Diabetes, scleroderma, oils and hormones
糖尿病，硬皮病，油脂和激素
by Raymond Peat
The basic argument: Stress and aging make cells less responsive in many ways by damaging their ability to produce energy and to adapt. The polyunsaturated fats are universally toxic to the energy producing system, and act as a “misleading signal” channeling cellular adaptation down certain self-defeating pathways. Diabetes is just one of the “terminal” diseases that can be caused by the polyunsaturated vegetable oils. Coconut oil, in diabetes as in other degenerative diseases, is highly protective.
基本观点是:压力和衰老通过破坏细胞产生能量和适应能力，在许多方面降低了细胞的反应能力。多不饱和脂肪对能量产生系统普遍有毒，并作为一种“误导信号”，引导细胞通过某些自我挫败的途径进行适应。糖尿病只是多不饱和植物油可引起的“终末期”疾病之一。椰子油对糖尿病和其他退行性疾病具有高度保护作用。
When the oral contraceptive pill was new (Enovid), it was found to produce signs of diabetes, including decreased glucose tolerance. Spellacy and Carlson (1966) suggested that an elevation of circulating free fatty acids might be responsible, and remarked that “Free fatty acids can block the Krebs cycle, with relative insulin action resistance resulting.” “The potential danger of the oral contraceptives is one of prolonged pancreatic stimulation.” Recent papers are reporting that the estrogen used to “treat menopause” causes an increase in free fatty acids. Spellacy and Carlson suggested that estrogen's effect was mediated by growth hormone, and that is now the consensus. Women are much more likely than men to develop diabetes.
当口服避孕药刚刚问世时(Enovid)，人们发现它会产生糖尿病的症状，包括糖耐量下降。Spellacy和Carlson(1966)认为可能与循环中游离脂肪酸的升高有关，并指出“游离脂肪酸会阻碍克雷布斯循环，导致相对的胰岛素作用抵抗。”“口服避孕药的潜在危险是长期的胰腺刺激。”最近的论文报道说，用于“治疗更年期”的雌激素会导致游离脂肪酸的增加。Spellacy和Carlson认为雌激素的作用是由生长激素介导的，这是现在的共识。女性比男性更容易患糖尿病。
Ephraim Racker observed that free unsaturated fatty acids inhibit mitochondrial respiration, and recent studies are finding that free linoleic and linolenic acids act as intracellular regulators, stimulating the protein kinase C (PKC) system, which is also stimulated by estrogen and the (cancer promoting) phorbol esters. They stimulate the cell while blocking the energy it needs to respond.
Ephraim Racker观察到游离不饱和脂肪酸抑制线粒体呼吸，最近的研究发现游离亚油酸和亚麻酸作为细胞内的调节器，刺激蛋白激酶C (PKC)系统，这也是由雌激素和(促进癌症)佛波酯刺激的。它们刺激细胞，同时阻断细胞反应所需的能量。
Scleroderma, or systemic sclerosis, is a supposedly mysterious condition in which tissues harden, with an excessive deposition of fibrous material. Besides hardening the skin, it can involve fibrosis of the heart and other organs, and can cause changes in blood vessels of the kidneys like those seen in some types of hypertension, and often involves Raynaud's phenomenon and osteoporosis of the fingers. (Silicone functions as an adjuvant, making exposure to irritants, solvents or infections more harmful. This seems to be the reason for the association between breast implants and scleroderma.) Another type of disease that involves hardening of the skin is scleredema, in which the skin thickens with an accumulation of “mucin” between collagen bundles, and in which fibroblasts are overactive in producing collagen. (Varga, et al.) This condition is believed to often follow a “febrile illness” and is associated with diabetes. My interest in these conditions comes from my awareness that estrogen promotes collagen formation, and that changes in the connective tissue are deeply associated with the processes of stress and aging, following the ideas of Metchnikov and Selye.
硬皮病，或系统性硬化症，被认为是一种神秘的状况，组织硬化，纤维物质过度沉积。除了皮肤变硬，它还会导致心脏和其他器官的纤维化，并会导致肾脏血管的变化，就像某些类型的高血压所见的那样，通常还会涉及雷诺氏症和手指骨质疏松症。(硅作为一种佐剂，使接触刺激物、溶剂或感染更有害。这似乎就是隆胸和硬皮病之间存在关联的原因。)另一种与皮肤硬化有关的疾病是硬化性水肿，在这种疾病中，皮肤增厚，胶原束之间的“粘蛋白”聚集，纤维母细胞过度活跃地生产胶原蛋白。(Varga等)这种情况通常伴随着“发热性疾病”，并与糖尿病有关。我对这些情况的兴趣来自于我的意识，即雌激素促进胶原蛋白的形成，结缔组织的变化与压力和衰老的过程密切相关，这是Metchnikov和Selye的观点。
Many people are still committed to the various old theories of diabetes, though a few are showing ways in which multiple causes can lead to diabetes. Increasingly, old age itself is seen to be “like diabetes (Meneilly, et al.; Smith, et al.), and the situation is ripe for a recentering of our understanding of diabetes around some of the general facts about aging and stress.
许多人仍然坚持各种关于糖尿病的旧理论，尽管一些人已经表明多种原因可以导致糖尿病。越来越多的人认为老年本身“就像糖尿病”(Meneilly等;史密斯等)，现在的情况已经成熟，可以让我们围绕衰老和压力的一些普遍事实来重新认识糖尿病。
Diabetes mellitus, as named, refers to excessive urination and sugary urine, but it is now often diagnosed in people who neither urinate excessively nor pass glucose in the urine, on the basis of a high level of glucose in the blood. Many other signs (abnormal mucopolysaccharide metabolism with thickening of basement membranes, leakage of albumin through capillary walls and into the urine, a high level of free fatty acids in the blood, insensitivity of tissues to insulin, or reduced sensitivity of the beta cells to glucose) are considered diagnostic by some people, who believe that the worst aspects of the disease can be prevented if they can diagnose early and take preventive measures. This attitude derives largely from the genetic theory of causation, though it incorporates a belief that (environmental) intervention can ameliorate the course of the disease. When I wrote Nutrition for Women, I mentioned that the sudden appearance of diabetes in non-European Jews when they moved to Isreal made the genetic theory of diabetes untenable, and since then other studies have made the similar point that environmental factors seem crucial. (Shaltout, et al.) Many people are arguing for the racial/genetic theory of diabetes, but they are failing to consider some simple dietary factors, especially the high consumption of unsaturated seed oils and the combination of nutritional deficiencies and environmental stress.
