic consequences of those amino acids.

參考

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Am J Pathol 1985 Dec;121(3):531-51. Sex hormones, immune responses, and autoimmune diseases. Mechanisms of sex hormone action. Ansar Ahmed S, Penhale WJ, Talal N. “Immune reactivity is greater in females than in males. In both experimental animals and in man there is a greater preponderance of autoimmune diseases in females, compared with males. Studies in many experimental models have established that the underlying basis for this sex-related susceptibility is the marked effects of sex hormones. Sex hormones influence the onset and severity of immune-mediated pathologic conditions by modulating lymphocytes at all stages of life, prenatal, prepubertal, and postpubertal.”

J Appl Physiol 1996 Feb;80(2):464-71. Effects of changes in dietary fatty acids on isolated skeletal muscle functions in rats. Ayre KJ, Hulbert AJ The effects of manipulating dietary levels of essential polyunsaturated fatty acids on the function of isolated skeletal muscles in male Wistar rats were examined. Three isoenergetic diets were used: an essential fatty acid-deficient diet (EFAD), a diet high in essential (n-6) fatty acids [High (n-6)], and a diet enriched with essential (n-3) fatty acids [High (n-3)]. After 9 wk, groups of rats on each test diet were fed a stock diet of laboratory chow for a further 6 wk. Muscle function was examined by using a battery of five tests for soleus (slow twitch) and extensor digitorum longus (EDL; fast twitch). Tests included single muscle twitches, sustained tetanic contractions, posttetanic potentiation, sustained high-frequency stimulation, and intermittent low-frequency stimulation. Results for muscles from the High (n-6) and High (n-3) groups were very similar. However, the EFAD diet resulted in significantly lower muscular tensions and reduced response times compared with the High (n-6) and High (n-3) diets. Peak twitch tension in soleus muscles was 16-21% less in the EFAD group than in the High (n-6) and High (n-3) groups, respectively [analysis of variance (ANOVA), P < 0.01). During high-frequency stimulation, EDL muscles from the EFAD rats fatigued 32% more quickly (ANOVA, P < 0.01)]. Also, twitch contraction and half-relaxation times were significantly 5-7% reduced in the EFAD group (ANOVA, P < 0.01). During intermittent low-frequency stimulation, soleus muscles from the EFAD group generated 25-28% less tension than did the other groups (ANOVA, P < 0.01), but in EDL muscles from the EFAD group, endurance was 20% greater than in the High (n-6) group (ANOVA, P < 0.05). After 6 wk on the stock diet, there were no longer any differences between the dietary groups. Manipulation of dietary fatty acids results in significant, but reversible, effects in muscles of rats fed an EFAD diet.

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J Neurochem 1988 04 50（4）:1185-93。 誘導細胞內超氧自由基的形成星形小學文化的多不飽和脂肪酸花生四烯酸和。 PH值，陳社發，陳羽交流“其他的多不飽和脂肪酸，包括亞油酸，亞麻酸和二十二碳六烯酸，也有效地刺激NBF形成星形膠質細胞，而飽和的棕櫚酸和不飽和油酸是無效的。 這些不飽和脂肪酸類似的效果觀察丙二醛形成細胞和培養液中的乳酸積累。 這些數據表明，細胞膜的完整性和細胞代謝是由花生四烯酸等多不飽和脂肪酸的攝動。“

安神經病學神經1983年6月13（6）:625-32。 腦水腫，腦內注射花生四烯酸誘導。 陳PH值，菲什曼天雨，Caronna J，Schmidley JW，PrioleauĞ，李J“腦內注射的多不飽和脂肪酸（多不飽和脂肪酸），包括亞麻酸（18:3）和花生四烯酸（20:4），造成腦顯著增加水和鈉的內容隨之減少鉀的含量和Na + - 和的K + - 腺苷三磷酸酶的活性依賴。 有毛和微觀水腫的證據。 不飽和脂肪酸和單不飽和脂肪酸，有效地誘導腦水腫。 [125I]牛血清白蛋白的空間在24小時內增加了兩倍和三倍，以18:3和20:4，表明血管性水腫，腦血管內皮細胞的通透性增加“，”這些數據表明，花生四烯酸等不飽和脂肪酸有的能力，促使血管性和細胞性腦水腫，進一步支持這一假設降解磷脂和多不飽和脂肪酸，尤其是​​花生四烯酸的積累，開始在各種疾病狀態下的腦水腫的發展。“

