用户工具

站点工具


萨拉迪诺谈普发生酮普发生癌

萨拉迪诺谈普发生酮普发生癌


萨拉迪诺谈普发生酮普发生癌话题

你们好吗 ,

欢迎来到《争议想法》 ,

我今天要甩出很多东西 ,

尝试保留在一个简短的《争议想法》视频中 ,

但是我昨天录制了一个高脂彼得的播客 ,

这非常了不起 ,

在那对话中我想强调一些非常有趣的论文给你们来说 ,

甚至在该播客播出之前 ,将在两周内播出。

我有一个与戴夫·费尔德曼一起播出的播客 ,

我们谈到了他的氧化磷脂实验 ,

这非常令人着迷 ,

我可能会在脂蛋白上做一个《争议想法》视频 ,

但请检查这篇论文 ,

这是我所见过的关于多不饱和脂肪与饱和脂肪的比较有趣的论文之一 ,

以及关于多不饱和脂肪会导致不适当胰岛素的观念

线粒体水平的敏感性导致本质上的脂肪细胞肥大与增生 ,

但是线下还有很多步骤 ,

所以本文着眼于生酮饮食中饱和脂肪与多不饱和脂肪的代谢差异 ,

如果您跳到结果部分 ,

我认为在汤姆伍德播客简短地看了这篇论文 ,

两周后我在播客中用彼得的更多研究 ,

但我想向大家展示一下 ,

开放图是饱和脂肪的 ,

封闭图是灰色的 ,不饱和脂肪的图 ,

如果你看这个,乍一看与基线相比变化 ,

您可能会认为多不饱和脂肪看起来更好 ,

因为它们正在制造更多的β-羟基丁酸酯。

生酮是神奇的 ,

所需葡萄糖含量较低。胰岛素水平较低 ,

而众所周知的低密度脂蛋白胆固醇水平较低 ,

这会引起动脉粥样硬化 ,

甘油三酸酯水平会进一步降低 ,

如果查看所测的胰岛素敏感性 ,

我相信通过钳形测试可以看到多不饱和脂肪导致胰岛素敏感性增加 ,

我们希望胰岛素敏感性是对的 ,

如果您正在做生酮饮食 ,

那么您不希望对胰岛素敏感 ,

那么正常的人类生理学就是 ,

当您进行生酮饮食时 ,

您绝对应该具有胰岛素抵抗性

生酮饮食的重点是为葡萄糖保留红血球 ,

在大脑 ,睾丸 ,卵巢 ,肾上腺 ,肾脏等 ,

这些葡萄糖比不依赖的肌肉更依赖葡萄糖。

不想在进行生酮饮食时对胰岛素敏感 ,

因此该实验在人类中的真正有趣之处在于

说明了我一直在与布拉德·马歇尔讨论

与本·比克曼的友好辩论以及即将播出的高脂彼得播客中讨论的观点 ,

如果您听了布拉德·马歇尔播客的话 ,

饱和脂肪和多不饱和脂肪在线粒体水平上有很大不同。

我在这里谈论的是fadh2与nadh的fn比值 ,

转化为活性氧 ,

表示胰岛素抵抗或脂肪和葡萄糖营养素停止进入细胞 ,

如果对胰岛素敏感性持续不当 ,

将继续持续进入葡萄糖 ,

甘油三酸酯和游离脂肪酸的导入会导致糖原和脂肪酸沉积 ,

脂肪细胞会生长。

您不希望细胞对胰岛素敏感 ,

这项研究在人类生酮饮食中清楚地表明了

生酮时不适当的持续胰岛素敏感性

短期内饮食基于多不饱和脂肪 ,

您可能会认为这很好 ,

因为酮体含量较高或甘油三酸酯含量较低 ,

但是这是因为脂肪细胞正在生长 ,

或者细胞对胰岛素的敏感性仍然不合适 ,

这是我们不想要的 ,

这是饱和脂肪应该通过产生活性氧而在体内发出的信号 ,

因此这是人类证明了很多相同的结果

分子病理学分子机制和我们一直在讨论电子传输链 ,

我们在布拉德·马歇尔对话谈到了电子传输链复合物的所有其他

1复合物2琥珀酸脱氢酶电子转移蛋白脱氢酶甘油醛3-磷酸脱氢酶都加入了q辅酶q部分

当这些通过复杂的事物进入时会导致备份 ,

从而导致超氧化物的反向电子传输生成 ,

从而导致过氧化氢和胰岛素抵抗的细胞信号传递 ,

这是身体生存所需要的 ,

如果没有胰岛素抵抗 ,您将会死掉。

细胞是这样充满了营养素信号

多不饱和脂肪会产生不适当的持续信号 ,

表明细胞可以接受更多营养素 ,

这是一件坏事 ,

塞满亚油酸的身体会使脂肪细胞生长 ,

它们变得肥大 ,

您曾听过比克曼和我所做的播客

最近《争议想法》是我向您展示的证据表明 ,

亚油酸代谢产物 ,

特别是4 h/e 4羟基壬醇与脂肪细胞肥大有关 ,

损害了脂肪生成 ,

从而导致脂肪细胞增生 ,

这就是脂肪细胞的分裂增长 ,

如果你不想以后出现病理性胰岛素抵抗 ,

但是肥大的脂肪细胞生病了 ,

释放炎性介质 ,释放游离脂肪酸 ,

您会出现代谢功能障碍 ,

所以多不饱和脂肪逐渐将您推向代谢功能障碍的道路

不是说所有的多不饱和脂肪在数量上都是不好的

它不是有毒的东西 ,

但数量很重要 ,

过量的进化上不一致地消耗大量的多不饱和脂肪 ,

特别是亚油酸是脂肪细胞生长变得肥大的信号 ,

妨碍了脂肪生成 ,

从而导致了脂肪细胞增生变大 ,人变胖和生病。

导致游离脂肪酸泄漏 ,

也就是说代谢功能异常又称为代谢综合症又称为糖尿病时 ,

这就是一个问题 ,

那就是不希望成为慢性病根源的

昨天发布的播客克里斯·基诺比(Chris Kenobi)