糖尿病，顾名思义，是指排尿过多和含糖尿，但现在往往是在血液中葡萄糖水平高的基础上，既不排尿过多，也不排出尿液中的葡萄糖的人被诊断为糖尿病。许多其它迹象(黏多醣代谢异常与基底膜的增厚,白蛋白通过毛细血管壁和泄漏到尿液中,高水平的血液中游离脂肪酸,组织对胰岛素不敏感,或减少敏感的β细胞葡萄糖)被一些人认为是诊断,他们认为，如果能及早诊断并采取预防措施，这种疾病最糟糕的方面是可以预防的。这种态度很大程度上源于因果关系的遗传理论，尽管它包含了(环境)干预可以改善疾病进程的信念。当我写《女性营养》时，我提到非欧洲犹太人移居以色列后突然出现糖尿病，这使得糖尿病的基因理论站不住脚，从那以后，其他研究也提出了类似的观点，即环境因素似乎至关重要。(shalout, et al.)许多人主张糖尿病的种族/遗传理论，但他们没有考虑到一些简单的饮食因素，特别是不饱和籽油的高消耗以及营养不足和环境压力的结合。
I have known adults and children who were diagnosed as diabetic, and given insulin (and indoctrinated with the idea that they had a terminal degenerative disease) on the strength of a single test showing excessive glucose. When I taught at the naturopathic medical school in Portland, I tried to make it clear that “diabetes” (a term referring to excessive urination) is a function, and that a high level of glucose in the blood or urine is also a function, and that the use of insulin should require a greater diagnostic justification than the use of aspirin for a headache does, because insulin use itself constitutes a serious health problem. (And we seldom hear the idea that “diabetes” might have a positive side [Robinson and Johnston], for example that it reduces the symptoms of asthma [Vianna and Garcialeme], which get worse when insulin is given. Normal pregnancy can be considered “diabetic” by some definitions based on blood sugar. I got interested in this when I talked to a healthy “diabetic” woman who had a two year old child whose IQ must have been over 200, judging by his spontaneous precocious hobbies. Old gynecologists told me that it was common knowledge that “diabetic” women had intellectually precocious children.)
我认识一些被诊断为糖尿病的成人和儿童，他们仅仅因为一次血糖超标就注射了胰岛素(并被灌输了他们患有晚期退行性疾病的想法)。当我在波特兰的自然疗法医学院教书时，我试图让人们明白“糖尿病”(指排尿过多)是一种功能，血液或尿液中葡萄糖含量高也是一种功能，使用胰岛素比使用阿司匹林治疗头痛需要更大的诊断理由，因为使用胰岛素本身就构成了严重的健康问题。(我们很少听到“糖尿病”可能有积极的一面的想法[罗宾逊和约翰斯顿]，例如它减轻哮喘的症状[维安娜和加西亚eme]，当给予胰岛素时，哮喘病会变得更糟。正常妊娠可以被认为是“糖尿病”的一些定义基于血糖。当我和一位健康的“糖尿病”妇女交谈时，我对这个问题产生了兴趣。她有一个两岁的孩子，从他自发的早熟的爱好来看，孩子的智商肯定超过了200。老妇科医生告诉我，“糖尿病”女性的孩子智力早熟，这是常识。)
When non-diabetic apes were given insulin treatments, they developed some of the same “complications of diabetes” that are seen in humans, and antibodies to insulin were found in their retinas, suggesting that some “complications of diabetes” were complications of insulin treatment. Patients were seldom well informed of the arguments against the use of insulin, but the justification for the new genetically engineered human insulin is precisely that it avoids immunological damage.
当非糖尿病类人猿接受胰岛素治疗时，它们出现了一些与人类相同的“糖尿病并发症”，并且在它们的视网膜中发现了胰岛素抗体，这表明一些“糖尿病并发症”是胰岛素治疗的并发症。患者很少了解反对使用胰岛素的理由，但新的基因工程人类胰岛素的理由恰恰是它可以避免免疫损伤。
Insulin was introduced into medicine in the 1920s. According to the Britannica Book of the Year for 1947, page 265, “Mortality from diabetes in 1920 in the United States was 16.0 per 100,000, 14,062 deaths, but in 1944, it was 26.4 per 100,000, 34,948 deaths.”
胰岛素在20世纪20年代被引入医学。根据1947年《大英百科全书》265页，“1920年美国糖尿病死亡率为每10万人16.0人，14062人，但在1944年，这一数字为每10万人26.4人，34948人。”
One of the theories of the cause of diabetes is that a virus damages the beta cells in the pancreas, and the main argument for that in the 1970s was that the onset of diabetes in children can often be dated to a time shortly after a severe viral infection. It is true that intense sickness and a high fever (and high doses of drugs given to treat the sickness) can cause very high levels of glucose in the blood, and even glucose in the urine, but this is a fairly well recognized consequence of stress. High doses of cortisone (prednisone, etc.) typically cause elevated glucose levels. Cushing's syndrome usually involves hyperglycemia. Normally, this is just a functional response to an excess of glucocorticoids, but studies in dogs suggested that intense and/or prolonged stress can damage the insulin-secreting cells in the pancreas. Dogs had half of their pancreas removed, to increase the burden put on the remaining tissue, and after a large dose of cortisone the dogs became (and remained) diabetic.
关于糖尿病的一个理论是，一种病毒会破坏胰腺中的细胞，而在20世纪70年代，这一理论的主要论点是，儿童糖尿病的发病通常可以追溯到严重的病毒感染后不久。的确，严重的疾病和高烧(以及为治疗疾病而服用的高剂量药物)会导致血液中葡萄糖含量非常高，甚至尿液中葡萄糖含量也很高，但这是相当公认的压力后果。大剂量的可的松(强的松等)通常会导致血糖水平升高。库欣综合征通常伴有高血糖。正常情况下，这只是对过量糖皮质激素的功能性反应，但对狗的研究表明，紧张和/或长期的压力会损害胰腺中的胰岛素分泌细胞。狗的胰腺被切除了一半，增加了剩余组织的负担，在大剂量的可的松之后，狗变成了(并且仍然是)糖尿病患者。
One of the problems associated with diabetes is the calcification of blood vessels, though now there is more emphasis on fatty degeneration. Other blood vessel problems include hypertension, and poor circulation in general, leading to gangrene of the feet, impotence, and degeneration of the retina. In muscles, and probably in other tissues of diabetics, capillaries are more widely spaced, as if the basal oxidative requirement were lower than normal. However, mitochondria contain more respiratory enzymes, as if to partly compensate for the poor delivery of oxygen to the cells. Osteoporosis or osteopenia is a common complication of diabetes, and seems to be associated with the calcification of soft tissues.
与糖尿病相关的问题之一是血管的钙化，尽管现在更多地强调脂肪变性。其他血管问题包括高血压、血液循环不良，导致足部坏疽、阳痿和视网膜退化。在肌肉中，可能还有糖尿病患者的其他组织中，毛细血管的间距更大，似乎基础氧化需求低于正常水平。然而，线粒体含有更多的呼吸酶，似乎在一定程度上弥补了向细胞输送氧气的不足。骨质疏松症或骨质减少是糖尿病的常见并发症，似乎与软组织的钙化有关。
F. Z. Meerson's description of the stress-injured heart is very similar to the general changes that occur in chronic diabetes. He found that the stressed heart becomes rigid and unable to contract completely, or to relax completely. Excess calcium enters cells, and fatty acids are mobilized both locally and systemically, and both of these tend to damage the mitochondria. In diabetes, fatty acids are mobilized and oxidized instead of glucose, and calcium enters cells, increasing their rigidity and preventing relaxation of muscles in blood vessels. (I'm not sure whether it is relevant to cell physiology, but the presence of an excess of free unsaturated fatty acids, and of calcium, in cells makes me think of the insoluble soap that these substances form in other situations, including the intestine. It seems that this could form a harmful deposit in cells, blocking many metabolic processes.)
