目录
Keith Littlewood
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基思・利特尔伍德解析甲状腺功能对人体健康的影响
**基思・利特尔伍德的职业背景与研究方向**
基思・利特尔伍德讲述了自己独特的职业轨迹。他曾在军队服役四年,退役后一度感到迷茫,偶然间因健身教练缺席而接手健身指导工作,由此进入健身行业。之后,他的职业范围逐渐扩展到康复、疼痛管理,再到功能医学和营养学领域。
他对雷佩特的研究成果及其他科学家的观点产生浓厚兴趣,认为许多有价值的早期研究在当今行业中被忽视,转而更关注简化的机制研究。为此,他投入多年时间研读相关资料,形成了自己的理解体系,并攻读了内分泌学硕士学位,目前正着手开展博士研究,聚焦污染对激素(尤其是甲状腺激素)的影响。
如今 50 岁的他,仍觉得自己刚刚起步。他认为甲状腺功能影响人体生理的方方面面,理解甲状腺功能及其紊乱机制是值得投入余生研究的课题。他的工作是为全球客户提供指导,帮助他们解决与激素相关的各类功能问题,核心在于从基础营养、环境因素等方面入手,找出身体负面输出的根源,助力客户做出改变。他并非阴谋论者,但深知企业对数据的干预、伪造等问题,如本・戈德亚克的《糟糕的科学》就揭示了相关现象。他强调,像胆固醇这样的指标,其与心脏病的关联并非定论,朱庇特试验的数据就存在隐瞒等问题。他的目标是让人们明白自己能掌控健康,通过适当指导找到改善生理状态的方法,减少对药物的依赖。
**甲状腺功能的广泛影响与评估方式**
基思・利特尔伍德认为,甲状腺功能是人体生理的层级机制,其影响渗透到各个方面。理解甲状腺功能如何被扰乱,是值得投入时间研究的。他致力于让人们认识到自身对健康的掌控力,通过指导帮助他们找到促进生理协调、维持长期有序状态的方法,从而减少干预需求。
在评估甲状腺功能时,血液检测有一定作用,但不能完全依赖。有些人血液检测结果正常,却存在便秘、脱发、胆固醇偏高、心率异常等症状。评估需结合营养状况、生活环境、情绪压力等多方面因素。
不同甲状腺协会对正常范围的界定存在差异,如促甲状腺激素(TSH)的正常范围约为 4 至 5mIU/L,但有研究指出,在妊娠和抑郁症案例中,TSH 不应超过 2.5mIU/L。雷佩特曾表示,从未见过促甲状腺激素高于 2 的健康人。基思认同这一观点,他认为垂体反应是一种应激的 fallback 机制,若甲状腺外周转化(如肝脏、肾脏、肌肉组织中的转化)高效,就无需依赖这种机制。多项研究表明,垂体激素(如生长激素、催乳素、促甲状腺激素)过量与疾病进展相关,且有医生认为,促甲状腺激素达到甲状腺功能减退的诊断标准可能需要数年时间,而临床医生往往忽视三碘甲状腺原氨酸(T3)和反三碘甲状腺原氨酸(反 T3)的变化。
除血液检测外,体温、心率等也是重要参考指标。甲状腺功能不足可能导致心率过缓,因甲状腺激素不足使心脏组织无法获得足够 T3,影响收缩和舒张功能,进而导致纤维化、动脉钙化和胆固醇沉积;也可能因甲状腺功能严重抑制,身体依赖肾上腺素而出现心动过速。通过规律饮食等调整,可观察到心率变化,判断身体是否不再依赖肾上腺素。
**皮质醇与甲状腺功能的相互作用**
在功能医学领域,存在下丘脑 - 垂体 - 肾上腺轴(HPTA)的概念,涉及反馈循环,皮质醇与甲状腺功能存在密切相互作用。当人处于压力状态时,会分泌更多肾上腺素和皮质醇;当存在炎症(如 C 反应蛋白升高)时,皮质醇也会增加,因为它具有抗炎作用。
肾上腺的功能依赖甲状腺,甲状腺功能低下会影响皮质醇的产生,但身体可能会有补偿机制。同时,压力状态和饮食不足会促使身体产生更多糖皮质激素(如皮质醇),这些激素会抑制促甲状腺激素的分泌。因此,压力过大时,促甲状腺激素的检测结果可能看似正常甚至偏低,仅靠血液检测难以准确评估甲状腺功能。
在某些情况下,肾上腺需要支持,如补充孕酮或孕烯醇酮以保障激素转化。确保足够的胆固醇、维生素 B6、维生素 A 等,对皮质醇的生成也很重要。此外,体温和脉搏可辅助判断甲状腺功能,低体温可能提示甲状腺功能低下,但心率快也可能是甲状腺功能严重抑制、身体依赖肾上腺素的表现,规律饮食后心率下降可作为判断依据。
**B 族维生素与甲状腺激素的关联**
基思・利特尔伍德提到,虽然他有段时间未深入研究,但理解是 B 族维生素(尤其是硫胺素、核黄素)在电子传递链和有氧代谢中作用关键,缺乏可能导致代谢功能障碍。
女性对 B 族维生素的需求可能更高,因为雌激素水平过高会影响肝脏功能,若 B 族维生素不足,雌激素代谢会受影响,这可能与自身免疫问题、甲状腺功能亢进有关,甚至可能涉及肿瘤发生。维持足够的 B1、B2 水平,对维持肝脏等组织的有氧代谢至关重要。因此,在考虑甲状腺治疗前,补充 B 族复合维生素是有益的,虽然有机 acids 检测可评估相关情况,但他更倾向于通过基础观察,优先补充 B 族维生素。
**海鲜中 Omega-3 脂肪酸的争议**
基思・利特尔伍德认为 Omega-3 脂肪酸的作用存在争议。很多人认为 Omega-3 脂肪酸具有心脏保护和抗炎作用,但他对此持不同观点。
从细胞膜角度看,过量 Omega-3 脂肪酸会使细胞膜变得通透。有研究显示,大量 DHA(一种 Omega-3 脂肪酸)会导致细胞膜渗漏,某些毒素也有类似作用。Omega-3 脂肪酸甚至被用于癌症治疗,通过增加细胞膜通透性,增强化疗药物的效果。
关于 Omega-3 脂肪酸与心脏健康、长寿的关联,基思认为现有研究存在不足。韩国的一项大型研究显示,胆固醇值在 5.5 至 6.4 或 5 之间与长寿相关,胆固醇值较低者反而寿命较短,这对传统观点提出挑战。仅通过食物问卷得出 Omega-3 脂肪酸改善心脏健康、延长寿命的结论,忽略了其他影响因素,不够严谨。
此外,DHA 与甲状腺转运蛋白(如转甲状腺素蛋白)的结合能力强,会取代甲状腺素(T4)。转甲状腺素蛋白虽不是最主要的甲状腺结合蛋白,但在大脑中是主要载体,若被不饱和脂肪酸取代,可能导致大脑局部甲状腺功能低下,这与阿尔茨海默病可能存在关联,但相关机制需进一步研究。
基思认为,不应大量补充 Omega-3 脂肪酸,通过适量食用海鲜(如牡蛎、虾)获取即可,这些食物还能提供硒、锌等支持甲状腺功能的营养素。单不饱和脂肪酸(如橄榄油)对细胞功能有保护作用,而过量摄入脂肪(尤其是不饱和脂肪酸)可能带来问题。
**碳水化合物摄入量与甲状腺功能的关系**
基思・利特尔伍德在指导客户时,不专注于具体的碳水化合物克数或身体成分,而是关注改善客户的能量水平、消化功能、睡眠质量和生育能力等。他鼓励客户自行尝试不同比例的碳水化合物摄入,如占饮食的 50%、60% 或 70%,找到适合自己的方式。
他认为,每天碳水化合物摄入量低于 100 克对很多人来说可能不合适。对于长期限制碳水化合物摄入的人,突然大量增加摄入可能产生不适。他建议客户根据自身情况调整,找到能改善身体状态的碳水化合物比例。
**果糖与甲状腺功能的关联**
基思・利特尔伍德认为果糖本身并非问题,过量摄入才可能带来影响。当葡萄糖过量时,可能激活多元醇通路,导致果糖积累,这一过程与糖尿病进展相关,但根源可能是甲状腺功能不佳导致的胰腺和肝脏功能异常,而非果糖本身。
肝脏功能受甲状腺影响,若肝脏无法有效处理葡萄糖,将其转化为甘油三酯等物质,可能引发问题。镁缺乏也可能与多元醇通路的激活有关。甲状腺功能不佳、有氧代谢异常、缺乏必要的辅助因子(如 B 族维生素)等,都可能导致葡萄糖代谢问题,进而影响果糖代谢。因此,不应将代谢问题归咎于果糖,而应关注甲状腺功能和整体代谢状态。
**甲状腺功能改善的案例与反 T3 的意义**
基思・利特尔伍德明确表示自己不是医生,不能诊断疾病或开具甲状腺激素药物,而是为客户提供信息,让他们自行研究并做出决定。对于身体状况脆弱(如面临心脏病发作风险)的人,是否使用甲状腺激素需谨慎,但对大多数人而言,使用甲状腺激素是安全的。
他接触过许多客户案例,甲状腺功能改善后,体重问题、睡眠质量、胆固醇水平、生育能力、便秘等状况都得到改善,身体变暖,脑雾减轻,甚至有因疫苗受损者的脑雾症状也大幅缓解。改善甲状腺功能并非一定要使用甲状腺激素,补充硒、锌等辅助因子(甲状腺受体是锌指结构)、牛磺酸(对甲状腺有益,能改善睡眠)、亚甲蓝(可提高甲状腺激素水平)等也有帮助。B 族维生素缺乏可能导致类似甲状腺功能不足的症状,补充后可能改善。当前环境中的污染、压力、营养不良、食物氧化等因素,都会影响有氧代谢,进而影响甲状腺功能。
在癌症研究中,肿瘤细胞处于相对甲状腺功能低下状态,存在高水平的甲状腺素(T4)、反三碘甲状腺原氨酸(反 T3)和脱碘酶 3,后者会进一步降解 T3,并促进其在肝脏的代谢。研究表明,限制 T4 生成(使用药物)可减少反 T3,对肿瘤有保护作用并使其缩小,但同时需补充 T3,以恢复肿瘤的正常甲状腺功能,停止糖酵解和乳酸生成,转向有氧代谢,促使周围细胞正常凋亡。
反 T3 是 T4 经内环脱碘产生的。在炎症状态下,T4 可能更多转化为反 T3,因为 T3 无法被有效利用,可能与甲状腺受体受污染物影响等因素有关。通过游离 T3 与反 T3 的比值(如应高于 20)或总 T3 与反 T3 的比值(如 10 至 15,游离 T3 处于上限 20% 以上),可了解代谢状况。反 T3 与其他甲状腺激素结合分析,能提示代谢问题,肿瘤中反 T3 水平高是因其微环境不允许 T3 发挥作用,维持糖酵解和瓦堡效应,浪费葡萄糖。
**令人期待的甲状腺相关研究领域**
基思・利特尔伍德的研究旨在探讨不同激素引发的不同反应,关注甲状腺素(T4)、反三碘甲状腺原氨酸(反 T3)与整合素 AVB3 受体(非基因组途径)的关系,及其在纤维化、肿瘤形成和血管生成、转移中的作用。他认为,关于甲状腺激素(如左甲状腺素)的使用及其影响,需要更多研究。
他还对细胞膜研究充满期待,如吉尔伯特・林、弗拉基米尔・梅特维夫和杰拉尔德・波拉克的研究,涉及细胞膜结构、有序水以及细胞与其他结构的界面等。传统观点认为饮食中的不饱和磷脂会增加细胞膜流动性,但有研究质疑这一观点,且关于细胞膜上大量泵的存在也存在疑问。他认为,这些领域若能得到更多研究,可能带来突破性进展。
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Hey everyone and welcome to the Boost Your Biology podcast. My name is Lucas and I am the founder of Ergogenic Health. Together in this podcast series, we will go underground to explore cutting edge health and human performance insights that you simply cannot search on Google to help you upgrade your existence. So without any further ado, let's jump into today's episode.
03:02
Ladies and gentlemen, welcome back to the Boost Your Biology podcast.
03:08
Today, I have a supremely special guest. Joining me in is Keith Littlewood. Keith, welcome to the show, man. Thanks for having me. Awesome. Keith, do you want to maybe let my listeners know a little bit about maybe your journey and how you got so fascinated into, I guess, optimizing human health? Sure. I failed massively at school, but the only qualification I was good at was biology, but there's nothing really kind of pulled out of that.
03:33
I was always going to go into the army. I was actually going to go into the RAF, but the career center was too far away. So I opted for the army and working with helicopters. And I did four years with the army and I came out of there pretty lost and didn't know what I wanted to do and ended up falling into a gym induction at a leisure center because the instructor wasn't there. And they asked me to take it because I was a leisure assistant at about 23, 24. And from being in the fitness industry as a fitness instructor to personal trainer, rehab into fitness,
04:01
therapy, pain management, and then into kind of some functional medicine, nutritional-based stuff. I then kind of got interested in the works of Ray Peete,
04:11