我们讨论了所有这些以及真正的历史流行病学 ,人类学和干预学证据 ,

这些证据主要是此处的主要驱动因素

是过量的多不饱和脂肪。

多不饱和脂肪和生酮饮食 ,

如果看到参考文献 ,

那将是一件令人着迷的事情 ,

因为您不希望在进行生酮饮食时保持胰岛素敏感性 ,

这是人类体内明显的证据 ,

这些机制正在发挥作用 ,

这是另一种令人着迷的论文

胰岛素诱导的cd36到质膜的转运是可逆的 ,与glut4相似。

里面说的是 ,

如果当您暴露于多不饱和脂肪时

您的细胞对胰岛素的敏感性不适 ,

可以将cd36很好地放入细胞膜中。

cd36是这些蛋白质中的一种 ,

它将参与到脂肪酸 ,游离脂肪酸的进入 ,

并且会导致脂肪细胞充满脂肪 ,

导致其他细胞充满脂肪 ,

就像glut4是一种葡萄糖转运蛋白 ,

响应cd36胰岛素将葡萄糖吸收到细胞中一样 ,

所以当对胰岛素敏感性不当 ,

正在输入过量的葡萄糖 ,多余的脂肪 ,

细胞没有停止的信号发出“我已经好了” ,

正在通过大量的亚油酸向细胞发出令人困惑的信号 ,

我们不应该这样做

从进化上讲 ,因为它们不存在于自然界中 ,

所以它们不存在于自然界中 ,

所以现在真的很有趣的东西是

与克里斯·基诺比播客中另一个有趣的话题 ,

那就是认为现在人们的寿命更长 ,实际上是愚蠢的。

没有充分的证据表明预期寿命更长了 ,

因为婴儿死亡率较低 ,

但是如果成年后才导致(死亡) ,那将歪曲数据。

今天的人类与100年前的人类大约相同 ,

比现在患有更多的慢性病 ,

我们生存的时间相同 ,

但是我们生活得更糟 ,

生命力更差

我们做自己想做事情的能力较弱 ,

因为我们患有更多的慢性病 ,

所以不要不要被这样的观念愚弄了:现在的寿命更长 ,

是寿命相同 ,婴儿死亡率更低 ,

这使得平均预期寿命看起来更长了 ,

但是人类寿命仍然与我们与詹姆斯·克里斯(James Clement)谈论的

相同发病率曲线的平方和事实 ,

正如克里斯·瑞安(Chris Ryan)在他的书中谈到的那样 ,

较高的婴儿死亡率在历史上不恰当地使数据朝着较小的预期寿命倾斜 ,

实际上这并不能代表人类寿命。

克里斯先生从历史资料中给我发了一些很酷的文章 ,

我会和你们分享故事 ,

我想这是个美国原住民绅士 ,

所以这是1870年9月15日晚间的电讯报 ,

如果您看这篇文章 ,您会再次看到历史参考 ,这只是一种历史

有趣的是 ,

他对美国本地人绅士鹰很感兴趣 ,

他经常一次将多达20加仑的纯蜂蜜装在鹿皮中 ,

装袋背着斜挎 ,