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ZH Nevropatol Psikhiatr進出口衛隊Korsakova 1990年，90（11）:47-50。 多發性硬化症和校正血液的流變學特性的變化]。 流變血屬性，Redchits乙二醇，謝列茲尼奧夫，Svetailo李，Margosi​​uk內華達州，許多多發性硬化症患者45 Stulin編號，Smertina唱片卡爾洛夫弗吉尼亞州，薩文機管局在俄羅斯進行了檢查。 與對照組相比，根據檢查組的表現引起血漿粘度，加速紅細胞聚集。 26.2％的患者表現出的血液粘稠度明顯增加。 據推測，這些變化有助於微循環的惡化，並加劇脫髓鞘過程。 再加上其他致病性治療方法通過血漿置換血液的流變屬性修正了有效。

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Acta Neurol Scand 1982 Oct;66(4):497-504, Platelet aggregation and multiple sclerosis. Neu IS, Prosiegel M, Pfaffenrath V Measurements of blood platelet aggregation were carried out in 30 patients suffering from multiple sclerosis (MS) and in 15 healthy individuals. Compared with the control group, the MS patients showed an increase in both spontaneous and induced (ADP and serotonin) platelet aggregation. The possible pathogenetic significance of these results is discussed.

Neurology 1975 Aug;25(8):713-6. Schwann cells and regenerated peripheral myelin in multiple sclerosis: an ultrastructural study. Ogata J, Feigin I Tissue of a multiple sclerosis plaque in the brachium conjunctivum of the pons known to contain peripheral myelin by light microscopic studies were removed from the paraffin block and processed for electron microscopic studies. The cells related to the peripheral myelin possessed the ultrastructural characteristics of Schwann cells, with basement membranes and associated collagen fibers. No continuity was seen with the peripheral within the central nervous tissues by selective maturation of multipotential primitive reticular cells, a phenomenon consistent with the view that Schwann cells are mesenchymal in character.

東北實驗醫學1999年12月; 189（4）:259-65。 升高血漿纖溶酶原激活物抑制物1（PAI-1）復發型多發性硬化症患者。 小野寺H，中島我，藤原ķ，永田ţ，糸山Ÿ“多發性硬化症（MS）是中樞神經系統炎性脫髓鞘疾病，涉及血管內皮細胞的活化和炎症焦點最早的變化之一。”血漿PAI-1的水平顯著提高，在活躍的MS病例較穩定的MS和控制。“這些結果表明，PAI-1血漿水平與MS疾病活動相關聯的是一個MS復發的良好指標。”

J分子醫學1997年3月75（3）:174-86。 一氧化氮在多發性硬化的作用。 帕金森，米特羅維奇B，美林，摩根富林明乙腦“已升高一氧化氮的生物合成與非特異性免疫介導的細胞毒性和慢性炎症性自身免疫性疾病包括類風濕關節炎，胰島素依賴型糖尿病，發炎性腸道疾病，多發性硬化症的發病機制“

美聯儲PROC 1987 01 46（1）:91-6。 neuroimmunologic疾病的發病機制中的凝血系統的作用。 帕特森PY，蘇梅CS，Kwaan慧聰“我們的研究和隨後的纖溶凝血系統的牽連內或壁面上發起的炎症特徵EAE的事件cerebrovasculature。凝血和纖維蛋白裂解”我們推測，關鍵事件促發EAE的是循環MBP反應的免疫效應細胞MBP腦血管內皮細胞表面上的immunodeterminants結合。 凝血和纖溶隨後發生在腦血管內皮細胞的效應細胞具有約束力的網站。 推出生物活性肽裂解纖維蛋白開放血腦屏障，從而為級聯炎症事件最終對EAE臨床表現的舞台。“