kind of a really broad reference of kind of, you know, information he's put out based upon his work and thought process and some really solid thinking from other scientists that I think is glossed over to a degree, but that's just generally how kind of business and industry operates these days, not looking at some of the older, you know, research that's really quite potent in favour of kind of more reductionist mechanisms. And so I got interested into that
04:40
reading his stuff and many other people's stuff for years, which I kind of, I think I've developed a lot of my, I'd say, understanding. I still feel like I don't know much at the moment. I still feel like I'm scratching the surface permanently. And I decided to put some of that kind of learning to the test and did a postgrad and a master's in endocrinology. And now I'm just knocking on the door of my PhD, which I've just started looking at
05:05
the effects of pollution and hormones, particularly thyroid hormones. So it's kind of been a journey like that. And I'm kind of at the ripe old age of 50 now, but I feel I'm just getting started. So I think if you kind of take on board something like thyroid, we just mentioned off areas like thyroid takes you into many areas, all areas of function, you know, it permeates every aspect of physiology. And I think getting an understanding of something that's such a
05:30
hierarchical mechanism of the human body and understand how it gets distorted, I think feels like a worthy lifetime of what's left of my lifetime approach to develop an understanding of it. So, you know, I make my living working with people around the world, coaching them through different areas of function that are often related to hormones. But a lot of it comes back to basic nutrition, first of all, understanding your environment, understanding what tweaks we can bring in to make some change, understanding how…
05:59
All the previous kind of inputs to your system are generally creating the negative outputs that you're experiencing. So my job is really to go in and help people resolve that and give them understanding of what they can do to create change. I wouldn't say I'm a conspiracy theorist, but I'm certainly well aware of
06:17
corporate interference and quashing of data, falsification of data. And you only need to read books like kind of Ben Goldacre's Bad Science as an example to get an idea of what companies have been capable of and have been influenced by kind of other kind of
06:32
anthropologists like Joseph Dummit, Drugs for Life, Gilbert T. Welch, Overdiagnosed, and various books like that that kind of give you an idea of some of the problem that people are facing and perhaps why, you know, one of my main assertions that thyroid blood tests can be a complete waste of time if you don't know the environment or
06:50
or the stress that someone's under, how much food they're eating. And while if you go and look at a clinical trial that's assessed something related to thyroid, unless you understand what the individual in the trial is exposed to, it's really difficult to get an idea of something that's effective or not. Yeah. I mean, you've got a really interesting background and some of the work you're putting out there, man, is highly respected. And I really appreciate people like yourself who
07:15
I guess, become an expert in this particular realm when it comes to thyroid health. So it's sort of, I'd love to, you know, explore some of the, you know, the far reaching effects of thyroid hormones in the body and sort of help to explain to my listeners why it has such broad reaching effects. Sure. Well, I still don't classify myself as an expert of any sorts because when you're starting a PhD, you realize some of the level of understanding you have is probably, you
07:41
not as good as you thought it was. So as much when I was starting my master's degree, I thought I knew nothing. I feel I know even less now. And part of that is probably looking at aspects of, you know, molecular science and how small and reductionist we can get and
07:56
I kind of put a post out this week about Hans Selye, who kind of really focused on the concept of supermolecular biology, understanding life, what's functioning, what's happening to the organism as such. And I think it's quite useful to keep a keen eye on what's happening at the molecular level, but understanding the broader implications for physiology and life, blood tests, and more importantly, symptom expression. So, you know, that's kind of…
08:24
what I'm really interested in is trying to get a broader grasp of how we can understand all the problems that are related to thyroid suppression. And I think ultimately get people to understand what they're in control of. I'm a big fan of Ivan Illich's work. He's made a really good argument that, you know,
08:42
technically people can be made into patients at the checkup. They're a person, now they're a patient. And that can come from, you know, very arbitrary numbers about what constitutes good and what constitutes bad. And, you know, there are probably many things that you kind of think, well, that's not right. And, you know, I kind of see those values not meaning what they're supposed to mean in a clinical perspective. And I think it just, again, it just comes down to creating more customers over time and being a customer from cradle to grave, not being…
09:10
kind of, you know, raise your kids in the way that you want and to the juxtaposition, not being able to die in the manner that you choose to die. So, you know, I think there's some implications of industry that I think permeate into people's daily lives. I think what I'm really motivated to do is to really make people understand that they are in charge of it and perhaps with a little hand-holding, they can see the path themselves about what creates more cohesion in biology and
09:39
concept of long range order and structure and self-ordering processes about how people maintain their physiology over a long time and don't need much interventions. They don't need to be put onto statins. They don't need to go on antihypertensives. Don't get me wrong. There are probably cases where people do really need that. However, when you understand the tenets that, you know, cholesterol is a really easy one to pick on.