F. Z. Meerson对压力损伤心脏的描述与发生在慢性糖尿病中的一般变化非常相似。他发现，受到压力的心脏变得僵硬，不能完全收缩，也不能完全放松。过量的钙进入细胞，脂肪酸在局部和全身动员，这两种情况都倾向于破坏线粒体。在糖尿病中，脂肪酸代替葡萄糖被调动和氧化，钙进入细胞，增加细胞的硬度，防止血管中的肌肉松弛。(我不确定这是否与细胞生理学有关，但细胞中存在过量的自由不饱和脂肪酸和钙，使我想到这些物质在其他情况下形成的不溶性肥皂，包括肠道。这似乎会在细胞中形成有害的沉积物，阻碍许多代谢过程。)
For many years, histologists have observed that calcium and iron tend to be deposited together in “devitalized” tissues. Now we know that cell death from a great variety of causes involves the cell's absorption of increased amounts of calcium. Simply the lack of energy increases the amount of calcium in a cell, and stimulation or excitation does the same, creating or exaggerating a deficiency of energy. In low thyroid people, many (if not all) tissues are very easily damaged. Since glucose is needed by liver cells to produce the active (T3) form of thyroid, diabetes almost by definition will produce hypothyroidism, since in diabetes glucose can't be absorbed efficiently by cells.
多年来，组织学家观察到钙和铁倾向于在“失活”组织中一起沉积。现在我们知道，细胞死亡的原因有很多，包括细胞对钙的吸收增加。简单地说，缺乏能量会增加细胞中的钙含量，刺激或兴奋也会增加钙含量，造成或夸大了能量的缺乏。在甲状腺功能低下的人群中，许多(如果不是全部)组织很容易受损。由于肝脏细胞需要葡萄糖来产生活性甲状腺(T3)，糖尿病几乎就定义而言会产生甲状腺功能减退，因为在糖尿病中葡萄糖不能被细胞有效吸收。
In the form of cell damage caused by the “excitotoxins,” glutamic and aspartic acids, the damage seems to require both stimulation, and difficulty in maintaining adequate energy production. This combination leads to both calcium uptake and lipid peroxidation. When cells are de-energized, they tend to activate iron by chemical reduction, producing lipid peroxidation. This could explain the presence of chemically active iron, but an actual increase in the iron concentration suggests that there has been prolonged injury (oxidative stress) to the cell, with increased production of the heme group, which binds iron.
在由谷氨酸和天冬氨酸等“兴奋性毒素”引起的细胞损伤中，损伤似乎既需要刺激，也难以维持足够的能量产生。这种结合导致钙吸收和脂质过氧化。当细胞失去活力时，它们倾向于通过化学还原来激活铁，产生脂质过氧化。这可以解释化学活性铁的存在，但铁浓度的实际增加表明细胞受到了长期的损伤(氧化应激)，与铁结合的血红素组的产生增加了。
Hans Selye found that he could produce scleroderma (hardening and calcification of the skin) in rats by giving them a toxic dose of a heavy metal, and then irritating the skin a little by plucking hair. Iron is now tending to be recognized as a factor in inflammation. Vitamin E was able to prevent the development of scleroderma under Selye's experimental conditions, suggesting that the irritation allowed the heavy metal to cause oxidative damage to the skin. Selye found other ways to cause calcification of tissues, including the walls of arteries, but he directed most of his attention to the role of “pro-inflammatory” hormones. A decreased blood supply was often used to predispose an organ to calcification. In diabetes, a characteristic feature is that the blood supply is relatively remote from cells in muscle and skin, so the oxygen and nutrients have to diffuse farther than in normal individuals, and the ATP level of cells is characteristically lower than normal. In blood cells, both red (Garnier, et al.) and white cells are probably more rigid in diabetes, because of lower ATP production, and higher intracellular calcium and sodium.
Hans Selye发现，他给老鼠注射有毒剂量的重金属，然后拔毛稍微刺激皮肤，可以使它们患上硬皮病(皮肤硬化和钙化)。铁现在被认为是引起炎症的因素。在Selye的实验条件下，维生素E能够防止硬皮病的发展，这表明刺激允许重金属对皮肤造成氧化损伤。Selye发现了导致组织(包括动脉壁)钙化的其他方法，但他把大部分注意力放在了“促炎”激素的作用上。血液供应减少常被认为是器官易发生钙化的原因。糖尿病的一个特征是血液供应距离肌肉和皮肤的细胞相对较远，所以氧气和营养物质要比正常人扩散得更远，细胞的ATP水平也明显低于正常人。在血细胞中，糖尿病患者的红细胞(Garnier等)和白细胞可能更坚硬，因为ATP生成较低，细胞内钙和钠较高。
Magnesium in the cell is largely associated with ATP, as the complex Mg-ATP. When ATP is “used” or converted to ADP, this lower-energy substance associates with calcium, as Ca-ADP. In a hypothyroid state, the energy charge can be depleted by stress, causing cells to lose magnesium. ATP is less stable when it isn't complexed with magnesium, so the stress-induced loss of magnesium makes the cell more susceptible to stress, by acting as a chronic background stimulation, forcing the cell to replace the ATP which is lost because of its instability. In this state, the cell takes up an excess of calcium.
细胞中的镁主要与ATP有关，如镁-ATP复合物。当ATP被“使用”或转化为ADP时，这种能量较低的物质与钙结合，即钙-ADP。在甲状腺机能减退状态下，能量电荷会因压力而耗尽，导致细胞失去镁。当ATP不与镁结合时，它就不那么稳定，因此应激引起的镁的损失使细胞更容易受到压力，这是一种慢性背景刺激，迫使细胞替换因不稳定而失去的ATP。在这种状态下，细胞会吸收过量的钙。
The picture that I think explains many of the features of diabetes is that an energy deficit produces an alarm state, causing increased production of adrenalin and cortisol. Adrenalin mobilizes fat from storage, and the free fatty acids create a chronic problem involving 1) blocked ATP production, 2) activation of the protein kinase C system (increasing tension in blood vessels), 3) inhibition of thyroid function with its energetic, hormonal, and tissue-structure consequences, 4) availability of fats for prostaglandin synthesis, and 5) possibly a direct effect on clot dissolving, besides the PAI-1 (plasminogen activator inhibitor) effect seen in diabetes (Ceriello, et al., Udvardy, et al., Vague, et al.). (Estrogen has many pro-clotting effects, and one of them is a decreased activity of vascular plasminogen activator. K. E. Miller and S. V. Pizzo, “Venous and arterial thromboembolic disease in women using oral contraceptives,” Am. J. Obst. Gyn. 144, 824, 1982. In 1968, D. G. Daniel et al., reported that estrogen promotes thromboembolism by increasing clotting factor IX in the blood.)