所以他也喜欢蜂蜜 ,

他一直是白人的坚定朋友

19岁那年就拥有了高大身材和强大力量。

他娶了一个妻子 ,并在1831年生了两个孩子 ,

妻子去世了 ,而这位老酋长在同年去世 ,

享年93岁或94岁。这是在1831年 ,

所以这表示他在90岁时而不是19岁时娶了一位年轻妻子 ,

这真是太酷了 ,这只是对美国原住民的历史回顾 ,

他在1831年活到93岁 ,

人类已经长寿是大部分时间 ,

现在的婴儿死亡率降低了 ,这是一个完全独立的问题 ,

我可以进入一个不同话题的播客 ,

这可能是由于抗生素和儿童卫生时代所致 ,

总体而言 ,孕妇有进展情况 ,但人类健康寿命没有改善 ,

实际上我不会说寿命变得更短 ,是因为由于慢性病的大量增加 ,

我们拥有重要生命的时间现在越来越少 ,

请收听克里斯·索诺比的播客 ,以获取更多有关此的更多信息 ,

因此播客中出现了另一种情况

与彼得在一起的时候 ,我们没有太多时间可以谈论新冠病毒。

我最近没有再谈论这个话题 ,

因为说实话 ,这个讨论对我来说很无聊 ,

我认为很明显 ,在过去的六七个月里 ,

我一直在说的事实是 ,

基础代谢健康决定了对这种病毒的反应方式。

最近CDC发布的估算显示 ,

病死率不到0.1% ,低于流感 ,

这些(信息)都遍及整个互联网 ,

尽管我确实认为可以验证

我从一开始就说的许多新陈代谢健康的内容 ,

但我并不需要重新发布 ,这完全取决于上下文 ,

如何才能变得新陈代谢健康?吃动物性食物,从头吃到尾

如果您需要更多的营养 ,

那么您就可以从饮食中消除加工过的种子油 ,

但是最近我在高脂彼得博客上看到了这篇文章 ,

塔克·古德里奇也谈论了它 ,

讨论了新冠病毒蛋白的游离脂肪酸结合 ,

有趣的是什么 ,是亚油酸 ,

他们所说的是在这个结合域内有许多亚油酸需求 ,

并且亚油酸结合稳定了锁定构象 ,

从而在人体细胞中降低了ace2的释放 ,

在人体细胞中亚油酸补充与新冠药物会合或抑制病毒复制 ,

这在某种程度上听起来像亚油酸可能对对抗新冠有益 ,

但如果您读了文章的结尾 ,那么我们就会得出一些有趣的结论

新冠接合亚油酸可以赋予组织独立的机制 ,

通过该机制病原体冠状病毒感染可以驱动免疫失调和炎症 ,

我们的发现为两者之间提供了直接的结构联系

亚油酸对新冠病理学和病毒本身 ,

表明s蛋白中的la结合和多模式la信号通路均代表了针对新冠感染的极好的治疗干预点 ,

因此最终关注对您我一样有意义

在汤米·伍德播客的对话中听到的是 ,

如果在代谢方面不健康 ,

是否会中性粒细胞淋巴细胞比例失调?