10:04
Because you just go back to the Jupiter trials and know that they were cut short. The data was withheld from, you know, peer review. No one's really ever had a good chance to look at the proper trial data, but it was cut short for a reason. And there are some very obvious reasons why that was cut short. And so when you understand that cholesterol is an example of
10:23
is not necessarily related to kind of heart disease any more than, you know, anything else could be. I mean, we understand that the cholesterol accumulating in an artery is because there is damage going on in that particular area. There's calcification of the arteries, as an example. And when you bring that back, we know that thyroid hormone has a huge impact on cholesterol values, you know, whether it's receptors, whether it's cholesterol enzymes, liver function,
10:49
accumulation of issues like non-alcoholic fatty liver disease accumulation of fatty acids you know inability to use glucose efficiently and this is where i think unpackaging thyroid and looking at the problems associated with studies and um you know understanding that suppression of thyroid values or just an inaccurate thyroid value because of what's going on at the receptor what's going on metabolically this can be a problem and that's what i i'm really interested in doing
11:18
Yeah. You sort of mentioned, Keith, around the inability to utilize sugar or I guess glucose. Do you want to sort of expand upon that and sort of mention the implications in terms of thyroid function and carbohydrate metabolism? Yeah. So, I mean, if you look at some of the nutrition in the world,
11:36
I would say that current fads within nutrition is that carbohydrates are still being vilified to a degree. I think I saw a post yesterday from David Perlmutter saying, I'm sorry, honey, I was wrong about you. And it's like, I was criticizing someone and saying he was a really good scientist for admitting he's wrong. And I was like, well, you know, he's a doctor. You only need to go back to basic undergraduate studies and understand that carbohydrate is the essential source of the metabolism.
12:04
And we still get many people, I think, jumping on the bandwagon that just because they can't utilize carbohydrates, that carbohydrates the issue. And we know there are many tenets to kind of insulin, pancreatic thyroid signaling from glup transporters or glute transporters to essentially the thyroid itself. And, you know, there are dozens and dozens of studies based around metabolic syndrome that show that when you make someone new thyroid,
12:29
blood values come back to relatively normal expression. Well, why is that? Well, the pancreas, just like every other organ and every tissue in the body, is thyroid-dependent.
12:38
And when you have aspects about thyroid signaling, remember the pancreas produces many things. It produces enzymes, digestive enzymes. It produces insulin, a couple of other things in there as well. But if the energy to the pancreas is substantially decreased, the ability to respond with insulin production over time can be substantially decreased. And there's kind of an energy pathway between high insulin values based upon the glucose values. Because if you can't keep getting glucose into the cell because the thyroid is not working efficiently…
13:08
perhaps the electron transport chain or the aerobic mechanism is impaired, which means that you're not able to use carbohydrates efficiently. So if you take it perhaps to an N-range example in diabetics, we know that fatty acid oxidation in the heart
13:22
It's a primary kind of pathway, but the heart needs to be flexible. It still needs to function using carbohydrates. You know, that glucose fatty acid Randall cycle is still very prevalent for the heart. So we know that the failing heart can't utilize glucose efficiently, and we've seen an abundance of fatty acids being utilized as well. Now, when fatty acid oxidation is also impaired and we lose the ability to oxidize fats, primarily because
13:47
Carbohydrates have a higher respiratory quotient, so they produce more carbon dioxide. Fats don't. Fats also come with the negative byproduct when it's chronic of chronic lipid peroxides, increased superperoxides or superoxides. And when this gets problematic, we tend to be wasteful of enzymes that are protective like superoxide dismutase, glutathione, and nitroglycerides.
14:14
Then we start to see, you know, rampant production of, say, nitric oxide to try and vasodilate because there's issues with kind of
14:21
blood supply we can understand how the heart starts to degrade and then we see all these negative things and one of these negative things is seeing you know fatty acids being oxidized we see high glucose within the blood because it can't be used efficiently and we see high triglycerides as well particularly metabolic syndrome so this is perhaps one of the most basic failings of thyroid physiology now if you go and you're looking at someone who's stressed as an example and
14:47
And there are various tenants because some people are prone to overeating. Some people are prone to undereating. Some people eat just the right amounts of food. But if someone's stressed not eating properly, say they're prone to skipping breakfast. And we all know that, you know, one of the
15:01
first signs of stress is a loss of appetite, right? We don't like to produce hydrochloric acid, which is thyroid related. We don't feel hungry because we're permanently producing adrenaline and cortisol, you know, as well as the kind of lack of appetite, you know, the inability to sustain deep sleep is glucose related.
15:23
not being able to get to sleep, waking up chronically at multiple times, and then not feeling very hungry because you've been kind of dipping in and out of that stress state throughout the night. That, to me, is thyroid failing. And there can be other tenants with, you know, inflammation in various tissues and particularly the gastrointestinal tract. We've got to a point where we're kind of, you know, not feeling hungry, not able to digest our food. And this also comes back to pancreatic signaling as well, is that
15:51
If you can't stimulate the pancreas to produce the enzymes, you're not going to feel as hungry because you can't keep breaking down the food. The GI tract is getting problematic. And this was where everybody's kind of shifts away from glucose metabolism to kind of the microbiome and going, yeah, but the microbiome's out. We really need to replenish that. And it's like once you get the thyroid functioning and you produce enough stomach acid,
16:13
you produce enough pancreatic enzymes, you know, food gets broken down efficiently and goes into, it's sterile, goes into the rest of the digestive tract and into the intestines. And therefore metabolism is kind of, is optimal. You've got optimal breakdown of nutrients and you get optimal assimilation. So the kind of pancreatic signaling comes back to,
16:34
If the thyroid is suppressed, so digestion is suppressed. So is the ability to take up carbohydrates and use it efficiently at the cell. And then we have all the other issues that spill over and perhaps into kind of brain function. And perhaps the end range of this is where we're seeing altered physiology within the brain, diabetes to the brain, Alzheimer's or Parkinson's.