我认为这幅图解释了糖尿病的许多特征，能量不足会产生一种警报状态，导致肾上腺素和皮质醇的增加。肾上腺素将储存的脂肪动员起来，而游离脂肪酸则会造成一种慢性问题，包括1)ATP生成受阻，2)蛋白激酶C系统的激活(血管紧张加剧)，3)甲状腺功能受到其能量、激素和组织结构的抑制，4)脂肪可用于前列腺素合成，5)除了在糖尿病中看到的PAI-1(纤溶酶原激活物抑制剂)作用外，可能对凝块溶解有直接影响(Ceriello等，Udvardy等，Vague等)。雌激素有许多促凝作用，其中之一是降低血管纤溶酶原激活物的活性。K. E. Miller和S. V. Pizzo，“使用口服避孕药的妇女的静脉和动脉血栓栓塞性疾病”，Am。j .水果。妇科。144,824,1982。1968年，D. G. Daniel等人报道雌激素通过增加血液中的凝血因子IX促进血栓栓塞。)
Increased entry of calcium into cells is complexly related to increased exposure to unsaturated fatty acids, decreased energy, and lipid peroxidation. Osteoporosis, calcification of soft tissues and high blood pressure are promoted by multiple stresses, hypothyroidism, and magnesium deficiency. The particular direction a disease takes–diabetes, scleroderma, lupus, Alzheimer's, stroke, etc.–probably results from the balance between resources and demands within a particular organ or system. Calcium overload of cells can't be avoided by avoiding dietary calcium, because the bones provide a reservoir from which calcium is easily drawn during stress. (In fact, the reason calcium can temporarily help prevent muscle cramps seems to be that it makes magnesium more available to the muscles.)
钙进入细胞的增加与不饱和脂肪酸暴露增加、能量减少和脂质过氧化密切相关。骨质疏松症、软组织钙化和高血压是由多种应激、甲状腺功能减退和镁缺乏引起的。一种疾病的特定方向——糖尿病、硬皮病、狼疮、阿尔茨海默病、中风等——可能是由特定器官或系统内资源和需求之间的平衡造成的。避免饮食中的钙不能避免细胞的钙超载，因为骨骼提供了一个储钙库，在压力下钙很容易被吸收。(事实上，钙可以暂时帮助防止肌肉抽筋的原因似乎是它让肌肉更容易获得镁。)
If we want to stop a disease that involves abnormal calcification or contraction of muscle (see Zenere, et al.), we can increase our consumption of magnesium, and to cause cells to absorb and retain the magnesium, we can increase our thyroid function. The use of coconut oil provides energy to stabilize blood sugar while protecting mitochondria and the thyroid system from the harmful effects of unsaturated fats.
如果我们想要阻止一种涉及异常钙化或肌肉收缩的疾病(见Zenere等)，我们可以增加镁的摄入，并使细胞吸收和保留镁，我们可以提高甲状腺功能。椰子油的使用为稳定血糖提供能量，同时保护线粒体和甲状腺系统免受不饱和脂肪的有害影响。
In 1947, B. A. Houssay found that a diet based on sugar as a source of energy was more protective against diabetes than a diet based on lard, while the most protective diet was based on coconut oil. Lard reflects the pigs' diet, and is usually extremely unsaturated, especially since it became standard to fatten them on soybeans and corn. Essentially, his study seems to show that unsaturated (pork) fat permits diabetes to develop, sugar is slightly protective, and coconut oil is very protective against the form of diabetes caused by a poison.
1947年，B. a . Houssay发现以糖为能量来源的饮食比以猪油为能量来源的饮食更能预防糖尿病，而最具保护性的饮食是以椰子油为基础的。猪油反映了猪的饮食，而且通常是极不饱和的，特别是在用大豆和玉米增肥成为标准后。从本质上说，他的研究似乎表明，不饱和(猪肉)脂肪会导致糖尿病的发生，糖有轻微的保护作用，椰子油对由毒素引起的糖尿病非常有保护作用。
At the same time, A. Lazarow was demonstrating that a low protein diet made animals more sensitive to diabetes, and that cysteine, glutathione, and thioglycolic acid (antioxidants) are protective against diabetes. The chelator of metals, BAL (British anti-lewisite), was also found to protect against diabetes.
同时，a . Lazarow证明低蛋白饮食使动物对糖尿病更敏感，半胱氨酸，谷胱甘肽和巯基乙酸(抗氧化剂)对糖尿病有保护作用。金属螯合剂BAL(英国抗刘易斯)也被发现可以预防糖尿病。
Taken together, those studies suggest that the oxidizable unsaturated fats are involved in the process of producing diabetes. At the same time, other studies were showing that the unsaturated oils suppress the thyroid, and that coconut oil increases the metabolic rate, apparently by normalizing thyroid function. Hypothyroidism is known to include deposition of mucopolysaccharides in tissues, increased permeability of capillaries with leakage of albumin out of the blood, elevated adrenalin which can lead to increased production of cortisol, decreased testosterone production, high risk of heart and circulatory disease, including a tendency to ulceration of the extremities, and osteoporosis, all of which are recognized “complications of diabetes.” Broda Barnes gave all of his diabetic patients a thyroid supplement, and found that none of them developed the expected complications of diabetes.
综上所述，这些研究表明可氧化的不饱和脂肪参与了糖尿病的产生过程。与此同时，其他研究表明，不饱和油脂抑制甲状腺，椰子油增加代谢率，显然是通过正常化甲状腺功能。众所周知，甲状腺机能减退包括粘多糖在组织中的沉积，毛细血管通透性增加，白蛋白从血液中漏出，肾上腺素升高，导致皮质醇分泌增加，睾酮分泌减少，心脏和循环系统疾病的高风险，包括四肢溃烂和骨质疏松症，这些都是公认的“糖尿病并发症”。布罗达·巴恩斯(Broda Barnes)给他的所有糖尿病患者服用了甲状腺补充剂，发现他们没有出现预期的糖尿病并发症。
Recently, a high safflower oil diet was found to cause diabetes (Ikemoto, et al.), and obesity itself is thought to be a factor in developing diabetes. The hormone patterns associated with obesity can be seen as either cause or effect of the obesity (or both cause and effect), since, for example, low thyroid can increase both estrogen and cortisol, which support the formation of fat, and the fat cells can become a chronic source of estrogen synthesis.
最近，高红花油饮食被发现会导致糖尿病(ikmoto, et al.)，肥胖本身被认为是糖尿病发生的一个因素。与肥胖相关的激素模式可以被视为肥胖的原因或结果(或因果关系),因为,例如,低甲状腺可以增加雌性激素和皮质醇,支持脂肪的形成,和脂肪细胞可以成为长期雌激素合成的一个根源。
On a diet lacking the “essential” unsaturated fatty acids, Benhamou (1995) found that nonobese diabetic mice didn't develop diabetes, that is, the unsaturated fats themselves, without obesity, are sufficient to cause diabetes. (Also see Girard; Golay, et al., and Kusunoki, et al.)