如果您想对此进行回听 ,免疫代谢会失调吗?请回到该播客 ,

但最终的问题是免疫系统将能够正确反应 ,

并且过量的亚油酸也将使新冠病毒能做其想做的事情 ,

如果我在急救室,我肯定不会接受静脉注射

亚油酸用于ICU患者 ,

我非常希望看到红细胞或人血清中亚油酸的平均水平与新冠结果相关 ,

基于我所学到的一切 ,

我认为是亚油酸代谢综合症等

我认为新冠很有可能将外流亚油酸用于消极的方式进行信号传导 ,

又使病毒在体内复制使亚油酸水平很高 ,

因此我们再次谈论新冠病毒 ,

我将分享一些对我来说很有趣的事情 ,

我的一个朋友做了这个网站 ,使人们垂涎三尺 ,

呃 ,我认为这是一个不错的网站 ,您应该看一下 ,

然后检查自己的风险 ,然后才能参加测验 ,

这实际上是一项很好的测验 ,将考查中性淋巴细胞比率 ,

我认为这种对免疫代谢的思考是人类为了预防冠状病毒感染

或更准确地预防冠状病毒而必须进行的基础代谢健康的基础 ,

这将是改变的基础是:当处于冠状病毒空间之内时 ,

这个测验令人惊讶 ,

我们可以找到这样的标题 ,

即麝香麝香将不会用计时病毒疫苗 ,

如果您相信这种话 ,可以称比尔·盖茨为指关节。

伊隆·马斯克说他不容易感染冠状病毒 ,

也不担心他或他孩子的健康 ,

这是一个大胆的声明 ,

我可能会同意 ,我并不担心会出现严重的冠状病毒 ,

我从一开始讲 ,

如果代谢健康 ,我们将轻松地过掉这种病毒传播 ,

这就是在我所有朋友中看到的 ,

我认识的每个人没有谁感染过冠状病毒 ,

我不知道自己是否感染过没有 ,

但是我想

如果您正在考虑基础代谢健康 ,如果您在代谢方面健康 ,

那么如果没有营养不足或存在潜在问题 ,

慢性病毒影响基本上就不会发生 ,

我想谈的最后一件事是与克里斯·诺比(Chris Nobi)谈过的一篇论文 ,

但在播客中我们没有谈及 ,

是讲由ip脂肪 ,必需脂肪酸和乳腺癌发生所引起的 ,

在该文中令人着迷的是 ,

可以查看乳腺癌的最终发病率 ,

患癌的大鼠所占的百分比 ,

以及饲喂含有不同水平的efa的大鼠的总产量。

这里的efa百分比是亚油酸的百分比 ,

饮食中的亚油酸就是efa

在这件事中 ,您现在可以看到 ,

随着饮食中亚油酸的含量从0.5%增至5% ,

乳腺癌的数量猛增 ,然后趋于平稳 ,

这是因为发生率之间存在着非常明确的几何关系

小鼠生癌是一种动物模型 ,

但我认为其中许多涉及多不饱和脂肪的动物模型都可以高度转化为人类 ,

因为在线粒体电子传输链nadh水平上涉及许多相同的机制 ,

在癌症的生长方面 ,以后我将在后面详细讨论 ,

我在与布拉德·马歇尔播客中谈到这一点 ,

当达到一定水平时 ,癌症的生长速度就会下降 ,

无法直接将其转化为人类数据 ,

但是大多数人的饮食中有多少亚油酸是多少高于这个值

甚至可能超过5%、10%、 12%、 13% ,

所以如果研究的所有人类数据都沿着横线部分 ,

那么高亚油酸与低亚油酸摄入看起来可能没有什么不同 ,

因为至少就这种癌症结局而言 ,该水平已经趋于稳定。

怀疑其他端点的结果可能相似 ,

但这是我想让康明斯谈论的事情 ,

如果正在研究人群,重新查看亚油酸含量的高低 ,

低水平的人最好将亚油酸的含量降至极低 ,

因为亚油酸的含量极低 ,

大约低于饮食中亚油酸的热量含量的百分之二或更少

如果找不到这样的人 ,

可以在无素饮食社区(或称聪明从头吃到尾的低亚麻酸社区)之外很难找到这样的人 ,

那么将不会研究我所相信的真实表象是人体中亚油酸作用的频谱 ,

因此不要被低亚油酸与高亚油酸的研究所误导 ,

如果它们全部处于图表横线平坦部分 ,

有发生率是因为两者都仍处于亚油酸的有毒水平 ,

因此本周仅使用一些有趣的文章 ,希望对你们有所帮助 ,

。。。

让我们知道您的想法。

记住这一切 ,我一直在思考这个概念 ,这继续引起我的共鸣 ,

我们不能忽视 ,根本不能忽视我们来自哪里 ,

作为人类 ,我们不能成为2020年失忆症的受害者。

作为人类 ,我们不能忘记的很多方面 ,

因此 ,感谢您成为回忆的一部分 ,

如果这能引起您的共鸣 ,

我会知道 ,并感谢大家的支持 ,

但您仍然应该始终保持精进

https://www.youtube.com/watch?v=1Xd6srWklJs

  what is up you guys welcome to another edition of controversial thoughts i figured out how to unmirror my video on zoom so this one is now properly situated and you can see all of our heart and soil supplements there behind me we got two new ones coming out this week histamine and immune and blood builder super stoked about that they come out on thursday which is tomorrow obviously my podcast fundamental health over there you can see that so i'm gonna throw around a bunch of stuff today try and keep this to a shorter controversial thoughts video but i recorded a podcast yesterday with peter from hyperlipid and it was amazing and there were a couple of really interesting papers in that conversation that i wanted to highlight for you guys even before that podcast comes out that podcast will be out in two weeks next week i have a podcast coming out with dave feldman we talked about his oxidized phospholipids experiment which is super fascinating i will do probably a controversial thoughts video on lipoprotein little a and lipids between now and then but check this paper out so this is one of the more interesting papers that i have seen regarding the polyunsaturated fat versus saturated fat ideas and the notion that polyunsaturated fats cause inappropriate insulin sensitivity at the level of the mitochondria leading to essentially adipocyte hyper trophy versus hyperplasia but that's many steps down the line so this is a paper looking at the differential metabolic effects of saturated versus polyunsaturated fats in ketogenic diets if you skip to the results section i think i looked at this paper briefly with tommy wood i went over it more with peter in the podcast in two weeks but i wanted to show you guys this one the open graphs are saturated the closed graphs the gray graphs are polyunsaturated if you look at this mean change from baseline at first glance you might look you might think that polyunsaturated fats look better because there's more beta-hydroxybutyrate they're making ketones ketones are magical right there's lower levels of glucose there's lower levels of insulin there's lower levels of ldl cholesterol which we know all know causes atherosclerosis wink wink and uh there is a lower there's a further decrease in triglycerides and if you look at the insulin sensitivity measured i believe by a clamp test you can see that polyunsaturated fats caused increased insulin sensitivity and we want insulin sensitivity right wrong if you are doing a ketogenic diet you do not want to be insulin sensitive normal human physiology is that you