16:57
as an example. So I think understanding that if you can regulate your thyroid, you can regulate
17:04
the pancreas and insulin production efficiently. And there can be other reasons that I've been working with a young lady in Australia, actually, who's a type one diabetic, who she was actually eating pretty good anyway. She was eating regularly, eating some really good foods, including kind of carbohydrate rich foods like orange juice and things like that, which diabetics are told, you know, to stay away from. And we actually got onto some progesterone and the progesterone significantly decreased the amount of insulin that she needed to use. So
17:32
So there are kind of other tenants within, you know, thyroid physiology that permeate to kind of, you know, the gonads, sex hormone production, allowing other structures to work efficiently, which spill over into, you know, less need for the pancreas to be utilized all the time, you know, less stress on the pancreas, but there's less stress on the liver. If you have an optimal, say, aerobic system that's functioning, your ability to use carbohydrates is solid. It's there. And for me,
17:57
That's a prime example of someone who's healthy. And we know that when we lose the ability to use this aerobic mechanism and we kind of fall back on chronic glycolysis, chronic lactate production as an example, this is the pathway for sustained disease, especially cancers.
18:13
And, you know, even if it's not kind of going to cancer via mutation within the mitochondria or the cells and the aerobic function, this is where we start to see disordered systems, pancreatic signaling, tissues within the cardiovascular system, accumulation of various products within the central nervous system and the brain. So
18:33
I think, you know, it sometimes becomes hard to focus on, say, just the pancreatic signaling from the thyroid, because again, that becomes part of a systemic problem. But everyone likes to break it down and go, it's a carbohydrate issue. You need to cut carbohydrates out. You need to go keto. You need to go carnivore. And people can actually, you know, do some, create some useful changes and go, yeah, I feel really good. I've lost some weight. And, you know, for most people, that's the primary reason
19:02
symptom of success for them right that that's the marker for them and they don't really kind of look at the other things so you find a lot of people they come out of a keto carnival diet and they try to bring carbohydrates back in and might be a man that's efficient might be not and then they start going on gaining weight again or you know i'm having all these problems i'm not my sleep is still not improving and that's a thing i see from a lot of people coming from keto and carnival hair loss
19:28
sleep not improving blood sugar's not improving and all you're doing is removing glucose from the system for a lot of people that i've seen is you don't restore glucose metabolism efficiently because you haven't addressed thyroid function and if you haven't addressed thyroid function the pancreatic signaling isn't going to restore you know and all of the other mechanisms associated with some of the aerobic system you know not shifting away from glycolysis don't get me wrong this is kind of
19:56
Some of the end range stuff that you might see, unless you're going and testing lactate and things like that, perhaps it's just a guess. But we know that, you know, within cancer, as an example, that sustained glycolysis, fermentive metabolism is a cause of many problems, primarily because it shuts down thyroid as well. There's some really interesting stuff I've been looking at recently as part of my research is showing that actually cancers, they're actually the tissue is hypothyroid. Just that cancer…
20:24
tumour itself. And there's been some cases of, you know, shutting down T4 and reverse T3, but giving someone T3 still, and it's actually shrinks the tumours quite substantially. So a lot of people might think that, hang on, you just need to get thyroid working, adequate T4, making sure that's converting to T3. Truth.
20:44
That's a very potent mechanism. But sometimes there is very kind of nuances when you see kind of disease like cancer physiology as an example, that there is a very different nuance to the tissues. And this is why I think maintaining thyroid function throughout life is
21:02
is going to be the marker for longevity. And that's when you start getting into, you know, another whole discussion about a lot of people say that you see decreased thyroid hormones in people who are older. And it's like, well…
21:14
Actually, you could actually say that they're at the point now where their thyroid is even more starting to fail. The other people, you've been assessing them and saying they've been dying of cardiovascular disease. But if you don't really know how the thyroid's functioning, you're just assuming that their thyroid values were normal and they were dying in what we call a euthyroid state. So again, as we said, thyroid physiology goes through many tenets.
21:37
of discussion from society through to nutrition, through to longevity, digestion, sleep, fertility, everything. Yeah, really, really fascinating stuff. I think you did a great job at sort of breaking that down. What came up for me there, Keith, was in terms of assessing someone's thyroid hormone production, how much emphasis do you place on blood work versus external symptoms and things like that? I think any information that you can get is useful.
22:06
I've seen people who look totally normal in blood tests. And again, the clinical presentation that you would expect someone to pick up when they're going to see a clinician might be constipated, might be hair fall, might be high cholesterol values. It might be, you know,
22:24
bradycardia might be tachycardia you know there are various nuances to looking at how you might assess someone and again it comes back to understanding nutrition it comes back to understanding environment someone's living in emotional stress that they might be under so i do think the thyroid blood tests are useful i'm not saying that they're all totally useless and don't mean anything they're just
22:46
a tool that can be used to make a decision. But again, it also comes back to what you perceive as normal. And most thyroid associations will say that if it's, you know, about four to five MULs, depending on the measurement you're looking at and what area of geography you're looking at, is that that's completely normal. And I mentioned this to someone the other day in a podcast. It's like, well, if you look at some of the
23:15
suggested diagnosis now within pregnancy and also within depression, there's quite a few papers that have said, I think there are some standpoints that says you shouldn't let the TSH go above 2.5. So if you're kind of suggesting that both depression and pregnancy require lower TSH values with
23:40
what are perceived to be normal free T4 values, then you're talking about sustaining life optimally through the gestational period. Why do you think that doesn't extend to kind of normal function and life, you know, outside of pregnancy? And this is where I think the problem is.
23:57
And also, you know, I'll quote Ray Peet, who said he never saw anyone that was actually healthy with a TSH above two. I think that's pretty spot on, to be honest. And I've always perceived the pituitary response as a stress response. It's a fallback mechanism. Not to say that, you know,
24:15
It's not important, but to the extent that we can maintain optimal peripheral conversion of thyroid hormones, particularly the liver, kidneys, muscle tissues, just an example, if that is efficient, we don't have to keep falling back on these mechanisms. And we know that a lot of the pituitary hormones, when they're produced in excess, growth hormone, prolactin, TSH even as an example, are associated with disease progression. So
24:43
And there are many doctors that have suggested it can take years before TSH gets to the point where it's over kind of hypothyroidism. Right. And you know,
24:53
clinicians wanting to see that TSH value above five, reduce T4 as an example, and really not kind of understanding what goes on with T3 and also reverse T3. So pulling those blood tests out and also comparing total T4 and T3, I think is useful as well, rather than saying, well, you know, the free T3 and T4, they're the most bioavailable. These are what we should be looking at. You know,
25:19
If you don't know what's going on with the thyroid carrier protein, transthyretin, albumin to a degree, obviously thyroid binding globulin, these are going to give us perhaps…
25:30
wayward values that really don't mean anything what's going on at the receptor how much thyroid hormone is being taken up now that's kind of you know the more gene expressing mechanisms rather than the metabolic mechanisms so if you're seeing people with you know reduced body temperature as an example low heart rate and the low heart rate can be
25:53
you know, the sign that the thyroid isn't allowing the heart tissue to get enough T3 and therefore doesn't contract and relax efficiently. Therefore it becomes slower, becomes fibrotic, you know, arteries are prone to calcification and then cholesterol being deposited there. So I think that without going meandering too far off and bring myself back in to the original question, I think the blood tests are useful, but they can't be relied upon. Yeah. Cool. Yeah.
26:21
Yeah, I mean, that makes sense. I mean, I've been personally been, you know, taking my morning temperatures and I do quite a lot of blood testing myself to assess my own thyroid hormones and my TSH sort of sits around maybe 0.8 or 1-ish. T3 is pretty much maxed out as high as possible and then T4 is moderate within range. And, yeah, one thing that did pop up, though, is –
26:48
What are the implications of cortisol and how does cortisol fit into the whole, you hear people talk about you don't want to be relying on cortisol to bring you energy. So do you want to sort of link the cortisol there? Sure. Well, obviously there are some people I think in the functional medicine world, when I remember studying, talked about the concept of the HPAT or HPTA, the hypothyroid pituitary thyroid syndrome.