Benhamou(1995)在缺乏“必需”不饱和脂肪酸的饮食中发现，非肥胖的糖尿病小鼠没有患上糖尿病，也就是说，不肥胖的不饱和脂肪本身就足以引起糖尿病。(也看到吉拉德;Golay等，Kusunoki等)
Estrogen and the polyunsaturated fatty acids (PUFA), linoleic and linolenic acid, alike activate the protein kinase C (PKC) system of cellular activation. Many of the functions of PUFA are similar to the functions of estrogen (e.g., antagonism to thyroid function, promotion of age pigment/lipofuscin), so this information showing that they both act similarly on the same basic regulatory pathway is important. Estrogen increases secretion of growth hormone (GH; it's closely associated with prolactin, also increased by estrogen), and GH causes an increase in free fatty acids in the blood. Estrogen promotes iron retention, so it sets the stage for oxidative stress. At least in some systems, both estrogen and PUFA promote the entry of calcium into the cell.
雌激素和多不饱和脂肪酸(PUFA)、亚油酸和亚麻酸一样激活细胞激活的蛋白激酶C (PKC)系统。多不饱和脂肪酸的许多功能与雌激素的功能相似(例如，拮抗甲状腺功能，促进年龄色素/脂褐素)，因此这一信息表明它们在相同的基本调控途径上发挥相似的作用是重要的。雌激素增加生长激素(GH;它与催乳素密切相关，雌激素也会增加催乳素)，生长激素会增加血液中的游离脂肪酸。雌激素促进铁的保留，所以它为氧化应激奠定了基础。至少在某些系统中，雌激素和pufa都能促进钙离子进入细胞。
In diabetes, there is a generalized excess activation of the PKC system. The starch-based diet, emphasizing grains, beans, nuts, and vegetables, has been promoted with a variety of justifications. When people are urged to reduce their fat and sugar consumption, they are told to eat more starch. Starch stimulates the appetite, promotes fat synthesis by stimulating insulin secretion, and sometimes increases the growth of bacteria that produce toxins. It is often associated with allergens, and according to Gerhard Volkheimer, whole starch grains can be “persorbed” from the intestine directly into the blood stream where they may block arterioles, causing widely distributed nests of cell-death. I have heard dietitians urge the use of “complex carbohydrates” (starch) instead of sugar. In the first physiology lab I took, we fed rats a large blob of moist cornstarch with a stomach tube, and then after waiting a few minutes, were told to dissect the rat to find out “how far the starch had gone.” In such a short time, we were surprised to find that not a trace of the starch could be found. The professor's purpose was to impress us with the rapidity with which starch is digested and absorbed. Various studies have demonstrated that starch (composed of pure glucose) raises blood glucose more quickly than sucrose (half fructose, half glucose) does. The sudden increase of blood glucose is sometimes thought to contribute to the development of diabetes, but if it does, it is probably mediated by fat metabolism and the hormones other than just insulin.
在糖尿病中，PKC系统普遍过度激活。以淀粉为基础的饮食，强调谷物、豆类、坚果和蔬菜，以各种理由被推广。当人们被敦促减少脂肪和糖的消耗时，他们被告知要多吃淀粉。淀粉会刺激食欲，通过刺激胰岛素分泌促进脂肪合成，有时还会增加产生毒素的细菌的生长。它通常与过敏原有关，根据格哈德·沃克海默(Gerhard Volkheimer)的说法，整粒淀粉颗粒可以从肠道“吸收”直接进入血液，在那里它们可能会阻塞小动脉，导致广泛分布的细胞死亡巢。我曾听到营养学家敦促使用“复合碳水化合物”(淀粉)而不是糖。在我参加的第一个生理学实验室里，我们用胃管给老鼠喂了一大团潮湿的玉米淀粉，几分钟后，我们被要求解剖老鼠，看看“淀粉吃了多少”。在这么短的时间里，我们惊奇地发现一点淀粉都找不到。教授的目的是让我们对淀粉消化和吸收的速度留下深刻印象。各种研究表明，淀粉(由纯葡萄糖组成)比蔗糖(一半果糖，一半葡萄糖)提高血糖的速度更快。血糖的突然升高有时被认为是导致糖尿病的原因，但如果真的是这样，它可能是由脂肪代谢和激素介导的，而不仅仅是胰岛素。
Brewer's yeast has been used successfully to treat diabetes. In the l930s, my father had severe diabetes, but after a few weeks of living on brewer's yeast, he recovered and never had any further evidence of diabetes. Besides its high B-vitamin and protein content, yeast is an unusual food that should be sparingly used, because of its high phosphorous/calcium ratio, high potassium to sodium ratio, and high estrogen content. The insulin-producing beta cells of the pancreas have estrogen receptors, but I don't know of any new research investigating this aspect of yeast therapy. In rabbit studies, diabetes produced by alloxan poisoning, which kills the beta cells, was cured by DHEA treatment, and beta cells were found to have regenerated in the pancreatic islets.
布鲁尔酵母已成功用于治疗糖尿病。在20世纪30年代，我的父亲患有严重的糖尿病，但在靠啤酒酵母生活了几个星期后，他康复了，再也没有任何糖尿病的迹象。除了维生素b和蛋白质含量高外，酵母是一种不常见的食物，应该少用，因为它的高磷/钙比，高钾/钠比，高雌激素含量。胰腺中产生胰岛素的细胞有雌激素受体，但我还不知道有任何关于酵母疗法这方面的新研究。在兔子研究中，四氧嘧啶中毒产生的糖尿病杀死了β细胞，通过脱氢表雄酮治疗治愈了糖尿病，并发现β细胞在胰岛中再生。
I think the basic anti-aging diet is also the best diet for prevention and treatment of diabetes, scleroderma, and the various “connective tissue diseases.” This would emphasize high protein, low unsaturated fats, low iron, and high antioxidant consumption, with a moderate or low starch consumption. In practice, this means that a major part of the diet should be milk, cheese, eggs, shellfish, fruits and coconut oil, with vitamin E and salt as the safest supplements. It should be remembered that amino acids, especially in eggs, stimulate insulin secretion, and that this can cause hypoglycemia, which in turn causes cortisol secretion. Eating fruit (or other carbohydrate), coconut oil, and salt at the same meal will decrease this effect of the protein. Magnesium carbonate and epsom salts can also be useful and safe supplements, except when the synthetic material causes an allergic bowel reaction..