神經毒性1998年八月至十月，19（4-5）:599-603。 半胱氨酸代謝產物同型半胱氨酸，同型半胱氨酸和磺基酸對人類神經細胞株在體外效應。 帕森斯包，華林濕度，拉姆斯登DB，威廉姆斯交流“半胱氨酸（胱氨酸）是一種非必需氨基酸，通過N-甲基-D-天冬氨酸（NMDA）受體的谷氨酸受體亞型引起的興奮屬性.. 半胱氨酸水平升高與神經系統疾病，如老年性癡呆（AD）和帕金森病（PD）是已知的協會。“這些結果表明，毒性反應是特定細胞類型半胱氨酸及其代謝物，這可能反映在觀察AD和PD等疾病的神經退行性疾​​病的模式。“

WMJ 1983 Mar-Apr;55(2):146-50. [Effect of tryptophan excess in a diet on amino acid composition of skin collagen and on an initial stage of protein biosynthesis in rat liver]. Pechenova TN, Sushkova VV, Solodova EV, Gulyi MF Protein deficiency and tryptophane load against its background lead to the acid-soluble collagen synthesis in the rat skin. The amino acid composition of the collagen differs from the norm. This is accompanied by changes in the free amino acid pool of blood serum and liver, under tryptophane load the free amino acids pool of the liver increasing twice as high. At the same time protein deficiency increases and tryptophane load decreases the level of tRNA amino acylation with tryptophane in the animal liver. Thus, protein deficiency and tryptophane load against its background cause deep changes in the protein biosynthesis.

Fed Proc 1987 Jan;46(1):91-6. Role of the clotting system in the pathogenesis of neuroimmunologic disease. Paterson PY, Koh CS, Kwaan HC “Our studies of the clotting system and ensuing fibrinolysis implicate coagulation and cleavage of fibrin within or on the luminal surface of the cerebrovasculature as events initiating the inflammation characterizing EAE.” “We postulate that the critical event precipitating EAE is binding of circulating MBP-reactive immune effector cells to MBP immunodeterminants on the surface of cerebrovascular endothelial cells. Coagulation and ensuing fibrinolysis occur at sites of binding of effector cells to cerebrovascular endothelium. Release of biologically active peptides cleaved from fibrin open the BBB, thereby setting the stage for the cascade of inflammatory events culminating in clinical manifestations of EAE.”

Rev Esp Fisiol 1983 Mar;39(1):39-44. Intralipid and free plasmatic tryptophan in vitro. Pena JM, Aulesa C, Vinas O, Bosch J, Farriol M, Schwartz S “In an attempt to investigate the role of the lipidic emulsion Intralipid in the development of metabolic encephalopathy in a patient showing high free tryptophan levels, the relationship between lipidic emulsion and free tryptophan was examined in in vitro experiments. The addition of intralipid to normal serum produces an immediate increase in non-esterified fatty acids and a parallel rise in free tryptophan. Moreover, when serum with intralipid is incubated at 37 degrees C, the lipases release new non-esterified fatty acids and the free tryptophan increases proportionally.” “It is concluded that intralipid causes an increase in free tryptophan levels. It is known that in vivo free tryptophan modulates 5-hydroxytryptamine synthesis and thus may be considered a possible causal agent for encephalopathy.”

Med Hypotheses 1980 May;6(5):545-557. Fatty acids, fibrinogen and blood flow: a general mechanism for hyperfibrinogenemia and its pathologic consequences. Pickart LR, Thaler MM Plasma fibrinogen is elevated in various stressful states and conditions in which active mobilization of free fatty acids (FFA) occurs. Reduction of plasma FFA by an assortment of hypolipidemic drugs is consistently followed by a decrease in the accompanying hyperfibrinogenemia. A direct link between FFA and fibrinogen has been demonstrated in animals, and in experiments employing incubated liver slices. Based on these clinical and experimental observations, we postulate that hepatic fibrinogen synthesis is stimulated by FFA. Since fibrinogen is a major determinant of whole blood viscosity, erythrocyte aggregation, and sludging of red cells in terminal and pre-terminal blood vessels, we propose that microcirculatory blood flow may be impaired in the presence of chronically elevated plasma FFA levls. Consequently, hypolipidemic drugs may be effective in prevention of circulatory complications associated with FFA-induced hyperfibrinogenemia.