27:13
adrenal axis, which draws upon the feedback loops that we have. There is a substantial interplay between the two. We know that when people are stressed out, they're prone to producing more adrenaline and cortisol. When people are inflamed, perhaps markers that you can see, something like C-reactive protein as an example, we know that there's often more cortisol because
27:36
Cortisol is an anti-inflammatory hormone. It does a great job of kind of lowering inflammation. And to the extent that, I mean, there are various things to probably unpack with cortisol is that the adrenal glands are thyroid dependent.
27:51
So all glands are thyroid dependent. So if you're in a low thyroid state, your ability to produce cortisol can be diminished, but there might be a compensatory mechanism going on. But also when we're stressed and when we're kind of not eating enough, you produce more of the glucocorticoids like cortisol and they have an inhibitory effect on TSH. So the more kind of stress that we're under, it makes the TSH look relatively normal and indeed even low.
28:18
So that's why a lot of people, unless you understand how much stress someone's under, if you're chronically skipping meals and going through that process of liberating energy via gluconeogenesis and the production of energy by breaking down fats and sometimes proteins as a fuel, then this has a suppressive effect on thyroid hormones, particularly TSH. So it's important to understand that if you're producing a lot of these kind of
28:45
adrenal hormones, it can, again, make the blood tests look completely normal. You can get to a point, I think, where adrenals do need support as well. I used to be quite set in stone that the thyroid was the
29:00
Always the issue. And I think there can be sometimes a need for supporting the adrenals more. Might be something like progesterone or pregnenolone to make sure they're getting more of the base hormone for hormone conversion if needed. So I think that's always useful to pack and make sure, you know, you've got adequate cholesterol values, adequate B6, adequate vitamin A to support
29:20
cortisol but again yes rampant cortisol can have a negative effect on thyroid function and i think there are things to work out you know but again we could come back to things like temperature as an example pulse can also be useful because pulse rate we tend to think of low thyroid function associated with bradycardia as an example but it could can also be tachycardia if someone's thyroid is so suppressed and they're running off you know chronic adrenaline production
29:49
So that's why, you know, it's very easy sometimes to look at someone's heart rate and think, oh, God, they're hypothyroid. And it's like, well, the temperature's low. They look like they're kind of hypo, not that the visual representation is always accurate. But then when you start giving them regular meals, you notice their heart rate drop down below 100%.
30:10
And it's because they're not running off adrenaline all the time. They're not trying to liberate energy from this gluconeogenesis, which is, you know, we, we, you term it kind of perhaps the stress response, but it's like, it's a normal pathway that's there to back us up. But to the extent that it's chronically maintained and you're breaking down factors as a fuel all the time, and perhaps proteins, then this can be kind of detrimental in itself. So, but it's, you know, we,
30:33
we will switch between, like for example, females during the menstrual cycle when, you know, during the follicular phase, go through glycolysis within the uterus and the surrounding structures because estrogen's primary function is often…
30:47
stimulates glycolysis and also what's going on around the rest of the structures there to help it get through the menstrual cycle. And then progesterone comes in, has this anti-estrogen effect and switches back towards oxidative metabolism. So there are various switches that are going on and off all the time. And it's kind of
31:04
It's similar to the cortisol pathway to the extent we're kind of using that all the time and not doing enough to kind of inhibit it. We shouldn't suppress it totally. We need it to a degree, but it's like when it's rampant, it's going to have a negative effect on thyroid function. You know, you can start to see issues related to, you know, pain issues, arthritic issues, you know, the loss of anti-inflammatory hormone production, which can be problematic.
31:30
There's also something else I'd like to discuss, Keith, and that is sort of the implications and the roles of the various B vitamins in conjunction with thyroid hormones. So do you want to sort of explain their complementary roles?
31:45
Sure. It's not something I've looked at for some time, but my understanding is particularly with electron transport chain, aerobic metabolism, I think thiamine deficiency is implicated in a lot of aerobic metabolism dysfunctions, as can be B2 and other vitamins as well. So I think
32:04
What's quite interesting to point out is that particularly with females, probably have a higher need because when there's an abundance of oestrogen and the liver becomes impaired, if they don't get enough B vitamins, their ability to metabolize oestrogen becomes compromised.
32:21
So if you think you get a kind of a double whammy of decreased liver function, decreased aerobic metabolism, and if the estrogen is chronic, glycolysis production can be a part of that. And I think that's one of the implicated pathways
32:34
in oncogenesis and cancer. And we know that estrogen is a significant component of this pathway. And so this is where I think maintaining those B1, B2s in particular is very important for maintaining aerobic metabolism, primarily for liver function, but other tissue function as well. I think it almost kind of adds into the idea that why females are 10 times more likely to suffer from autoimmune issues or
32:59
hyperthyroidism. So we could argue that in some cases that understanding if someone's got enough B vitamins can be a useful support. And I think that's something we want to kind of tick the box for prior to kind of thinking about thyroid therapy. And that's why I'd rather go with just a B complex for most people, because it can be quite useful.
33:21
I'm not really someone who goes down the route of lots of testing. I've done that before. You know, if people have got the money, they can go in and do an organic acids test and look at the profiling there. But I've kind of got to the stage now where the way I like to work is minimal testing, feeling what's going on, looking at the basics like temperature and pulse, sleep quality, digestion, mood, sleep.
33:43
you know all of these aspects don't get me wrong i will use those tests if things i'm doing aren't working they're always a fallback but at the end of the day i think you know just you know we can get a lot of those nutrients from food to support what's going on sometimes with females there's a need to to go with that you know after that if the b vitamins are adequate then it might be that the thyroid is being suppressed whether it's high estrogen we know whether it's uh environmental pollutants whether it's stresses whether it's inheritable traits but yeah i
34:11
yeah, I think that the components of B vitamins are essential to understand that energy production can be inhibited by a lack of B vitamins for sure. Awesome. Awesome. So Keith, I'd love to get your perspective on, might be a little bit controversial, are the omega-3s from seafood? I'd love to hear about your thoughts there. Sure. So this is quite a contentious area and I've kind of
34:38
tried to unpack my level understanding with this. And a lot of people kind of go with the ideas that omega-3 is a heart protective and anti-inflammatory.
34:48
They tend to have an effect where they suppress the pathways of inflammation. One of the primary mechanisms, and still I'm happy to be proved wrong on this, and I kind of read a lot of Ray Peet's work that influenced me on this, I think omega-3 should be kept to a very bare minimum. And again, when we look at the disease states, like in the diabetic heart as an example, or
35:09
or kind of neurological issues like Parkinson's, there's often an abundance of these and an excess of these. So we have to kind of wonder why are these in excess? And I think another component of this is the supposed cardiac risk. And there's a lot of studies and suggestions and narrative that cholesterol, as an example, is lowered by increasing the omega-3s within the diet. And I think this is not perhaps always
35:37
a positive pathway. But if you're looking at the concept of cardiac risk, cardiac risk, I remember when I was a fitness instructor, we had seven things with the American College of Sports Medicine that were defined as cardiac risk. And I think that things are pretty similar now. But if your cholesterol was high,
35:53
that's a level of cardiac risk right now depending on where you sit i mean i see many blood tests coming from clients in the u.s and you've got these big red numbers in cholesterol going and it's like i'm looking at again that cholesterol value is absolutely fine and there are some huge studies there's a really big one that came out of korea showing that you know cholesterol values of 5.5 to 6.4 or 5 are absolutely pretty normal and
36:17
were associated with increased longevity, but anybody who had lower cholesterol values was dying earlier. So there's still kind of many contentious issues with kind of heart disease, longevity, and the idea of cardiac risk. And I think omega-3s,
36:33
One of the primary reasons I think they might be problematic is what they do to the cell membrane. And when there's an abundance of them, they tend to make the cell membrane quite leaky. You see a lot of people going, you need membrane fluidity. And I think membrane fluidity is a bit of a misnomer. And I won't pretend…
36:49
I'm an expert on any level of this, but again, and there's another contentious area within biology about how the cell membrane functions. So people suggest that when you kind of, it's very easy to put phospholipids, unsaturated phospholipids into the cell membrane just by increasing them in the diet. And this is supposed to make them more fluid. But there's quite a few studies that have shown that when you have an abundance of say DHA, the omega-3,
37:16
at the cell membrane, it makes it quite leaky. Now you can actually go and stab holes in cell membranes and they still don't get leaky, but you can give them omega-3s at the membrane and it does make them leaky. And there are various other kind of poisons that have this effect as well. Now omega-3 is being used within cancer therapies as well to make chemotherapy more efficient. So it makes the cell membrane leakier, chemotherapy kind of toxic agents can go into the cancer cell
37:46
and make the cell die, go through apoptosis, this kind of programmed cell death. Now, I think if you're looking at that, you're going, well, if it makes chemotherapy more toxic, what is the accumulation of these products over time? But a lot of people keep focusing on the idea that cardiac risk is going down simply just by having a lower cholesterol value.