should absolutely be insulin resistant when you are doing a ketogenic diet that's the whole point of a ketogenic diet is to spare glucose for the red blood cells the brain the testicles the ovaries the adrenals the kidneys things like that that are more glucose dependent than the muscles you don't want to be insulin sensitive when you are doing a ketogenic diet so what's really interesting about this experiment in humans is it illustrates the notion that i have been discussing with brad marshall a little bit with the friendly debate with ben bickman and in the podcast coming with peter from hyperlipid in two weeks that saturated fats and polyunsaturated fats do very different things at the level of our mitochondria if you listen to the podcast of brad marshall you know what i'm talking about here is the fn ratio the fadh2 to nadh ratio which translates into reactive oxygen species which signal insulin resistance or a stop to the cellular ingress of nutrients both fat and glucose and if you have inappropriate continued insulin sensitivity you will get continued ingress continued importation of glucose and triglycerides and free fatty acids which leads to glycogen and fatty acid deposition your adipocytes will grow you do not want your cells to be inappropriately insulin sensitive which this study in a ketogenic diet in humans clearly illustrates the inappropriate persistent insulin sensitivity when ketogenic diets are based on polyunsaturated fats in the short term you might think it's good because your ketones are higher or your triglycerides are lower but what's happening is that your adipocytes are growing or your cells remain inappropriately insulin sensitive that is what we do not want that is what saturated fats are supposed to signal in your body by generating reactive oxygen species so this is human evidence that a lot of the same molecular pathology molecular mechanisms that i've been discussing the electron transport chain we talked about this at brad marshall all these other on-ramps in the electron transport chain complex 1 complex 2 succiny dehydrogenase electron transferring flavor protein dehydrogenase glyceraldehyde 3-phosphate dehydrogenase all feeding into that q the coenzyme q moiety leading to a backup when things are coming in through complex one leading to reverse electron transport generation of superoxide leading to hydrogen peroxide and cellular signaling of insulin resistance which is what your body needs to survive you would be dead without insulin resistance it's how your cells signal were full of nutrients polyunsaturated fats create an inappropriate persistent signal that the cells can accept more nutrients which is a bad thing stuffing your body full of linoleic acid grows your adipocytes they become hypertrophic you've listened to the podcast with ben bickman and the last controversial thoughts i did i showed you evidence that linoleic acid metabolites specifically four h and e four hydroxynonol are connected with adipocyte hypertrophy impaired adipogenesis which is leading to adipocyte hyperplasia which is the ex the growth of fat cells by division that's what you want if you don't want to become insulin resistant pathologically later on but big fat cells hypertrophic fat cells get sick quote unquote they release inflammatory mediators they release free fatty acids and you get metabolic dysfunction so gradually polyunsaturated fats push you along the road to metabolic dysfunction now i'm not saying all polyunsaturated fats are bad in all quantity they're not a toxic thing but the amount matters excess evolutionarily inconsistent consumption of massive amounts of polyunsaturated fats specifically linoleic acid is a signal to your adipocytes to grow to become hypertrophic to limit adipogenesis to limit hyperplasia to become big and fat and sick the button bursts on the pants you get free fatty acids leaks and that is when metabolic dysfunction aka metabolic syndrome aka diabetes really starts and that is a problem that is what you do not want you guys that is at the root of chronic disease listen to the podcast they released with chris kenobi yesterday we talked about all that and the real good historical epidemiological and anthropologic and interventional evidence that the the main driving factor here is excess polyunsaturated fats you can get that study on polyunsaturated fats and ketogenic diets if you see the reference there but that is a