Seyfried Rejects Genetic Model to Frame Cancer as Metabolic Defect

塞弗里德驳斥基因模型，将癌症定性为代谢缺陷 主流肿瘤学将癌症视为基因突变而非由葡萄糖和谷氨酰胺发酵驱动的线粒体代谢紊乱，从而误判了癌症本质。 托马斯·塞弗里德（Thomas Seyfried）教授指出，主流肿瘤学聚焦于基因突变存在根本性缺陷，并认为癌症是由受损的线粒体氧化磷酸化以及依赖葡萄糖和谷氨酰胺的代偿性发酵驱动的。他解释了环境毒素、慢性压力和不良饮食如何损害线粒体健康，同时提出了结合血糖酮体指数（GKI）、热量限制、禁食、高压氧疗法以及“压迫-脉冲”（press-pulse）方案来饿死癌细胞并提高疗效的治疗策略。此外，塞弗里德还阐释了肿瘤转移的机制，批评了现代肿瘤学的体制教条，并强调应通过易于获取的代谢监测工具赋予患者自主掌控权。 托马斯·塞弗里德（Thomas Seyfried）教授指出，全美每天约有 1,700 人死于癌症，而主流医学界忽视了癌症本质上是线粒体代谢疾病而非遗传基因缺陷。 (0:00) 癌细胞的核心能量来源是葡萄糖和谷氨酰胺，当线粒体有氧呼吸受损时，细胞会退回到古老的发酵途径以维持不受控的增殖。 (25:19) 癌症相关基因突变并不具备 100% 的外显率，遗传异常与环境毒素本质上是通过干扰线粒体的氧化磷酸化效率，诱发补偿性发酵。 (33:25) 塞弗里德团队开发了葡萄糖酮指数（GKI）来追踪从消耗碳水到燃烧脂肪的代谢转变，并指出慢性压力和睡眠不足会推高血糖并损伤线粒体。 (37:42)

Professor Thomas Seyfried argues that cancer is fundamentally a mitochondrial metabolic disease driven by impaired respiration and compensatory fermentation, rather than a genetic disorder caused by DNA mutations. Contending that mainstream oncology misdiagnoses the disease's origin, Seyfried advocates for metabolic therapies targeting cancer's dual fuels—glucose and glutamine—to manage tumors without systemic toxicity. Mitochondrial Dysfunction and the Oncogenic Paradox (15:00) Rooting his hypothesis in Otto Warburg’s research, Seyfried contends that cancer originates from chronic damage to mitochondrial structure and respiration rather than genetic mutations. When oxidative phosphorylation fails, cells revert to ancient, pre-oxygen fermentation pathways to survive. According to Seyfried, this bioenergetic shift resolves Albert Szent-Györgyi's "oncogenic paradox," explaining why diverse environmental insults—including radiation, chronic inflammation, intermittent hypoxia, microplastics, and synthetic chemicals like PFAS—all trigger malignancy by degrading delicate inner mitochondrial membranes and cristae. Seyfried challenges the prevailing Somatic Mutation Theory (SMT), noting that cancer-associated mutations like BRCA1 or TP53 are not 100% penetrant, and known driver mutations frequently exist in healthy tissue. In his view, DNA mutations and genomic instability are downstream consequences of elevated reactive oxygen species (ROS) leaking from damaged mitochondria, rather than the primary cause of oncogenesis. Starving Cancer: Glucose, Glutamine, and Metastasis (25:19) Because fermentation yields only 2 to 4 ATP per fuel unit—compared to 34 to 36 ATP from respiration—Seyfried explains that cancer cells require massive nutrient influx, relying strictly on two fuels: glucose and the amino acid glutamine. Glucose drives glycolytic fermentation, while glutamine fuels mitochondrial substrate-level phosphorylation (mSLP). Crucially, Seyfried asserts that cancer cells cannot burn fatty acids or ketones due to structural mitochondrial defects; intracellular lipid droplets represent protective storage rather than fuel consumption. Consequently, Seyfried argues that dietary carbohydrate restriction alone is insufficient; therapy must simultaneously block glutamine. He points to repurposed drugs, like the antiparasitic mebendazole, as dual-pathway inhibitors. Regarding metastasis, which causes most cancer deaths, Seyfried rejects standard cancer stem cell models. He posits instead that metastatic cells are macrophage-tumor hybrids that retain the immune cell's ability to migrate through circulation while remaining metabolically dependent on glucose and glutamine. The Glucose Ketone Index and Therapeutic Synergy (49:23) To quantify mitochondrial health and therapeutic efficacy, Seyfried developed the Glucose Ketone Index (GKI), which divides blood glucose (mg/dL converted to mmol/L by dividing by 18) by blood ketone levels (mmol/L). While modern diets and sedentary lifestyles keep most individuals in the high-risk "Red Zone" (GKI > 9.0), Seyfried targets the "Zone of Prevention" (3.0 to 9.0) and deeper therapeutic zones (GKI ≤ 3.0, and ≤ 1.0) to manage disease. Under therapeutic ketosis, Seyfried states healthy cells enter a protective "bunker mode," while tumor cells become vulnerable, lose their immunosuppressive lactic acid shields, and cannot repair oxidative DNA damage. He argues this allows clinicians to administer significantly lower, less toxic doses of conventional chemotherapy (such as cisplatin) or hyperbaric oxygen therapy (HBOT). He cites cases like Pablo Kelly, who survived 10 years with an inoperable glioblastoma managed primarily through metabolic therapy. Institutional Resistance and Misconceptions on Cachexia (66:10) Seyfried criticizes the oncology establishment, pointing out that approximately 1,700 Americans die from cancer daily (~70 per hour) despite massive funding for mutation-targeted treatments. He attributes institutional resistance to legal "standard of care" constraints, medical curricula omitting bioenergetics, and financial disincentives surrounding non-patentable lifestyle and dietary protocols. Seyfried also disputes the clinical argument that ketogenic diets trigger cancer cachexia. He contends that true cachexia is a pathological wasting syndrome driven by the tumor scavenging host muscle tissue for glutamine—a process intensified by high-dose toxic chemotherapy—whereas therapeutic ketosis selectively reduces fat while preserving lean muscle. Furthermore, he condemns hospital practices that feed cancer patients high-sugar nutrition shakes, arguing they inadvertently supply the precise fuels required for tumor proliferation. Seyfried acknowledges that strict metabolic management requires substantial discipline and medical guidance, likening the medical field's reluctance to the historical resistance against the Copernican heliocentric model. Because mainstream institutions largely ignore metabolic oncology, his ongoing research through organizations like the MORE Alliance relies on private philanthropy rather than pharmaceutical or government grants.

波士顿学院的托马斯·塞弗里德（Thomas Seyfried）教授主张，癌症在本质上并非源于基因突变，而是一种由线粒体呼吸功能损伤引起的代谢性疾病；通过限制肿瘤赖以生存的葡萄糖与谷氨酰胺，并利用生酮状态保护正常细胞，能够从生物能学机制上有效遏制肿瘤生长。 呼吸损伤与致癌悖论的代谢解答 (15:00) 塞弗里德追溯诺贝尔奖得主奥托·瓦尔堡（Otto Warburg）的研究指出，健康细胞利用功能完备的线粒体通过氧化磷酸化（OxPhos）高效率产生34至36个ATP分子，而在电子显微镜下，癌细胞的线粒体常表现出内膜嵴缺失或解体的“幽灵线粒体”状态。当呼吸功能因累积损伤降至临界阈值以下时，细胞便会退化回史前单细胞生物的古老生存机制——在胞质与线粒体基质内进行代偿性发酵。这种发酵每单位营养仅生成2至4个ATP并伴随乳酸分泌，同时丧失了正常呼吸对无序增殖的抑制调控，驱使细胞陷入失控分裂。 这一机制解释了阿尔伯特·圣捷尔吉（Albert Szent-Györgyi）提出的“致癌悖论”：辐射、化学毒物（如PFAS、微塑料、草甘膦）、慢性炎症、病毒感染及睡眠呼吸暂停引起的间歇性缺氧等截然不同的致癌因素，其共同终点都是对线粒体结构和功能的慢性破坏。塞弗里德据此批判了占据主导地位的体细胞突变理论（SMT），强调BRCA1或TP53等致癌突变均非100%外显；基因突变实质上是线粒体呼吸衰竭后活性氧（ROS）过量产生导致的下游继发结果，而非癌症的始发驱动因素。 葡萄糖与谷氨酰胺的双重燃料阻断 (25:19) 癌细胞依赖低效的发酵途径维持生存，因而必须通过细胞核逆行信号转导上调转运体，极度渴求两类特定底物：葡萄糖与谷氨酰胺。葡萄糖主要支持胞质糖酵解，而血液中最丰富的氨基酸——谷氨酰胺，则在线粒体基质底物水平磷酸化（mSLP）过程中提供发酵动力。塞弗里德澄清，正常人体细胞能高效利用脂肪酸降解生成的酮体，但癌细胞因线粒体受损而完全缺乏燃烧酮体的生化能力；显微镜下癌细胞蓄积的脂滴并非其消耗脂肪的证据，而是一种无法代谢脂质时的保护性隔离。 因此，单一的生酮饮食往往不足以彻底消灭肿瘤，治疗方案必须同时切断谷氨酰胺供应通道。塞弗里德提倡联合使用具有双重代谢抑制特性的再利用药物（如抗寄生虫药甲苯咪唑 mebendazole）协同阻断糖酵解与谷氨酰胺分解。在其实验证据与临床转化案例中，英国胶质母细胞瘤患者巴勃罗·凯利（Pablo Kelly）在拒绝常规放化疗的情况下，通过严格代谢疗法维持高酮低糖，使原发不可手术的恶性肿瘤边界清晰并缩小，历经四次减积手术生存达10年，且最终并非死于脑肿瘤复发。 葡萄糖酮指数与代谢干预评估 (49:23) 为建立客观量化线粒体健康与抗癌代谢深度的工具，塞弗里德团队开发了葡萄糖酮指数（Glucose Ketone Index, GKI）。该指标将以mg/dL为单位的血糖数值除以18换算为mmol/L，再除以血酮读数（mmol/L）得出标准化比值。在该图谱中，GKI大于9.0属于代谢综合征高发的“红区”；3.0至9.0为维持线粒体弹性的“预防区”；1.0至3.0为能够抑制肿瘤血管生成与炎症的“治疗区”；低于1.0则达到“深度治疗性生酮状态”。 塞弗里德同时驳斥了常规医学对生酮可能引发酸中毒的担忧，指出酮症酸中毒是1型糖尿病患者血酮达到15至20 mmol/L且伴随极高血糖的病理急症，而0.5至3.0 mmol/L的营养性生酮则是人类应对远古食物匮乏的天然生理基线。在断食干预方面，针对禁食第3天易出现的烦躁不安和睡眠剥夺等“生理撞墙期”，塞弗里德建议在纯水断食前推行为期约一周的极低碳饮食作为过渡阶梯，以平稳度过脑部对葡萄糖类似戒断反应的不适期。 常规肿瘤治疗范式危机与协同策略 (66:10) 塞弗里德对肿瘤学现状表达了严厉抨击，援引美国每天约1700人（每小时约70人）死于癌症、2026年预计年死亡逾62万人的严峻现状，直指以基因突变为靶向的研发模式耗费巨资却收效有限。他指出，医院营养科为防止恶病质（Cachexia）而向化疗患者供应富含高果糖浆和精制糖的高热量流食的做法是灾难性的，这直接加速了肿瘤的葡萄糖摄取；真实的恶病质其实是晚期肿瘤为获取谷氨酰胺而驱动宿主肌肉剧烈分解的病理产物。在转移机制上，塞弗里德提出肿瘤扩散并非纯干细胞行为，而是巨噬细胞与肿瘤干细胞融合形成的杂交细胞在宿主创伤修复信号引导下穿透组织，此类高转移性细胞同样深陷对葡萄糖和谷氨酰胺的发酵依赖。 塞弗里德主张将代谢疗法与常规疗法有机结合作为协同手段：生酮状态诱导健康细胞进入低代谢增殖的防御“掩体模式”，使临床医生能够大幅降低顺铂、卡铂等化疗药剂量或辅以高压氧治疗（HBOT），在增强肿瘤杀伤的同时显著减轻脱发、组织出血和系统毒性；同时，代谢阻断消除了肿瘤周围由乳酸和琥珀酸构成的免疫抑制屏障，使CAR-T或PD-1/PD-L1免疫疗法更易穿透。他将现代肿瘤学对代谢理论的抵触比作哥白尼和伽利略时代地心说体制的惯性，并表示其创立的MORE联盟正致力于推动以患者为中心的代谢肿瘤学临床教育。 塞弗里德坚称癌症本质上是具有普适代谢通路的单一边界疾病，但他亦提醒，癌症患者普遍存在复杂的系统性基础代谢损伤，实施生酮与热量限制方案必须在专业医生监护下配合非侵入性影像动态跟进。该疗法目前主要依靠私人慈善基金支持，若要在临床实践中全面铺开，仍面临主流肿瘤学体制、医学院传统教学框架及缺乏药企专利赞助等多重现实阻力。

## Background 本期视频由 YouTube 频道《The Diary Of A CEO》于 2026 年 7 月 16 日发布。节目简介指出，全美每天约有 1,700 人死于癌症，波士顿学院生物学教授托马斯·塞弗里德（Thomas Seyfried）认为主流肿瘤学界百年来误判了癌症本质，并深入剖析癌症作为线粒体代谢疾病的机理、肿瘤赖以生存的双重燃料，以及如何通过生酮饮食与血糖酮体指数（GKI）等代谢干预策略协助控制肿瘤。 ## TL;DR 塞弗里德教授指出癌症并非基因突变疾病，而是由环境毒素、久坐、高加工碳水及慢性压力导致线粒体长期受损、迫使细胞退回到原始无氧发酵（瓦氏效应）的代谢性疾病。恶性肿瘤细胞主要依赖葡萄糖与谷氨酰胺这两种燃料苟活，且由于线粒体结构缺陷无法利用脂肪酸与酮体。通过生酮饮食、断食以及辅助药物切断燃料供应，可将患者机体置于低 GKI 状态，这不仅能保护健康细胞、削弱肿瘤屏障，还能大幅降低传统化疗与放疗的毒性剂量并提升疗效。此外，团队提出的“压榨-脉冲”（Press-Pulse）治疗策略结合高压氧等手段，在胶质母细胞瘤和晚期转移癌患者中实现了长期高质量带瘤生存。 ## Atmosphere & style 对谈在深沉、严肃而又极富紧迫感的氛围中展开，塞弗里德教授既有资深科研学者的严谨较真，又带着面对当下每天数千人丧命却受阻于医疗体制既得利益时的义愤填膺。主持人巴特利特循循善诱，不断充当普通大众的提问者，要求将复杂的生化机理转化为通俗易懂的常识，现场甚至拿出仪器刺破手指实测 GKI，极具临场感与代入感。整场对话不仅是一次硬核的癌症生物学认知颠覆，更充满了对绝望病患的人文关怀与赋权希望，给人一种兼具震撼、警醒与求真力量的观听体验。 ## Bulletin - [02:42](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=162s) 波士顿学院的托马斯·塞弗里德教授指出，主流医学将癌症误诊为基因疾病长达百年，癌症本质上是线粒体呼吸功能慢性受损引发的代谢疾病，细胞被迫重启远古厌氧发酵机制苟活增殖。 - [01:08:07](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4087s) 根据美国癌症协会最新数据，全美每天约有 1,700 人死于癌症（每小时 70 人），全年预计死亡超 62.6 万人、新增确诊病例逾 211 万例，传统放化疗的高毒性应对未能有效遏制这一危机。 - [24:21](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1461s) 癌细胞受制于线粒体结构缺失（幽灵线粒体），无法有效燃烧脂肪或酮体，仅依赖葡萄糖和谷氨酰胺这两种燃料进行底物水平磷酸化发酵维持生存。 - [01:30:47](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=5447s) 塞弗里德团队提出“压榨-脉冲”（Press-Pulse）代谢疗法与血糖酮体指数（GKI），通过生酮和热量限制压低血糖，结合间歇性靶向药物阻断谷氨酰胺，辅以极低剂量化疗即可精准打击恶性肿瘤与转移病灶。 ## Key takeaways - [02:42](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=162s) 线粒体代谢学说：癌症并非原发于细胞核的基因病，而是细胞质内线粒体氧化磷酸化功能遭到不可逆慢性损害后导致的代谢紊乱。 - [15:00](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=900s) 破解“致癌悖论”：各种毫无关联的致癌因素（吸烟、致癌病毒、微塑料、草甘膦、慢性炎症等）最终均指向破坏线粒体呼吸链这一共同核心病理。 - [01:08:07](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4087s) 经典核质置换实验证实：肿瘤细胞核置入健康细胞胞浆后停止失控生长，而健康细胞核置入受损胞质却发生癌变，确凿证明线粒体而非细胞核决定了细胞癌变表型。 - [20:25](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1225s) 电镜下的“幽灵线粒体”：人类所有恶性肿瘤细胞的线粒体嵴几乎完全损毁或缺失，物理结构的崩溃直接导致其丧失高效氧化磷酸化产能能力。 - [24:21](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1461s) 双燃料依赖：由于丧失呼吸功能，癌细胞的能效暴跌，只能疯狂通过底物水平磷酸化消耗葡萄糖和谷氨酰胺两种燃料苟延残喘。 - [26:43](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1603s) 逆向信号转导与原癌基因：受损线粒体会向细胞核发出能量窒息警报，促使细胞核被动激活原癌基因以敞开营养转运闸门，这属于原始保命代偿而非基因主动致癌。 - [29:54](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1794s) 现代环境与旧石器基因冲突：过量加工碳水、久坐不动、慢性压力和睡眠缺失破坏线粒体，导致发达国家癌症高发，而传统生活方式原住民和野外狼群几乎不患癌。 - [32:55](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1975s) 外显率漏洞：Tay-Sachs 等真正的基因遗传病外显率达 100%，而 BRCA1 等癌症易感基因突变均不完全外显，仅属继发风险因素，其机制仍是通过削弱线粒体功能起作用。 - [49:23](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=2963s) 血糖酮体指数（GKI）：将摩尔浓度下的血糖除以血酮所得的单一数值，是评估线粒体健康与抗癌代谢状态的关键生物标志物，GKI 越低代表肿瘤能源被限制得越彻底。 - [53:01](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3181s) 厘清酮症酸中毒与营养性生酮：酮症酸中毒是 1 型糖尿病胰岛素崩溃下的血糖血酮双失控危象，而适度断食产生的营养性生酮是人类演化出的自然清洁供能状态。 - [59:10](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3550s) 生酮状态作为化疗载体：生酮诱导健康细胞进入“地堡防御模式”，同时切断癌细胞修复 DNA 所需的葡萄糖，使极低剂量的化疗药物即可发挥杀伤作用并减轻全身毒性。 - [01:01:29](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3689s) 恶病质的真实机制：恶病质并非生酮减重，而是恶性肿瘤在缺乏能量时代偿性分解患者肌肉组织以汲取谷氨酰胺，属于肿瘤发酵引发的消耗性危机。 - [01:10:22](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4222s) 医院营养补充误区：主流临床为了维持化疗患者体重常投喂高果葡糖浆、甜点和精制碳水代餐，这在代谢层面上直接为极度渴求葡萄糖的恶性肿瘤输送养料。 - [01:26:48](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=5208s) 高压氧疗法协同增效：正常细胞能耐受高压氧带来的活性氧（ROS）应激，而呼吸缺陷的癌细胞无法承受，生酮配合高压氧可安全且特异性地灭杀癌细胞。 - [01:30:47](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=5447s) 肿瘤转移的真相与巨噬细胞杂交：单纯肿瘤干细胞无法转移，转移灶由巨噬细胞与肿瘤细胞异常融合形成，这类杂交细胞天生具备组织穿透力且高度依赖谷氨酰胺驱动发酵。 - [01:40:47](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=6047s) 自下而上的科学范式革命：如同哥白尼日心说颠覆托勒密地心说，线粒体代谢学说正面临药企利益与主流医学教育体系的阻碍，需依靠公开透明的临床成果和公众科学素养倒逼医疗变革。 ## Detailed walkthrough ### [00:00](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=0s) 机密信封与被忽视的癌症代谢真相 对话伊始，主持人在托马斯·塞弗里德（Thomas Seyfried）教授面前注意到了一个标有“机密”（confidential）字样的信封。塞弗里德教授透露，信封里装的是一篇处于禁发期（embargo）的重要论文，即将作为《Frontiers in Science》的封面领衔文章发表。该论文提出了一套能有效控制癌症且能让患者存活极长时间的治疗策略，堪称“给绝望者带来希望”。然而，塞弗里德直言，整个主流肿瘤学界至今仍不理解他对癌症起源的看法——事实上，所有慢性疾病和癌症的根源都可以追溯到线粒体受损。 面对主流学界的冷漠与抗拒，塞弗里德表现出强烈的愤慨：“谁能不恼火呢？这个国家每天有 1,700 人死于癌症，也就是每小时 70 人，而且情况每年都在恶化，人们究竟什么时候才能清醒过来？”他指出，现代人身处一个充斥着高度加工碳水化合物、缺乏运动、情绪压力沉重和睡眠习惯恶劣的环境，正在对线粒体造成慢性损害。他以犬科动物作比：癌症是家犬的头号死因，因为家犬被关在公寓里、一天只遛一次、摄入加工食品，最终导致肥胖与癌症；相比之下，野外的狼奔跑捕食天然食物，极少罹患癌症。塞弗里德强调，他们绘制了一套“生物能量健康路线图”（bioenergetic road map to health），只要置身于所谓的“预防区”（zone of prevention），患上癌症或慢性疾病的几率就会极低。 - 全美每天约有 1,700 人死于癌症，折合每小时 70 人，死亡数据逐年攀升。 - 破坏线粒体的现代生活方式四大要素：精制碳水过量、缺乏身体活动、情绪压力、长期睡眠不足。 - 对比案例：家养宠物犬头号死因为癌症，而野生狼群几乎不患癌。 ```mermaid flowchart TD accTitle: 现代环境对线粒体与健康的破坏链条 accDescr: 图表展示现代生活方式因素如何损伤线粒体并推向慢性病与癌症，而维持线粒体健康则进入预防区。 subgraph Hazards["现代环境毒素与生活方式"] H1["高加工碳水化合物"] H2["缺乏运动与久坐"] H3["慢性情绪压力与缺觉"] end subgraph Impact["细胞能量中枢受损"] M1["线粒体功能受损与氧化应激 (ROS)"] end subgraph Outcome["终末健康状态"] O1["癌症与各类慢性代谢疾病"] O2["进入预防区：健康与长寿 (低风险)"] end Hazards --> M1 M1 -->|未受保护 / 持续损伤| O1 M1 -.->|改变代谢生活方式 / 保护线粒体| O2 ``` --- ### [02:42](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=162s) 癌症起源于线粒体：瓦氏效应与细胞发电厂 主持人随后切入正题，询问塞弗里德教授毕生致力于研究的核心目标。塞弗里德表示，他的团队致力于在“无毒性”的前提下有效控制癌症，而这一理论的基石正是德国著名科学家奥托·瓦尔堡（Otto Warburg）在 1920 至 1940 年代的研究发现——癌症本质上是一种“线粒体代谢疾病”，而非主流观念所认定的基因疾病。这意味着癌症的源头在于细胞质中被称为“细胞动力源”的线粒体，而不是细胞核内部的基因序列。 现场展示了一个线粒体物理模型。塞弗里德借此澄清了人们的刻板印象：虽然教科书上常把线粒体画成独立的豆状结构，但它在细胞内部实际上是一个动态响应的“管状网络”（tubular network），会根据细胞内外的刺激实时调整。更为关键的是，在受精卵形成的最初时刻，胚胎发育所需的所有线粒体全部来自母亲卵子的细胞质，存在于细胞核之外的胞浆中。塞弗里德指出，除意外事故外，正是线粒体决定了人类的生物学寿命上限；人类无法活到 400 岁，小鼠寿命大约为 2.5 年，而大象的寿命与人类相仿，物种间寿命的差异根本上取决于线粒体的损耗耐受程度与衰退速度。 - 科学史渊源：奥托·瓦尔堡（Otto Warburg）于 20 世纪 20 至 40 年代率先奠定癌症的线粒体呼吸损伤学说。 - 遗传学现实：受精时胚胎全部的线粒体均遗传自母亲的卵细胞质（细胞质遗传），完全位于细胞核之外。 - 衰老与寿命机制：线粒体具有代谢“保质期”（expiration date），物种的寿命极限由其维持高效能量制造的能力所决定。 --- ### [05:05](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=305s) 线粒体的系统控制权：细胞命运的司令官 塞弗里德进一步阐述了线粒体在机体中的非凡地位。它绝非单纯提供燃料的附属构件，而是掌控细胞内外环境的绝对主宰。不仅单个细胞内的环境受其统辖，它还跨越组织和细胞壁进行系统性通讯，调控着诸如肝脏组织群落、肺部群落、结肠群落以及大脑中的神经元和神经胶质细胞群落。这种遍布全身的通讯网络构成了整个机体的代谢健康基石。 针对主持人的疑问——“线粒体既像大脑，又像发动机舱？”，塞弗里德给出了肯定的回答，并特别强调其“大脑”属性的神秘与强大：线粒体会直接向细胞核下达指令，何时分裂、何时减速完全由线粒体控制。当特定器官的一群细胞中，线粒体因环境毒素等各种因素遭到不可逆损伤时，便会诱发慢性疾病，而癌症则是其中最具创伤性和最具破坏力的终极形态。 - 跨细胞组织调控：线粒体释放的信号协调邻近细胞（肝、肺、结肠、神经元及胶质细胞群落）的代谢与微环境。 - 逆向核调控：线粒体并非被动听命于细胞核，相反，它直接指导细胞核启动或停止细胞分裂程序。 - 疾病诱因：不同器官细胞群中线粒体的损伤模式各异，构成了各种慢性退行性病变及最严重的癌变表型。 --- ### [07:24](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=444s) 呼吸燃烧、ATP 货币与活性氧（ROS）的致命破坏 塞弗里德详细解构了细胞内线粒体能量代谢的物理与化学过程。所谓的致癌物（carcinogens），本质上就是破坏线粒体内脆弱膜结构中蛋白质和脂质的化学物质。线粒体内部的复杂褶皱（嵴膜）包含了利用氧气进行能量转化的核心机器。人体呼吸吸入的氧气充当了呼吸链中电子的“最终受体”，使得高能货币三磷酸腺苷（ATP）源源不断地从管状网络中生成，用以维持酶反应和全部生理运作。 他用内燃机燃烧汽油的比喻来解释这一机制：汽车引擎燃烧辛烷时，打断碳氢键产生内爆推动活塞，并排放废气；细胞同样在“燃烧”食物分子中的碳氢键，但这不是瞬间失控的爆炸，而是一套极其精密、渐进分级的生物化学过程，其清洁副产物仅为二氧化碳（$CO_2$）和水。然而，当细胞面临致癌物刺激，或者因睡眠呼吸暂停（sleep apnea）导致每次长达 30 秒以上的间歇性缺氧（intermittent hypoxia）时，细胞内就会产生大量活性氧（ROS，即自由基）。这些 ROS 就像让金属生锈一样破坏线粒体 delicate 的内膜；如果损伤过于剧烈且急性，细胞将丧失所有能量来源并走向凋亡（apoptosis）或坏死（necrosis）。 - 能量生成本质：吸入的氧气作为最终电子受体，通过受控氧化降解食物中的碳氢键，产生驱动生命运作的化学能量货币 ATP，清洁产物为 $CO_2$ 和 $H_2O$。 - 致癌机制核心：致癌物与间歇性缺氧均促发活性氧（ROS）急剧上升，侵蚀并破坏线粒体内膜的精细脂质与蛋白质复合物。 - 急性损伤转归：当能量供给发生灾难性断崖下跌时，细胞会直接触发程序性死亡（凋亡）或病理性坏死。 ### [09:45](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=585s) 远古发酵通路与线粒体基质中的能量代偿 线粒体并非一朝一夕丧失功能的，往往是历经数月乃至数年的慢性损伤，才使得这一细胞器彻底失去产生充足能量的能力。令人惊奇的是，当现代线粒体呼吸受损时，细胞会启动深埋于进化历程中的远古应急通路进行代偿。在地球生命演化的早期，生命体诞生于没有氧气的幽暗环境中，单细胞生物为了生存而肆意疯狂增殖。那时它们既没有复杂的细胞调控，也没有线粒体，完全依赖细胞质中的发酵作用获取能量。随后，一次划时代的内共生事件发生了：一个具备细胞核、依靠细胞质发酵的细胞，吞噬合并了某种细菌——也就是线粒体的前身。从那一刻起，细胞拥有了双重供能系统：一种是存在于细胞质中的古老低效发酵，另一种则是能够利用氧气高效生成大量能量的氧化磷酸化系统。 托马斯·塞弗里德（Thomas Seyfried）教授指出，他们团队与匈牙利塞梅维什大学（Semmelweis University）的全球顶级学者克里斯托斯·奇诺普洛斯（Christos Chinopoulos）合作取得了一项重大发现：不仅细胞质可以发酵，在线粒体内部的基质（Matrix）深处——即分解食物的三羧酸循环（TCA cycle / Krebs cycle）发生之地——同样隐藏着来自无氧时代的底物水平磷酸化（Substrate-level phosphorylation）古老发酵通路。在线粒体呼吸链因慢性损伤遭到破坏后，这套古老的远古发酵机制便会苏醒，竭力弥补缺失的能量。线粒体基质开始利用谷氨酰胺（Glutamine）这种发酵燃料疯狂抛出三磷酸腺苷（ATP）。原本演化出来进行高效有氧能量代谢的精密细胞器，在绝境中沦为了靠远古发酵苟延残喘的机器。 这种损伤的性质决定了细胞的生死：如果针对氧化磷酸化的破坏是急性的，细胞便会迅速死亡。最典型的例子就是氰化物（Cyanide）中毒，氰化物会立即结合在线粒体利用氧气合成能量的关键蛋白质上，使整个能量系统瞬间瘫痪，“基本上就是把你窒息死亡”，甚至连喝下含有氰化物的饮料也是当场毙命；叠氮化物（Azide）等剧毒物质也是同理。然而，对于慢性病和癌症而言，线粒体所承受的绝非这种瞬时打击，而是经年累月的慢性压力。在骨骼、肺部、膀胱或大脑等特定组织中，线粒体会向细胞核发出求救信号：“我正在窒息，我没有获得足够的能量！”接到求救的细胞核随即开启细胞表面的转运蛋白，疯狂从外界汲取燃料，试图通过非氧依赖的发酵通路维持能量供应。 - 线粒体起源于数十亿年前的细菌内共生，带来了利用氧气进行高效代谢的新能源形式。 - 塞弗里德与奇诺普洛斯合作证实：线粒体基质内的三羧酸循环深处存在古老的无氧产能通路，能通过谷氨酰胺发酵产生 ATP。 - 急性呼吸抑制（如氰化物中毒）会瞬间致死，而慢性呼吸损伤则会诱使细胞回退至古老的发酵自救机制。 --- ### [15:00](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=900s) 破解“致癌悖论”：细胞失控增殖的古老宿命 健康状态下，线粒体依赖氧气将燃料完全氧化，呼出二氧化碳并通过尿液排出水分与废物，维系着整个人体精密而高效的代谢稳态（Metabolic homeostasis）。然而，长期的吸烟、缺乏运动、接触微塑料（Microplastics）、“永久性化学物”（Forever chemicals/PFAS）、草甘膦（Glyphosate）除草剂、致癌病毒感染以及慢性炎症，都在日复一日地侵蚀线粒体的高效产能架构。塞弗里德指出，这正是彻底破解困扰医学界百年的“致癌悖论”（Oncogenic Paradox）的关键钥匙。该悖论最初由匈牙利著名科学家、因发现维生素 C 而荣获诺贝尔奖的阿尔伯特·圣捷尔吉（Albert Szent-Györgyi）提出：医学界早已发现环境中存在成百上千种截然不同的诱癌因素（病毒、炎症、致癌物、间歇性缺氧、罕见的胚系突变等），但科学界却始终无法解释——这些风马牛不相及的致病因子，究竟是通过怎样一个共同的病理生理机制，最终殊途同归地导向了同一种结果，即细胞分裂失控（癌症）？ 塞弗里德直言，这个共同机制正是线粒体的呼吸损伤。线粒体不仅是发电站，更是决定细胞何时分裂、何时停止分裂的“命运指挥官”。当线粒体遭受慢性损伤而失灵，细胞就不得不退回到远古生命形态的生存模式——那是一个氧气尚未出现、单细胞生物不受拘束、毫无节制疯狂分裂的时代。主持人史蒂文·巴特利特（Steven Bartlett）随后用通俗的语言打了个生动的比方：“在这个线粒体中，藏着来自数十亿年前远古细菌的遗传记忆。古老的细菌极其自私，只顾自己生长增殖，从不与外界沟通，与其他细胞毫无协同性可言。融合成为现代形态后，它学会了为了整个生物体的利益而生长；可一旦遭受损伤，它就退化回那种原始自私的生长模式，根本不在乎宿主的死活，这也就是癌症的本质。”塞弗里德赞同了这个形象的概括，强调正是这种向原始无氧生存程序的“返祖回退”，触发了失控的癌变进程。 ```mermaid flowchart TD accTitle: 致癌悖论的统一解机制 accDescr: 各种环境致癌因素损伤线粒体导致呼吸链破坏，迫使细胞启动远古发酵并失控增殖 subgraph Causes["多源环境致癌压力 (致癌悖论)"] A1["慢性炎症 / 致癌病毒"] A2["微塑料 / 永久性化学物 / 草甘膦"] A3["吸烟 / 缺乏运动 / 间歇性缺氧"] end subgraph Impairment["共同病理核心"] B["线粒体氧化磷酸化遭受慢性损害"] C["细胞发出能量窒息信号并唤醒远古基因"] end subgraph Consequence["返祖代偿与癌变"] D["激活无氧发酵通路: 葡萄糖与谷氨酰胺"] E["脱离多细胞机体调控: 恢复原始自私增殖 (癌症)"] end Causes --> B B --> C C --> D D --> E ``` --- ### [17:39](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1059s) 瓦伯格效应的真相与心肌梗死的代谢启示 回溯历史，德国生理学家奥托·瓦伯格（Otto Warburg）很早就洞察到了癌症的能量本质。瓦伯格提出，癌症本质上是一个能量代谢问题：为什么癌细胞即使处于 100% 充足氧气浓度的环境中，依然疯狂进行发酵，并向外排出海量的发酵代谢废物——乳酸（Lactic acid）？