38:06
So we don't know what the sustained effects are chronically with that. And I still don't see any studies that show that people who have omega-3s live longer. And, you know, when you're looking at studies that are just looking at kind of food questionnaires, you can't really make any assumptions. And I think this comes down to the organization and coherence of a cell. And I think an abundance of these fatty acids is causing problems. And so, you know, I'm sitting on the fence with this for now, but that's, I'm sitting on the fence when I say,
38:35
I don't think that chugging down on omega-3s is going to increase anybody's lifespan. I think keeping them to a minimum because they're an abundance of foods. If you eat a good amount of seafood like oysters or shrimp, you will get a certain amount of these foods in there. You also get an abundance of other really good thyroid-supportive nutrients like selenium and zinc as an example.
38:57
You've got to kind of unpack some of the assumptions made from food questionnaires simply by just saying, OK, the omega three to six ratio needs to be improved for cardiac health and that will restore longevity. And it's like, well, let's see all the other factors that perhaps lead to making somebody more robust or kind of fragile over time. So my belief system is
39:20
that omega-3s, as an example, shouldn't be taken in abundance. I think even the polyunsaturated fatty acids, you know, some are quite protective. I mean, you know, olive oil, quite protective. And in fact, some of these kind of monounsaturated fatty acids as well seem to be quite protective, particularly with cell function. It's when we get an abundance of fats that I think in the diet that can be problematic. They can
39:46
also kind of bind to, in fact, you know, there's some really interesting studies that show that DHA has a quite a high capacity to bind to transthyretin, which is a thyroid carrier protein, and displaced T4. Now, saturated fatty acids can do this at a higher level, but they're more prone to kind of hijacking by the unsaturated fatty acids. And transthyretin
40:09
is not the most abundant thyroid carrier protein, thyroid binding protein is, but trans-thyretin is the kind of primary carrier within the brain. So if you're getting displacement of, you know,
40:22
trans-thyretin with fatty acids, particularly unsaturated fatty acids, then you're going to get relative or local states of hypothyroidism, as an example, within the brain. And I think this is where there's some really interesting areas to look at with regards to Alzheimer's, because a lot of people seem to think that there are low levels of DHA, and this might be the reason that people get Alzheimer's. But actually, you know,
40:48
We come back to the kind of the cell membrane as an example. The unsaturated phospholipids are the first fatty acids that can be removed from the cell to be used as a fuel.
40:58
So if you've got a diabetes of the brain and it can't use glucose efficiently, then you're going to see the fats being utilized at a faster rate because glucose can't be used. And you'll see an abundance of perhaps glucose in these areas. So I think, you know, there's a correlation between low omega-3s in the central nervous system in Alzheimer's, specifically in dementia, not Parkinson's. In fact, with Parkinson's in certain areas,
41:23
particularly around the substantia nigra, you're seeing an accumulation of fatty acids like you are in the heart, particularly DHA. And this is where there are quite a few studies that when you make someone new thyroid, the Parkinson's and Alzheimer's symptoms seem to drastically decrease. So again, I think the capacity of
41:44
omega-3s to distort thyroid function and how to look at that appropriately within a broad range of kind of studies and tests is what we should be looking at rather than just you know going down the cardiac risk i know i wasn't really succinct about that but i think there's there's quite a lot to talk about with it oh that's that's cool i'd like to yeah share my experience with omega-3 supplement
42:07
When I was younger, you know, like at the end of sort of high school, I was using quite a lot of omega-3 supplements. Then one day I sort of decided, well, what would happen if I just stopped taking them? And then I remember like an alleviation of this like heaviness and dullness and brain fog. I'm like, you know, this is weird because like, you know, after years of using omega-3s, I thought they were helping with
42:29
cognition and things like that but i no longer use any omega-3 supplements i might use you know have some seafood two to three times a week yeah primarily my main protein source is you know red meat so yeah the studies on cognition is like there are several studies that
42:47
I think mothers being exposed to higher levels of unsaturated fatty acids and fish oils in particular, and also in baby formula. And actually they've fared worse in cognition and developmental tests. Now, there are plenty of studies that show that perhaps there might be useful, but there are certainly no clear-cut studies that say, yes, this has a very good effect. And we know that actually the brain…
43:16
in utero and when it's first born has very low levels of unsaturated fatty acids. And I think that's the reason behind that. So it's like, if there are studies showing that the development's getting worse, I think these are the studies that we need to look at and kind of pay attention to. Yeah. What I'd love to touch on, Keith, is how do you go about sort of calculating or estimating how many grams of carbohydrates one needs to support thyroid function? Like, how do you sort of go about that?
43:46
Yeah. I mean, it depends how you want to be specific. When I coach clients, I'm not saying here you need 200 grams of carbohydrate a day. I'm not really into that. I'm not into body composition. That's not really what I'm interested in. I'm interested around getting rid of people's energy, digestion, improving sleep issues, making them more fertile. So I encourage the clients to play around with that themselves. So it might be someone needs
44:11
50% carbohydrates might be 60 or 70 within the diet. And I kind of just get them to play around with that. You know, there's certainly a minimum value. I don't think people do very well under 100 grams of carbohydrate a day. And you specifically see people coming in thinking just throwing loads of carbohydrates after they've kind of been restricting them for a long period of time is going to do wonderful things. It's like your body's probably not going to be quite used to that. So I kind of look at trying to avoid kind of weight gain with clients.
44:40
You know, I kind of do go through the process of getting people to eat five or six smaller meals a day to start with and playing around with that. And then I might get them going back to three square meals a day because that's what they're good with, getting a bit of hunger in between. But some people, you know, I'm just playing around with kind of sensations of hunger and just…
44:58
managing to maintain sleep through the night, avoiding weight gain if kind of they've had a hard time utilizing carbs before. But yeah, you know, getting people up somewhere between 100 and 200 grams of carbohydrate, depending on their need. Some people need even a bit more if they're super athletic. So
45:17
I don't have too much specifics and nuance with that as a value. And certainly if you're kind of more interested in kind of body comp, then there are people more skilled at that who can do that.
45:27
And what about in terms of the source of the carbohydrates? There's something we haven't discussed, and that is fructose. Yeah, I don't think fructose is bad. I think like anything, you can consume too much of it. I think also coming back to the idea of the pancreatic insulin signaling, a lot of people blame fructose. But for an example, you can activate something called the polyol pathway,
45:54
And that's kind of implicated in diabetes progression because the end product of that is fructose accumulation via, you get a blockage, I think it's succinate dehydrogenase, and this starts accumulating kind of more fructose. And I think that that's just when there's an abundance of glucose, this tends to take place. And everyone blames it, go, oh, it's the fructose accumulating. But if the liver, if the pancreas isn't functioning again because of the thyroid,
46:20
not working efficiently. And if the liver is accumulating kind of glucose into triglycerides, as an example, and other fatty acids, the liver's not functioning, the liver's sluggish, the liver's not converting enough T4 to T3, then this can end up blaming the amount of
46:37
carbohydrates and particularly fructose, but it might be this polyol pathway that's driving that response. So I think it's important not to keep blaming fructose. I think it's good to kind of, you know, have a different source, you know, glucose rich foods, you know, fructose, which I don't think is demanding on the liver as people make out, but it's just this, this kind of activation of the polyol pathway. Magnesium deficiency can be implicated in that.