fascinating thing now because you do not want to remain insulin sensitive when you are on a ketogenic diet clear evidence in humans that these mechanisms are in play this is another fascinating paper insulin-induced translocation of cd36 to the plasma membrane is reversible and shows similarity to that of glut4 what they're saying here is that if your cells remain insulin sensitive inappropriately when you are exposed to polyunsaturated fats you are putting cd36 in the cell membrane well what is cd36 doing cd36 is one of these proteins that is going to be involved in the ingress of fatty acids free fatty acids and it's going to cause your fat cells to fill up cause the other cells to fill up with fat just like glut4 is a glucose transporter that's going to pull glucose into the cell in response to insulin cd36 is kind of like a fat transporter so when you're inappropriately insulin sensitive you are importing excess glucose excess fats your cells don't have the signal that says stop i'm done you're giving confusing signals to your cells by having massive levels of linoleic acid which we're not supposed to have evolutionarily because they don't occur in nature they do not occur in nature so really interesting stuff there now the other interesting piece of the podcast with chris kenobi that we talked about was the notion that humans are living longer today which is just silly i actually don't think there's any good evidence we're living any longer today the life expectancy looks like it's longer because we have a lower infant mortality rate but that's skewing the data if you live to adulthood as i talk about with chris the length of the life of a human is about the same today as it was 100 years ago we have more chronic disease than we do than we did then today that's very clear and we're living about the same amount of time but we're living worse we have less vitality we have less ability to do the things we'd like to do because we have more chronic disease so don't be fooled by the notion that we are living longer today we are living the same there is lower infant mortality which makes it look the average life expectancy look longer but humans are still living the same amount we talked about this with chris with james clement the squaring of the morbidity curve and the fact that as chris ryan has talked about in his books a higher infant mortality rate inappropriately skews the data towards smaller life expectancies historically which are actually not representative of the amount of time that humans lived one of my friends chris meister sent me some pretty cool articles from a historical source that i'll share with you guys about a um [Music] and i guess a native american gentleman so this is from the evening telegraph uh september 15 1870 and if you look at this article you'll see the historical reference again this is just kind of historical interesting to a native american gentleman called chickasaw he would frequently bring in for sale at one time as much as 20 gallons of pure honey in deerskins uh bags slung to his back so he liked honey too he was always a firm friend of the whites a man of gigantic stature and herculean strength in his nine uh in his 19th year uh he took a wife and by her had two children in 1831 she died and the old chief did not long survive her dying in the same year aged 93 or 94. this is in 1831 so this says in his 90th year not 19th year in his 90th year he took a young wife so how cool is that it's just a historical recounting of a native american who lived to 93 years old in 1831 humans have been living long amounts of time for i would say the majority of revolution we had lower rates of infant mortality today which is a whole separate issue i can go into a different podcast that's probably due to sanitation antibiotics and childhood you know overall uh progression in terms of the way that women have babies but the lifespan the health span of humans has not improved has not in fact i'd say it's gotten shorter because the amount of time that we have vital life is now lower due to the massive increase in chronic disease listen to the podcast of chris sonoby for a whole lot more about that so one other thing that sort of came up in the podcast with peter that we didn't have a whole lot of time to talk about was sars kovi 2. now i haven't been talking about this much recently because honestly the discussion's just gotten kind of boring to me i think