在正常生理机制下，氧气的存在本该彻底关闭无氧发酵（巴斯德效应），让系统恢复高效代谢稳态。为了让听众更直观地理解，塞弗里德举了心肌梗死（Heart attack）的残酷例子：当突发心梗、呼吸心跳骤停时，患者体内血液会瞬间被两大发酵代谢废物填满——一种是乳酸，另一种则是他们最新证实的琥珀酸（Succinic acid）。大脑神经元无法承受这种发酵低效产能太久，若不立刻抢救便会死亡；但只要心肺复苏成功，心脏重新跳动、恢复正常呼吸，血液中积聚的乳酸和琥珀酸便会迅速消退无踪，因为只要有氧气和功能完好的线粒体，人体根本不需要依靠发酵苟活。 然而，癌细胞的诡异之处就在于：即便在氧气极度充沛的条件下，它们依然停不下来发酵。瓦伯格由此断言：癌细胞的线粒体必定遭受了不可逆的永久性损伤。但在当时，瓦伯格没有透射电子显微镜，缺乏现代分子生物学工具，只能完全基于纯粹的生物化学推论立论。随后几十年里，主流医学界对瓦伯格发起了猛烈攻击，理由是许多实验发现部分癌细胞依然在消耗氧气、摄入氧气，因此主流学界武断地宣称“瓦伯格错了，线粒体并没有损坏”。塞弗里德在此揭示了他们团队彻底推翻主流认知的关键突破：癌细胞确实在消耗氧气，但消耗氧气根本不是为了通过正常的氧化磷酸化高效合成 ATP；相反，由于呼吸链结构缺陷，癌细胞吸入氧气后产生的是大量极具破坏性的活性氧自由基（ROS, Reactive Oxygen Species）。这些肆虐的自由基反过来进一步攻击细胞，制造了当今主流肿瘤学界苦苦追踪、不断测序的成千上万种 DNA 突变。那些基因突变根本不是癌症的源头，仅仅是线粒体呼吸功能损坏后引发的下游附带损伤而已。 - 心脏骤停缺氧时，血液中会迅速飙升两大发酵产物：乳酸（Lactic acid）与琥珀酸（Succinic acid）；复苏供氧后产物立即清除。 - 癌细胞在常氧状态下依然持续发酵（瓦伯格效应/有氧糖酵解），表明其呼吸控制机制发生了永久性不可逆损伤。 - 主流医学界误以为癌细胞耗氧即代表呼吸正常；塞弗里德团队证实其耗氧主要是生成了导致基因突变的活性氧自由基（ROS），而非用于产生能量。 ### [20:25](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1225s) 电镜下的“幽灵线粒体”与肿瘤学家的盲区 人类对抗癌症的根本困境在于失控的细胞增殖。现代医学为了阻断这种失控，不断向患者体内倾倒各种极端手段——使用剧毒药物化疗、高能射线放疗，或是通过外科手术直接切除。然而，如果将癌细胞置于高分辨率电子显微镜下观察，就会发现其内部的能量引擎——线粒体——早已千疮百孔。线粒体内膜高度折叠的“嵴”（cristae）几乎全部消失或严重变形，呈现出所谓的“幽灵线粒体”（ghost mitochondria）：外壳看似完整，内部却空空如也。 Thomas Seyfried 强调，生物学中有一条坚不可摧的底层公理：“结构决定功能（Structure determines function）”。一旦细胞器的物理结构发生畸变，其生理功能必然出现严重障碍，根本无法再通过正常的氧化磷酸化（Oxidative Phosphorylation）高效生成能量。Seyfried 语带讽刺地调侃道，除了肿瘤学家（Oncologists），全天下的生物学家都明白这个常识。当主持人 Steven 笑着追问“那肿瘤学家是干什么的？你又是什么？”时，Seyfried 幽默地回答：“他们是专门研究癌症的人，而我只是个生物学家。” - **幽灵线粒体（Ghost Mitochondria）**：在电子显微镜下，癌细胞的线粒体嵴完全缺失或结构严重扭曲，沦为无功能空壳。 - **生物学底层原则**：结构畸变必然导致氧化磷酸化能量代谢受损，这是所有恶性肿瘤的通用病理特征。 ```mermaid flowchart TD accTitle: 线粒体结构损伤导致功能衰竭的病理链条 accDescr: 展示线粒体在物理结构崩溃后，如何从正常氧化磷酸化滑向低效的异常状态。 subgraph StructuralDamage["结构崩溃"] A["环境毒素/缺氧/慢性炎症"] --> B["线粒体嵴 (Cristae) 破损与缺失"] B --> C["形成空壳般的“幽灵线粒体”"] end subgraph FunctionalFailure["功能障碍"] C --> D["破坏呼吸链与膜接触界面 (MAMs)"] D --> E["氧化磷酸化 (OxPhos) 能量衰竭"] end ``` --- ### [21:22](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1282s) 跨越百年的印证：从瓦伯格假设到线粒体相关膜病变 为了验证线粒体缺陷的普适性，Seyfried 曾耗费一年多时间深挖早期的电镜文献。当年的奥托·瓦伯格（Otto Warburg）受限于时代技术，无法直接看清亚细胞微观结构，只能凭借精密的生物化学测定提出假设；而 Seyfried 查阅了大量肿瘤电子显微切片，证实所有恶性肿瘤细胞无一例外都存在线粒体数量、形态与功能的严重缺陷。此外，他与全球顶尖的癌症电子显微学专家海梅·阿里斯门迪-莫里略（Jaime Arismendi-Morillo）深度合作发表论文，不仅证实了线粒体自身的损毁，更发现细胞质中线粒体与其他细胞器之间的连接纽带——线粒体相关内质网膜（MAMs）同样全部发生结构病变。 这种严重的器质性破坏直接切断了正常的细胞氧气利用路径。即便用氰化物（Cyanide）、叠氮化物（Azide）完全阻断细胞呼吸，甚至将其置于完全无氧的环境中，癌细胞依然能够存活并疯狂分裂。原因在于它们早已抛弃了氧气代谢通道，退回到了原始古老的无氧发酵（Fermentation）模式。只要细胞还能通过发酵维持能量供给，它就不会启动细胞凋亡程序。 - **电镜文献实证**：人类迄今观察过的所有恶性肿瘤细胞，均存在线粒体数量减少、超微结构损毁的共性。 - **线粒体相关膜（MAMs）病变**：内质网与线粒体之间的物理接触界面发生异常，直接干扰钙离子信号传导与细胞命运调控。 - **抗缺氧/抗毒素生存**：即使暴露于致命的呼吸链毒剂（氰化物、叠氮化物）或无氧环境，发酵状态下的癌细胞依然能继续生存。 --- ### [24:21](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1461s) 贪婪的能量吞噬者：葡萄糖与谷氨酰胺 正常的线粒体氧化磷酸化是生物演化出的极高能效系统，每消耗一分子底物可利用氧气生成大约 34 至 36 个 ATP。相比之下，失去正常线粒体功能的癌细胞只能依赖古老的发酵途径，其产能效率断崖式下跌，往往只能产生微不足道的 2 到 4 个 ATP。为了弥补这种巨大的能量缺口并满足不受限增殖的需要，癌细胞必须建立起庞大的后勤供给通道，变得极度“贪婪”，疯狂从宿主环境中掠夺两项核心燃料：**葡萄糖（Glucose）**与**谷氨酰胺（Glutamine）**。 谷氨酰胺是人体血流中含量最丰富的氨基酸。在进化历程中，谷氨酰胺发酵是机体在窒息或缺血时保全细胞生命的关键后备方案，也是肠上皮细胞与免疫系统快速增殖的主力能源。虽然生化上因人体可通过糖分自主合成而将其归为“非必需氨基酸”，但对于依赖发酵的肿瘤而言，它却是绝对不可或缺的救命稻草。Steven 在此做了一个精辟的总结：当线粒体退化至史前原始机制时，癌细胞为了在极低产能效率下苟活，彻底沦为自私贪婪的掠夺者，切断与机体整体的协同节律，无休止地吞噬养分并无序自我克隆。 - **能效断崖式暴跌**：正常氧化磷酸化产生约 34-36 个 ATP，而发酵代偿途径仅能产生约 2-4 个 ATP。 - **癌细胞的两大核心燃料**： 1. **葡萄糖**：通过无氧糖酵解提供基础能量与碳骨架。 2. **谷氨酰胺**：血液中最丰富的氨基酸，为肿瘤提供线粒体底物级磷酸化能量及氮源。 --- ### [26:43](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1603s) 婴儿为何患癌？逆向信号转导与致癌悖论 面对这种代谢退化模型，Steven 提出了一个极为尖锐且具有普遍痛点的问题：如果癌症是后天生活方式导致线粒体受损的产物，那为何连生活习惯完全空白的 3 岁幼儿甚至 6 个月大的婴儿都会罹患恶性脑瘤？Seyfried 直言，这并非婴儿自身的“主动生活选择”，而是源于“被动暴露”。现代工业社会充斥着大量全氟/多氟烷基化合物等“永久化学品”（Forever Chemicals）与脂溶性致癌物，它们极易穿透母体胎盘屏障，在胚胎早期发育的关键窗口期，直接渗透并破坏胎儿大脑细胞幼嫩脆弱的线粒体。 一旦细胞内的线粒体能量系统被不可逆地摧毁，便会激活名为“线粒体应激反应”（Mitochondrial Stress Response）的**逆向信号转导（Retrograde Signaling）**机制。垂死的线粒体向细胞核发出求救警报，迫使细胞核扮演被动呼应的角色——激活所谓的“原癌基因（Oncogenes）”。原癌基因的本质并非凭空制造癌症，而是打开细胞膜上的营养闸门，海量吞噬葡萄糖与谷氨酰胺来维持低级发酵，重返生命早期缺乏调控的原始单细胞增殖状态。这就是著名的“致癌悖论（Oncogenic Paradox）”：无论是慢性炎症释放的炎性细胞因子破坏线粒体能量代谢、长期严重的睡眠呼吸暂停所致的“间歇性缺氧（Intermittent Hypoxia）”，还是外界化学毒物，最终都收敛于同一终点——线粒体呼吸受损迫使细胞进行代偿性发酵。对于细胞而言，如果不启动这种原始发酵来代偿，下场就只有死亡。 - **胎盘屏障穿透**：脂溶性致癌物与工业“永久化学品”可穿过母体胎盘，在胚胎期损毁胎儿细胞线粒体，从而诱发婴幼儿实体瘤。 - **逆向信号转导（Retrograde Signaling）**：由受损线粒体向细胞核发送逆向压力指令，激活原癌基因以敞开营养摄取大门。 - **间歇性缺氧（Intermittent Hypoxia）**：睡眠呼吸暂停等病症可反复重创线粒体氧化磷酸化效率，诱发代偿性无氧发酵。 - **代偿性生存法则**：发酵是细胞在线粒体呼吸功能彻底报废后，为了避免细胞坏死而启动的终极保命机制。 ```mermaid flowchart LR accTitle: 逆向信号转导与原癌基因激活流程 accDescr: 展示受损线粒体如何向细胞核发出警报，激活原癌基因并引起暴食与恶性增殖。 subgraph Trigger["上游损伤"] A["永久化学品 / 间歇缺氧 / 慢性炎症"] --> B["线粒体受损 / OxPhos 衰竭"] end subgraph Signaling["逆向通讯"] B --> C["线粒体应激反应 (逆向信号)"] C --> D["细胞核应答"] end subgraph MetabolicShift["代谢退化与发酵"] D --> E["原癌基因 (Oncogenes) 开启闸门"] E --> F["巨量掠夺葡萄糖与谷氨酰胺"] F --> G["史前原始发酵与失控增殖"] end ``` ### [29:54](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1794s) 现代生活方式与癌症地理差异：旧石器基因与现代环境的冲突 主持人提到一个引人深思的流行病学现象：尼日尔（Niger）、冈比亚（Gambia）、尼泊尔（Nepal）等贫穷国家的癌症发病率一直处于全球最底端；与此相对，澳大利亚、新西兰和美国等高收入发达国家却拥有世界上最高的癌症发病率。针对这一反差，Thomas Seyfried 博士指出其根本症结在于现代技术与环境。人类在生理学本质上依然是“旧石器时代的人类”（Paleolithic man），机体经过数百万年的演化，拥有极强的高效储能能力，以应对历史上反复出现的饥荒期。 然而，现代社会创造了一个全新的异质环境：大量高度加工的高碳水化合物食物、普遍缺乏运动的久坐生活、严重的心理与情绪压力、恶劣的睡眠质量，再加上环境中无处不在的致癌物暴露。这些现代生活因素层层叠加，对细胞内至关重要的细胞器——线粒体——造成了长期的慢性损伤。在某些器官中，若特定细胞群的线粒体遭到不可逆的持续伤害，细胞就会启动失控的异常增生，从而演变为乳腺癌、肺癌等恶性肿瘤。50万年前的旧石器时代祖先，以及现代依然遵循传统生活方式生活、极少受到现代饮食和作息冲击的人群，癌症发病率都极低。 Seyfried 博士援引了著名人道主义医生阿尔伯特·史怀哲（Albert Schweitzer）的历史记录。史怀哲在非洲行医期间，特意在当地部落原住民中寻找癌症病例，却震惊地发现癌症在这些人中极其罕见。原因在于他们保持着大量体力活动、食用天然有机食物、没有现代社会的剧烈精神压力，也未接触工业化学品。Seyfried 进一步举了犬类的演化例子：所有的家犬都由灰狼演化而来，野外的灰狼终日在自然中奔跑、吃天然猎物，几乎从不患癌；而生活在公寓里的现代宠物狗，每天仅由遛狗员牵出去走一趟，往往变得肥胖不堪，癌症更成为了家犬的第一死因。维持线粒体的活力与健康，是避免细胞遭受慢性损伤、降低各类慢性退行性疾病（包括2型糖尿病、肥胖症、高血压甚至神经精神疾病）的核心。 ```mermaid flowchart TD accTitle: 现代环境诱发癌症机制 accDescr: 现代环境多重压力损伤线粒体导致异常发酵与癌症 subgraph ENV["现代生活环境压力"] A["高加工碳水化合物"] B["缺乏运动 / 久坐"] C["慢性压力与睡眠剥夺"] D["环境化学毒素暴露"] end subgraph MITO["线粒体功能受损"] E["线粒体氧化磷酸化效率崩溃"] F["线粒体受损启动补偿性发酵供能"] end subgraph CANCER["病理结果"] G["异常钙信号通路 / 邻近调控失效"] H["失控的恶性细胞增生（癌症）"] end ENV --> E E --> F F --> G G --> H ``` --- ### [32:55](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1975s) 癌症是基因病吗？外显率漏洞与线粒体损伤假说 针对大众和主流肿瘤学界坚信“癌症是基因遗传病”的观点（例如乳腺癌易感基因 BRCA1 或引发多种恶性肿瘤的 Li-Fraumeni 综合征），Seyfried 博士给出了有力反驳。他提到其团队成员 Bob Kaplan 博士在《Oncology》期刊上发表的梳理遗传风险的重磅论文：在纯粹的单基因遗传病中，例如戴萨克斯症（Tay-Sachs disease）或先天性代谢缺陷病，基因突变是“100%外显”（100% penetrant）的——只要携带该突变，就百分之百会发病。然而，医学界至今未发现任何一个能达到 100% 外显率的癌症基因突变；大部分所谓的“癌症基因”都是不完全外显的（incompletely penetrant），这证明它们充其量只是继发性风险因素（secondary risk factors），绝非原发病因。 Bob Kaplan 的深入研究进一步揭示，每一个与癌症风险挂钩的基因突变，最终其生物学效应都落脚在同一处：以某种机制破坏线粒体内氧化磷酸化（oxidative phosphorylation）的能量转换效率。不仅基因突变如此，诸如致癌化学物质、致癌病毒（例如导致肝癌的肝炎病毒、引发宫颈癌的人乳头瘤病毒 HPV）也是同样的机理——病毒蛋白或产物侵入线粒体内部，或直接在线粒体内复制，从而彻底破坏其产能效率。当有氧呼吸衰退，细胞便被迫开启原始的“补偿性发酵”（compensatory fermentation），通过异常的钙信号传导导致细胞不再服从周围正常组织的微环境调控，最终走向不受拘束的无序生长。 Seyfried 博士解释完这一链条后，充满激情地确认道：“我讲得足够清楚了吗？只要我能让你听明白，我们就能让每一个人都理解这个事实。” 主持人回应解释自己之所以频繁追问“为什么”并要求通俗解释，是因为节目听众中有一群在押的年轻管教人员（young offenders），他们曾对主持人反馈说“我很想听那一期，但里面用的词汇太深奥了，我根本听不懂”。Seyfried 赞同这种担忧，同时笑称在学术界这属于标准专业术语，绝非自视甚高；但幸运的是，如今听众完全可以借助 AI 工具将复杂的学术表达快速降维、“精简通俗化”（dumb it down），让人人都能掌握自身健康背后的科学真相。 - **遗传学对比**：真正的单基因代谢遗传病（如 Tay-Sachs）突变具有 100% 的致病外显率，而乳腺癌 BRCA1、Li-Fraumeni 综合征等肿瘤基因突变均不完全外显，属于继发风险。 - **病理共性**：基因变异、环境致癌物和病毒感染殊途同归，最终均指向损伤线粒体有氧呼吸功能，强迫细胞切换为无氧发酵。 --- ### [37:46](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=2266s) 保护线粒体的处方：从葡萄糖到酮体（GKI 机制初探） 主持人向 Seyfried 提问：对于一个当前未被诊断出癌症、希望尽一切可能降低患癌概率的普通人而言，既然关键在于防止线粒体承受过度氧化应激与损伤，那么日常生活中应该遵循怎样的具体“处方”？ Seyfried 博士指出，正是为了解决这一量化难题，他们团队开发出了**葡萄糖-酮体指数（Glucose Ketone Index, GKI）**计算器——这是首个能帮助普通人直观评估线粒体健康水平的生物标志物工具。人体的代谢核心在于能量燃料的切换：从以碳水化合物（糖）为燃料，切换到以脂质（脂肪）为燃料。当主持人追问何为脂质燃料时，Seyfried 明确指出其核心形式就是“酮体”（ketones）。 Seyfried 解释了人体储能机制演化的精妙逻辑。人体内广泛分布的脂肪组织（adipose tissue，包括腹部外周脂肪）是数百万年来为了抵御极端严酷自然环境和饥荒而演化出的“高效机器”。在生物学上，“葡萄糖是黄金”，人体要么将其立即燃烧供能，要么将其转化为脂肪储存起来。当机体停止摄入糖分时，体内储存的脂肪便会释放进入血液循环，被运送至肝脏。在肝脏内，长链脂肪酸就像被送入粉碎机的大树枝一样，被高效分解成微小的水溶性代谢产物——酮体。酮体具有高度水溶性，除了无法供能给缺乏线粒体的红细胞（erythrocytes）之外，能完全取代葡萄糖，成为大脑、肌肉及体内绝大多数正常组织细胞的高效清洁能量来源。 ### [39:46](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=2386s) 进化遗留的脂肪储备与现代慢病危机 人类的线粒体在漫长进化中学会了极其高效地榨取葡萄糖中的能量。在过去数十万年的远古时期，食物匮乏是常态，如果人类无法将多余的热量高效转化为脂肪储存起来，早在五十万年前整个物种就已经彻底灭绝。然而在当下现代社会，环境中充斥着海量的高度加工碳水化合物，身体的本能又不会轻易通过尿液排泄这些能量（除非患有未受控制的糖尿病），结果就是全部被转化为脂肪堆积，演变为一场波及全球的肥胖流行病。这种原本保护人类祖先生存的演化机制，在久坐不动、充斥高压与垃圾食品的现代环境下，反而对线粒体造成了巨大毒害。 长期压力、缺乏运动与过度进食共同构成了一个高危闭环。当人处于急性压力下（例如与人争吵、商业谈判崩盘），皮质类固醇（corticosteroids）会迅速激增，推高血糖并引发全身性系统炎症。短期的压力反应并无大碍，但现代人的生活充斥着“慢性压力”——一边吃着充满反式脂肪与糖分的 Twinkie 点心，一边坐在沙发上刷着充斥坏消息的手机屏幕（doom scrolling）。这会导致活性氧类（ROS）等反应性分子不断生成，持续削弱线粒体正常产生 ATP 的效率。面对这种损伤，体内细胞会出现两种极端走向：无法通过代偿性发酵供能的细胞会慢慢死亡，引发神经退行性疾病或器官衰竭；而能够重启远古厌氧发酵机制的细胞，则会彻底走向不受控的疯狂增殖，即癌症。 ```mermaid flowchart TD accTitle: 现代生活压力对线粒体命运的影响 accDescr: 展示现代生活方式如何导致线粒体受损，进而分化为细胞死亡或癌变两种结局。 subgraph S1["现代环境压力源"] A["高加工碳水 + 暴食"] B["缺乏运动 / 久坐"] C["慢性压力与皮质类固醇激增"] end subgraph S2["细胞与线粒体损伤"] D["过量活性氧 (ROS) 生成"] E["线粒体氧化磷酸化效率崩溃"] end subgraph S3["分化结局"] F["无法进行发酵代偿：细胞死亡\n(帕金森病、失智症等慢病)"] G["启动古老厌氧发酵：失控增殖\n(癌症 Tumorigenesis)"] end A --> D B --> D C --> D D --> E E --> F E --> G ``` - 神经元通常无法依靠发酵存活：例如在帕金森病中，黑质致密部（substantia nigra）的多巴胺神经元一旦线粒体受损就会直接凋亡，因此神经元本身极少发生癌变；大脑中的恶性肿瘤几乎全部起源于神经胶质细胞。 - 癌症、2型糖尿病、心血管疾病与失智症（包括阿尔茨海默病）本质上共享同一个底层病理机制：特定组织细胞内线粒体呼吸功能的慢性或急性破坏。 --- ### [42:27](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=2547s) 睡眠的修复机制与旧石器时代祖先的代谢强韧度 针对睡眠对代谢的影响，托马斯·塞弗里德教授指出，良好的睡眠本质上是让全身及线粒体卸下负荷、恢复能量代谢效率的“生理停机维护”。当人睡个好觉醒来时，全身感到焕然一新，正是因为线粒体获得了喘息并能重新有效调控微环境。相反，如果长期熬夜、精神高度紧张，身体各器官的线粒体无法完成自我修复，不仅会直接诱发神经精神问题和消化道紊乱，还会进一步恶化为2型糖尿病与癌症。 现代人与旧石器时代祖先的身体负荷形成了鲜明对比。远古人类为了追捕野牛或猛犸象等大型动物，必须付出极高强度的体力消耗。以色列近期针对数十万年前穴居人的一项古人类学研究显示，人类祖先往往倾向于猎杀并食用兽群中最强壮的成年个体，他们深知骨髓与肌肉饱含生命力和强健的代谢能量，但这反过来使兽群中的老幼失去保护，间接加速了这些巨型动物的灭绝。旧石器时代的祖先身形宛如刀刻般健美精悍，完全没有2型糖尿病、癌症或阿尔茨海默病等慢性病的困扰；他们的主要死因是急性感染、外伤和婴儿夭折。人类现代身体的基因组依旧属于那个时代，而将机体拉回到低血糖、高酮体的代谢状态，正是复刻这一古老而健康的生理平衡。 - 追捕猎物与高强度生存活动让远古人类的线粒体时刻维持在高效率的能量输出状态，肌肉与大脑均具备极强的代谢适应力与耐力。 - 现代医学需要解决的不是祖先面对的外伤与感染，而是由能量过剩和代谢失调引发的慢性内源性疾病。 --- ### [45:13](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=2713s) 绝密信封、 Frontiers 论文与 GKI 的诞生渊源 在演播室的桌面上放着一个引发主持人史蒂文极大好奇的保密信封。塞弗里德解释，信封内是一篇尚处于限期禁发（embargo）状态的重磅论文，即将作为领头文章发表在《Frontiers in Science》上。该论文系统阐明了如何维持线粒体健康以及如何精准管理机体的能量代谢效率。有趣的是，期刊除了准备面向专业学术界的完整版论文，还专门针对 8 至 14 岁的青少年制作了一份名为“Young Minds”的通俗降维版本；塞弗里德的同事笑称，绝大多数普通成年人可能更愿意读那份青少年版，因为专业版中关于线粒体内生物能量学（bioenergetics）的复杂机制会让非专业读者望而生畏。 谈及血糖酮体指数（Glucose Ketone Index, GKI）的研发历史，塞弗里德分享了一位改变他研究路径的真实患者故事——美国律师特鲁迪·杜庞特（Trudy Dupont）。特鲁迪不幸罹患了罕见且极难手术的脑干神经胶质瘤，在阅读了塞弗里德的著作《癌症作为代谢疾病》（Cancer as a Metabolic Disease）后，她主动联系并严格采纳了代谢疗法，成功将原本仅剩几个月的预期寿命延长了10年之久（虽然后来不幸离世）。 众所周知，肿瘤细胞极度依赖葡萄糖发酵生存（瓦氏效应），且由于线粒体结构与功能受损，癌细胞根本无法有效氧化脂肪酸或燃烧酮体作为能量。如果癌细胞强行燃烧脂肪，其受损的电子传递链会导致活性氧失控从而自我瓦解，因此肿瘤细胞只能将未利用的脂肪酸以脂滴形式储存在细胞质中；学术界常有人误读这一现象，声称“癌细胞充满脂肪滴证明它需要脂肪酸供能”，塞弗里德斥责这种观点完全本末倒置。 为了追踪特鲁迪的代谢状态，塞弗里德最初让她通过指尖采血，分别单独汇报血糖和血酮的数值。然而，单纯监测单项数据在临床实际中带来了巨大的混乱： - 特鲁迪因脑干肿瘤影响行走平衡，平日需拄拐杖并使用无障碍车位。 - 某天她外出办事，发现专属残疾人车位被他人占用，顿时怒火中烧、气愤不已。 - 她气冲冲跑上楼后立即扎手指测血糖，结果读数瞬间飙升到了惊人的 186 mg/dL（而正常代谢疗法目标区通常在 50–65 mg/dL 左右）。 - 特鲁迪陷入极度恐慌，立刻发邮件给塞弗里德绝望地哭诉：“我要死了！我的血糖爆表了，肿瘤马上要疯狂生长了！” - 塞弗里德冷静地询问她当时的血酮水平，她回答血酮依然保持在 0.4 至 0.9 mmol/L 之间，并没有显著波动。 这次突发状况让塞弗里德深刻意识到，情绪和急性应激导致的血糖剧烈波动，会让患者产生不必要的恐慌。单看血糖或单看血酮都无法全面反映真实的肿瘤营养微环境。为了解决这一痛点，塞弗里德与团队成员乔希（Josh）决定将两者的摩尔浓度统一整合为单一比例公式，由此正式创立了能够综合评估患者抗肿瘤代谢状态的“血糖酮体指数（GKI）”。 ### [49:23](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=2963s) 血糖酮体比指数（GKI）的诞生与远古人类的线粒体状态 托马斯·塞弗里德（Thomas Seyfried）解释了血糖酮体比指数（Glucose Ketone Index, 简称 GKI）的计算逻辑：由于临床上血糖通常以毫克/分升（mg/dL）为单位计量，而血酮则以毫摩尔/升（mmol/L）计量，为了消除单位混乱并获得一个在各种生理状态下都极其稳定的数值，研究团队将血糖先换算为毫摩尔/升（即除以 18），再除以血酮的毫摩尔浓度。这一公式最初是受到癌症患者特鲁迪（Trudy）案例的启发而研发出来的。随后，塞弗里德与学生德里克·李（Derek Lee）以及克里斯托斯·希诺普洛斯（Christos Chinopoulos）联合绘制了比率图表，并逐渐意识到这个指标本质上直观反映了人体线粒体的健康水平。 当 GKI 处于较低区间时，人体便进入了类似旧石器时代远古人类的生理代谢区。塞弗里德风趣地指出，远古人类绝不可能去吃什么糕点、蛋糕或甜食，他们处于生酮状态并不是出于自律的“选择”，纯粹是因为恶劣的生存“环境”。他们经常经历长期的间歇性断食，平日活动量极大，因此体内的氧化磷酸化器官（线粒体）完好无损，几乎不会患上现代意义上的慢性代谢病或癌症。 ### [50:25](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3025s) 演播室现场测定 GKI：从“预防区”到“暴食常态” 主持人史蒂文·巴特利特（Steven Bartlett）当场拿出随身携带的 Keto-Mojo 仪器进行实时自测。塞弗里德教授笑着打趣道，他自己出门也总是随身带着这台小仪器。现场测得史蒂文的血酮值为 0.4 mmol/L，血糖值为 90 mg/dL。通过简易换算：先将血糖 90 除以 18 得出 5.0 mmol/L，再除以酮体 0.4 mmol/L，算出的 GKI 最终读数为 12.5。塞弗里德对照图表确认，12.5 稳妥地落在了“预防区”（Prevention Zone，即黄色至绿色过渡带）。 史蒂文分享了自己此前进行纯肉饮食（Carnivore Diet）的经历：他连续一周狂吃肉眼牛排、培根、鸡蛋和羊肉，成功将 GKI 降到了 10 左右；他笑称牛排实在太美味，自己吃得有点超标，否则完全可以降得更低。塞弗里德肯定了这种效果，并解释人类在进化过程中本质上是食腐与狩猎物种，原本的生存模式是在偶尔捕获猎物时“大快朵颐”，之后面临长期饥饿，身体早已适应了周期性的营养匮乏。然而，现代人却演变成了“每天都在大摆筵席”，一天吃五顿还零食不断，身体长期处于高血糖、低酮体的胰岛素狂飙状态。 ```mermaid flowchart LR accTitle: GKI Calculation and Metabolic Zones accDescr: 血糖与血酮的计算逻辑，以及不同比值对应的代谢危险与预防区域划分。 subgraph Calc["GKI 换算逻辑"] A["血糖 (mg/dL) ÷ 18"] --> B["血糖 (mmol/L)"] B & C["血酮 (mmol/L)"] --> D["GKI = 血糖 ÷ 血酮"] end subgraph Zones["代谢健康分级"] D --> E["红区 (GKI > 50-500)<br>高糖/零酮/慢性病与癌症高危"] D --> F["黄绿区 (GKI 9-12)<br>旧石器人类常态/慢性病预防区"] D --> G["深绿区 (GKI < 1-3)<br>治疗级生酮/肿瘤饿死控制区"] end ``` ### [53:01](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3181s) 红色高危区与酮症酸中毒的医学认知误区 塞弗里德严肃指出，那些长期摄入高碳水化合物、大量精制糖、零运动且频繁进食的现代人群，长期滞留在所谓的“红色区域”（Red Zone）。在极端的临床病例中，有人血糖高达四五百毫克/分升，同时体内的酮体读数完全为零，计算出来的 GKI 甚至高达 500，这是滋生肥胖与恶性肿瘤的绝佳温床。“我们可以偶尔踏足红区，但绝不能终身定居在红区。” 很多主流临床医生一听到“生酮”便条件反射式地大呼“酮症酸中毒（Ketoacidosis）”，塞弗里德对此严厉驳斥，直言“饶了我吧！”他厘清了病理性酸中毒与营养性生酮的本质鸿沟： - **酮症酸中毒**：属于病理性危机，仅见于无法分泌胰岛素的 1 型糖尿病患者或严重失控状态，此时患者由于胰岛素应答全面崩溃，血糖和酮体同时极度失控飙升，血酮往往高达 15 至 20 mmol/L。 - **营养性生酮**：史蒂文测出的 0.4 mmol/L 乃至正常人轻度断食产生的酮体，是完全符合人类演化生理的温和状态。 - **2 型糖尿病等慢性病**：其本质是长期的过量摄入损害了细胞线粒体的氧化磷酸化能力，由此引发的一系列退行性病变。 ### [54:37](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3277s) 饿死癌细胞的“双燃料”封锁：葡萄糖与谷氨酰胺 在深入探讨能量生物学（Bioenergetics）时，塞弗里德详细说明了利用低 GKI 对抗癌症的核心机理：癌细胞因为线粒体存在严重的结构和功能缺陷，根本无法利用酮体作为能量底物；相反，当人体进入绿色深层生酮区、血酮上升时，正常细胞代谢活力大增，而酮体对癌细胞不仅毫无助益，甚至在一定浓度下对其具有微毒性。通过剥夺葡萄糖，肿瘤内部的异常炎症反应消退，异常的新生血管网（Angiogenesis）也会被瓦解，原本狂躁恶性的肿瘤逐渐变得“温顺而惰性”。 然而，光靠断绝葡萄糖依然无法彻底杀死肿瘤，因为癌细胞还依赖第二种至关重要的燃料——氨基酸**谷氨酰胺（Glutamine）**。血液中无时无刻不在流淌着充沛的谷氨酰胺，为细胞质发酵和线粒体底物水平磷酸化持续提供动力。因此，塞弗里德团队主张必须结合老药新用（Repurposed Drugs）实施组合拳： - 在高阶儿童胶质瘤等重磅研究中，他们重点验证了广谱抗寄生虫老药**甲苯咪唑（Mebendazole）**。 - 该药被证实能同时双靶点阻断葡萄糖与谷氨酰胺的代谢通路。 - 塞弗里德特别强调：“我只谈论在自己实验室中经过严格测试并发表过学术论文的成果。现代肿瘤学界至今没有认清的是：癌细胞脱离了葡萄糖和谷氨酰胺根本无法生存，且它们绝对无法切换到利用脂肪酸或酮体维持生命。” ### [58:02](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3482s) 格利欧母细胞瘤幸存十年的奇迹：巴勃罗·凯利的案例 当史蒂文追问这一套疗法是否能彻底消灭癌症时，塞弗里德非常坦诚地表示，科研团队绝不轻易使用“治愈（Cure）”这一字眼，但它确实能够长期将恶性肿瘤控制在惰性状态。 为了佐证其真实疗效，塞弗里德讲述了来自英国德文郡（Devon）的胶质母细胞瘤（Glioblastoma）患者巴勃罗·凯利（Pablo Kelly）的震撼故事： - 凯利最初被确诊为**完全无法手术切除（Inoperable）**的原发脑胶质母细胞瘤，常规医学体系建议对他进行放疗和化疗毒药轰炸。 - 崇尚自然疗法的凯利拒绝了放化疗，全面采用了塞弗里德的代谢疗法。 - 令人震惊的是，在代谢疗法的干预下，原本弥漫浸润的恶性肿瘤边界变得异常清晰清晰（Demarcation）。神经外科医生见状大感意外，主动表示可以动刀切除。 - 凭借代谢治疗结合后续的 4 次减瘤手术（Debulking surgeries），这位曾被宣判死刑的患者打破了胶质母细胞瘤几个月或一两年的生存期魔咒，顽强地生活了整整 10 年，期间还组建家庭并生育了两个孩子。 ### [59:10](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3550s) 生酮状态作为代谢载体：大幅提升化疗与放疗疗效 在回顾了胶质母细胞瘤患者因最后一次肿瘤切除术引发脑出血去世、而非死于肿瘤本身的案例后，对话转向了代谢疗法如何与传统癌症治疗协同工作。Seyfried 教授指出，让患者处于营养性生酮状态（Nutritional Ketosis）时，生酮环境会充当一种“代谢载体”（Metabolic Vehicle），极大地促进药物向肿瘤细胞的输送。这种机制使得医生能够大幅降低化疗药物的剂量，同时反而取得更大、更显著的治疗效果。 Seyfried 教授分享了他们在土耳其伊斯坦布尔和希腊诊所的实际临床实践。面对晚期胰腺癌、晚期乳腺癌等绝症患者，他们先诱导患者进入一定程度的生酮状态，再施用顺铂（Cisplatin）、卡铂（Carboplatin）等标准传统化疗药物，但剂量大幅削减。这些原本预后极差的患者很多能够存活四到五年甚至更久。这背后的生物学机制在于：当人体进入禁食或生酮状态时，健康细胞会启动类似于“避难地堡模式”（Bunker Mode）的保护机制——它们减缓分裂速度、保存能量并增强自我防御；而癌细胞缺乏这种进化演变出的代谢关闭开关，依然在疯狂尝试分裂。当化疗毒素袭来时，处于防护状态的健康细胞受损极小，而暴露且快速分裂的癌细胞则承受了全部打击。 ```mermaid flowchart TD accTitle: 生酮状态对健康细胞与癌细胞的分化影响 accDescr: 展示进入生酮状态后，健康细胞进入防御状态，而癌细胞因缺乏保护机制被低剂量化疗精准打击 Keto["患者进入营养性生酮状态"] subgraph Healthy["健康细胞响应"] H1["进入'地堡防御模式'"] H2["减缓细胞分裂 / 保守能量"] H3["抵抗化疗毒性 / 避免受损"] end subgraph Tumor["癌细胞响应"] T1["缺乏代谢关闭开关"] T2["继续疯狂分裂 / 葡萄糖供应被切断"] T3["无法修复氧化损伤 / 迅速凋亡"] end Keto --> H1 --> H2 --> H3 Keto --> T1 --> T2 --> T3 ``` - 化疗会在肿瘤内部产生巨大的氧化应激（Oxidative Stress）与 DNA 损伤，癌细胞需要消耗海量的葡萄糖来进行修复；生酮状态切断了葡萄糖供应，导致癌细胞无法修复 DNA 损伤而迅速死亡。 - 发酵代谢的废弃产物（如乳酸和琥珀酸）实际上构成了肿瘤抵御化疗与放疗的“生化护盾”；只有同时切断葡萄糖和谷氨酰胺这两种发酵燃料，才能彻底卸下肿瘤的防御外壳。 --- ### [01:01:29](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3689s) 精准免疫疗法的误区与恶病质真相 Seyfried 教授进一步探讨了精准免疫治疗（如 PD-1、PD-L1 抑制剂或 CAR-T 等疗法）在临床中的局限。主流医学往往在患者经历放化疗失败、身体极度虚弱时才使用免疫疗法。此时肿瘤正处于极具侵略性的最强状态，免疫疗法很难正面击溃它，通常只能带来微弱的部分缓解（Partial Response），主流肿瘤学界甚至将延长 6 个月寿命视为重大突破，而代谢疗法则着眼于延长 5 到 6 年以上。正确的策略应是先施加代谢压力使肿瘤缩小、变惰性（Indolent），在保全患者自身免疫系统、肠道微生态和身体机能的前提下，再辅以极低剂量的精准靶向药物彻底清除残留病灶。 针对主流肿瘤医生因害怕“恶病质”（Cachexia，一种导致患者肌肉和脂肪极度消耗的衰竭综合征）而极力反对生酮饮食的现象，Seyfried 教授从生物化学机制上进行了纠正： - **恶病质（病理性消瘦）**：由于肿瘤疯狂发酵需要谷氨酰胺，它会主动分解患者的肌肉组织来摄取谷氨酰胺作为能量，导致病理性的肌肉萎缩。 - **生酮减重（治疗性减重）**：处于营养性生酮状态下的体重减轻属于生理性的治疗性减重，能从源头上抑制肿瘤对机体资源的掠夺。 --- ### [01:06:10](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3970s) 体细胞突变理论的破局与主流认知障碍 主流肿瘤学目前完全建立在“体细胞突变理论”（Somatic Mutation Theory, SMT）之上，认为癌症从根本上是由随机 DNA 基因突变驱动的遗传疾病，因此研发重点全在针对 DNA 和细胞分裂的毒性治疗上。加之主流医学界要求必须有耗资巨大的多中心双盲 Phase 3 临床试验才能将方案列入标准疗法，而饮食与代谢干预几乎不可能获得药企的大额资助，导致肿瘤科医生缺乏开具代谢处方的官方授权，甚至常常对患者说“能吃什么就吃什么”。 Seyfried 教授指出，许多肿瘤医生并非存心不良，而是现行医学教育体制从未教过他们癌症深层的生物化学与代谢本质。美国国家癌症研究所（NCI）等权威机构在官网上依然宣称癌症是基因疾病，却忽视了大量在无基因突变情况下依然发生癌变的“野生型癌症”（Wild-type Cancers），以及正常人体细胞中同样普遍存在所谓“致癌驱动基因突变”却并未失控生长的最新测序事实。这再次引出了核心争论：驱动癌细胞疯狂生长的，究竟是细胞核内的基因突变，还是细胞质中受损的线粒体？ ### [01:08:07](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4087s) 线粒体决定细胞命运与破损的治癌系统 托马斯·塞弗里德（Thomas Seyfried）教授与主持人史蒂文·巴特利特（Steven Bartlett）回顾了经典的核质置换实验：如果将肿瘤细胞的细胞核移入去核的正常细胞中，细胞并不会发生癌变，异常失控的生长完全停止；相反，若将正常细胞的细胞核移植到去核的肿瘤细胞胞浆中，细胞却依然会出现失控生长。这一确凿的事实无可辩驳地证明，驱动癌症的并非细胞核内的基因突变，而是细胞质中的线粒体。"是线粒体掌控着我们的命运，"塞弗里德直言，主流肿瘤学界至今既不理解也不愿接受这一点，反而拿所谓的“双盲交叉试验尚未完成”当作挡箭牌。在他看来，这根本不是尊重科学，而是医疗体系为了保护自身利益与破损机制所编造的推托之辞。 ```mermaid flowchart TD accTitle: 核质置换实验机制图 accDescr: 对比肿瘤细胞核移入正常胞质与正常核移入肿瘤胞质的不同实验结果 subgraph Experiment1 ["实验 A：转移肿瘤核"] direction TB N1["肿瘤细胞核"] --> C1["去核正常细胞胞质（健康线粒体）"] C1 --> R1["细胞正常生长（无失控增殖）"] end subgraph Experiment2 ["实验 B：转移正常核"] direction TB N2["正常细胞核"] --> C2["去核肿瘤细胞胞质（受损线粒体）"] C2 --> R2["细胞失控生长（发生癌变）"] end ``` 当主持人问他是否对此感到极其愤怒时，塞弗里德毫不掩饰自己的激动：“史蒂文，面对这种现实，谁能不愤怒？”在美国，每天有整整 1,700 人死于癌症，换算下来相当于每小时夺走 70 条生命，且这一数据逐年恶化。塞弗里德指出，上一期节目引用的还是旧数据，而根据美国癌症协会（American Cancer Society）针对 2026 年的最新预测，仅这具一年就将有超过 62.6 万人因癌症离世。电视广告中每天都在大肆宣传波士顿各大医疗机构的“重大突破”，筹款活动接连不断，但患者的死亡人数却在不断攀升。“为癌症筹了那么多钱，问责机制究竟在哪里？人们什么时候才能清醒过来？你绝不可能通过对一个人进行辐射和下毒来让他们恢复健康！”塞弗里德强调，战胜癌症必须从生物学和生物化学机制入手；他提供了严谨的科学底层逻辑，而临床医生则需要将其落实到日常诊疗中。 - **核质置换科学事实**：正常线粒体可以抑制致癌表型，而受损线粒体即使搭配正常细胞核仍旧会导致细胞失控生长。 - **2026 年美国癌症死亡预测**：全年预计 626,000 人死亡，平均每天约 1,700 人，每小时约 70 人。 - **主流疗法困境**：铺天盖地的“新突破”并未降低死亡率，塞弗里德谴责传统放疗与化疗缺乏对疾病代谢生化本质的考量。 --- ### [01:10:22](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4222s) 医院饮食悲剧与“代谢肿瘤学”的崛起 根据美国癌症协会 2025 至 2026 年公布的统计数据，新增确诊病例呈现严峻的爆发态势：2026 年全美预计新增确诊病例超过 211 万例，相当于每天有约 5,800 人被诊断患癌。其中肺癌依旧是头号杀手，其致死人数甚至超过了结直肠癌和胰腺癌的总和。与此同时，乳腺癌、前列腺癌、胰腺癌、黑色素瘤以及 HPV 相关的口腔癌等高危癌种发病率全线飙升。面对如此严峻的局势，主流医院在临床护理上的认知误区却令人痛心疾首。为了防止患者在残酷的化疗期间体重暴跌，营养师往往叮嘱患者“只要能咽得下去，想吃什么就吃什么”。 塞弗里德与主持人痛陈这种做法在代谢层面上简直是一场彻底的悲剧。为了强行拉高热量摄入，医院给患者递上高果葡糖浆和精制糖调配的代餐奶昔、冰淇淋以及高碳水舒适食品。这种做法虽然短期保住了体重，却直接导致患者血液中充斥着葡萄糖与胰岛素，宛如给体内的恶性肿瘤“直接浇灌养料”。不过，星星之火正在点燃：全球已有少数前沿的整合肿瘤医生开始尝试在化疗前利用生酮饮食（Ketogenic Diet）和断食策略，先保护正常细胞、削弱肿瘤活力，然后再以更低、更精准的化疗剂量进行打击。塞弗里德正是该方案的核心开拓者，并正在联合各方成立 MORE 联盟（Metabolic Oncology Research and Education，代谢肿瘤学研究与教育联盟），以此继承奥托·瓦尔堡（Otto Warburg）百年前开创并由波士顿学院团队完善的代谢治疗路线。 - **新增确诊数据**：2026 年全美预计新增超 211 万癌症病例（平均每天约 5,800 例）。 - **主要高发癌种**：肺癌致死率最高；乳腺癌、前列腺癌、胰腺癌、黑色素瘤和口腔癌发病率持续走高。 - **医院饮食误区**：为了维持体重盲目投喂糖浆、冰淇淋和高碳水食品，直接导致高血糖与高胰岛素，加速滋生肿瘤。 - **MORE 联盟目标**：汇聚医学研究与临床力量，推动以生酮限制和靶向给药为核心的代谢肿瘤学规范。 --- ### [01:12:58](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4378s) 挑战绝症：胶质母细胞瘤与胰腺癌的生存希望 针对临床上最棘手的恶性肿瘤，塞弗里德表示现代主流医学在长达一个世纪的时间里几乎毫无建树。以致命的脑胶质母细胞瘤（Glioblastoma）为例，百年来标准疗法的改善微乎其微，它曾先后夺走了参议员泰德·肯尼迪（Ted Kennedy）、约翰·麦凯恩（John McCain）以及乔·拜登总统的儿子博·拜登（Beau Biden）的生命，在传统医学中几乎被直接宣判为死刑。然而，塞弗里德郑重表示：“我们并不宣称彻底治愈了癌症，但通过代谢疗法，我们正在让这些胶质母细胞瘤患者活得远比预期长得多，胰腺癌同样取得了绝佳的控制效果。” 塞弗里德发出公开挑战：如果有人给他机会组建团队，他愿意用自己的代谢疗法直接对抗任何制药巨头的任何前沿临床试验。他的团队不仅明确知晓背后的分子机制，更配备了成熟的临床医生与代谢营养师，能够立即投入实战。他们的核心目标是通过非毒性方式有效遏制癌细胞能量供给，让癌症晚期患者显著延长寿命，维持优良的生活质量并重新回归社会，而非在昂贵且痛苦的无效治疗中消耗生命。 - **胶质母细胞瘤的顽疾**：过去 100 年常规治疗缺乏突破，常规预后极差，被广泛视作绝症。 - **代谢干预的临床优势**：在胶质母细胞瘤和胰腺癌案例中，通过切断肿瘤能源供应已取得极佳的生存期延长效果。 - **公开对决挑战**：塞弗里德直言愿将代谢疗法与各大跨国药企的新药临床试验进行公开对照检验。 --- ### [01:14:00](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4440s) 假若执掌大权：塞弗里德的终结癌症蓝图 在对谈中，主持人打趣地发起假设：“托马斯，如果你今天当选美国总统，甚至直接成为无需受限的最高决策者，你的首要目标是阻止每天 1,700 人的癌症死亡悲剧，你会推行怎样的施政纲领？”塞弗里德笑着调侃政客们普遍缺乏基本的科学素养，随后严肃地勾勒出他的改革路径。首先，在临床治疗端，他绝不会全盘推翻现有体系或强行取缔利润高达数十亿美元的抗癌药物，而是通过代谢前置干预，让医生以更低剂量、更安全的方式协同用药，极大减轻毒副反应。 而在预防层面，塞弗里德将“公众教育”列为第一优先级。但他特别强调，绝不能由政府出台强制命令去规定民众“能吃什么”或“不能吃什么”。医疗图表与科学数据的意义在于为个体赋权，让每个人知晓风险所在。食品带来的愉悦感固然存在，理性的公民在了解机制后自会懂得“偶尔享用但不能长期生活在那种致病环境中”。此外，塞弗里德指出了极其严峻的社会公平问题：贫困地区的“食物荒漠”（Food Deserts）充斥着廉价的劣质垃圾食品，而 Whole Foods 等高端超市中健康的优质肉类与天然食材价格高昂，普通穷人根本负担不起进入“代谢健康安全区”的成本。要想真正逆转每年数十万人丧命的癌症危机，首要任务就是降低天然健康食材的门槛，并帮助大众坚决避开高度加工的精制碳水化合物。 - **协同给药策略**：保留现有化疗药物，但在代谢控制前提下大幅削减使用剂量，保障疗效的同时降低毒性。 - **健康赋权而非行政强制**：反对政府强制干预个人餐盘，主张通过代谢教育让患者自主做出知情选择。 - **解决食物荒漠与贫困困境**：关注底层人群因经济压力只能被迫依赖垃圾食品的社会不公，提出应从国家层面降低健康食物的成本。 - **首要饮食建议**：优先在日常生活中剔除高度加工的精制碳水化合物（Highly Processed Carbs）。 ### [01:16:49](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4609s) 保护线粒体：运动、药物争议与抗癌生活方式清单 托马斯·塞弗里德（Thomas Seyfried）教授强调，健康的核心在于维持线粒体（mitochondria）这一细胞器的生物能量效率。只要保护好线粒体，就能协同降低失智症、糖尿病和肥胖症的发病风险。当主持人史蒂文·巴特利特（Steven Bartlett）问及当下风靡的降糖减重药物 Ozempic 以及 GLP-1 受体激动剂能否作为走捷径的解决方案时，塞弗里德教授持谨慎保留态度：虽然 GLP-1 类药物确实能有效降低血糖，但目前尚无明确研究证明它能否提升血酮水平。在他看来，酮体才是直接增强线粒体生物能量效率、维持线粒体健康的关键，单纯降糖而不产生充足酮体，未必能达到预期的代谢保护效果。 ```mermaid flowchart TD accTitle: 线粒体健康与生活方式干预 accDescr: 展示保护线粒体与损害线粒体的两类相反生活方式对比 subgraph Protect["保护线粒体（降低慢性病与癌症风险）"] P1["适度运动与肌肉活动"] P2["消除食物沙漠与杜绝超加工食品"] P3["心理减压（音乐疗法、冥想、社交与快乐）"] P4["提升血酮水平 / 维持低 GKI"] end subgraph Damage["损毁线粒体（诱发代偿性发酵与癌变）"] D1["超加工垃圾食品 / 高果糖玉米糖浆"] D2["极差睡眠与长期沙发久坐（刷手机）"] D3["孤立无援与长期的情绪压力"] D4["合成农药与环境毒素损伤氧化磷酸化"] end Protect -->|维持生物能量效率| Healthy["健康细胞与抗癌微环境"] Damage -->|迫使细胞依赖发酵产能| Cancer["细胞生长失控与肿瘤恶化"] ``` 接着，两人梳理了促进代谢健康的核心要素：教育、消除导致廉价垃圾食品泛滥的“食物沙漠”（food deserts）、杜绝超加工食品、坚持运动，以及积极舒缓情绪压力。塞弗里德分享了一位来自东亚（日韩会议）学者的讽刺性总结——“如何快速患上癌症”： - 长期顿顿吃垃圾食品； - 保持极其恶劣的睡眠； - 屁股绝不离开沙发，整天盯着电视屏幕或手机进行“毁灭性刷屏”（doom scrolling）； - 坚决不运动，杜绝朋友社交，完全杜绝快乐。 这一反讽清单不仅是罹患癌症的“快车道”，也是几乎所有慢性退行性疾病的催化剂。 --- ### [01:19:10](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4750s) 动态监测、AI 赋能与赋予患者饮食自主权 针对日常代谢追踪，塞弗里德指出大多数人虽不需要天天刺破手指测血糖酮体比（GKI），但随着持续血糖监测仪（CGM）和新一代持续血糖-血酮联合监测仪的问世，自我量化正在变得极其简便。他的实验室团队成员（如 Lucas Lou 等人）正在研发结合人工智能的手机应用程序：用户只需拍下某种食物的照片，AI 就能即时预测该食物会将自己的代谢状态归入图表中的哪一个健康或风险区间（如安全区或高危红区）。 塞弗里德强烈主张“患者赋权”（patient empowerment）。他认为任何政府、总统或国王都不应该强行规定普通人必须吃什么，每个人都应当拥有代谢知识，自主测试并作出选择。针对经常有人问他“我到底该吃什么”，他的答复是“吃任何你想吃的，只要测试你的代谢数值，看它落在图表的哪个区间”： - **地中海饮食变体**：希腊的研究团队采用热量限制的低碳地中海饮食（三文鱼、沙丁鱼、橄榄油、牛油果配合运动），在胶质母细胞瘤（Glioblastoma）患者身上取得了惊人的长期生存成效； - **纯肉食饮食（Carnivore）**：吃搭配贝阿恩斯酱（béarnaise sauce）的肋眼牛排，同样能够压低血糖并大幅拉升血酮； - **植物性饮食**：只要经过精心设计、不依赖精制糖，素食者同样能达成低 GKI。 针对具体食物成分，塞弗里德痛斥高果糖玉米糖浆（HFCS）是“最糟糕的垃圾食品”，对工业种子油（如芥花籽油、大豆油等）则指出个体间因年龄、种族、性别及生活方式的不同存在代谢差异。而当巴特利特提到合成农药会让淋巴瘤患病风险激增 41% 时，塞弗里德一针见血地指出其根本病理：这些毒素全部都在损伤线粒体的氧化磷酸化机制，迫使受损细胞启动代偿性底物水平发酵，最终走向失控的增殖。他坦言目前肿瘤学界极度缺乏对线粒体生物学与生物化学的深刻理解，建议大众关注像英国的尼克·莱恩（Nick Lane）以及道格·华莱士（Doug Wallace）等线粒体生物学领域顶尖学者的前沿研究。 --- ### [01:22:23](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4943s) 断食撞墙期破解法与模拟断食的抗癌机制 当话题切入断食（fasting）实践时，巴特利特承认自己从未尝试过长达一周的纯水断食。塞弗里德提到了作家瓦拉尔·西姆切克（Veral Simck）新书中的概念——纯水断食进行到第 3 天左右会遭遇极其痛苦的“撞墙期”（the wall）：身体陷入剧烈不适、严重失眠、双腿抽动或不宁腿症状（Jimmy legs），极易导致放弃。西姆切克发现抿上极其微量的葡萄糖汁即可帮助平稳渡过难关。 为了让癌症患者更平顺、无痛地跨越这道生理障碍，塞弗里德团队与临床医生设计了一套渐进方案： - **前期准备**：在进行纯水断食前，先进行约一周的极低碳/零碳水饮食（Zero-carb diet），以肉类等高蛋白高脂肪食物为主； - **戒断糖瘾**：葡萄糖对大脑具有类似可卡因的极强成瘾性，骤然断糖会引发震颤与焦虑；通过预先零碳水适应，让患者平稳走出代谢“红区”过渡到“黄区”； - **顺畅过渡**：当大脑适应低碳供能后再切入纯水断食，神经系统受到的生理创伤会大幅减少，如同顺畅地穿过了一扇紧闭的闸门。 巴特利特随后引用了瓦尔特·隆戈博士（Dr. Valter Longo）关于“模拟断食饮食”（fasting-mimicking diet, FMD）的临床研究：断食能急剧下调胰岛素样生长因子-1（IGF-1），强力激活细胞自噬，并剥离癌细胞的代谢屏障，使常规肿瘤治疗的有效性提升高达三倍。塞弗里德对此表示完全赞同，指出这层屏障正是癌细胞发酵排出的代谢废物（如乳酸和琥珀酸），断食能直接剥夺这些发酵原料。然而，当被问及若身为统治者是否会强制人人佩戴 CGM 动态血糖仪时，塞弗里德果断表示“绝不强制”。他认为唯有确诊癌症且极度渴望维持绿区代谢指标的患者，或者有主动健康诉求的人，才有必要借助监测设备来认知自己的代谢边界。他随后以在墨西哥与一位首席医生的深入交流为例，进一步阐明了这种监测对患者心理与饮食行为的微妙影响。 ### [01:25:22](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=5122s) 动态血糖监测与患者自主权：从被动警报到身体感知 Steven Bartlett 和 Thomas Seyfried 教授探讨了监测设备在生活中的实际体验。Steven 提到，当一个人戴着连续血糖监测仪（CGM）去参加聚会尽情享乐时，如果手臂上的设备不停发出尖锐刺耳的哔哔警报声，很多人会烦躁地一把撕下设备直接扔进垃圾桶——没人愿意在开心狂欢时被别人在耳边喋喋不休地训斥。相比之下，自己主动选择用采血针扎手指测血糖，是一种自主自愿的决策，而不是被设备强行指手画脚。 尽管如此，Steven 承认佩戴一两次 CGM 具有极高的教育意义：它让人真切地意识到，自己塞进嘴里的每一样食物都会在短短 10 分钟内对血糖产生直接且巨大的影响；而当随后的血糖剧烈暴跌、遭遇“低血糖撞墙”（crash）时，身体所经历的疲劳与不适感，能瞬间将日常行为与真实的生理感受紧密联系在一起。 Seyfried 教授对此表示高度赞同，并举了英国 stage 3 胶质瘤患者 Andrew Scarborough 的例子。Andrew 依靠该疗法成功生存了约 15 年，他扎手指测量了无数次，如今仅凭自身的感觉就能准确判断身体处于哪个代谢区间。Seyfried 指出，对于刚刚确诊且面临终末期判决的患者而言，手臂上的监测设备是宝贵的导航仪，能帮助他们稳定留在理想的“绿色安全区”（green zone），从而以更高的生命质量活得更长久。他强调，相比于医学界那些“如同刻在花岗岩上”死板不可动摇、任何偏离都可能导致医生吊销执照的传统标准治疗（Standard of Care, SOC），代谢疗法完全是由患者自主驱动的（patient-driven），充满了基于个体状态调整的灵活性。 --- ### [01:26:48](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=5208s) 高压氧疗法与代谢疗法的协同抗癌机制 两人随后深入讨论了高压氧疗法（Hyperbaric Oxygen Therapy, HBOT）在癌症治疗中的强力协同效果。Steven 援引了一项 2013 年的研究，指出在系统性转移癌的小鼠模型中，虽然生酮饮食本身就能显著减缓肿瘤生长，但如果将生酮饮食与高压氧疗法结合，肿瘤的缩小速度和生存期的延长幅度会呈现出极其震撼的协同倍增效应。Seyfried 自豪地确认，这篇具有里程碑意义的论文正是他和南佛罗里达大学的 Dominic D'Agostino 教授等人共同完成并发表的。 Seyfried 解释了其背后的生物物理学机理：高压氧会在细胞内产生巨大的氧化应激（oxidative stress）。正常的健康细胞拥有完整健全的线粒体氧化磷酸化功能，能够有效应对并中和这种应激；然而癌细胞的线粒体氧化磷酸化缺陷，根本无法承受高浓度的活性氧（ROS）。因此，通过营养性生酮将癌细胞逼入绝境，再配合高压氧，就能在完全不伤及正常组织的前提下，对癌细胞实施特异性的精准灭杀。 这与现有的标准放化疗形成了刺眼的对比。Seyfried 严肃地指出：“放疗是在用各种毒素破坏全身。”更讽刺的是临床上常见的恶性循环：当患者历经艰辛通过饮食调整身体时，肿瘤科医生往往冷嘲热讽称“这根本没用”，随即施加高剂量的放化疗；而这些治疗带来的极度全身压力与应激，直接把患者的生理指标瞬间推入爆表的“红色危险区”（red zone），反过来由于皮质醇激增和血糖暴涨，变相喂饱并强化了肿瘤。Seyfried 澄清自己并不完全反对化疗，但化疗必须在正确的代谢背景下应用——当身体处于营养性酮症状态时，仅需使用极低剂量的化疗药物，即可达到杀伤效果，同时避免迫使肿瘤细胞发生突变并产生耐药性。 --- ### [01:28:50](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=5330s) 环境毒素、微塑料与线粒体损伤的根源 话题转向日常生活中的环境致癌隐患，特别是微塑料（microplastics）和全氟/多氟烷基物质（PFAS，俗称“永久化学品”）。Steven 提到，在 2023 年底，国际癌症研究机构（IARC）已正式将常用于不粘锅涂层和食品包装的某些永久化学品升级为人类一类致癌物（Group 1 Carcinogen），其机制证据表明它们会诱导表观遗传改变并严重抑制免疫系统，理应被全面禁用。此外，未经充分过滤的市政自饮水系统中频繁检测出砷（arsenic）、镉（cadmium）等重金属，这些同样被 IARC 列为一类致癌物。 Seyfried 情绪激动地指着桌上的线粒体模型表示，现代医学忽视了一个最根本的底层共性：他在重新梳理奥托·瓦尔堡（Otto Warburg）的全部开创性著作后证实，无论是永久化学品、微塑料、还是水体中残留的工业毒素和重金属，它们在细胞微观层面造成的后果是完全一致的——它们直接破坏线粒体这一细胞器，造成活性氧（ROS）损伤，削弱氧化磷酸化的产能效率。当细胞无法通过正常呼吸获取能量时，为了自保苟活，就会发生代偿性的逆转，疯狂利用葡萄糖和谷氨酰胺进行发酵，最终引发失控的恶性增殖。Seyfried 断言，几乎所有的慢性疾病和癌症，本质上都源于对线粒体的慢性持续损伤。好在人体的线粒体拥有惊人的自我修复潜能，只要通过代谢干预将身体维持在健康的代谢区间内，哪怕接触到了环境毒素，机体也能最大限度地抵御并修复这种损伤。 --- ### [01:30:47](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=5447s) 揭秘癌症转移的真相：“压榨-脉冲”策略 在被问及当前尚未探讨的最关键议题时，Seyfried 毫不犹豫地提出了癌症致死的头号元凶——肿瘤转移（Metastasis）。他直言，局部局限性肿瘤相对容易长期控制，真正导致绝大多数癌症患者丧命的是癌细胞扩散至全身。乳腺癌扩散至肝脏、肺部和大脑，肺癌向脑部转移，往往令传统全身化疗束手无策。 对于转移的成因，Seyfried 揭示了一个颠覆主流认知的机制： 主流学界热衷于炒作“癌症干细胞”（stem cell tumor），但他通过实验室培育证实，纯粹的肿瘤干细胞即便生长得异常凶猛且布满血管，也根本无法发生转移。真正的转移细胞，是在局部形成未愈合的慢性创口时，机体免疫系统派出巨噬细胞前往试图修复，结果巨噬细胞与肿瘤细胞发生非正常融合，诞生了一种具有高侵袭性的“巨噬细胞-肿瘤杂交细胞”（macrophage-tumor cell hybrid）。巨噬细胞本身在人体内就具备天生在血液和各组织间穿梭游走的通行权，这赋予了杂交细胞无与伦比的迁徙与转移能力。 尽管这些转移杂交细胞极其顽固，Seyfried 团队却发现了它们的致命软肋：它们是高度依赖谷氨酰胺（glutamine-driven）和葡萄糖的“发酵狂徒”。因此，由他和 Dominic D'Agostino、Joe Maroon 共同创立的“压榨-脉冲”（Press-Pulse）治疗策略展现出了巨大的潜力： ```mermaid flowchart TD accTitle: Press-Pulse Therapeutic Strategy accDescr: A flowchart illustrating the Press-Pulse strategy for targeting metastatic cancer cells while preserving healthy tissues. subgraph PressStage["持续压榨 (Press)"] A["热量限制与生酮饮食"] --> B["压低系统性血糖水平"] B --> C["削弱原发与转移肿瘤能量供给"] end subgraph PulseStage["间歇脉冲 (Pulse)"] D["靶向药物 (如DON类似物)"] --> E["阻断谷氨酰胺利用"] E --> F["精准打击转移性巨噬细胞杂交细胞"] end PressStage --> Synergy["协同效应: 诱导肿瘤消退"] PulseStage --> Synergy Synergy --> Outcome["保护并强化已被浸润的正常器官机能"] ``` - **持续压榨（Press）**：通过生酮饮食和热量限制，长期且持续地将宿主血糖压制在极低水平，剥夺肿瘤的基础能量来源。 - **间歇脉冲（Pulse）**：采用特定靶向药物对谷氨酰胺代谢进行短暂、高强度的间歇性阻断，给极度依赖谷氨酰胺的转移杂交细胞致命一击。 - **辅以极低剂量免疫治疗**：在不破坏机体免疫监视的前提下，实现转移灶的逐步清除（resolution），同时不仅不损害反而增强了已被肿瘤浸润的原有器官的生命力。 面对 YouTube 评论区成千上万身患绝症或陪伴患癌亲人苦苦挣扎的绝望观众，Steven 询问 Seyfried 最想对他们说什么。Seyfried 动情而又沉重地感慨：核心的悲剧在于，当科学界已经拥有了这样一套毒性极低、机制明确且行之有效的慢病化管理策略时，主流医疗体制却迟迟不肯采纳和推行。他寄希望于这类深度对话能够唤醒大众，把掌控生命的权利重新交回到患者自己手中。 ### [01:34:07](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=5647s) 挑战医疗既得利益与科学范式：从地心说到癌症代谢 托马斯·塞弗里德（Thomas Seyfried）尖锐地指出，许多公众尚未意识到，他们的亲人根本没有必要为了某些依靠“维持患者患病状态”来牟取暴利的医疗产业而沦为牺牲品。当大众被灌输“面对癌症你无能为力”的观念时，塞弗里德强调事实恰恰相反——只要掌握了正确的代谢生物学知识，患者完全有能力主动作为。然而，阻碍这一转变的根源在于：现代肿瘤医生在医学院接受的全部教育都将癌症定义为基因疾病，他们从未真正研读过细胞代谢相关的生化文献，甚至根本不了解癌症生物学与生物化学的底层逻辑。 为了说明颠覆既定认知有多么艰难，塞弗里德用科学史上的哥白尼革命作比喻。在长达 1800 年的时间里，整个西方世界都盲信亚里士多德的学说与克劳狄乌斯·托勒密（Claudius Ptolemy）的数学计算，坚信地球是宇宙中心的“地心说”。直到哥白尼提出若将太阳置于中心、地球仅是一颗普通行星，那些复杂的运行数学才变得合理；随后开普勒发现行星轨道是椭圆而非正圆，伽利略通过望远镜观察到木星卫星并精确预测了行星轨迹。然而，在这一真理确立的过程中，乔尔达诺·布鲁诺（Giordano Bruno）因挑战正统地心说被罗马天主教会活活烧死在火刑柱上。塞弗里德直言，无论面对的是宗教集团还是坐拥庞大利益的工业帝国，撼动根深蒂固的权力结构都极其凶险。 ```mermaid flowchart TD accTitle: 科学范式转移的历程对比 accDescr: 对比历史上天文学地心说到日心说的范式颠覆过程，与当前从癌症基因论向线粒体代谢论的范式转变。 subgraph Astronomy["天文学范式转变"] A["托勒密地心说<br/>(统治1800年)"] --> B["哥白尼与伽利略<br/>(提出日心说并验证)"] B --> C["突破既得利益与正统阻力<br/>(布鲁诺殉道)"] end subgraph Oncology["肿瘤学当前面临的变革"] D["癌症基因突变学说<br/>(主导现代临床标准)"] --> E["线粒体代谢学说<br/>(以瓦尔堡假说为基石)"] E --> F["重构治疗逻辑与临床协作<br/>(挑战高利润工业体系)"] end ``` ### [01:36:08](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=5768s) 继承瓦尔堡的衣钵与防范“学术冷箭” 当主持人史蒂文·巴特利特（Steven Bartlett）问及挑战主流体系是否对他个人的学术生涯造成危险时，塞弗里德表现出科研学者的执着与笃定。他坦言自己并不担心世俗意义上的威胁，真正让他时刻保持警惕、甚至夜不能寐的，是“被未知数据迎头痛击（blindsided）”——即出现任何一条颠覆其理论框架的切实反例。为了防止这种情况发生，他和他的学生团队时刻紧盯最新发表的文献。每当有论文宣称“癌症细胞能够燃烧脂肪酸或酮体提供能量”时，他们便立即深挖实验细节，结果发现每一次研究人员都在培养基中残留了葡萄糖或谷氨酰胺，从而造成了是脂肪酸在供能的假象。 塞弗里德谈到，他们的研究建立在生化巨擘奥托·瓦尔堡（Otto Warburg）的肩膀之上。在全盘推崇“基因致癌论”的狂潮中，瓦尔堡的发现被粗暴地抛弃和践踏。而塞弗里德最新的论文正是对瓦尔堡当年遗留的漏洞进行校正与弥补，将癌症研究重新引回正轨。他坚信，只要将癌症定性为“线粒体代谢紊乱”，其所有的细胞表型和病理特征都能得到无懈可击的解释。这一理论并非要彻底排斥现有的化疗等有毒化学药物，而是指导临床医生转换用药策略，在特定的代谢窗口期以低毒、高效的方式实施精准打击。 - 科学界曾将奥托·瓦尔堡的代谢理论边缘化长达半个世纪，错误地全力押注于寻找癌症基因开关。 - 塞弗里德团队反复核查反方文献后证实，脱离葡萄糖与谷氨酰胺，癌细胞无法仅依靠脂肪酸或酮体维持生存与恶性增殖。 - 代谢疗法的核心在于改变化学治疗药物的应用时机与组合方式（“压迫-脉冲”策略），而非盲目排斥现代医学工具。 ### [01:37:48](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=5868s) 行动指南：GKI 指数监测与临床协同考量 面对饱受癌症折磨的患者及其家属，主持人询问目前最切实的行动步骤是什么。塞弗里德建议，患者及其家属首先应当主动阅读相关论文以获取认知武装，随后配合知情的医生，将身体指标调控至目标代谢区间。史蒂文指出，普通患者可以通过市面上销售的手持测量设备（如约 20 至 30 美元的 Keto-Mojo 仪器）进行指尖采血，直接读取血糖与血酮水平；新型设备甚至无需手动将血糖值除以 18 进行单位换算，即可一键生成血糖酮体指数（GKI），这极大降低了居家量化管理的门槛。 塞弗里德特别提醒，进入理想的低 GKI 治疗区间并非易事，绝不能盲目冒进。癌症患者通常不是完全健康的个体，往往伴随高血压、糖尿病等多种慢性并发症。此外，部分个体存在肉碱（Carnitine）缺乏等代谢异常，导致脂肪酸无法顺利转运生成酮体；如果在不了解自身状况的情况下盲目追求深度生酮，可能会引发严重不适甚至昏厥送医。因此，实施代谢干预必须在充分掌握生化特性的专业临床医师指导下进行，并结合 PET 扫描、MRI 等无创影像技术密切监控肿瘤变化。 - **GKI 测量工具**：利用家用血糖尿酮仪进行指尖采血，设备内置换算程序可直接得出 GKI 读数。 - **生化个体差异**：体内缺乏左旋肉碱会导致脂肪酸向酮体转化受阻，此类患者需要针对性的营养补充支持。 - **临床安全边界**：对于伴有基础疾病的患者，极度严格的生酮方案需在医生严密监控下平稳推进，切忌脱离医疗监督单独操作。 ### [01:40:04](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=6004s) 能量之源：为绝望者带来生机与民间研究资助 节目进入尾声，主持人抛出了每一期节目的传统保留问题：“在你的生命中，什么赋予了你最大的能量？什么又是你经历过最大的能量消耗？”塞弗里德毫无迟疑地回答，赋予他无穷力量的正是揭开生命本源奥秘的这一过程。大自然允许人类窥视人体运作的底层生物学与生物化学密码，而他们将这些知识转化为救治慢性病与癌症患者的工具，将过去含糊不清的“我在生酮”转变为精准可量化的 GKI 数字，让深陷绝望的病患重获生机。 塞弗里德动情地表示，这项研究的目的绝不是为了赚取数十亿美元的利润，而是为了让那些被主流医学判定死刑的患者活得更久。他经常收到三四年前被诊断为绝症的患者发来的邮件，惊喜地发现对方不仅健在，甚至刚刚陪妻子度完假回来，这种回馈是支撑他不断前行的核心动力。由于该方向与传统医药产业的商业模式存在根本冲突，塞弗里德的研究无法获得常规的官方或企业大额资助，其所有的实验室经费全部依赖于私人慈善机构（例如特拉维斯·克里斯托弗森的基金会等）。塞弗里德幽默而真诚地感慨：“如果有人曾被医生断言只能活 6 个月，而 6 年后依然健康地活着，不妨给支持我们工作的民间基金会投进几个便士。” - **资助渠道**：研究资金高度依赖民间慈善与非营利机构（如癌症代谢疗法基金会、伊丽莎白·安·韦瑟斯乳腺癌研究基金）。 - **学术输出**：塞弗里德团队持续在各类学术期刊发表同行评议论文，通过详实数据推动癌症认知的范式转移。 - **核心动力**：突破预后极限、延长晚期患者高质量生存期的真实临床反馈，构成了支撑研究的最主要精神能量。 ### [01:42:44](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=6164s) 肿瘤学界的误区与患者社群的情感支持 在探讨如何获取准确医疗信息时，托马斯·塞弗里德（Thomas Seyfried）教授直言，相较于心脏病学或骨科置换手术等领域已经达到最前沿的水准，现代肿瘤学界依然是一片充斥着错误认知与误解的“巨大荒原”（vast wasteland of misinformation or misunderstanding）。医生与专家们普遍未能理解癌症的线粒体代谢本质，导致大众难以在常规医疗体系中获得正确的指导。 主持人史蒂文·巴特利特（Steven Bartlett）回顾了双方此前的对话，指出上一期节目的传播规模极为惊人——在 YouTube 上突破了 1000 万次观看，各大音频平台也获得了约 500 万次播放，累计触达超过 1500 万人。更重要的是，节目不仅启发人们向医生提出更有针对性的问题，更在评论区自发形成了一个互助社区。史蒂文特别向听到这里的听众呼吁：一旦确诊癌症，独自面对互联网搜索、播客和 AI 工具往往是一段极其孤独、令人惶恐的旅程；他鼓励大家在评论区留下爱与支持，分享严谨求证过的有效资源，为深处逆境的人们提供情感依托。 - 主持人与塞弗里德教授的上一期对话全网播放量已突破 1500 万次（YouTube 达 1000 万次，音频平台约 500 万次）。 - 评论区成为了全球癌症患者与家属交流抗癌心路历程、缓解孤立无援感的情感绿洲。 --- ### [01:44:09](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=6249s) 自下而上的变革与终身不辍的科研使命 面对主持人的由衷赞誉，塞弗里德教授表达了感谢，并强调大众媒体在破除信息壁垒中起到了至关重要的桥梁作用。医疗体制本身极难自发改变，但随着越来越多成功的临床案例报告相继发表，公众对代谢疗法的认知与需求将形成一股自下而上的倒逼力量，最终推动整个抗癌体系的重塑。 塞弗里德教授明确表示自己绝不会停下脚步，波士顿学院（Boston College）的学生们对此充满热情并积极参与其中。他强调“科学素养”（scientific literacy）是每个人在现代社会中掌握自身健康命运的关键。播客在温馨的致谢与推荐下一期视频的结语中圆满结束。 - **自下而上的医疗变革路径**：真实临床成功案例报告的持续发表，将激发患者群体的强烈诉求，进而倒逼主流医疗体系升级。 - **年轻一代科研传承**：波士顿学院的学生正深入投身于癌症代谢疗法的基础与转化研究。 - **核心倡导**：普及大众科学素养，用求真严谨的科学逻辑武装患者，是摆脱疾病恐惧、重获健康主导权的根本力量。 ## Notable quotes > [00:00](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=0s) 谁能不恼火呢？这个国家每天有 1,700 人死于癌症，也就是每小时 70 人，而且情况每年都在恶化，人们究竟什么时候才能清醒过来？ — Thomas Seyfried > [15:00](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=900s) 在这个线粒体中，藏着来自数十亿年前远古细菌的遗传记忆。古老的细菌极其自私，只顾自己生长增殖，从不与外界沟通，与其他细胞毫无协同性可言。融合成为现代形态后，它学会了为了整个生物体的利益而生长；可一旦遭受损伤，它就退化回那种原始自私的生长模式，根本不在乎宿主的死活，这也就是癌症的本质。 — Steven Bartlett > [20:25](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1225s) 他们是专门研究癌症的人，而我只是个生物学家。 — Thomas Seyfried > [32:55](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=1975s) 我讲得足够清楚了吗？只要我能让你听明白，我们就能让每一个人都理解这个事实。 — Thomas Seyfried > [45:13](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=2713s) 我们要死了！我的血糖爆表了，肿瘤马上要疯狂生长了！ — Trudy Dupont > [53:01](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3181s) 我们可以偶尔踏足红区，但绝不能终身定居在红区。 — Thomas Seyfried > [54:37](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=3277s) 我只谈论在自己实验室中经过严格测试并发表过学术论文的成果。现代肿瘤学界至今没有认清的是：癌细胞脱离了葡萄糖和谷氨酰胺根本无法生存，且它们绝对无法切换到利用脂肪酸或酮体维持生命。 — Thomas Seyfried > [01:08:07](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4087s) 为癌症筹了那么多钱，问责机制究竟在哪里？人们什么时候才能清醒过来？你绝不可能通过对一个人进行辐射和下毒来让他们恢复健康！ — Thomas Seyfried > [01:19:10](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=4750s) 吃任何你想吃的，只要测试你的代谢数值，看它落在图表的哪个区间。 — Thomas Seyfried > [01:40:04](https://www.youtube.com/watch?v=kBm8Ho-_RXM&t=6004s) 如果有人曾被医生断言只能活 6 个月，而 6 年后依然健康地活着，不妨给支持我们工作的民间基金会投进几个便士。 — Thomas Seyfried ## Mentioned Thomas Seyfried, Steven Bartlett, The Diary Of A CEO, Otto Warburg, Albert Szent-Györgyi, Christos Chinopoulos, Jaime Arismendi-Morillo, Albert Schweitzer, Bob Kaplan, Trudy Dupont, Derek Lee, Pablo Kelly, Dominic D'Agostino, Valter Longo, Nick Lane, Doug Wallace, Veral Simck, Andrew Scarborough, Joe Maroon, Giordano Bruno, Nicolaus Copernicus, Galileo Galilei, Johannes Kepler, Claudius Ptolemy, Ted Kennedy, John McCain, Beau Biden, Travis Christofferson, Frontiers in Science, Cancer as a Metabolic Disease, Keto-Mojo, MORE 联盟 (Metabolic Oncology Research and Education), Boston College, Semmelweis University, National Cancer Institute (NCI), American Cancer Society, International Agency for Research on Cancer (IARC), Foundation for Cancer Metabolic Therapies, Elizabeth Ann Weathers Breast Cancer Research Fund ## Video description 1,700 Americans will die from cancer today. 70 every single hour. Professor Thomas Seyfried says it doesn't have to be this way, and that mainstream oncology has misunderstood cancer for 100 years. Thomas Seyfried, PhD, is a professor of biology at Boston College and one of the world's leading researchers on the metabolic origins of cancer. He is author of the book 'Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer' and co-developer of the Glucose Ketone Index (GKI) and the “press-pulse” therapeutic strategy. He explains: ◼ Why he believes cancer is a mitochondrial metabolic disease, not a genetic one ◼ Why cancer cells feed on two fuels and the strategy his team uses to starve tumors ◼ How a ketogenic diet lowers your GKI and makes chemo and immunotherapy work better ◼ The environmental drivers quietly damaging your mitochondria ◼ How his team is keeping glioblastoma patients alive for years, and why almost no patient is ever told this option exists The views expressed are those of the guest, and this conversation is intended for general informational purposes only. This podcast and its associated materials should not be used as a substitute for professional medical advice, diagnosis, or treatment. 00:00:00 Intro 00:02:42 The New Discovery About Cancer 00:03:43 What Role Do Mitochondria Play in Cancer? 00:08:12 ATP & Fermentation: How Your Cells Make Energy 00:15:00 The Oncogenic Paradox Finally Explained 00:20:19 Ghost Mitochondria: Cancer Under the Microscope 00:25:19 Glucose & Glutamine: The Fuels That Feed Cancer 00:26:32 Why Do Children & Babies Get Cancer? 