47:00
But I think it's just kind of the accumulation of the glucose when thyroid signaling isn't optimal, when the electron or the aerobic metabolism isn't working efficiently. You know, it might be some cofactors that aren't in there, might be some thyroid cofactors, might be going back to B vitamins and energy production again. This might be just one of the reasons why we're seeing these kind of high values.
47:20
or it might just come back to some of the signaling mechanisms between the glute transporters. But I still think that can be substantially related to thyroid function. Awesome. Awesome. Hey, I'd love to dive into, I guess, some situations and unusual cases where you've corrected thyroid
47:40
thyroid hormone production or you've added in thyroid and some unrelated or unknown health issue just goes away. I'd love to hear about some stories there. Gosh, there are so many. But it's important to say I'm not a doctor. I can't diagnose. I never give people thyroid hormone. I furnish them enough information for them to make decisions. So they educate themselves. I don't think, don't get me wrong, if you're
48:07
very fragile and immediate risk of a heart attack. It's not even something you should be thinking about, but taking thyroid is very safe for most people. And they, they're quite capable of making their decisions once they've read enough research around it. So I encourage people to do the reading, to make decisions themselves. If there are permanently low temperatures, things aren't improving sleep, you know, blood glucose values, cholesterol, it's something that you should be considering. But, you know, I've seen kind of clients, you know, sometimes it
48:33
It's the weight issue. Sometimes it's totally unrelated to weight. I've certainly seen clients, you know, sleep through the night when they have adequate thyroid hormone.
48:42
You know, sometimes you can argue the idea is that you don't need thyroid hormone because there are a certain amount of people like 65, 70% of clients I work with, their thyroid is suppressed because they're not getting enough carbs in or they're not eating enough food. Therefore, the thyroid doesn't get a chance to function properly. But then there are a certain number of clients that do need that response. And I've seen anything from cholesterol values improve. I've seen clients get pregnant. I've seen constipation resolve.
49:12
It's pretty the full gamut of thyroid symptoms. People get warmer, brain fog lift. I've seen clients who are damaged by a vaccine historically improve their thyroid function. The brain fog's lifted substantially.
49:27
There are just many things that I think that thyroid can resolve. And it doesn't necessarily always need to be thyroid hormone. There are thyroid supporting things. We talk about the cofactors like selenium and zinc. Bear in mind the thyroid receptors are zinc fingers.
49:42
and that may have an impact but you know there are aspects from supplements or compounds like taurine which can be pro-thyroid which i think is really really good i think seeing my sleep kind of improves reasonably well by starting touring which i think has been quite nice certainly a deeper sleep and i also think methylene blue which kind of tends to increase thyroid hormones as well i've seen some do some wonderful things so as much as i'm kind of pro-thyroid i
50:07
I think there are a number of things that people can consider. And going back to the B vitamins again, it might seem like it's a thyroid deficiency, but it might be a simple B vitamin deficiency that's driving that. But I think the more that we're seeing kind of rampant pollution and stress and malnutrition, abundance of pollution in foods, kind of highly oxidized foods that tend to cause problems with the aerobic metabolism. And, you know, we go back to that.
50:31
point with cancer tumours that are very low in thyroid and the aerobic system doesn't work very well. You know, there are clear cases there where adequate T3 has done some wonderful things, not in my work, but in these kind of advanced kind of cancer cases where I think that's very potent and very impressive. So I think that there can be
50:51
Like I said, I can't think specifically right now, putting me on the spot, but I was in clients' digestion, mood, fertility, sleep, cholesterol values, blood glucose values, HbA1c values improve, menstrual cycle. It can be something that restores as well. Usually there's some interplay between higher estrogen levels, lower progesterone levels, nutrition.
51:13
that could play a big part in that as well. So it doesn't necessarily mean that they need thyroid, but again, I have seen some substantial changes with it for sure. Yeah. I think the clear cut takeaway there is the amazing adaptogenic potential of thyroid in the body. You just sort of mentioned some of those things that's corrected. Yeah.
51:33
And, I mean, I've seen that happen, you know, with other people as well. Like you see them correcting a lot of things. There was one stealth marker we didn't really get a chance to discuss, but I'd like to quickly touch on it is reverse T3. It's one of those markers that rarely gets assessed. Yeah. Let's talk about maybe why it's neglected and what's its function in the body.
51:58
Well, if you go to, again, if you go to, I've got some big classic endocrine textbooks there that don't even mention it. It's like they don't even mention premenstrual syndrome in there. Like it doesn't exist in your kind of classic endocrine textbooks. And reverse T3 sometimes get a very small mention or it's just totally ignored. Some clinicians, a lot of clinicians tend to think it's totally pointless. It's not metabolically active. It's primary kind of consideration is,
52:26
And again, used by integrative practitioners is the role that it might be acting as a metabolic break. T4 should convert to T3.
52:34
when the outer ring is deiodinated. So T4 is kind of an iodine molecule is removed to give us this kind of nice kind of, you know, very functional metabolic kind of health restoring action of T3. Now, if there's an excess of T4, it might be deiodinated to the inner ring, which is reverse T3. So you can unpack this in a couple of different values. If you think there's rampant inflammation going on,
53:01
then you might come to the conclusion that T4 is being converted to reverse T3 because T3 can't be used efficiently. Why might that be happening? Could it be an issue with the thyroid receptor? We get certain pollutants that act as something called a ligand binding where it kind of fits into the thyroid receptor. That might be an issue. And therefore, we might assume that if there are higher values of reverse T3, it might be because T3 is not being used.
53:28
There's another point to that, and I'll just kind of quickly suggest that, is that if you have a high reverse T3 and you compare that with a ratio of, say, free T3 or total T3, you can get an idea of where, if that needs to be a certain value. So, for example, some people suggest that a free T3 to reverse T3 ratio should be higher than 20.
53:52
Now, depending on what values you're looking at, you need to kind of add a couple of zeros on them, divide it by the reverse T3. Then there's the component that some people look at doing a total T3 test and dividing that by the reverse T3 to come up with a ratio. And some suggest that should be between 10 and 15 with an upper reference range of free T3 above 20%.
54:15
So I kind of like that one because that's quite useful because you're comparing the total T4 with the reverse T3 and kind of making the distinction that free T3 should be upper range. And I think that upper range of free T3 is where we should always be at because it's constantly being turned over and it should be being turned over. Now, bringing it back to the disease state again, a tumor often has high levels of T4, high levels of reverse T3, high levels of deodinase 3,
54:44
which also ends up degrading T3 down further and also sends it down its kind of degradation pathway at the liver. So you get kind of upregulation of the, you know, sulfation and glucuronidation of T3. The problem is, again, it suggested that T4 and reverse T3, when they're elevated, could be implicated in tumor formation.
55:08
Now T4 and reverse T3 have a specific non-genomic effect that are associated with fibrosis. So I think, again, it's kind of not sitting on the fence, but understanding that yes, reverse T3 could be higher when there's rampant inflammation going on, which may suggest that T3 is not being utilized or assimilated, taken up at the appropriate sites.
55:32
but in cancer cells as an example is that reverse t3 can be very elevated because the tumor itself has a specific microenvironment that doesn't allow t3 to be used it maintains glycolysis and this fermentive or the walberg effect maintains wasteful use of glucose and some of the studies what they can suggest is that as i said if you kind of
55:56
make someone hypothyroxinemic, i.e. restrict their ability to use T4, so give them a thyroid kind of a slowing medication, that stops them producing T4, which then stops them producing reverse T3. And that seems to have a very protective effect on tumours and shrinks tumours quite substantially. However, what they found is that you need to give someone T3 to have this effect. So it's restoring…
56:23
the tumor status to euthyroid, which stops glycolysis, which stops this kind of increased lactate production, switches to kind of aerobic metabolism and allows cells around it to go through this kind of usual program cell death. And, you know, with cancer cells, they kind of, you know,
56:41
the concept of increased telomeres and what they call replicative immortality. Cancer cells want to keep going on and on forever, and they don't care what's going on around them. They just keep breaking tissues and fuel sources around them. And that's in a relative state of hypothyroidism. So just without rambling too much, just to understand that
57:01
There are cases when perhaps reverse T3 combined with other thyroid hormones can be useful to get an idea of if there's a problem metabolically, but also a high reverse T3 without looking at the T3 and perhaps TSH levels will always generally look normal within this. But the T3 within that specific area might be kind of very, very low. So it's important to understand that there are various nuances to looking at reverse T3.