it's abundantly clear that the things that i've been saying for the last six to seven months are true that it's our underlying metabolic health that determines how it will respond to this virus recent cdc estimates were released showing case fatality rates of less than 0.1 percent that's lower than the flu these are all over the internet i didn't feel the need to repost even though i do feel it validates many of the things i was saying from the beginning be metabolically healthy it's all about context how do you become metabolically healthy eat animal foods nose to tail eliminate uh processed seed oils from your diet if you guys need more nosotel nutrition that's what we do at heart in soil you can check us out heart and soil dot co if you need desiccated organs if you can get fresh organs that's fantastic but there was recently this article that i saw on peter's blog hyperlipid tucker goodrich also talked about it discussing the free fatty acid binding pocket uh of the sars kov2 spike protein what's interesting is that this is linoleic acid and what they say here is that within this binding domain there are many um linoleic acid needs and linoleic acid binding stabilizes the locked s conformation giving rise to reduced ace2 in vitro in human cells linoleic acid supplementation synergizes with cov2 uh uh drug rendezvous or suppressing sars cov2 replication which in a way makes it sound like linoleic acid could be beneficial for fighting sars covi2 but if you read the end of the paper there are some interesting things that come out of that as well we hypothesized that linoleic acid acid sequestration by cyrus kovi 2 could confer a tissue independent mechanism by with by which pathogenic coronavirus infection may drive immune dysregulation and inflammation our findings provide a direct structural link between linoleic acid cova-19 pathology and the virus itself and suggests that both la binding pocket within the s protein and the multimodal la signaling access represent excellent therapeutic intervention points against sars kobe 2 infections so ultimately the concern here which would make sense to me as you heard in the conversation with tommy wood is that if we are metabolically unhealthy are we going to have a disorder neutrophil lymphocyte ratio are we going to have disordered immuno metabolism go back to that podcast if you want to review that but ultimately the question is is our immune system going to be able to respond properly and could excess linoleic acid also be enabling cyrus cov2 to do what it wants to do i would certainly not be accepting intravenous infusions of linoleic acid if i were in the icu or if i were administering them to patients in the icu i would very much like to see average levels of linoleic acid in the red blood cells or the serum of people in correlation with sars kobe 2 outcomes i think that would be fascinating based on everything that i have learned about linoleic acid metabolic syndrome et cetera i think it is very possible that exodus linoleic acid could both be used by sars kovi to to do its signaling in a negative way and to [Music] be needed for sars kov2 replication in the body i would not want my linoleic acid levels to be high since we are talking about cyrus kov2 again i'll share a couple of things that are interesting to me one of my friends did this website stop covet cold uh i think this is a great site you should check it out you can check your covered risk you can take a quiz which is actually a really good quiz which will look at your neutral lymphocyte ratio and i think this type of thinking about the immune metabolism the underlying metabolic health that humans can have to um to prevent coronavirus infection or prevent severe courses with coronavirus more accurately will be what is needed to change but that quiz there is pretty freaking amazing uh while we are on the um sort of the tabloid space of um the coronavirus conversation we can find this headline that elon musk will will not be taking a chronovirus vaccine and calls bill gates knucklehead if you believe the new york post uh elon musk said that his he was not susceptible to coronavirus or concern for the health of him or his kids which that was a bold statement that i would probably agree with i am not concerned about getting a severe course of coronavirus i have said this from the very beginning that if we are metabolically healthy we will move through this virus with ease