00:29:25 Why Wealthy Countries Have More Cancer 00:32:55 Is Cancer Genetic? 00:37:58 The Prescription: The Glucose Ketone Index 00:40:23 How Stress & Poor Sleep Fuel Cancer 00:44:54 What's Inside the Confidential Envelope? 00:45:58 The Patient Who Inspired the Discovery 00:50:25 Measuring Your Glucose Ketone Index Live 00:53:01 The 'Red Zone' Link To Cancer 00:58:02 The Man Who Survived Glioblastoma for 10 Years 00:58:55 Using the Keto Diet to Supercharge Chemo 01:07:32 The Experiment That Could Prove Cancer Isn't Genetic 01:08:30 1,700 Cancer Deaths a Day: Seyfried's Warning 01:13:41 Seyfried's Plan to End the Cancer Epidemic 01:16:25 What Foods You Should Actually Eat 01:21:58 Fasting Protocols & Hitting 'The Wall' 01:26:48 Hyperbaric Oxygen Therapy & Cancer 01:28:30 Microplastics & 'Forever Chemicals' 01:30:47 How Cancer Spreads: Metastasis Explained 01:37:27 The #1 Actionable Takeaway 01:39:45 Energy, Hope & Final Words Independent Fact Check: https://stevenbartlett.com/wp-content/uploads/2026/07/DOAC-Dr.-Thomas-N.-Seyfried-Independent-Research-Further-Reading.pdf Thomas Seyfried's Metabolic Health Assessment: https://stevenbartlett.com/wp-content/uploads/2026/07/Proposed-glucose-ketone-index-GKI-zones.webp Thomas' latest research paper https://link.thediaryofaceo.com/7btDwc6 Follow Professor Thomas: ◼Instagram - https://link.thediaryofaceo.com/1MRuOwr ◼X - https://link.thediaryofaceo.com/DDF9xxr ◼Substack - https://link.thediaryofaceo.com/HKsGFcF ◼ Professor Seyfried's Biology Department - https://link.thediaryofaceo.com/HKwWhwD ◼ Foundation for Cancer Metabolic Therapies - https://link.thediaryofaceo.com/6Ehj3Hh ◼ Elizabeth Ann Weathers Breast Cancer Research Fund - https://link.thediaryofaceo.com/Bf10aHy A message from Professor Seyfried: “If you would like to support research on the mitochondrial metabolic theory of cancer, please consider donating to our research. Please remember that no donation amount is too small or too large.” The Diary Of A CEO: ◼ Join DOAC circle here - https://doaccircle.com/ ◼ Buy The Diary Of A CEO book here - https://smarturl.it/DOACbook ◼ The 1% Diary is back - limited time only: https://bit.ly/3YFbJbt ◼ The Diary Of A CEO Conversation Cards: https://linkly.link/2hm7r ◼ Get email updates - https://bit.ly/diary-of-a-ceo-yt ◼ Follow Steven - https://g2ul0.app.link/gnGqL4IsKKb Sponsors: Wispr - Get 14 days of Wispr Flow for free at https://wisprflow.ai/steven Eight Sleep - http://eightsleep.com/steven use code STEVEN for up to $350 off. 30-day at-home trial. Free returns. Ekster Link: https://link.thediaryofaceo.com/GSNEWnm [Source](https://www.youtube.com/watch?v=kBm8Ho-_RXM)

[0:00] Thomas Seyfried: 谁能不恼火呢？这个国家每天有 1,700 人死于癌症，也就是每小时 70 人，而且情况每年都在恶化，人们究竟什么时候才能清醒过来？ [15:00] Steven Bartlett: 在这个线粒体中，藏着来自数十亿年前远古细菌的遗传记忆。古老的细菌极其自私，只顾自己生长增殖，从不与外界沟通，与其他细胞毫无协同性可言。融合成为现代形态后，它学会了为了整个生物体的利益而生长；可一旦遭受损伤，它就退化回那种原始自私的生长模式，根本不在乎宿主的死活，这也就是癌症的本质。 [20:25] Thomas Seyfried: 他们是专门研究癌症的人，而我只是个生物学家。 [32:55] Thomas Seyfried: 我讲得足够清楚了吗？只要我能让你听明白，我们就能让每一个人都理解这个事实。 [45:13] Trudy Dupont: 我们要死了！我的血糖爆表了，肿瘤马上要疯狂生长了！ [53:01] Thomas Seyfried: 我们可以偶尔踏足红区，但绝不能终身定居在红区。 [54:37] Thomas Seyfried: 我只谈论在自己实验室中经过严格测试并发表过学术论文的成果。现代肿瘤学界至今没有认清的是：癌细胞脱离了葡萄糖和谷氨酰胺根本无法生存，且它们绝对无法切换到利用脂肪酸或酮体维持生命。 [68:07] Thomas Seyfried: 为癌症筹了那么多钱，问责机制究竟在哪里？人们什么时候才能清醒过来？你绝不可能通过对一个人进行辐射和下毒来让他们恢复健康！ [79:10] Thomas Seyfried: 吃任何你想吃的，只要测试你的代谢数值，看它落在图表的哪个区间。 [100:04] Thomas Seyfried: 如果有人曾被医生断言只能活 6 个月，而 6 年后依然健康地活着，不妨给支持我们工作的民间基金会投进几个便士。

[33:25] Thomas Seyfried: If I can make you understand this, we can make everybody understand this. [34:25] Young offender (quoted by Steven Bartlett): I can't listen to that episode because the words you used were too big. [43:14] Steven Bartlett: What is in that envelope in front of you? [85:06] Thomas Seyfried: standard of care [88:49] Thomas Seyfried: press-pulse [97:37] Thomas Seyfried: GLP-1 inhibitor [100:04] Thomas Seyfried: few shekels [100:04] Thomas Seyfried: hope to the hopeless

[0:00] You have an envelope in front of you [0:01] there that says confidential on the [0:03] front of it. What is in that envelope? [0:04] >> It's a paper that's under embargo [0:06] because the world thinks it's going to [0:07] be very important and it's going to be a [0:09] lead article in the frontiers in science [0:11] because this is a strategy to manage [0:13] cancer effectively and we have a lot of [0:15] evidence to keep these people alive a [0:17] hell of a lot longer. We have given hope [0:19] to the hopeless [0:20] >> and you have a perspective on treating [0:22] cancer and other metabolic diseases that [0:24] others don't have. [0:25] >> Yes. But the problem is the field [0:27] doesn't understand what I'm saying about [0:29] the origin of cancer. So everything [0:31] comes back to mitochondria and all [0:33] chronic diseases in cancer are the [0:35] result of damage to this and the science [0:37] is telling us this. But the field of [0:38] cancer has yet to accept it. That is a [0:42] tragedy. [0:42] >> Are you pissed off about this? [0:43] >> Well, who wouldn't be? There's 1,700 [0:46] people a day in this country dying from [0:49] cancer. That's 70 an hour. And it gets [0:51] worse every single year. When is the [0:53] people going to wake up? So give me a [0:55] prescription of how I should live my [0:57] life to keep my mitochondria healthy. [0:58] >> So it all comes down to what you do to [1:01] maintain the health and vitality of the [1:02] mitochondria that reduce the risk. But [1:05] we are now in a new environment where we [1:07] have massive amounts of highly processed [1:08] carbohydrates, inactivity, emotional [1:11] stress, poor sleep habits and you [1:13] chronically damage this organel. And [1:15] then if you look at the domestic dog, [1:17] cancer is the number one killer of the [1:18] domestic dog. But wolves in the wild [1:20] rarely have cancer. But the wolf is out [1:23] running around eating natural foods. Yet [1:24] the dog is in an apartment somewhere [1:26] gets a dog walker once a day, right? And [1:28] the next thing the dog is obese and full [1:30] of cancer. [1:31] >> And I want to give people actionable [1:32] things that they can think about. [1:33] >> So this is what's really important. This [1:35] is a bioenergetic road map to health. [1:38] This is what we call the zone of [1:39] prevention. It's very hard to get cancer [1:41] or chronic diseases when you're in these [1:43] zones. [1:44] >> So let's talk about that. [1:45] >> So [1:48] this is super interesting to me. My team [1:49] given me this report to show me how many [1:51] of you that watch this show subscribe. [1:52] And some of you have told us according [1:54] to this that you are unsubscribed from [1:56] the channel randomly. So favor to ask [1:58] all of you, please could you check right [1:59] now if you've hit the subscribe button [2:01] if you are a regular viewer of the show [2:02] and you like what we do here. We're [2:04] approaching quite a significant landmark [2:05] on this show in terms of a subscriber [2:07] number. So, if there was one simple free [2:09] thing that you could do to help us, my [2:11] team, everyone here, to keep this show [2:13] free, to keep it improving year over [2:15] year and week over week, it is just to [2:17] hit that subscribe button and to double [2:18] check if you've hit it. Only thing I'll [2:20] ever ask of you. Do we have a deal? If [2:22] you do it, I'll tell you what I'll do. [2:23] I'll make sure every single week, every [2:26] single month, we fight harder and harder [2:27] and harder and harder to bring you the [2:28] guests and conversations that you want [2:30] to hear. I've stayed true to that [2:31] promise since the very beginning of the [2:32] DEO, and I will not let you down. Please [2:36] help us. Really appreciate it. Let's get [2:37] on with the show. [2:40] [music] [2:41] [singing] [2:42] >> Professor Thomas Seaf Freed, what is it [2:45] that you've committed your life to [2:46] doing, Thomas? [2:47] >> Well, we're right now committed our [2:50] lives to managing cancer effectively [2:53] uh without toxicity which is based on [2:56] based on the science that I and other [2:59] others have done in this field. [3:01] >> You have a perspective on treating [3:02] cancer and other metabolic diseases that [3:04] others don't have. the mainstream should [3:07] I say. [3:08] >> Oh yeah. Well, mainstream doesn't have [3:09] it for sure. But it's based on science. [3:11] I mean I'm my work is based on what Otto [3:15] Warberg the famous German scientist said [3:18] from the 1920s30s and 40s. He clearly [3:21] showed that cancer was a mitochondrial [3:23] metabolic disease. [3:25] >> What does that mean mitochondrial [3:27] metabolic disease? [3:28] >> Okay. It means that the origin of the [3:30] disease resides in the organel called [3:33] the mitochondrian. It's it's in the [3:36] cytoplasm of the cell. It used to be [3:39] called still is the the powerhouse of [3:42] the cell. Gives the cell the energy. [3:44] >> I think we have a mitochondria. Could [3:45] one of my team bring in a mitochondria? [3:47] >> Well, this is you have a a mitochondria [3:50] in here. Oh, here we go. [3:51] >> You got one each here. [3:52] >> Yeah. Well, see, this is the little [3:53] organel that you see. It looks like a [3:56] bean shape, but it's actually a tubular [3:58] network. These are tubes [4:01] >> and they respond dynamically inside the [4:04] cell to uh both internal uh activities [4:08] as well as external activities. So you [4:11] have to realize that at the time of [4:13] conception [4:15] uh all of the mitochondria for the [4:17] developing embryo are in the cytoplasm [4:20] from the mother. [4:21] >> The cytoplasm [4:22] >> the mitochondria are not in the nucleus. [4:24] They're in the cytool. Oh, outside of [4:26] the [4:26] >> outside of the nuke, but in the cell [4:28] body itself. So all of the mitochondria, [4:31] they determine our destiny. They will [4:33] determine how long you will live on the [4:35] planet if if you don't have an [4:37] unfortunate accident or something like [4:39] this. They have an expiration date. [4:41] Different species die at different [4:44] times. You don't find people living 400 [4:46] years. Mice live about two and a half [4:48] years. Elephants live, you know, as long [4:50] as we do or whatever. But that's all [4:52] determined by this organel. So you can [4:54] see I have wrinkles and this kind of [4:56] thing. This is from living on the planet [4:58] and this is from wear and tear on this [5:00] organel which allows us to make energy [5:04] efficiently. [5:05] >> So when this organel starts to falter [5:07] with age uh you die you die from old [5:10] age. This organel has to be protected [5:13] and respected if you would like to live [5:15] a normal lifespan. But in diets and [5:18] lifestyles and way we are today we we we [5:21] damage this organel and this organel [5:24] then can present itself damage to this [5:26] organel which is a tubular network [5:28] inside the cell. But let me say [5:30] something else. It not only controls the [5:33] internal environment of the cell. It [5:35] also controls the neighboring cells. The [5:38] liver neighborhood the lung neighborhood [5:40] the colon neighborhood the brain [5:41] neighborhood the gal neighborhood the [5:43] neuron neighborhood. But they're all [5:44] come from the same origin in that [5:46] cytoplasm and they determine the overall [5:50] metabolic health of your body. It's a [5:52] systemic they communicate [5:54] uh with each other across cells across [5:56] tissues. I'll tell you this organel [5:59] controls [snorts] a lot of what goes [6:02] what that nucleus does. It tells the [6:04] cell when to divide. It tells the cell [6:08] when to slow down. [6:09] >> It's kind of like a brain but also like [6:10] an engine room. [6:12] >> It's kind of like that. Certainly [6:13] certainly the brain part of it is really [6:16] mysterious uh in the sense of of how it [6:20] controls the destiny of the cell in the [6:22] body. So sickness [6:25] sickness disease cancer what do we know [6:28] about the role that this little thing [6:30] plays in these chronic diseases and [6:32] illnesses and cancers that so many [6:33] people suffer with? [6:34] >> Yeah. Well, this is the organel that [6:36] becomes damaged. Um and it can be [6:38] damaged in many many different ways. uh [6:41] for cancer is what [clears throat] we [6:43] have spent a lot of our time on and now [6:46] we've moved into the whole chronic [6:47] disease issue because each each chronic [6:50] disease can have different [6:52] manifestations of ill health to the [6:55] mitochondria in a particular population [6:57] of cells. But in the case of cancer [6:59] which is what we call the most serious [7:02] of the chronic diseases creating the [7:05] most trauma uh the most emotional [7:08] distress but we have clearly shown based [7:12] on on many many works that any multiple [7:17] things from our environment can damage [7:19] this organel in a particular population [7:22] of cells in a particular organ. For [7:24] example, when you talk about [7:26] carcinogens, [7:27] it's a chemical that causes cancer. How [7:30] does that chemical cause cancer? It [7:32] damages the proteins and the lipids. [7:36] These little squiggles are delicate [7:39] internal membranes. They they contain [7:42] the proteins and the lipids that allows [7:44] us to generate energy when we breathe. [7:47] Okay, you're breathing. I'm breathing. I [7:49] take in oxygen. Oxygen serves as a kind [7:53] a a final acceptor for electrons that [7:56] allows ATP uh to come out of this little [7:59] and don't forget it's a tubular network [8:01] >> and ATP is the energy currency. [8:03] >> It's the chemical energy currency. It [8:05] allows us to enzymes to work allow [8:08] allows all the metabolic machinery [8:10] inside of a cell to work optimally. [8:12] >> So just to play this back to you so I [8:14] know I'm clear. Oxygen comes in because [8:16] I breathe in. I then eat food [8:18] >> in in that mitochondria. It does a [8:20] process and it spits out ATP as the [8:22] energy. [8:23] >> Well, and and the waste products of a [8:25] good energy metabolism would be CO2 and [8:28] water. So, when we burn gasoline in an [8:31] engine of a car, we break down the [8:33] octane, the carbon hydrogen bonds in an [8:35] octane and and we have an internal [8:37] explosion that drives pistons. Okay? The [8:40] exhaust is a lot of waste products uh [8:42] from breaking down the M that we're [8:44] doing the same thing inside the cell. [8:46] We're combusting carbon hydrogen bonds [8:49] and that combustion of carbon hydrogen [8:51] bonds is a graded process. So it's not [8:54] an immediate explosion. It's a it's a [8:56] you're you're breaking down the carbon [8:57] hydrogen bonds in a very precise way [9:00] producing ATP which then drives the [9:02] entire machinery of the neurons and the [9:04] rest of the body. [9:06] >> It can respond dramatically to energetic [9:08] stress, emotional stress. Anyway, I gave [9:11] you an example of a carcinogen uh [9:13] intermittent hypoxia like people who [9:16] have sleep apnea. They stop breathing [9:18] for 30 seconds or more in that general [9:20] and then they that creates rust RO and [9:23] that's what carcinogens do ROS. These [9:26] are called reactive oxygen species. They [9:29] damage those delicate membranes. And [9:32] then what happens if it's too acute, too [9:36] stressful, the whole cell will die. the [9:38] cell loses its energy and we get uh [9:41] apoptosis or necrosis cell death. But if [9:45] it's gradual chronic over years, months, [9:48] years, this organel [9:51] loses its ability to produce sufficient [9:53] energy. But the the cell compensates [9:58] interestingly enough by using these [10:00] ancient pathways heirlooms of our [10:03] evolutionary past. So um because all [10:07] life on the planet evolved in in oxygen [10:11] but without oxygen in the dark uh these [10:14] cells grew like crazy. There was no they [10:16] were single cells. They unbridled [10:18] proliferation and all this kind of [10:20] stuff. They didn't have mitochondria. [10:22] They had bacteria and the bacteria [10:25] which this organel came from was a [10:27] fusion between one cell uh that had a [10:31] nucleus and and was was fermenting [10:35] through the cytoplasm and this bacteria [10:37] which is the mitochondria came in and [10:39] now you have two different forms of [10:42] energy. You have um the energy in the [10:44] cytoplasm, the ancient fermentation, and [10:47] then you have this new form which can [10:48] take in oxygen and generate energy much [10:50] much more efficiently than the airlumic. [10:53] Listen, one of our big discoveries, if [10:56] you can believe it. But you see that [10:58] space in the middle there? [10:59] >> Yeah. [11:00] >> That's called the matrix. And that's [11:01] where the KB cycle, the TCA cycle, which [11:04] breaks down the food that we eat. But [11:07] they have an ancient part of a [11:09] fermentation mechanism inside because [11:11] before oxygen came every all life forms [11:14] were fermenttors. They they produced [11:16] energy without oxygen because there was [11:18] no oxygen. We had to wait for those [11:20] bacteria to make oxygen through a [11:22] photosynthetic process. But all [11:24] organisms were fermenttors in the [11:26] beginning after this organel came in and [11:28] was able to take in oxygen make energy [11:30] really really quick. But in that matrix [11:32] they have a uh in the cycle there's a [11:34] little pathway there that makes energy [11:37] without oxygen from the evolutionary [11:39] past. So we have it in the cytoplasm of [11:41] the cell because they can use they can [11:43] ferment in the cytoplasm. But this organ [11:46] that our big discovery with the work of [11:48] of Christounis from semlice university [11:51] he's the world leader on that little [11:53] pathway. When this organel becomes [11:57] impaired, [11:58] these ancient pathways of energy through [12:01] fermentation arise. Okay, they they try [12:04] to replace the lost energy from the [12:06] efficiency of this organel. That space [12:09] starts throwing out ATP [12:12] from glutamine. It's another [12:14] fermentation fuel and and it's making [12:18] it's making ancient energy in the [12:20] sophisticated organel that was that was [12:23] that that evolved to make efficient [12:25] energy. So let me let me tell you. So [12:28] you get you asked me what about damaging [12:30] this organel and what happens if the [12:33] damage to oxidative phosphorilation [12:35] >> what does that mean? [12:36] >> Which means energy through oxygen [12:38] [clears throat] [12:38] >> is too acute the cell will die. [12:43] Cyanide is a a perfect example of this. [12:46] You take a mouse or a rat or a person [12:48] and you drink Kool-Aid, the cyanide [12:50] laced Kool-Aid, you die because what [12:52] happens is that cyanide binds to the [12:55] protein that's going to um um use oxygen [12:59] for energy and the whole system shuts [13:01] down. [13:02] >> Suffocates you basically. [13:03] >> Yeah. You die in instantly. Um and there [13:05] are other things that can kill uh can [13:07] kill uh quickly aid and a variety of [13:10] other chemicals but for chronic diseases [13:12] it's usually u not an acute stress on [13:16] this organel it's a it's a chronic [13:18] stress and in cancer what happens in a [13:21] particular tissue whether it's bone lung [13:24] bladder brain they gradually compensate [13:27] with these ancient fermentation pathways [13:30] so so this thing this organel cell [13:35] signals to the nucleus I'm suffoc I'm [13:38] not getting enough energy. Um so the [13:41] nucleus turns on the transporters on the [13:44] surface of the cell to bring in fuels [13:48] that will elevate energy through what we [13:50] call uh oxygen independent mechanisms. [13:53] This is an oxygen dependent organel. [13:55] This gets most of its energy because we [13:57] breathe, all of our cells are using [13:59] oxygen and the CO2 that we're blowing [14:01] out and the water that will be collected [14:03] in the form of urine when you might put [14:05] uh other waste products in there. That's [14:08] efficient metabolic homeostasis. This [14:10] organel makes not only the cell but the [14:13] whole body in a state of of metabolic [14:16] homeostasis where all systems are [14:18] working at optimal efficiency. But with [14:21] chronic disruption, uh, smoking, uh, [14:25] lack of exercise, you can go right down [14:26] the list of all of the different things [14:28] that can elicit cancer, any kind of [14:31] carcinogens, microplastics, forever [14:33] chemicals, uh, uh, uh, glyphosate and [14:37] any of these kinds of things that would [14:39] chronically damage uh, the ability of [14:41] this organel to produce energy. Viruses, [14:44] ankcoenic viruses, inflammation. you [14:46] have chronic inflammation. Any of those [14:49] things damage this the sophisticated [14:52] ability of this organel to produce [14:53] sufficient energy. That's why that's why [14:57] um uh the ankcogenic paradox which we [14:59] solved. [15:00] >> What's the ankcogenic paradox? [15:01] >> That was the paradox that was first put [15:03] out by Albert St. Gorgi Hungarian [15:05] [clears throat] [15:06] uh scientist who received a Nobel Prize [15:08] I think for vitamin C. He said he said [15:11] he was very interested in cancer and [15:13] living systems. He said there's a [15:15] paradox. He said we know multiple things [15:19] in the environment can elicit cancer. [15:21] We've identified these ankcogenic [15:23] viruses, chronic inflammation, [15:25] carcinogens, intermittent hypoxia, rare [15:29] rare germline mutations. He said we [15:32] don't understand [15:33] the common pathophysiological [15:36] mechanism by which any of those [15:39] provocative agents would elicit [15:42] disregulated cell growth which is [15:44] cancer. When you talk about cancer, what [15:46] do people say what is cancer? It's cell [15:48] division out of control. It's [15:51] disregulated cell growth. This organel [15:55] determines when cells should divide and [15:57] when they should not divide. It [15:59] regulates the destiny of the cell. So [16:02] what happens when this organel becomes [16:04] chronically impaired? It falls back on [16:07] these ancient pathways, these or or [16:10] these or um uh pathways that existed [16:13] before oxygen came into the environment [16:15] where all the cells were disregulated in [16:17] the growth because they didn't have this [16:19] regulatory system which is the [16:21] mitochondria coming from a from a [16:23] bacteria. [16:23] >> So let me play that back to you in a way [16:24] just so I you know make sure I [16:25] understand. [16:26] >> I I know it can be kind of deep. [16:27] >> Okay. So in this mitochondria here that [16:30] I have in front of me, there is an [16:32] ancient um because this came from the [16:36] >> bacteria [16:36] >> a fusion of bacteras a long long time [16:38] ago. [16:39] >> Yeah. [16:39] >> The old bacteria [16:40] >> about several billion years ago [16:42] >> used to be very selfish and just think [16:44] about itself. It used to grow on its own [16:45] and didn't communicate with anybody. Had [16:47] its own way of growing and multiplying [16:49] that was really not um in cohesion with [16:51] anything else. That is still in there [16:54] somewhere. And although now in its [16:56] modern form because there's been that [16:58] fusion it grows thinking about the wider [17:01] organism [17:02] um when it becomes damaged [17:06] it falls back on that old selfish way of [17:08] growing and sometime and that's kind of [17:10] what can cause cancers. So if you if [17:13] there's stresses on this which could be [17:15] all the car carogenic things you [17:17] described then sometimes this falls back [17:20] on that prehistoric selfish way of [17:22] growing where it doesn't think about the [17:24] wider organism. [17:25] >> It's close um um in the sense of [17:29] thinking we don't know about that we [17:31] just know the consequences of what [17:33] happens when it falls back on those [17:35] ancient pathways. Now here's the [17:37] situation. [17:39] People knew from Otto Warberg said [17:42] cancer is a energy problem in the cell. [17:46] This why would the cells start to [17:49] ferment and produce a massive amount of [17:52] fermentation waste product which is [17:53] lactic acid. Even in the presence of [17:57] oxygen, 100% oxygen, they're still [17:59] fermenting. Why? That shouldn't happen. [18:02] Uh when you and I hold our breath or [18:04] have a heart attack, let me tell you [18:05] something. This is really remarkable and [18:07] this is another piece of information [18:09] that got us on this whole thing. When [18:11] people have heart attacks, uh they stop [18:14] breathing, the heart seizes, okay, the [18:16] bloodstream immediately fills with these [18:19] fermentation waste products which are [18:21] lactic acid and the other one which we [18:25] now know is suinic acid. Okay. Wow. [18:28] These two waste products. Now, if you [18:30] don't start breathing in a short period [18:33] of time, you're going to be dead. [18:34] >> Mhm. And you and what you die because [18:36] the neurons in your brain cannot sustain [18:40] this kind of fermentation energy for [18:42] very long. As soon as you the heart you [18:44] you give them cardiac massage and [18:46] whatever the guy's heart starts beating [18:48] again. The lac the waste products [18:51] of lactic acid and suinic acid go away. [18:54] They disappear because you're breathing [18:55] now. You don't need to ferment when you [18:57] have oxygen in the environment. And it's [18:59] and the mitochondria can can utilize the [19:01] oxygen in the environment. cancer cells [19:04] to Warberg said it's the weirdest thing. [19:07] These cancer cells um continue to [19:11] ferment even in 100% of oxygen. Why are [19:14] they doing that? And he speculated that [19:17] this organel was damaged. Irre [19:20] irreversible damage to the organel [19:23] happened in these cancer cells. He [19:26] didn't have an electron microscope at [19:28] the time. He didn't have the [19:30] sophisticated tools that we have today. [19:32] So he projected that all on biochemistry [19:35] at that time. He was a biochemist and he [19:37] said you don't should not produce [19:39] fermentation if you have ox oxygen [19:41] should shut that off and these guys [19:43] should return to a normal metabolic [19:44] homeostasis. And he said that's because [19:46] there's something irreplace irre [19:48] irreversibly damaged in this organel. So [19:51] a lot of people attacked him and they [19:52] said oh we don't have any evidence for [19:54] that. Here's the beautiful thing. Some [19:56] cancer cells continue to take in oxygen [19:58] and make ATP. Therefore Warberg must be [20:00] wrong. Uhhuh. We showed that that we [20:04] showed the cancer cell takes in oxygen, [20:06] but it's not making energy through ATP [20:08] in any great amount. It's using it for [20:10] ROS react these radicals that further [20:13] damage and cause the DNA mutations that [20:15] everybody is chasing. It's all [20:17] downstream effects of damage. [20:20] >> So what does this what does this mean in [20:21] simple terms? Because I'm aware a lot of [20:22] my [20:22] >> Well, it it means I say, okay, so so I [20:25] have disregulated cell growth. That's [20:27] ultimately what the problem we're [20:29] dealing with. We can't control how these [20:31] cells are dividing. We're throwing all [20:33] kinds of crazy stuff at them. Trying to [20:34] poison or radiate surgically remove [20:36] them. We're trying to do everything to [20:38] stop this disregulated cell growth. [20:40] >> Mhm. [20:41] >> So when we look at this organel under [20:43] the micro under the electron microscope, [20:45] we find these cry are often missing. You [20:47] have what they call ghost mitochondria. [20:49] You got the shell but nothing inside or [20:51] if they're inside, they're all deformed. [20:53] So we know there's a foundational [20:55] principle in biology. Structure [20:57] determines function. If the structure is [21:00] abnormal, the function will be abnormal. [21:02] This is known to all biologists except [21:05] oncologists. They don't seem to [21:07] understand it. [21:07] >> What's an oncologist? [21:08] >> Those are the people who study cancer. [21:11] >> So, what are you then? [laughter] [21:12] >> I'm a biologist. [21:14] >> You're a biologist. [21:15] >> Yeah. I mean, when we know that if the [21:17] organel is damaged, you're not going to [21:18] be able to produce energy efficiently by [21:20] oxidative phosphorilation. Okay. [21:22] >> I think you're a bit further down the [21:24] road, Thomas, than a lot of my viewers [21:25] are. for me hearing that there's this [21:27] energy engine in my cells that and [21:30] there's trillions of them or billions of [21:32] them and they also communicate with each [21:34] other and when this becomes stressed or [21:38] hurt or damaged because of lifestyle [21:40] choices that I make energy production [21:42] and inefficiency will change and that [21:44] could cause this to die or malfunction [21:46] in some way that is as for me I go I've [21:49] got it [21:49] >> okay that's a major step forward now we [21:53] build upon that yes now we build upon [21:55] that okay so so here's the situation [21:58] we've discussed cancer cells all of them [22:01] that we have ever looked at have defects [22:04] in the number structure and function of [22:07] that organel okay I have looked at I [22:10] published that big paper where I spent [22:13] uh over a year of my time going through [22:16] the ancient the well the early electron [22:18] microscopy literature warberg didn't [22:20] have that opportunity because that [22:22] technology was not there for him. So he [22:25] speculated that based on the [22:26] biochemistry, but I went back and I [22:29] looked at these um electron microraphs [22:31] of mitochondria in various cancers and [22:33] they're all damaged. There is few of [22:35] them that risk Christ are gone. I work [22:38] with some of the best like Aris Aris [22:40] Mendy Marillo uh who is a world leader [22:42] in beautiful electron microscopy of of [22:44] cancer cells and you can see and and all [22:47] the damage uh under his magnificently [22:49] beautiful and one we have a couple of [22:51] papers but let me tell you something [22:52] else Stephen in the cytoplasm these [22:55] organels are also in contact with other [22:58] cellular membranes like the endopplasmic [23:00] reticulum there's a lot of we call [23:01] organels inside a cell you have the [23:04] nucleus you have the mitochondrian [23:07] you you you have loss. There's intimate [23:10] contacts between some of the other [23:11] membranes, mitochondrial associated [23:14] membranes we see and they're also [23:16] abnormal when you look at them under the [23:18] electron microscope. [23:19] >> The ones it's talking to are abnormal. [23:21] >> Yeah. The ones you can see the the [23:22] mitochondria are abnormal and the [23:24] membranes that contact them are [23:25] abnormal. Okay. And that intimate [23:27] contact [23:28] >> uh I'll get into the calcium signaling a [23:30] little bit later which controls the [23:32] destiny of the cell. Why the cell is [23:34] growing out of control? Well, first of [23:36] all, it's fermenting. Okay, that means [23:37] it's getting energy from sources other [23:40] than oxidative phosphorilation. You can [23:41] take a cancer cell and and treat it with [23:44] cyanide or aid or in absence of and it's [23:47] still living. It's still growing because [23:49] it's not using [23:50] >> the oxygen path. [23:51] >> They're not using the oxy falling back [23:53] on on on oxygen independent mechanisms [23:56] which are called fermentation. So I [23:58] understand that to be that there's a [24:00] malfunction in a mitochondria which [24:02] means that it no longer uses its oxygen [24:04] pathway [24:05] >> as sufficiently as it should. There's [24:07] always some residual level [24:08] >> and it finds another way to make the [24:10] energy which is how it survives. [24:11] >> Yes. [24:11] >> And then it stops communicating with the [24:13] rest of the cell. [24:14] >> Well, it actually communicates with the [24:15] nucleus [24:16] >> to open up the floodgates to bring in [24:18] the fuels that drive this fermentation [24:20] energy. [24:21] >> It gets more and more greedy. It it has [24:23] to because you're you're taking an [24:25] organel that produces energy highly [24:27] efficiently. Okay. Um like 34 to 36 ATPs [24:32] >> with oxygen [24:33] >> with oxygen. And now you're you're [24:35] trying to replace that with fuels that [24:38] give you two uh two moles of energy. Uh [24:42] >> so it's inefficient [24:43] >> very and then and then you get you get [24:45] two out of the in so you're getting [24:46] four. So you you you have to take in in [24:49] order to make up the efficiency you must [24:52] have a tremendous logistic you must have [24:54] tremendous supply [24:56] >> of [24:56] >> of the fuels that will give us energy [24:58] >> which are [24:59] >> glucose the sugar [25:01] >> and the amino acid glutamine [25:03] >> okay [25:03] >> okay our bodies are loaded with [25:05] glutamine that's the most abundant amino [25:06] acid in our bloodstream and evolution [25:08] provided that for us because if we stop [25:11] breathing we use that fuel to keep the [25:13] cells alive we our gut is controlled by [25:16] glutamine Our immune system uses [25:18] glutamine. [25:19] >> What is glutamine? [25:20] >> It's an amino acid. Okay. [25:22] >> Which we make from food. [25:23] >> Yeah. Which we can make from food. True. [25:25] Or they call essential and non-essential [25:27] amino acids. Essentials are from that we [25:30] must eat. We must have certain foods [25:31] that provide these. Glutamine is [25:33] considered a non-essential amino acid. [25:36] It's an essential amino acid [25:37] biochemically called non-essential [25:39] because we can make it from sugar. [25:42] >> But basically, it's the most abundant [25:44] amino acid in our body. I think I get it [25:46] now. [25:47] >> Okay, feed me back. Tell me, let me let [25:49] me test you. There should be a button [25:52] just down below here. And if it says [25:53] subscribed, you're already subscribed. [25:55] If it says subscriber, that means you're [25:58] not yet. And if you're not subscribed, [25:59] please could you do us a favor and hit [26:00] that button? It helps the show more than [26:02] you know. And according to the [26:03] algorithm, you're someone that watches [26:05] our show, but you haven't yet hit that [26:06] button. Thank you so much. [26:08] When we fall, the mitochondria falls to [26:11] that prehistoric pathway where it starts [26:13] making energy in a really really [26:14] inefficient way without using oxygen in [26:17] the same way. It starts relying now on [26:20] glucose and glutamine um to produce that [26:22] energy which is a much less efficient [26:24] source of energy. So it gets a bit more [26:26] greedy. It needs much more to make the [26:28] same amount of ATP which is energy. [26:30] >> Mh. [26:30] >> So these a cancer cell can be very very [26:32] greedy. It's not responding to oxygen in [26:34] the same way and