Neurologia 1996 Aug-Sep;11(7):272. [Exacerbation of spasticity induced by serotonin reuptake inhibitors. Letter]. del Real MA, Hernandez A, Vaamonde J, Gudin M

J Neurol Neurosurg Psychiatry 1997 Mar;62(3):282-4. Ondansetron, a 5-HT3 antagonist, improves cerebellar tremor. Rice GP, Lesaux J, Vandervoort P, Macewan L, Ebers GC. “It has been previously shown that ondansetron, a 5-HT3 antagonist, can ameliorate vertigo in patients with acute brainstem disorders. A coincidental benefit was the improvement of cerebellar tremor in some patients with both vertigo and tremor. To further evaluate this effect, a placebo controlled, double blind, crossover study was conducted of a single dose of intravenous ondansetron in 20 patients with cerebellar tremor caused by multiple sclerosis, cerebellar degeneration, or drug toxicity.” “Thirteen of 19 patients were deemed to have improved spiral copying after treatment with ondansetron when compared with baseline performance.”

Neurologia 1993 Oct;8(8):252-5. [Retinal periphlebitis in multiple sclerosis. A prospective study]. Rio J, Colin A, Salvador F, Tintore M, Viguera ML, Montalban J, Codina A “In three cases (12.5%) retinal periphlebitis was observed.” “Given the absence of myelin in the retina, the presence of retinal periphlebitis suggests the existence of a vascular mechanism in the pathogenesis of multiple sclerosis.”

Int J Neurosci 1995 Dec;83(3-4):187-98. Premenstrual exacerbation of symptoms in multiple sclerosis is attenuated by treatment with weak electromagnetic fields. Sandyk R. “The present report concerns two women with chronic progressive stage MS who experienced, coincident with increasing functional disability, regular worsening of their symptoms beginning about a week before menstruation and abating with the onset of menstruation. These symptoms resolved two months after the initiation of treatment with EMFs.”

J Physiol Biochem 1998 Dec;54(4):229-37. The role of nitric oxide in the pathogenesis of multiple sclerosis. Santiago E, Perez-Mediavilla LA, Lopez-Moratalla N “The inducible NOS (iNOS) is associated with the development of a number of autoimmune diseases.” “Induction of the enzyme is effected by proinflammatory cytokines, immunomodulating peptides, and even beta-endorphin through a mechanism involving an increase in cAMP. An excessive production of NO has been implicated in the severe lesions observed in multiple sclerosis (MS).”

J Neurol 1980 Jan;222(3):177-82. Cerebrospinal fluid lipids in demyelinating disease. 二。 Linoleic acid as an index of impaired blood-CSF barrier. Seidel D, Heipertz R, Weisner B “The linoleic acid content of control CSF (1.6 +/- 0.8 nMol/ml) is considerably lower than the corresponding serum value (2.5–4.1 muMol/ml). Although CSF from MS patients contains a significantly higher linoleic acid concentration than controls the close correlation between CSF linoleic acid and CSF albumin is maintained. The high CSF concentration of cholesterol esters rich in linoleic acid, which are abundant in serum but represent only traces in CNS lipids, points towards an impaired BBB function as the cause of CSF linoleic increase. We are able to show that both albumin and linoleic acid are suitable as “serum markers….”

J Neurol Sci 1987 Feb;77(2-3):147-52. Chronic periphlebitis retinae in multiple sclerosis. A histopathological study. Shaw PJ, Smith NM, Ince PG, Bates D Retinal periphlebitis in multiple sclerosis is of particular interest in relation to our understanding of the pathogenesis of the demyelinating central nervous system plaques. Previous studies have largely been clinical, and there is little detailed histopathological information relating to this condition. We present the first detailed report in the neurological literature on the histological findings in chronic periphlebitis retinae associated with multiple sclerosis. The most significant abnormalities of the affected retinal veins were the presence of thick laminated collagen in the wall, associated with a scanty infiltration of plasma cells.