57:28
Amazing, amazing. My final question for you, Keith, is are there any areas of research that you're really, I know you sort of said the pollution, the implications there on thyroid health, but any areas of research you're really excited to see more of? I think there's so much thyroid research still not done yet.
57:48
My idea with my study is to look at how, you know, different hormones might elicit different responses. And it may be that we get to look at some of these markers. There are some studies on this role of T4 with reverse T3 and something called the integrin AVB3 receptor, which is like this non-genomic pathway. So it's metabolic. And T4, when it's high, can be implicated in fibrosis and tumor formation and also in
58:16
you know, angiogenesis and metastasis. So I think the concept of understanding the metabolic effects of
58:26
Perhaps when people are prescribed the standard thyroid hormone, levothyroxine, there are implications with that and shifting away to more appropriate mechanisms like T3 or T4, T3 combos. And that's the kind of research I'm kind of trying to diagnose, which is going to take place over the next six years. So that's something I'm really personally interested in. I do think that there's a kind of…
58:51
not a purposeful suppression of thyroid physiology, but when you think it ties into statin medication production, glucophage, metformin profit and industry, I think you can perhaps see why there's not as many studies on this as there should be. So that's what I'm interested in personally. I think anything I'm really interested in, because I don't understand it enough, is the concept of
59:16
membrane of the cell. And, you know, if you come across Gerald Pollack's work and Gilbert Ling's and how the idea that the cell membrane, that the lipid bilayer isn't as important as we think it is. And there are more complex proteins and ordered water structures that perhaps are more responsible for ions being absorbed into the cell rather than these complex pump pathways. And, you know, the questions of whether you have up to 400 pumps
59:42
in a perceived cell membrane. It's like, where do all these pumps go and where's the land space for them? So I think if that turns out to be kind of getting more research by certainly cleverer people than myself and looking at the idea of kind of Gilbert Lings and Trochan and Vladimir Metviv works and Gerald Pollack's work and the idea of structured water and interfaces between the cell and other structures, I think that's something that could be groundbreaking.
01:00:10
That's something I'd really like to see more of. Amazing. All right. Well, Keith, I want to let my listeners know, like if they want to connect with you and learn more about some of the things you spoke about today, you know, where can they find you? Sure. My website is balancedbodymind.com. It's kind of also reflecting my kind of therapy stuff, which I stopped doing last year. So I don't tend to do that much anymore. Instagram, Tomo Littlewood. People need to email Keith at balancedbodymind.com. So I appreciate the shout out. Thank you.
01:00:40
Awesome. So I'll make sure to leave those linked in the show notes for those listening in. But Keith, thank you so much for coming on the show. Pleasure. Thank you everyone for joining in to today's episode. For in-depth show notes and lessons learned, visit nofilter.media forward slash boost your biology. This has been a No Filter Media production. Say what you want.
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**Keith Littlewood:从失败到探索人类健康奥秘的旅程**
我的对优化人类健康的热情,源于一次“失败”——学校的学习经历。生物学是我唯一擅长的科目,但这并没有为我指明明确的职业道路。我曾计划加入空军,但最终选择了陆军,从事直升机相关工作。四年军旅生涯后,我感到迷茫,不知所措。23、24岁时,一次偶然的机会,我成为了一名健身教练,从此踏入了健身行业。
从健身教练到私人教练,再到康复训练、疼痛管理,最终深入功能医学和营养学领域,我的职业生涯经历了多次转变。**Ray Peete的研究对我影响深远。**他基于自身工作和思考,以及其他一些被忽视的科学家的研究成果,提出了许多深刻的见解。我发现,当今的商业和工业界往往更青睐还原论的方法,而忽略了一些更早期的、同样有效的研究。
多年来,我潜心阅读,不断实践,对内分泌学的理解也日益加深。目前,我正攻读博士学位,研究方向是污染对激素(特别是甲状腺激素)的影响。深入了解甲状腺功能及其紊乱,对于理解人体生理的各个方面至关重要,我认为这是一项值得我为之奋斗终生的事业。
我的工作是帮助世界各地的人们改善健康状况。我主要通过指导,帮助他们解决与激素相关的各种问题,例如能量、消化、睡眠、情绪等。我的工作重点在于营养、环境和生活方式的调整。
我清醒地认识到,企业干预、数据压制和伪造等现象确实存在,这些都严重影响着人们的健康。**甲状腺血液检测本身可能毫无意义,除非你充分了解个体所处的环境和压力水平。**评估甲状腺相关临床试验的有效性,也必须考虑试验参与者的暴露情况。
我并不认为自己是专家,因为在攻读博士学位期间,我越发意识到自己知识的匮乏。我对超分子生物学很感兴趣,它关注的是生物体的整体功能,而非仅仅停留在分子水平。我认为,既要关注分子水平的变化,也要理解这些变化对生理、血液检测和症状表达的更广泛影响。我的研究目标是更全面地了解与甲状腺抑制相关的问题,并帮助人们掌握自身健康的主动权。
在体检过程中,技术手段可能会将人轻易地定义为“病人”,仅仅因为一些任意的数值被定义为“好”或“坏”。我希望人们能够意识到,他们完全有能力掌控自己的健康,并在我的指导下找到改善生理机能的途径。我的目标是帮助人们长期保持生理机能的稳定和有序,而无需过多的医疗干预。
胆固醇本身并不一定与心脏病直接相关,它只是众多影响因素之一。动脉中胆固醇的积累,往往是由于该区域存在损伤。甲状腺激素对胆固醇值有显著影响。我的研究重点在于,甲状腺功能抑制或不准确的甲状腺值如何影响代谢,以及这如何成为健康问题的根源。
关于甲状腺激素、碳水化合物代谢以及相关营养素的补充,我有一些独特的见解:
- 碳水化合物并非洪水猛兽: 当前营养学界对碳水化合物的评价存在偏差。碳水化合物是人体代谢的主要能量来源。不能有效利用碳水化合物,并不意味着碳水化合物本身就是问题。胰腺、甲状腺以及葡萄糖转运蛋白之间存在复杂的相互作用。甲状腺功能障碍会影响胰腺的胰岛素分泌,进而影响葡萄糖的利用效率。
- 甲状腺功能与血糖代谢: 甲状腺功能障碍会影响胰腺功能,导致胰岛素分泌不足,从而影响葡萄糖的利用。这与代谢综合征密切相关。当甲状腺功能恢复正常后,血糖值通常也会恢复正常。
- 压力与甲状腺功能: 压力会导致食欲下降,影响消化,进而影响营养吸收,最终抑制甲状腺功能。
- B族维生素的重要性: B族维生素,特别是维生素B1和B2,对于维持细胞的能量代谢至关重要,特别是对于肝脏功能。女性由于雌激素代谢的特殊性,对B族维生素的需求更高。
- Omega-3脂肪酸的争议: Omega-3脂肪酸的益处和风险都值得商榷。过量摄入Omega-3脂肪酸可能会导致细胞膜通透性增加,这可能与一些疾病的发生发展有关。
- 反向T3(rT3): 反向T3是一个容易被忽视的指标,它可能反映了T3的利用效率。高水平的反向T3可能提示T3的利用存在问题,这与炎症、肿瘤等疾病有关。
- 甲状腺激素的适应性: 甲状腺激素具有强大的适应性,它可以影响人体多个系统,改善睡眠、消化、情绪、生育能力等。
我的研究方向之一是探索污染物对甲状腺激素的影响。我还对细胞膜的结构和功能,以及有序水结构在离子吸收中的作用非常感兴趣。
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