they they're a bit more [26:36] selfish. they start they start sort of [26:38] multiplying without thought of the [26:40] broader organism. [26:41] >> Yes. Yes. [26:43] >> So the question I have is how does this [26:45] happen? [26:46] >> Malfunctioning of the m what is it that [26:48] I've done? You know what I ask this [26:50] question? [26:50] >> Okay. Well, I Okay. [26:51] >> It's because children can get these [26:53] cancers [26:54] >> or a 90-year-old can get the cancer. And [26:57] it doesn't appear to me that a [26:58] three-year-old [27:00] has necessarily made life choices yet [27:02] that could [27:02] >> but as I said when you consider forever [27:05] chemicals uh that are in the environment [27:08] uh things that we have that we use in [27:11] our technologically advanced societies [27:13] can get through the placental wall and [27:16] get these into the ch into these [27:17] children's uh organs. Um you know you [27:21] have to put it together. We usually it's [27:23] a a constellation of things because [27:26] don't forget I said carcinogens. Some of [27:27] these carcinogens are fat soluble. Some [27:29] of these carcinogens can get in and [27:31] damage those during early stages of [27:33] development. People always say how you [27:35] explain brain cancer in in a in a [27:38] six-month old baby. Okay. What what did [27:41] he what what he he wasn't smoking and [27:43] drinking and partying all the time, but [27:45] but his the mitochondria and a [27:46] population of cells in his brain became [27:49] damaged. And that damage then led to [27:51] this disregulated cell growth because [27:54] the organel controls when cells should [27:56] divide and not divide. And then and then [27:59] where's the energy coming from? How do [28:01] you how do you take a highly [28:03] sophisticated piece of an organel and [28:05] making energy so incredibly efficient [28:08] and now we're using energy. [28:10] So uh this organel signals to the [28:13] nucleus called mitochondrial stress [28:15] response retrograde signaling. The [28:17] nucleus acts as a respondent to what [28:20] this organel wants. So the nucleus then [28:22] ankco genes which that you've heard a [28:25] lot about. They open the floodgates to [28:27] bring in the glucose and glutamine that [28:30] allow the cell to grow in a disregulated [28:32] way. So we've as you said they go back [28:35] to these ancient fermentation pathways [28:37] where there was no regulation because [28:39] this organel was not part of the problem [28:41] part of the situation the regulation. So [28:43] is there what are the lifestyle factors [28:45] that are causing this to were [28:46] drastically increasing the probability [28:48] of this happening. [28:49] >> It's not necessarily what the person did [28:51] or all cases it's what the person was [28:54] exposed to uh that could have elicited [28:57] this. That's the ankcoenic paradox. So [29:00] uh we have shown uh that inflammation [29:04] produces these cytoines when you have an [29:07] inflammatory heat in inflammation they [29:10] they damage the ability of this organel [29:12] to make energy efficiently. Chronic [29:14] inflammation is known to be a risk [29:17] factor for cancer. Chronic inflammation [29:21] intermittent hypoxia carcinogens. [29:23] >> What's intermittent hypoxia? [29:25] >> It's like the sleep apnea that kind of [29:27] thing. [29:28] Warberg had clearly shown that [29:30] intermittent hypoxia on cells would [29:32] damage the efficiency of oxidative [29:34] phosphorilation leading to a [29:36] compensatory fermentation. So you have [29:38] to compensate because let me tell you if [29:40] you don't compensate you're dead. The I [29:43] mean the cell dies. When we look at the [29:45] populations around the world that have [29:47] the most prevalence of cancer, it [29:49] doesn't appear to be [29:52] some of the [29:54] countries like Nijer, Gambia, Nepal [29:57] consistently rank at the very bottom for [29:59] cancer cancer incidents. Conversely, [30:02] high-income countries like Australia, [30:03] New Zealand, and the United States have [30:05] the highest rates of cancer. Why is [30:08] that? [30:09] >> It's because of our um technology. Uh we [30:12] are still paleolithic man and uh our [30:16] biology [30:18] has allowed us to store energy [30:21] efficiently [30:23] uh because of times of famine. We are [30:25] now in a new environment where we have [30:27] massive amounts of highly processed [30:29] carbohydrates, inactivity, emotional [30:31] stress, we have poor sleep habits. You [30:34] you pile all those together with availab [30:38] the exposure to carcinogens and whatever [30:41] and you chronically damage this organel [30:44] and uh [clears throat] in some organs [30:46] you can get breast cancer if it's a lung [30:48] if it's a whatever it is that organel [30:51] becomes chronically damaged in some [30:53] populations of cells in a particular uh [30:56] in a particular organ and and you can [30:58] elicit disregulated cell growth as the [31:01] result of that. You know what I find is [31:04] in in that in the paper that we have [31:06] with the chart uh if you can keep your [31:09] mitochondria healthy because don't [31:11] forget Paleolithic man our ancestors [31:13] from 500,000 years ago uh or modern men [31:18] like you said in these countries living [31:20] according to traditional ways with [31:22] minimal in interference from modern diet [31:25] and lifestyle issues have lower amount [31:27] of cancer in general and this is what [31:29] Albert Schwitzer found the the famous [31:32] humanitarian physician. He was [31:34] specifically looking for cancer in [31:35] African tribes and he said remarkably [31:38] it's extremely low. What what are these [31:40] guys doing where western society has has [31:43] a lot of cancer and these Africans have [31:45] living living according to the [31:47] traditional ways. So they have a lot of [31:49] exercise. They're eating all organic [31:50] foods. Uh they're not under the same [31:52] kind of stress or exposure to chemicals [31:54] that modern societies have. And you find [31:57] out you have very low cancer. Like for [31:59] example, uh dogs are all evolved from [32:01] the wolf. Uh wolves in the wild rarely [32:05] have cancer. The domestic dog, cancer is [32:07] the number one killer of the domestic [32:09] dog. What is the dog doing that the [32:11] wolf? The wolf is out running around [32:12] eating natural foods. The dog the dog is [32:14] in an apartment somewhere gets a dog [32:16] walker once a day, right? And the next [32:19] thing the dog dog is obese and full of [32:20] cancer. So it all it all comes down to [32:24] what what you do to maintain the health [32:26] and vitality of the mitochondria that [32:28] reduce the risk and that's what this [32:30] chart I'll show you has reduce the risk [32:33] of damaging this chronically. Okay. So [32:36] that can explain in large part why [32:39] modern societies are struggling with [32:42] chronic diseases not only cancer we have [32:44] diet type 2 diabetes we have obesity we [32:46] high blood pressure we we have a whole [32:48] even neuroscsychiatric problems. If you [32:51] can protect and keep this organel [32:53] healthy, you reduce risk. Now people [32:56] say, well, cancer has to be genetic [32:58] because we have inherited genes that put [33:01] us at higher risk like the Bracka one [33:03] for breast cancer and the leaf ramen for [33:05] variety of other cancers. Our paper in [33:08] this pile done by Bob Kaplan uh he went [33:11] through uh and looked at all the genetic [33:14] risk. [33:14] >> Which paper is it? [33:15] >> Um it's one of the ones published in [33:17] oncology. But none of these mutations [33:20] are 100% penetrant, meaning that they're [33:23] secondary risk factors. A primary risk [33:25] factor would be every time that mutation [33:27] is there, 100% of the people because I [33:29] work in Tesax's disease. I work in [33:31] inborn errors of metabolism. Those [33:33] mutations are 100% responsible for that [33:35] condition. There's no gene mutation [33:37] that's 100% pen. You have that gene, [33:39] you're going to 100% get cancer. Uh most [33:41] of them are are uh um are what they call [33:44] incompletely penetrint. So what does [33:46] that tell us about the nature of [33:47] >> well it tell and then we went back what [33:48] Bob did is he went back and he looked at [33:51] what every one of those gene mutations [33:54] in some way disturbs the efficiency of [33:57] oxidative phosphorilation in that [33:59] organel [34:00] >> in the mitochondria [34:01] >> in the mitochondria we we looked at we [34:02] have all the evidence all the risk [34:04] factor all the genetically just just the [34:07] front page there I was going to show you [34:09] the hard data but you got [laughter] so [34:11] anyway that all of them damage this the [34:14] efficiency of energy through through [34:15] through this organel. So that's like [34:18] carcinogens, that's like um viral [34:22] infections. The viruses that like [34:24] hepatoma and papilloma, they they their [34:27] their products will go in here and [34:28] damage it or they will replicate inside [34:30] this organel, screwing up the [34:31] efficiency, causing a compensatory [34:34] fermentation, causing the disregulated [34:37] cell growth through abnormal calcium [34:39] signaling, causing cells to no longer uh [34:42] be responsive to their neighbors. Is [34:44] that clear? If I can make you understand [34:46] this, we can make everybody understand [34:47] this. [34:48] >> Yeah. So, the the reason I uh spend a [34:50] lot of time asking why and asking for [34:52] clarification is because when I do the [34:55] show, I then go out into the real world [34:56] and I meet the people that listen. [34:57] >> Yeah. [34:58] >> And one of the groups of people that [34:59] listens are young offenders. And when I [35:01] went and visited them, I pointed at the [35:03] episodes that I thought would help them. [35:04] Yeah. And a young one of the young [35:05] offenders said to me, "I can't listen to [35:07] that episode because the words you used [35:08] were too big." [35:09] >> And I remember thinking to myself, [35:10] >> "Okay, that I get that all the time, but [35:12] guess what? Now we have AI and you can [35:15] take this statements and put it into AI [35:19] right on the and and it'll it'll it'll [35:22] dumb it down for you. [35:23] >> So So that's a tool that we previously [35:26] did not have. [35:27] >> So So I use that all the time. I said [35:30] when you hear me speak like this, don't [35:31] think I'm arrog [35:33] I I I these are the terms that we use [35:35] when you're part of the academy. Yeah. [35:37] >> Okay. But we can take those terms now [35:39] and AI can do a wonderful job in in in [35:41] synthesizing. Oh yeah, I know what he's [35:43] talking about now. But without that [35:45] tool, then it becomes like you said, [35:47] well, I can't understand anything. [35:49] >> I've got 60 seconds and I'm going to [35:51] show you how much I can get done because [35:53] of our sponsor called Whisper Flow. And [35:56] for those of you that don't know what it [35:57] is, it's a business I invested in that [35:59] turns your speech into text in any app [36:01] or device. I'm going to post into our [36:03] Slack channel, which rewards whichever [36:05] team member conducted the most [36:06] experiments this week. Hi everyone, here [36:08] is this week's experimentter of the [36:10] week. Congratulations to the Dire of SEO [36:13] trailer team which is Aunt, Liv, Dom, [36:16] and Cam. You guys have won. Okay, now [36:19] I'm going to open Gmail. So, here is one [36:21] of our founders on an email chain that I [36:22] want to connect my team with. All I have [36:24] to say is add my team's emails, and [36:27] Whisper will do exactly that. Now, a [36:30] quick message to Juan, who does my [36:31] schedule every single week. Hey, Juan, [36:33] can I record on Wednesday at 2? [36:35] Actually, no. Do you know what? Let's [36:36] record at 3 p.m. on Wednesday. Whisper [36:39] Flow is four times faster than typing [36:41] and it is incredibly easy to use. So, if [36:43] you want to give it a go, all you have [36:45] to do is head to whisperflow.ai/stephven [36:48] to download it today. If you know me and [36:51] if you've listened to this podcast [36:52] before, you'll know how obsessed I am [36:54] with sleep. I've been on a bit of a [36:55] journey with sleep. I see it as the [36:57] single most important thing that I'm [36:58] have the privilege of having control [37:00] over. And that's exactly what our [37:01] sponsor eight are. It's a very, very [37:04] intelligent piece of material to sleep [37:06] on. Here's what the Eight Sleep Pod [37:08] does. It monitors your body while you're [37:11] sleeping. And with their AI, it adjusts [37:14] the temperature for you using billions [37:17] and billions and billions of hours of [37:18] sleep data. And members have reported up [37:21] to a 34% deeper sleep and falling asleep [37:25] up to 44% faster. Me and my fianceé [37:29] Melanie sleep on different parts of the [37:31] bed and it adjusts my part of the bed to [37:33] my body and her part of the bed to her [37:36] body. So if you want to learn more about [37:37] this pod, go to 8 sleep.com/stephven. [37:42] Big opportunity. I am not kidding. Give [37:44] it a try. I really want to just make [37:46] sure I tick off the box of um cause [37:50] factors. So you mentioned stress, [37:53] >> you mentioned sleep. [37:55] >> I currently don't have cancer as far as [37:57] I'm aware. God forbid. Um but I but I [37:59] want to do everything I can to prevent [38:00] the probability. Yeah. [38:02] >> And I from what I've understood that [38:03] means protecting my mitochondrial [38:05] function. [38:06] >> Yes. [38:06] >> By living a lifestyle where I'm not [38:08] creating this sort of like crazy [38:09] oxidative stress on the mitochondria. [38:12] >> Right. [38:12] >> So give me a prescription of how I [38:14] should live my life to keep my [38:16] mitochondria healthy. [38:17] >> Well, that's why we developed the [38:18] glucose ke ketone index calculator. the [38:20] first biomarket tool that can allow [38:22] people to know the level of health of [38:24] their mitochondria because [38:27] um when you shift from carbohydrate fuel [38:30] to lip lipid fuel, [38:31] >> what's lipid fuel? [38:32] >> Fat. [38:34] >> So ketones, [38:35] >> ketones are a water- soluble breakdown [38:37] product of fatty acids. [clears throat] [38:39] >> Okay. So we store atapose tissue. We [38:42] store fat [38:43] >> which is the belly fat [38:45] >> all over. We have fat on our [38:47] >> on the outside. [38:48] >> Yeah. So on the outside that was there [38:50] because as a species we had to survive [38:54] in the most harsh environments and we [38:57] were um food was not always there. So we [39:00] had to survive all kinds of famine all [39:02] kinds of absence of food. Our bodies are [39:04] so our it's a machine that was home over [39:09] millions of years to be super efficient. [39:11] So glucose is gold sugar. Okay. You [39:16] either burn it or you can store it as [39:18] fat. Okay, that's that's the key. But [39:21] when you have you're not bringing in [39:23] sugar, that stored fat now moves into [39:25] the bloodstream, goes to the liver, and [39:27] it's like taking a branch and putting it [39:29] in a chopper and you outcome these [39:32] little soluble ketone bodies. They're [39:34] breakdown products of longchain fatty [39:36] acids. They can replace sugar for the [39:38] brain, for the muscles, for most other [39:41] cells in the body except ariththraittes, [39:43] but they can replace they can replace [39:46] the energy of glucose. Okay? So, uh, and [39:50] that's how we evolved. But we're now in [39:52] an environment where we have massive [39:54] amounts of highly processed [39:56] carbohydrates and we we don't want to [39:59] pee them out unless you have diabetes or [40:01] something. So, we store them as fat. So [40:03] we have an obesity epidemic as the [40:06] result of our evolutionary ability to [40:08] store energy which kept us alive as a [40:10] species because if we were unable to [40:12] store the fat in 500,000 we would have [40:14] all been extinct. You and I this [40:16] conversation would never exist. [40:17] >> We would never have existed as a species [40:19] except for our ability to store energy [40:22] and we burn energy efficiently in these [40:23] organels. So this is all a very highly [40:27] efficient machine. So when we lose that [40:29] ability, uh when we have so much energy [40:32] in the environment, stress, no exercise, [40:34] all this, we store more and more fat, we [40:37] produce an an environment that's very [40:40] damaging to this organal. [40:41] >> Well, say that again. So how does stress [40:43] impact that? [40:44] >> Stress elevates corticosteroids. When [40:46] you're under stress, you get into a [40:47] fight, you get into an argument, or [40:49] you're stressed out by business deal [40:51] going bad, whatever. uh corticosteroids [40:55] elevate elevate blood sugar contributing [40:57] to uh systemic inflammation. It's okay [41:01] for a short period of time to be pissed [41:03] off at something. But it's the chronic [41:04] stress, the chronic like looking at the [41:07] cell phone, doom scrolling, all this [41:08] kind of crazy stuff while eating the big [41:10] Twinkie, doom scrolling, eating [41:11] Twinkies, not moving. All of this [41:13] creates uh stress on this organel in [41:17] some population of cells. [41:19] >> It makes it work harder. It's damaging [41:21] because you produce reactive species [41:23] that damage the efficiency of this [41:25] organel to produce energy effectively [41:28] and that either will kill the cell [41:31] gradually if it can't comp use [41:33] compensatory fermentation or predispose [41:36] you to cancer. So either way is [41:39] unhealthy. So we have chronic disease. [41:41] Cancer is the number one big dog in the [41:43] chronic disease world. I mean it's the [41:44] one that people fear the most. um type [41:47] two diabetes, cardiovascular disease, [41:50] you know, dementia, uh all of these are [41:53] part of damage to this organel in one [41:55] way or another. In like I said for [41:58] Parkinson's disease, when that organel [42:00] gets damaged, the cells of the [42:01] substantion aigrate die. They are [42:03] incapable of compensating with [42:05] fermentation. So they up and die. Cancer [42:08] is very rare in neurons of the brain. [42:10] Neurons the gal cells of the brain form [42:13] these brain tumors mostly but neurons [42:15] [clears throat] can't compensate with [42:17] fermentation so they die. So you you [42:19] either get comp compensatory ancient [42:21] fermentation leading to disregulated [42:23] cell growth which we call cancer or we [42:25] get cell death leading to chronic [42:27] diseases. [42:27] >> What about sleep then? What's going on [42:29] with sleep that's causing [42:30] >> sleep is a way we can restore the energy [42:32] efficiency of the mitochondria [42:33] >> if we're well slept. [42:34] >> If we have good sleep. Yeah. You know [42:36] everybody feels good when you have a [42:37] good night's sleep. your body feels [42:38] rejuvenated because you're not you're [42:40] not stressing out. You're reducing the [42:43] ability of this organel to manage the [42:46] the the the metabolic uh environment. uh [42:49] if you're up all night and you're and [42:50] you're like stressed out and you're [42:52] never given this uh organel in a [42:54] particular cell in a particular part of [42:56] the organ of the body, you know, you you [42:59] get neuroscychiatric problems, you can [43:01] get digestive problems, you can get [43:03] cancer, you can get type 2 diabetes, you [43:06] have a whole and we put it in the paper [43:08] there, all the different stress, all the [43:09] different things that can chronically uh [43:11] or acutely damage oxidative [43:13] phosphorilation. [43:14] >> So sleep basically gives the [43:16] mitochondria a little bit of a break. [43:17] Yes. It's a it's it gives your whole [43:19] body a break, let's be honest. So, so, [43:22] but you you pile those things on [43:24] together. Lack of exercise. Our [43:26] ancestors, what do you think our [43:27] ancestors, you know, how hard it is to [43:28] run down and kill a big buffalo or a [43:30] woolly mammoth? I mean, you're you're [43:32] exhausted after doing something. As a [43:34] matter of fact, you chase these animals, [43:37] uh, you separate. And this is another [43:38] thing that was really interesting. Came [43:39] out of Israel. I think it was last year. [43:42] They looked at the cavemen, what they [43:43] were eating. they were eating the the [43:45] strongest members of the herd uh leading [43:48] to the indirect extinction of these [43:50] animals. They found out that if you can [43:52] eat the strongest member of the herd, [43:55] you'll get the vitality of that uh of [43:57] that or buffalo or elephant or whatever [44:00] the hell they were eating because they [44:01] knew the marrow and the and the the [44:04] physiology of that of that organism at [44:07] that point in its life could provide you [44:09] with the strength that that had. Now, [44:11] when you eat the strongest members of [44:13] the herd because you want to be tough, [44:15] you're putting the old and the young at [44:17] vulnerable to predators leading to the [44:19] extinction. Uh, and this is what a big [44:22] paper came out of out of uh, Israel. [44:24] They looked at these cavemen, what they [44:25] were eating like 500,000 years ago or [44:27] whatever they're doing. So, humans [44:28] indirectly caused extinction of other [44:30] species in part in not in part because [44:33] they were eating the toughest guys in [44:34] the herd. So, because they felt that if [44:37] I eat those guys, I'm gonna be strong [44:39] too. And in a way, they're right. But [44:41] all of it has to do with the energy [44:43] efficiency of your muscles, your brain, [44:45] your ability to be resilient, endurance. [44:49] I'm telling you, these guys were [44:52] chiseled. They they weren't dying from [44:54] type 2 diabetes, cancer, right? [44:57] Dementia. They were dying from [44:58] infections and injuries and child [45:01] mortality. Uh we're mostly killing our [45:03] paleolithic ancestors. But when you [45:06] bring your body back into a low glucose [45:07] ketone, you're actually going back like [45:09] you were. This is why we developed the [45:11] glucose ketone index. [45:13] >> What is in that envelope in front of [45:14] you? [45:15] >> Well, this is um it's a paper that's [45:16] under embargo because they they think [45:18] it's going to be the world thinks it's [45:20] going to be very important and um and it [45:23] is. [45:24] So, and what it is, this is a [45:28] um a way to keep that organel healthy. [45:31] So this is a way to manage uh um energy [45:36] efficiency in the body. [45:37] >> And this hasn't been released yet. [45:39] >> It hasn't been released. Okay. It's [45:41] coming out. It's a it's going to be a [45:42] lead article in the frontiers in [45:44] science. And not only that, we the paper [45:47] the paper was written [45:50] uh for the scientists and then the [45:53] journal decided to make a second copy [45:55] for they call young minds. So letting [45:58] kids that are like 8 to 12 or 14 years [46:00] old synthesize it down and and and one [46:04] of my colleagues said that's probably [46:05] what most people will be reading because [46:08] they don't want to know about the [46:09] bioenergetics that actually goes on [46:11] inside this organel to explain why this [46:14] chart means something. [46:15] >> And you've been working on this for some [46:16] time. [46:17] >> Well, I I I built the GKI. So let me [46:19] tell you the story. There was a woman uh [46:21] an American woman a lawyer Trudy Dupant [46:24] who uh developed um a kind of a brain [46:27] stem tumor and after I wrote my book [46:30] that book there that's my only book [46:32] anyway Trudy Trudy wanted to use this [46:35] metabolic therapy she stayed alive much [46:37] longer over 10 years with this we kept [46:40] the she eventually passed away [46:41] unfortunately but so I was measuring [46:44] because we knew that the tumor cells [46:47] needed sugar to grow out of Worberg [46:49] showed that and many other people show [46:51] that and they can't burn ketones because [46:54] because the fatty you need a very [46:57] efficient mitochondria to burn ketones [47:00] for energy. Our normal cells can burn [47:03] ketones for energy and that gives us [47:05] tremendous uh uh we can actually breathe [47:08] lower oxygen more energy if you have [47:10] efficient if you can burn ketones [47:12] efficiently in this organel. But if the [47:14] organel is damaged, they can't use the [47:16] ketones. They can't burn fatty acids or [47:18] ketones, which stores lipid drops. It's [47:20] one of these big papers here. These [47:24] Stephen, you can't believe how people [47:25] misinterpret information. They see [47:27] droplets of fatty acids in the cytoplan [47:29] say, you see the cancer cell needs all [47:30] that fatty acid. No, they can't. It's [47:32] there to protect them. If they try to [47:33] burn it, they blow this up and die. So [47:35] there is a storage of fat. They can't [47:37] burn fatty acids or ketone bodies. So, I [47:39] knew cancer needed glucose, and I knew [47:41] cancer couldn't burn fatty acids or [47:43] ketones because this organel is is [47:45] broken. [47:47] So, I'm measuring glucose and ketones [47:50] independently in Trudy. She's doing the [47:53] finger prick thing, sending me the [47:56] information back and saying, "Oh, here's [47:58] my glucose. Here's my ketones." [48:00] >> Okay, so I have a a ketone glucose [48:02] reader in front of me. [48:03] >> Right. Right. [48:04] >> If I put my blood on this strip, it [48:06] tells me my glucose levels. If I put my [48:08] blood on this strip, yeah, it tells me [48:09] my ketone levels. [48:10] >> Right. Right. But if you if you look at [48:12] them independently, [48:14] >> glucose is very volatile, very variable. [48:17] >> And this is why I developed the glucose [48:19] ketone ratio because Trudy had a parking [48:22] spot that was for handicapped because [48:25] she had a cane. Her brain stem gloma was [48:28] preventing her from walking as [48:30] effectively as normal people. So she [48:32] somebody took her parking spot. She was [48:35] So she ran upstairs and took [48:39] her blood sugar and it was 186 milligram [48:42] per deciliter. It was very very high. So [48:45] and I know she was on a ke ketoic diet [48:48] and and she emails me and says I'm going [48:50] to die. My cancer is going to grow fast. [48:51] What's going on? She said my blood sugar [48:53] is like 186 and you know it's supposed [48:55] to be you told me it was supposed to be [48:56] 60 or you know 50 65 or in that zone. [48:59] She says so I said what's your ketone [49:00] level? Oh, it's still, you know, like [49:02] you just had point4 millmer or I think [49:05] it was 0.9 millmer. I said, well, that [49:07] didn't change, right? No, just the sugar [49:09] changed. So, I said to the students that [49:12] were working with Josh Fidenbower, I [49:13] said, Josh, this this trying to measure [49:16] these two independently is a [49:18] You can't this is hard to figure out. [49:19] So, what we decided to do in miller [49:21] because glucose comes out in milligram [49:23] per deciliter whereas ketones come out [49:25] in millimmer. So we had to convert [49:27] glucose to millimmer and divide it by [49:29] the ketone in millimmer and then you get [49:31] a number that's not all over the world. [49:34] It's very stable. So so we were able to [49:38] because of Trudy that one cancer patient [49:41] we developed the ratio of of this. Then [49:44] later on we realized that this ratio is [49:47] a statement of how healthy your [49:49] mitochondria actually are. So when you [49:52] when you have these low ratio you're in [49:53] paleolithic man. you're back in the zone [49:56] where we didn't have chronic diseases [49:58] because we didn't have damage to the [50:00] organel that would cause those diseases. [50:02] So, paleolithic men think where are they [50:04] getting their pastries? Where where are [50:06] they getting their cakes and sweets and [50:08] all this other they didn't have it. They [50:10] weren't there because of of choice. They [50:12] were there because of circumstance. So, [50:14] our new and we learned paleolithic man [50:17] was always in some sort of a state of [50:20] some ketosis because they wouldn't have [50:21] food for periods. They were very active [50:24] in their exercise. They had they didn't [50:26] have chronic diseases, but they had [50:27] other kinds of diseases. So, so then um [50:31] my my my my student um Derek Lee, myself [50:35] and Christo Shinopoulos, we started to [50:38] make a ratio chart. Now, these are the [50:40] numbers that you get when you divide [50:41] your sugar by your ketones. [50:43] >> Okay. So, my sugar by my ketones. So, if [50:45] I did my glucose measure now on this [50:47] little [50:47] >> Okay, let's see what your GKI is. [50:49] >> Oh, you want me to do it? Okay. [50:50] >> Okay. What? You had a glucose. You had a [50:52] a ketone was 0.4 millmer. [50:54] >> Yeah. [50:54] >> Okay. What was your sugar? [50:56] >> I haven't. [50:56] >> So, we can divide. We can do the divi [50:58] division right now and tell you what you [51:00] have. [51:00] >> You can get these little uh ketone [51:02] >> Oh, yeah. It's a keto mojo. And you can [51:03] also get them now for for uh [51:06] >> Wow, these guys skilled at doing this. [51:08] >> I travel with one of these, [laughter] [51:10] believe it or not. [51:11] >> Yeah. [51:11] >> So, I I have one all the time. [51:13] >> Wow. [51:15] >> 90. [51:15] >> 90. Okay. So, you have to you have to [51:18] divide. You have to divide. You're not [51:19] getting the Doesn't this give you the [51:20] push button and give you the GKI right [51:22] away? Cuz the new ones have it. So, you [51:24] have to divide 90 by 18 and you get a [51:27] number. [51:28] >> Uh, five. [51:29] >> Five. So, divide five by 0.4. [51:32] >> 12.5. [51:33] >> Okay. So, here you are. [51:36] 12.5. You're down here in the in the in [51:39] the prevention zone. [51:40] >> Ah, nice. [51:41] >> Okay. So, so you This is where [51:44] Paleolithic man mostly lived. [51:46] Paleolithic man lived in the yellow [51:49] green zones because they didn't have [51:51] access to all of the things that would [51:53] drive up your blue blood sugar and keep [51:56] your key when your blood sugar goes [51:58] through the roof your ketones are really [51:59] low because insulin is now driving it [52:01] up. So So that's good. Um 12, huh? [52:05] >> So I I did the I did the carnivore diet [52:08] for a week. [52:09] >> Uh eating big ribe eyes. You like ribeye [52:11] steak? [52:12] >> Yes, of course. [laughter] [52:15] ribe eyes, bacon and eggs, lamb. I I so [52:18] I did it for a week and um I was able to [52:21] get down to 10. [52:23] >> Okay. [52:24] >> Okay. And I could get lower, but I was [52:25] loving the ribeye so much I ate a little [52:27] too much of it. Right. You have to [52:28] [laughter] be have some level of [52:29] discipline. Yeah. [52:30] >> So, [clears throat] uh so so but people [52:33] people this is what we call the zone of [52:35] prevention. It's very hard to get cancer [52:38] or chronic diseases when you're in these [52:40] zones because you're keeping this [52:41] organel quite healthy. When you live in [52:43] these zones consistently, [52:45] >> you you don't have to live consistently [52:47] because humans, we we evolved as a [52:49] scavenger species. We would engorgorge [52:51] ourselves because we knew it wasn't [52:53] happening every day. [52:54] >> Modern man is live is living in the [52:57] feast every single day. And that's why [52:59] we're are we have an out all the chronic [53:02] diseases. This is the red zone is the [53:06] zone of risk for chronic diseases and [53:08] cancer. And when you look at the obesity [53:11] epidemic, you look at all these things, [53:13] these guys are and it's it's like we can [53:16] visit the red zone. We don't want to [53:18] live in the red zone. [53:20] >> So if I was to visit the red zone, it [53:22] would look like meeting high [53:24] carbohydrate diets, lots of sugar. [53:26] >> Yeah. No exercise. [53:28] >> No exercise. [53:29] >> Yeah. And basically modern man. [53:31] >> And also eating five meals a day, like [53:33] snacking all the time. [53:34] >> Yeah. Oh, then you'd be, you know, we [53:36] have uh there's document cases. We have [53:38] them up to 500. [53:40] >> You can get GKIS of 500. [53:42] >> You have people with, you know, blood [53:44] sugars about 4 or 500 milligram per [53:46] deciliter. I mean, you could do the and [53:48] zero ketones. I mean, you you do the you [53:51] do the math. It's it's unbelievable. [53:52] >> You're basically saying, I want to keep [53:54] my my blood glucose levels [53:55] >> and you want to you want to have some [53:57] level of ketones [53:58] >> and high and my ketone levels somewhat [53:59] as high as I can. [54:00] >> Well, it's you don't want to go because [54:02] people then have the physicians [54:03] listening. They go, "Oh, he's going to [54:04] go with the keto acidosis." People give [54:06] me a break. Keto acidosis is like when [54:09] you have ketone levels of 15 to 20 [54:11] millmer. Are you kidding me? What is [54:13] yours? 