Am Heart J 2000 Aug;140(2):212-8. Low intracellular magnesium levels promote platelet-dependent thrombosis in patients with coronary artery disease. Shechter M, Merz CN, Rude RK, Paul Labrador MJ, Meisel SR, Shah PK, Kaul S.

J Neurochem 1996 Mar;66(3):1157-66. Mast cell activation causes delayed neurodegeneration in mixed hippocampal cultures via the nitric oxide pathway. Skaper SD, Facci L, Romanello S, Leon A. “Neurotoxicity required a prolonged period (12 h) of mast cell incubation, and appeared to depend largely on elaboration of the free radical nitric oxide by astrocytes.” “Myelin basic protein and 17 beta-estradiol had a synergistic action on the induction of mast cell-associated neuronal injury.” “Further, palmitoylethanolamide, which has been reported to reduce mast cell activation by a local autacoid mechanism, decreased neuron loss resulting from mast cell stimulation in the mixed cultures but not that caused by direct cytokine induction of astrocytic nitric oxide synthase.” “These results support the notion that brain mast cells could participate in the pathophysiology of chronic neurodegenerative and inflammatory diseases of the nervous system, and suggest that down-modulation of mast cell activation in such conditions could be of therapeutic benefit.”

International Journal of Microcirculation–Clinical and Experimental, 1996, Vol 16, Iss 5, pp 266-270. Hyperventilation enhances transcapillary diffusion of sodium fluorescein. J Steurer, D Schiesser, C Stey, W Vetter, MV Elzi, JP Barras, UK Franzeck. “Voluntary hyperventilation (HV) provokes hemoconcentration due to a loss of fluid from the intravascular space.” “The exact, mechanism of enhanced transcapillary diffusion of Na fluorescein is not known, The distinct increase in FLI without a significant change in microvascular skin flux suggests an HV-induced increase in capillary pressure or an enhancement in capillary permeability for water and small solutes.”

Kidney Int 1992 May;41(5):1245-53. Essential fatty acid deficiency normalizes function and histology in rat nephrotoxic nephritis. Takahashi K, Kato T, Schreiner GF, Ebert J, Badr KF.

Arthritis Rheum 1981 Aug;24 (8):1054-6. Sex steroid hormones and systemic lupus erythematosus. Talal N.

Clin Rheum Dis 1982 Apr;8(1):23-8. Sex hormones and modulation of immune response in SLE. Talal N.

Ann NY Acad Sci 1986;475:320-8. Hormonal approaches to immunotherapy of autoimmune disease. Talal N, Ahmed SA, Dauphinee M.

Ann Nucl Med 1998 Apr;12(2):89-94. Clinical significance of reduced cerebral metabolism in multiple sclerosis: a combined PET and MRI study. Sun X, Tanaka M, Kondo S, Okamoto K, Hirai S “The severity of cerebral hypometabolism was also related to the number of relapses.” “Our results suggest that measurement of cerebral metabolism in MS has the potential to be an objective marker for monitoring disease activity and to provide prognostic information.”

Fed Proc 1987 Jan;46(1):118-26. Pathway to carrageenan-induced inflammation in the hind limb of the rat. Vinegar R, Truax JF, Selph JL, Johnston PR, Venable AL, McKenzie KK “Antiserotonin agents inhibited the hypoalgesia and part of the edema. These findings and histological observations suggested that dermal mast cells were injured by C. The hyperalgesia and part of the edema were sensitive to arachidonate cyclooxygenase inhibitors (AACOIs). It is speculated that injured mast cells metabolize arachidonic acid and reactive intermediates, not prostaglandins, mediate the NPIR hyperalgesia and part of the edema.” “Arachidonic acid metabolism by neutrophils is speculated to produce the mediators of phagocytic inflammatory (PI) edema and hyperalgesia.”