that's what i have seen in all of my friends everyone that i've known who've had who's had a coronavirus i don't know if i've had it or not it's possible but uh i think that if you were metabolically healthy if you were thinking about your underlying metabolic health chronovirus will essentially be a pretty non-issue if you are not nutrient deficient or having under underlying issues the last thing i want to talk about is a paper that i talked to chris nobi about but we didn't have during the podcast it's this one by clement ip fat and essential fatty acid and mammary carcinogenesis what's fascinating in this paper is that you can look at the final incidence of mammary tumors percent of rats with tumors and total yield of rats fed diets containing different levels of efa the percent efa here is the percent of linoleic acid the dietary linoleate is the efa in this thing now you can see that the total number of mammary tumors skyrockets as you go from 0.5 percent to about five percent uh linoleic acid in the diet and then levels off what's interesting is there is a really clear geometric relationship between the incidence of memory tumors in rats again it's an animal model but i think many of these animal models involving polyunsaturated fats are highly translatable to humans because they involve many of the same mechanisms at the level of the mitochondrial electron transport chain nadh levels cancer growth i'll talk more about that in the future i talked about that in the podcast with brad marshall but when you get to a certain level the cancer growth levels off well we can't translate this directly to humans but what percentage of uh linoleic acid is in the diet of most humans it's much higher than this it's probably even beyond five percent 10 12 13 perhaps so if all of the humans studied are along the flat portion a high versus a low linoleic acid consumption might not look any different because there is a leveling off in terms of at least this cancer outcome i suspect the outcomes may be similar for other endpoints but this is something i talked to ivor cummins about that if you're studying populations of humans and you're looking at high versus low levels of linoleic acid the low group had better have a very low level of linoleic acid as an ancestrally low level of linoleic acid which is around the level of less than two percent or fewer calories from linoleic acid in your diet if you cannot find people in the population that would be very hard to find outside of someone in this community or a carnivore community or a very astute nose to tail low linolenic acid community you are not going to be studying a true representation of what i believe to be the spectrum of linoleic acid effects in the human body so do not be misled by studies of low versus high linoleic acid that do not show a difference if they are all on that sort of flattening out portion of the graph where there's no difference in incidence because they're both still at a toxic level of linoleic acid so just some using from this week some interesting articles hopefully that's helpful to you guys again super excited about the release of gut and digestion fire starter and now blood builder and histamine and unit hardened soil you can check us out heart and soil dot co you can always email me heart dr paul dr paul at heart and soil dot co if you have any questions it's it's meaningful to me to get more nosotel nutrition into your life because these are the nutrients that i believe help us thrive as humans we should not fear animal foods in any way shape or form and there are unique nutrients here if you can get fresh organs that's fantastic but if you can't i hope that our supplements which believe me are the highest quality we can find anywhere and we are developing a us-based supply chain as well will improve your life let us know what you think dr paul dr paul heart and soil dot co you guys are all part of the remembering it's something i continue to think about this concept continues to resonate with me that we cannot ignore we simply cannot ignore where we have come from as humans we cannot be we cannot fall victim to the amnesia of 2020. there are so many aspects of what it means to be a human that we cannot forget so thank you for being a part of the remembering if this resonates with you i let me know and thank you for all for your support and still you should always still stay radical
· 2020/10/06 17:24