我认为基本的抗衰老饮食也是预防和治疗糖尿病、硬皮病以及各种“结缔组织病”的最佳饮食。这将强调高蛋白，低不饱和脂肪，低铁，高抗氧化剂消耗，适度或低淀粉消耗。实际上，这意味着饮食的主要部分应该是牛奶、奶酪、鸡蛋、贝类、水果和椰子油，维生素E和盐作为最安全的补充。应该记住，氨基酸，尤其是鸡蛋中的氨基酸，会刺激胰岛素分泌，这会导致低血糖，而低血糖又会导致皮质醇分泌。在同一餐中吃水果(或其他碳水化合物)、椰子油和盐会降低蛋白质的作用。碳酸镁和泻盐也可以是有用和安全的补充，除非合成材料引起过敏肠道反应。
Although I started this newsletter with the thought of discussing the Mead acids–the unsaturated (n-9) fats that are formed under certain conditions, especially when the dietary polyunsaturated fatty acids are “deficient”–and their prostaglandin derivatives as a distinct anti-stress, anti-aging system, the loss of which makes us highly susceptible to injury, I will save that argument for a future time, leaving this newsletter as an addition to the view that an excess of the polyunsaturated fats is central to the development of degenerative diseases: Cancer, heart disease, arthritis, immunodeficiency, diabetes, hypertension, osteoporosis, connective tissue disease, and calcification.
虽然我在开始这篇时事通讯时，是想讨论米德酸——在特定条件下形成的不饱和脂肪(n-9)，特别是当饮食中的多不饱和脂肪酸“不足”时——以及它们的前列腺素衍生物作为一种独特的抗压力、抗衰老系统，失去多不饱和脂肪会使我们非常容易受伤，我将把这个论点留到以后讨论，留下这篇通讯作为对以下观点的补充:过多的多不饱和脂肪是退化性疾病发展的核心:癌症、心脏病、关节炎、免疫缺陷、糖尿病、高血压、骨质疏松症、结缔组织疾病和钙化。
REFERENCES WITH EXCERPTS AND COMMENTS A. A. Alzaid, et al., “Effects of insulin on plasma magnesium in noninsulin-dependent diabetes mellitus: Evidence for insulin resistance,” J. of Clin. Endocr. and Metab. 80(4), 1376-1381, 1995. ”…insulin resistance in subjects with NIDDM impairs the ability of insulin to stimulate magnesium as well as glucose uptake.“ A. B. Akella, et al., “Diminished Ca++ sensitivity of skinned cardiac muscle contractility coincident with troponin T-band shifts in the diabetic rat,” Circulation Research 76(4), 600-606, 1995.D. A. Antonetti, et al., “Increased expression of mitochondrial-encoded genes in skeletal muscle of humans with diabetes mellitus–Rapid publication,” J. of Clinical Investigation 95(3), 1383-1388, 1995. “The increased mitochondrial gene expression may contribute to the increase in mitochondrial respiration observed in uncontrolled diabetes.” (Low ATP with high respiration would suggest uncoupling; unsaturated fatty acids are known uncouplers of respiration from energy production.) S. Asakuma, et al., “The effects of antianginal drugs on energy expernditure during exercise in normal subjects,” Japanese Circulation Journal–English Edition 59(3), 137-145, 1995. “RQ (carbohydrate consumption relative to fat consumption) during exercise was significantly increased and VO2 was decreased after propranolol, metoprolol and amosulalol.” “These data suggest that propranolol, metoprolol and amosulalol [beta-blockers] increase the efficiency of energy expenditure during ordinary physical activity by increasing the utilization of carbohydrate and by decreasing the utilization of fat.” M. Bardicef, et al., “Extracellular and intracellular magnesium depletion in pregnancy and gestational diabetes,” Amer. J. of Obst. and Gyn. 172(3), 1009-1013, 1995. P. E. Beales, et al., “Baclofen, a gamma-aminobutyric acid-b receptor agonist, delays diabetes onset in the non-obese diabetic mouse,” Acta Diabetologica 32(1), 53-56, 1995. P. Y. Benhamou, et al., :“Essential fatty acid deficiency prevents autoimmune diabetes in nonobese diabetic mice through a positive impact on antigen-presenting cells and Th2 lymphocytes,” Pancreas 11(1), 26-37, 1995. C. D. Berdanier, “Diet, autoimmunity, and insulin-dependent diabetes mellitus: A controversy,” Proc. Soc. Exp. Biol. Med. 209(3), 223-230, 1995. “The majority of the genetic mutations that result in the phenotypic expression of the insulin-dependent diabetes mellitus genotype are in the immune system.” Antibodies to milk protein can be found in the patient, but these probably represent antigen mimicry, resulting from the loss of antibody specificity which is a feature of autoimmune disease. G. Bianchi, et al., “Thyroid volume in type 1 diabetes patients without overt thyroid disease,” Acta Diabetologica 32(1), 49-52, 1995. “An association between insulin-dependent diabetes mellitus (type 1) and thyroid diseases has long been reported….” P. Bjorntorp, “Insulin resistance: The consequence of a neuroendocrine disturbance?” Int. J. Obes. 19(Suppl. 1), S6-S10, 1995. “The decreased capillary density may…be of importance for the apparent insulin resistance.” R. Bouillon, et al., “Influence of age, sex, and insulin on osteoblast function: Osteoblast dysfunction in diabetes mellitus,” J. of Clin. Endocr. and Metab. 80(4), 1194-1202, 1995. ”…the osteoblast function is significantly decreased in diabetic patients….“ A. Ceriello, et al., “The defence against free radicals protects endothelial cells from hyperglycaemia-induced plasminogen activator inhibitor 1 over-production,” Blood Coagulation & Fibrinolysis 6(2), 133-137, 1995. “The hypothesis that oxidative stress may play an important role in the pathogenesis of diabetic complications is … supported by this study.” [GSH reduced PAI-1.] V. Coiro, et al., “Low-dose ovine corticotropin-releasing hormone stimulation test in diabetes mellitus with or without neuropathy,” Metabolism–Clinical and Experimental 44(4), 538-542, 1995. ”…basal and CRH-induced cortisol levels were significantly higher in diabetics than in normal controls.“ ”…even uncomplicated diabetes mellitus is associated with adrenal hyperfunction.“ S. R. Colberg, et al., “Skeletal muscle utilization of free fatty acids in women with visceral obesity,” J. Clin. Invest. 95(4), 1846-1853, 1995. “Visceral obesity is strongly associated with insulin resistance.” ”…visceral adiposity is clearly associated with skeletal muscle insulin resistance but this is not due to glucose-FFA [free fatty acid]substrate competition. Instead, women with visceral obesity have reduced postabsorptive FFA utilization by muscle.“ G. A. Colditz, et al., “Weight gain as a risk factor for clinical diabetes mellitus in women,” Annals of Internal Medicine 122(7), 481-486, 1995. C. Douillet and M. Ciavatti, “Effect of vitamin E treatment on tissue fatty acids and cholesterol content in experimental diabetes,” J. Nutr. Biochem. 6(6), 319-326, 1995. “Diabetes induced a decrease of monounsaturated fatty acids and particularly palmitoleic acid in all studied tissues: liver, aorta, plasma.” C18:3 n-6 and C20:4 n-6 were increased by diabetes. M. Garnier, et al., “Red blood cell sodium conent in NID diabetic patients with hemorheological abnormalities,” Clinical Hemorheology 15(3), 325-333, 1995. K. D. Gerbitz, et al., “Mitochondrial diabetes mellitus: A review,” BBA–Mol. Basis Dis. 1271(1), 253-260, 1995. This particular kind of diabetes, which is combined with deafness in 60% of the patients, involves a variant mitochondrial gene and occurs in about 1.5% of diabetics. “The underlying pathomechanism is probably a delayed insulin secretion due to an impaired mitochondrial ATP production in consequence of the mtDNA defect.” To know the “causal” value of this gene we have to know how often it occurs in people who never develop diabetes. It is interesting that it is suggested to operate by way of impaired ATP production, which can be the result of so many factors, such as excess unsaturated fats, low thyroid, low magnesium, low copper, etc. Pages 141-151 of the same journal as an article by D. C. Wallace, et al., “Mitochondrial DNA mutations in human degenerative diseases and aging,” which makes the point that “Generally, individuals inheriting these mitochondrial diseases are relatively normal in early life, develop symptoms during childhood, mid-life, or old age depending on the severity of the … mutation; and then undergo a progressive decline.” Their energy-producing systems are supposedly more susceptible to the effects of aging. J. Girard, “Role of free fatty acids in insulin resistance of subjects with non-insulin-dependent diabetes,” Diabetes Metab. 21(2), 79-88, 1995. “Studies performed in the rat suggest that impaired glucose-induced insulin secretion could also be related to chronic exposure of pancreatic beta cells to elevated plasma free fatty acid levels.” [This direct effect of free fatty acids on the beta cells is extremely important. Estrogen–probably via GH–increases free fatty acids, and adrenalin–which is elevated in hypothyroidism–increases the release of free fatty acids from storage. Free fatty acids impair mitochondrail energy production.] A. Golay, et al., “Effect of lipid oxidation on the regulation of glucose utilization in obese patients,” Acta Diabetologica 32(1), 44-48, 1995. [Free fatty acids strongly and quickly depress the ability to oxidize or store glucose.] A. Gomes, et al., “Anti-hyperglycemic effect of black tea (Camellia sinensis) in rat,” J. of Ethnopharmacology 45(3), 223-226, 1995. It “was found to possess both preventive and curative effects on experimentally produced diabetes in rats.” Y. Hattori, et al., “Phorbol esters elicit Ca++-dependent delayed contractions in diabetic rat aorta,” Eur. J. Pharmacol. 279(1), 51-58, 1995. [Diabetic tissue is more responsive to activation of protein kinase C by phorbol esters.] B. A. Houssay and C. Martinez, “Experimental diabetes and diet,” Science 105, 548-549, 1947. [Mortality was zero on the high coconut oil diet, 100% on the high lard diet. It was 90% on the low protein diet, and 33% on the high protein diet. With a combination of coconut oil and lard, 20%.] B. A. Houssay, et al., “Accion de la administracion prolongada de glucosa sobre la diabetes de la rata,” Rev. Soc. argent. de biol. 23, 288-293, 1947. S. Ikemoto, et al., “High fat diet-induced hyperglycemia: Prevention by low level expression of a glucose transporter (GLUT4) minigene in transgenic mice,” Proc. Nat. Acad. Sci. USA 92(8), 3096-3099, 1995. ”…mice fed a high-fat (safflower oil) diet develop defective glycemic control, hyperglycemia, and obesity.“ M. Inaba, et al., “Influence of high glucose on 1,25-dihydroxyvitamin D-3-induced effect on human osteoblast-like MG-63 cells,” J. Bone Miner. Res. 10(7), 1050-1056, 1995. J. S. Jensen, et al., “Microalbuminuria reflects a generalized transvascular albumin leakiness in clinically healthy subjects,” Clin. Sci. 88(6), 629-633, 1995. G. Jorneskog, et al., “Skin capillary circulation severely impaired in toes of patients with IDDM, with and without late diabetic complications,” Diabetologia 38(4), 474-480, 1995. A. M. Kahn and T. Song, “Insulin inhibits dog vascular smooth muscle contraction and lowers Ca++[i] by inhibiting Ca++ influx,” J. of Nutrition 125(6 Suppl.), S1732-S1737, 1995. F. Kuhlencordt, et al., “Examination of the skeleton in diabetic patients up to age 45,” Deutsche med. Wchnschr. 91, 1913-1917, 1966. “Some patients have a generalized osteoporosis-like process, and some have localized bone lesions….” M. Kusunoki, et al., “Amelioration of high fat feeding-induced insulin resistance in skeletal muscle with the antiglucocorticoid RU486,” Diabetes 44(6), 718-720, 1995. “These results suggest that glucocorticoids play, in a tissue-specific manner, a role in the maintenance and/or production of insulin resistance produced by high-fat feeding.” A. Lazarow, “Protection against alloxan diabetes,” Anat. Rec. 97, 353, 1947. A. Lazarow, “Protective effect of glutathione and cysteine against alloxan diabetes in the rat,” Proc. Soc. Exp. Biol. & Med. 61, 441-447, 1946. [While certain doses of cysteine, glutathione, and thioglycolic acid completely prevented alloxan diabetes, it was interesting that all of the rats receiving ascorbic acid became diabetic. To me, this argues for the free radical cause of diabetes, rather than just the sulfhydryl oxidation. Lazarow suggested that succinic dehydrogenase, and various other sulfhydryl enzymes, including those involved in fatty acid oxidation, might be involved.] R. B. Lipton and J. A. Fivecoate, “High risk of IDDM in African-American and Hispanic children in Chicago, 1985-1990,” Diabetes Care 18(4), 476-482, 1995. “The relatively early age at onset may point to an environmental factor associated with this high incidence of the disease.” G. S. Meneilly, et al., “Insulin-mediated increase in blood flow is impaired in the elderly,” J. Clin. Endocrinol. Metab. 80(6), 1899-1903, 1995. “Normal aging is characterized by resistance to insulin-mediated glucose uptake.” J. Ma, et al., “Associations of serum and dietary magnesium with cardiovascular disease, hypertension, diabetes, insulin, and carotid arterial wall thickness: The ARIC study,” J. Clin. Epidemiol. 48(7), 927-940, 1995. [Carotid wall thickness increased in women as serum Mg level decreased.] Y. Matsumoto, et al., “Creatine kinase kinetics in diabetic cardiomyopathy,” Amer. J. Physiol.-Endocrinol. Met. 31(5), E1070-E1076, 1995. F. Mercure and G. Vanderkraak, “Inhibition of gonadotropin-stimulated ovarian steroid production by polyunsaturated fatty acids in teleost fish,” Lipids 30(6), 547-554, 1995. “The inhibitory actions by PUFAs were not restricted to long-chain PUFAs, as linoleic and linolenic acids had similar actions in the goldfish. The inhibitory action of EPA on testosterone production was reversible upon removal of the PUFA from medium.” ”[Stimulated] …testosterone production … was attenuated by PUFAs….“ H. Mulder, et al., “Non-parallelism of islet amyloid polypeptide (amylin) and insulin gene expression in rat islets following dexamethasone treatment,” Diabetologia 38(4), 395-402, 1995. S. Nagasaka, et al., “Effect of glycemic control on calcium and phosphorus handling and parathyroid hormone level in patients with non-insulin-dependent diabetes mellitus,” Endocr. J. 42(3), 377-383, 1995. ”…hyperglycemia causes excess urinary calcium and phosphorus excretion in patients with NIDDM. In response to urinary calcium loss, PTH secretion is mildly stimulated. Bone formation seems to be suppressed in the hyperglycemic state in spite of increased PTH secretion.“ [These are the changes I would expect to see in hypothyroid people with high cortisol.] B. Oztas and M. Kucuk, “Influence of acute arterial hypertension on blood-brain barrier permeability in streptozocin-induced diabetic rats,” Neuroscience Letters 188(1), 53-56, 1995. S. Phillips, et al., “Neuropathic arthropathy of the spine in diabetes,” Diabetes Care 18(6), 876-869, 1995. J. F. Pouliot and R. Beliveau, “Palmitoylation of the glucose transporter in blood-brain barrier capillaries,” Bioch. et Bioph. Acta–Biomembranes 1234(2), 191-196, 1995. “Palmitoylation may be involved in the regulation of glucose transport activity in hyperglycemia.” R. Ramakrishnan and A. Namasivayam, “Norepinephrine and epinephrine levels in the brain of alloxan diabetic rats,” Neuroscience Letters 186(2-3), 200-202, 1995. [Epinephrine increased in striatum, hippocampus and hypothalamus, Norepinephrine increased in hypothalamus and decreased in pons and medulla.] J. G. Regensteiner, et al., “Effects of non-insulin-dependent diabetes on oxygen consumption during treadmill exercise,” Med. Sci. Sports Exerc. 27(6), 874-881, 1995. “The reduced rate of increase in oxygen consumption during increasing submaximal work loads in NIDDM suggests that limitations in oxygen delivery may impair exercise performance in otherwise healthy persons with diabetes.” A. A. Shaltout, et al., “High incidence of childhood-onset IDDM in Kuwait,” Diabetes Care 18(7), 923-927, 1995. The incidence of IDDM in children is high in the region and has apparently increased nearly fourfold in the last decade. This is especially significant, since diabetes that appears in childhood is especially important for the theory of genetic causation. This study should give the gene people real trouble. They might have to call in the “gene for bed-wetting” people to help with their case. M. A. Smith, et al., “Radical AGEing in Alzheimer's disease,” Trends in Neurosciences 18(4), 172-176, 1995. A. Tchernof, et al., “Relation of steroid hormones to glucose tolerance and plasma insulin levels in men: Importance of visceral adipose tissue,” Diabetes Care 28(3), 292-299, 1995. A. Tchernof, et al., “Reduced testosterone and adrenal C-19 steroid levels in obese men,” Metabolism–Clin. and Exp. 44(4), 513-519, 1995. ”…reduced concentrations of testosterone and adrenal C-19 steroid precursors are associated with increased body fatness rather than with excess visceral fat accumulation.“ [These results] ”…emphasize the importance of adrenal steroids as correlates of body composition in men.“ B. G. Trumper, et al., “Circadian variation of insulin requirement in insulin dependent diabetes mellitus–The relationship between circadian change in insulin demand and diurnal patterns of growth hormone, cortisol and glucagon during euglycemia,” Hormone and Metabolic Research 27(3), 141-147, 1995. “The results of the study showed that the early morning rise in the insulin demand is related to the increased early morning cortisol secretion and to the nocturnal peaks of growth hormone concentration.” M. Udvardy, et al., “Altered lysis resistance of platelet-rich clots in patients with insulin-dependent diabetes mellitus,” Thromb. Res. 79(1), 57-63, 1995. Suppression of clot-dissolving ”…was remarkably stronger in IDDM, along with the highest PAI-1 activity concentration ratio of the platelet lysates, compared to plasmatic levels.“ P. Vague, et al., “Hypofibrinolysis and the insulin resistance syndrome,” Int. J. Obes. 19(Suppl. 1), S11-S15, 1995. Hypofibrinolysis is observed among obese subjects and it has been shown that an excess of plasminogen activator inhibitor 1 (PAI 1) the main regulator of the fibrinolytic system, is closely associated to other components of the insulin resistance syndrome, namely, excessive body weight, high waist to hip ratio, elevated blood pressure, hyperinsulinemia and hypertriglyceridemia.” E. O. Vianna and J. Garcialeme, “Allergen-induced airway inflammation in rats: Role of insulin,” American J. of Respiratory and Critical Care Med. 151(3), 809-814, 1995. “Clinical asthma appears to be less severe when diabetes mellitus is superimposed.” A. Warley, et al., “Capillary surface area is reduced and tissue thickness from capillaries to myocytes is increased in the left ventricle of streptozotocin-diabetic rats,” Diabetologia 38(4), 413-421, 1995. G. C. Weir, “Which comes first in non-insulin-dependent diabetes mellitus: Insulin resistance or beta-cell failure? Both come first,” JAMA 273(23), 1878-1879, 1995. N. R. Williams, et al., “Plasma, granulocyte and mononuclear cell copper and zinc in patients with diabetes mellitus,” Analyst 120(3), 887-890, 1995. “…the copper and zinc status of these diabetic patients was reduced, providing further evidence of a role for these antioxidant” trace elements in this disease. T. Yamakawa, et al., “Augmented production of tumor necrosis factor-alpha in obese mice,” Clinical Immunology and Immunopathology 75(1), 51-56, 1995. “…the TNF-alpha derived from adipose tissues might be involved in the induction of peripheral insulin resistance…” T. Yamashita, et al., “Increased transendothelial permeation of albumin by high glucose concentration,” Metabolism 44(6), 739-744, 1995. M. B. Zemel, “Insulin resistance vs. hyperinsulinemia in hypertension: Insulin regulation of Ca++ transport and Ca++-regulation of insulin sensitivity,” Journal of Nutrition 125(6 Suppl.), S1738-S1743, 1995. B. M. Zenere, et al., “Noninvasive detection of functional alterations of the arterial wall in IDDM patients with and without microalbuminuria,” Diabetes Care 18(7), 975-982, 1995. [There is a reduced vasodilatory capacity in diabetes, and especially in patients who are leaking albumin.] D. B. Zilvermit, et al., “Oxidation of glucose labelled with radioactive carbon by normal and alloxandiabetic rats,” J. Biol. Chem. 176, 389-400, 1948. [Diabetic rats had the same rate of glucose oxidation as normal rats, in this experiment. This is an artificial form of diabetes that doesn't immediately involve an excess of unsaturated fatty acids, as occurs during stress, estrogen excess, hypothyroidism, or diets high in polyunsaturated fats which can cause a more “natural” kind of diabetes. The artificial alloxandiabetes forces the animal to oxidize an excess of fatty acids, and eventually should lead to the same kind of mitochondrial damage seen in natural diabetes.]