0.4. That's called nutritional [54:15] ketosis. That's how we evolved. When you [54:18] have type 1 diabetes where you can't [54:20] control sugar or or or insulin, you have [54:23] no insulin responsive. You're going to [54:25] get high levels of sugar and ketones. [54:27] This is this is a pathological [54:29] condition. Most of type two diabetes, [54:32] these are all pathologies based on [54:34] damaging oxidative phosphorilation. So [54:37] what this chart does is for the first [54:40] time and we put it together because we [54:42] did all the B in the paper discusses the [54:44] bioenergetics. What we're finding in [54:46] cancer is that if you can get into the [54:49] green zones where your blood sugar is [54:51] low and your ketones are elevated, you [54:53] hammer the hell out of these tumor cells [54:56] because they they they you're taking [54:58] away one of their two primary fuels [55:02] driving disregulated cell growth. Okay? [55:05] And as the and as the and as the ketones [55:08] go up, the rest of your cells in the [55:10] body are getting super healthy. The [55:13] tumor cells can't tap into the value of [55:16] a ketone because the organel needed in [55:19] the tumor cell to do that is corrupted [55:22] structurally and functionally is am I [55:26] clear about that? [55:27] >> Yes. [55:27] >> Okay. So ketones will make you healthy, [55:30] the normal cells of your body, but [55:32] cannot be used to help the cancer cell [55:35] because you need a good structural [55:37] functional organel to burn them. So they [55:39] become marginalized and if the ketones [55:42] go up, they're actually toxic to that to [55:44] that cell to some extent. So but they're [55:47] still alive. Uh the cancer cells are now [55:51] incapacitated. [55:52] there. Uh we we showed you get rid of [55:54] the abnormal inflammation, you get rid [55:56] of the angioen, the abnormal blood [55:57] vessels. You're taking an angry tumor [56:00] and making it much less angry, much less [56:03] inflamed, uh uh more indolent uh kind of [56:07] a tumor, but it's still there. It's not [56:09] because the other fuel that's keeping [56:12] this cancer cell going is the glutamine. [56:14] Okay. So now when you have the patient [56:18] in this green zone, this is for [56:20] management. Now, Stephen, this is [56:22] prevention is is never having to deal [56:25] with what I'm talking about. If you're [56:27] living in the yellow zone, the [56:28] probability of getting cancer or chronic [56:31] diseases is already reduced. Okay? But [56:35] now you have some poor guy out there. [56:37] He's living in the red zone his whole [56:38] life. He wants to manage the cancer that [56:40] he has. He he has to get down in the [56:42] green zone and try to stay there as long [56:44] as he can. But the cancer will still [56:46] grow because it has access to glutamine. [56:48] Okay? And glutamine is always here's the [56:50] bloodstream. Look at look at you have [56:52] this much blood. Cancer needs that. So [56:54] you always have a surfitit of glutamine. [56:57] So you have to come in now with drugs [56:59] and the drugs like repurposed drugs to [57:02] target the the glutaminolysis [57:04] with this one here this BMC big paper [57:07] here. [57:07] >> Mhm. [57:08] >> Okay. This paper and the new one we have [57:10] with the ketogenic for the high [57:12] childhood um high-grade gloma for kids. [57:15] So once once you get down here, you come [57:19] in with drugs that target glutamine. [57:21] I've looked at one and that's Mbendazol. [57:24] Okay. How did I come to that [57:25] realization? People knew that embendazol [57:27] had some therapeutic benefit about [57:29] cancer, but they don't believe it until [57:30] you show the mechanism. That paper shows [57:32] the mechanism. It targets glucose and [57:34] glutamine. That was this one targets [57:36] glucose and glutamine, the two fuels [57:38] driving the disregulated growth of the [57:40] tumor. Okay. So here's the here's the [57:43] mitochondria. [57:45] So it's getting the glucose and the [57:47] cytoplasm from the sugar uh and making [57:50] and it's fermenting that and then also [57:52] the the amino acid glutamine comes in. [57:55] You have to block the glycolysis and the [57:57] gluc these two pathways. You have to [57:59] restrict availability of glucose and [58:01] glutamine together at the same time. [58:04] Yeah. [58:04] >> I speak only about things that I have [58:06] tested in my lab and published papers on [58:09] like this. So you have to real the [58:11] cancer field doesn't understand that the [58:14] cancer can't grow without glucose and [58:17] glutamine and can't switch to fatty [58:19] acids or ketone bodies. [58:21] >> That's still not going to kill the [58:22] cancer though, is it? It's just going to [58:23] >> Yeah, we don't ever use the term cure [58:25] because some of these tumors, now let me [58:26] tell you, we have people like Pablo [58:29] Kelly from Devon, England, he had the [58:31] glyobblasto [58:33] uh he didn't take any radiation or [58:35] chemo. He just did metabolic therapy. He [58:37] lived for 10 years. He was diagnosed [58:39] with an inoperable glyopblast. They [58:42] wanted to irdiate and poison him with [58:44] the drugs. He said no. He was one of [58:45] these naturalistic kind of guys. And um [58:49] he he lived for 10 years and the tumor [58:52] became operable. He had four debulking [58:54] surgeries on an originally described [58:56] inoperable cancer cut out four times [58:59] because once we put the metabolic [59:00] therapy the circle the demarcation of [59:02] the tumor. Whoa. A neurosurgeon says I [59:04] think I can get this out. But he never [59:06] never got rid he lived with it for 10 [59:08] years. Had a couple of kids. He died [59:10] from a cerebral hemorrhage on the last [59:11] debulking surgery. He never died from [59:13] the tumor. [59:13] >> But you're saying you're saying that the [59:15] two work together in in tandem. You're [59:17] saying that the chemotherapy works in [59:20] >> the Now that's where that's another [59:21] thing. So what we do u this is very [59:24] interesting. So if you put the patient [59:27] in nutritional ketosis, the the [59:29] ketogenic [59:31] state of nutritional ketosis facilitates [59:34] the delivery of drugs to the tumor cell. [59:37] It actually makes you can use lower [59:39] doses of drugs and you and and and you [59:43] get bigger effect. The therapeutic [59:44] benefit increases with lower dosing. [59:47] >> So you want to be in ketosis when you do [59:48] these chemotherapy, radiation therapy. [59:50] >> Yeah. And then you use much lower doses. [59:52] This is what we're doing in a stimul [59:54] clinic. We're taking pancreatic cancers. [59:56] These guys live in four and five years. [59:58] What are we doing? And advanced breast [60:00] cancer and all these terminal cancers. [60:02] We put them into some level of ketosis [60:04] and then you come in with the standard [60:06] drugs, cis platin, carboplatin, whatever [60:09] you want to do, but you cut the dosages [60:11] down big time and then they have tremend [60:15] the the uh and this is what the title of [60:17] the paper is ketogenic diet uh as a [60:22] metabolic vehicle [60:24] uh for enhancing therapeutic efficacy. [60:28] The current body of research suggests [60:29] that being in a state of ketosis can act [60:31] as a helper therapy, enhancing the [60:33] cancer killing effects of chemotherapy [60:34] while simultaneously protecting healthy [60:36] cells. [60:36] >> Yeah. Yeah. Right. Right. [60:39] >> Progressive oncologists are currently [60:40] using ketogenic diets alongside standard [60:42] chemo to maximize its efficacy. [60:45] >> That's right. That's what we're doing in [60:46] Istanbul [60:49] and and and also in in in Greece. We're [60:52] doing we're doing those same things. So [60:54] you you can use this [60:55] >> when you enter a fasted or ketogenic [60:57] state. Your healthy cells essentially go [60:58] into bunker mode. They slow their [61:01] division, conserve energy, and build up [61:02] their defenses. Cancer cells, however, [61:04] do not have this evolutionary off [61:06] switch. They continue trying to rapidly [61:08] divide. When the toxic chemotherapy [61:09] hits, your shielded healthy cells [61:11] survive it much better. While the [61:14] exposed rapidly dividing cancer cells [61:16] take the full hit. [61:18] >> Yeah. [61:18] >> Oh, okay. Interesting. [61:20] >> Yeah. In other words, you make with the [61:22] tools you have work better. The problem [61:24] in the field of cancer today is they're [61:26] not using the tools in the correct way. [61:29] Now, let me give you another example. If [61:31] you take imunotherapies, you hear about [61:33] these things, chimeic acid, G receptor, [61:36] PDL, PD1, PDL1 inhibitors, they're [61:39] called precision medicines, right? So [61:42] look, they're designed [61:44] to attack a a molecule on the surface or [61:48] stop that cell from uh being resistant. [61:51] >> Mhm. [61:51] >> If you would try to attack and what they [61:53] do often times, they come at after [61:55] you've failed chemo and radiation, they [61:57] then come at you with an imunotherapy. [61:59] The metabolic pressure shrinks down your [62:01] tumor, makes it very indolent, [62:03] >> non-aggressive, and the rest of your [62:05] body is healthy. You're not going bald. [62:06] You're not bleeding gums. Your [62:08] microbiome isn't blown to hell. So, and [62:10] then you can come in with lowdose chemo [62:13] imunotherapy because what'sever left in [62:15] that remaining residual mass, they may [62:18] all have something in common for having [62:20] survived all this, right? So now you can [62:23] come in with a precision medicine and [62:24] possibly resolution. I thought this was [62:27] fascinating. It says chemotherapy [62:28] creates massive oxidative stress, i.e. [62:30] damage inside the tumor. To repair the [62:32] damage and survive, the cancer cell [62:33] requires massive amounts of glucose. So, [62:35] if the patient is in ketosis, the [62:37] tumor's glucose supply is essentially [62:39] cut off. It can't the cancer cell can't [62:41] repair the DNA damage caused by your [62:43] chemo, leading to faster tumor death. [62:46] Um, yeah, interesting. [62:48] >> Well, don't forget also, listen to this, [62:51] and there's another thing people go in. [62:53] What protects the tumor cell from chemo [62:55] and radiation is the waste products of [62:58] fermentation. The lactic acid and the [63:00] suxinic acid that are dumped out of this [63:03] raging beast prevent these other [63:06] therapies from working. So if you want [63:08] your therapy to work, you got to target [63:11] those two fuels together at the same [63:13] time. And when you do that now this cell [63:16] the shield is off. These things are [63:18] super vulnerable to even low doses of [63:20] chemo and radiation. And the [63:22] imunotherapies, look at if you have an [63:24] imunotherapy, you try to attack the [63:27] beast when it's at its strongest. H [63:28] you're not going to win. And this is [63:30] what happens. You get only partial [63:32] response. They in the field of cancer [63:33] today, they think living an extra six [63:35] months is a major breakthrough. We're [63:37] talking about living an extra five and [63:39] six years. This is what's really [63:41] important. I just um I was reading some [63:43] research to figure out if oncologists so [63:47] cancer doctors are currently [63:48] recommending the ketogenic diet and it [63:50] says the vast majority of mainstream [63:52] oncologists do not recommend the [63:53] ketogenic diet to the to their newly [63:55] diagnosed patients. Um in fact if a [63:58] patient brings it up many doctors will [63:59] actively advise against it and the [64:02] reasons for that number one is the fear [64:04] of cacettia. Cexia. Yeah. [64:07] >> Cexia. Cancer. Cexia is a severe wasting [64:10] syndrome where patients rapidly lose [64:11] muscle and fat. It is a massive problem [64:13] and a leading cause of mortality in [64:15] cancer patients. Because the ketogenic [64:16] diet suppresses appetite and often leads [64:19] to weight loss. Encologists are [64:20] terrified that a strict keto diet will [64:22] accelerate cexia and weaken the patient. [64:25] >> Well, that's because they they have not [64:27] heard what I just said with respect to [64:29] the biology and biochemistry. Okay. [64:31] Cexia there's two ways you can lose in [64:34] cancer patients. CEXIA is the ability of [64:36] the tumor cell to mobilize energy out of [64:39] the muscles. It's taking the glutamine [64:41] out of your muscles and feeding. This is [64:43] one of the two fuels that's driving the [64:45] beast is glutamine. Where are they [64:47] getting the glutamine from? They're [64:48] getting the glutamine not only from the [64:50] bloodstream, but they dissolve your [64:51] muscles as a uh as part of that part of [64:55] that process. So, when you put a patient [64:58] in nutritional ketosis, [65:00] the weight loss is therapeutic weight [65:02] loss. CEXIA is pathological weight loss. [65:05] Now, the only way you can lose weight is [65:07] you take a high dose of chemotherapy. [65:10] I travel all the time. So, I made a rule [65:12] in my life that I'll only travel with a [65:14] cabin bag. The problem with this is [65:15] there's not much space. And here's the [65:17] solution. It is called an extra 1% [65:20] travel pack. And I teamed up with Extra [65:22] to make this. Typically, I can only [65:24] bring some of my black shirts. And it's [65:25] a trade-off of which black shirt should [65:26] I bring? How many of these do you think [65:28] I can get in here? So, let's try 1 2 3 4 [65:32] 5 6 7 8 9 10 11 12 13 14. Let's try 15. [65:41] 16 17 18 19 20 21 22 23 24. [65:46] Okay, so that's 24 black t-shirts. [65:49] Here's where the magic comes in. Zip it [65:51] up. Make sure it's nice and sealed. And [65:52] then you use this little contraption. [65:55] Stick it on there. I can now take more [65:57] than 20 black shirts with me, which will [65:59] last me 3 weeks. So, if you travel [66:02] frequently and you want to get one of [66:03] these so you can save more space and be [66:04] away for longer, go to extra.com and use [66:07] code DOAC for 10% off our collection. [66:10] And I think some of the background [66:12] context here is that mainstream oncology [66:14] operates on the um sort of sematic [66:16] mutation therapy, which is the belief [66:18] that cancer is fundamentally a genetic [66:20] disease driven by DNA mutations. And [66:23] because their training focuses on [66:24] genetics, their treatments are designed [66:26] to target DNA and cell division like [66:28] heradiation targeted genetic therapies [66:30] rather than manipulating um cellular [66:33] metabolism. And lastly, as mentioned, I [66:36] think we talked about this earlier, [66:37] mainstream medicine requires massive [66:39] multic-enter double blind phase 3 [66:41] clinical trials before a protocol [66:43] becomes the standard of care. So dietary [66:45] interventions rarely get the level of [66:47] funding. So on ancologists lack the [66:48] institutional green light to prescribe [66:50] them to patients and they tend to say to [66:52] them eat what you can. [66:54] >> I I don't blame them. They're good. Many [66:56] of them are good people. The problem is [66:58] the system doesn't train them to [66:59] understand the biology and biochemistry [67:01] of the disease they're treating. Uh some [67:03] of them become very resistant to this. [67:05] They say get angry because if I why [67:06] didn't I why wasn't I told this? Well, [67:09] first of all, they're not reading these [67:10] papers. Uh you ask them about it. They I [67:12] never read it. Well, how are you going [67:13] to know anything if you don't read the [67:14] literature? Um, listen to this. The [67:17] National Cancer Institute, the NCI, on [67:19] their website, on their website says [67:21] cancer is a genetic disease caused by [67:23] what you just said. Okay, they I well I [67:26] said why don't they put the articles in [67:28] there showing all the tumors they can't [67:30] find any mutations. The somatic mutation [67:33] theory says that cancer is caused by [67:35] random genetic mutations. So now new [67:39] sequencing of normal people like you and [67:42] me are finding mutations in all these [67:44] driver genes in cells in our body that [67:46] aren't in disregulated cell growth. So [67:48] we're calling them wild type cancers. [67:49] What do you mean a wild type cancer? [67:51] >> You lost me. [67:52] >> Okay. The nucleus of a tumor cell, a [67:54] raging tumor cell. [67:56] >> What's causing him that cell to grow? Is [67:58] it the mitochondria and the cytoplasm or [68:00] is it the mutations in the nucleus? [68:03] Okay. So according to the sematic [68:05] mutation theory, it's the mutations in [68:07] the nucleus that are causing the [68:08] disregulated cell growth. You take that [68:10] nucleus and put it into into a [68:13] enucleated normal cell. [68:15] >> Yeah. And there's no cancer. [68:16] >> No can there's no disregulation. [68:18] >> There must be something else. [68:19] >> Then you take the nucleus of the normal [68:21] cell and put it into the cytoplasm of a [68:24] tumor cell and you get disregulated cell [68:27] growth. [68:27] >> So it must be something other than the [68:28] nucleus. [68:29] >> Yes. The mitochondria. [68:30] >> Interesting. And it says [68:31] >> so with mitochondria controlling our [68:32] destiny and and and the the field of [68:36] cancer has yet to understand it, accept [68:40] it, and then say, "Well, we can't do any [68:42] of this until we double the line [68:43] crossover." That's just what do you [68:44] mean? The science is telling us this. [68:46] That's your way of protecting a broken [68:48] system. [68:49] >> Are you pissed off about this? Cuz you [68:50] do seem pissed off about this. [68:51] >> Well, who wouldn't be, [68:54] Stephen? [68:55] There's 1,700 [68:58] people a day in this country dying from [69:00] cancer. I don't know the English. [69:02] Listen, that that comes out to 70 an [69:04] hour. And it gets worse every single [69:07] year. And the last time I was on the [69:08] show, you guys use some old data. Look [69:11] it up today. It's 2026. American Cancer [69:14] Society says this year in 2026 we will [69:18] have 626,000 [69:21] souls leave the planet from cancer. [69:25] Okay, this 2026 and every year it gets [69:28] worse. So when you hear all the [69:30] breakthroughs, we have we have [69:32] television ads in Boston for the cancer. [69:35] Breakthrough after breakthrough after [69:37] breakthrough. All these different they [69:40] come on and and and and all we do is get [69:42] more dead cancer patients. Raise money [69:44] for cancer. Where's the where's the [69:46] accountability for all the money you're [69:48] raising? When are the work when is the [69:49] people going to wake up? You don't make [69:51] someone healthy by irdiating and [69:54] poisoning them. You've got to understand [69:56] the biology and the biochemistry of the [69:58] disease. I have the concepts and the [70:00] proofs, but the physician who works with [70:03] the patient on a clinic basis, they're [70:05] the ones that must apply this to the [70:07] clinic. So, there's two different things [70:08] here. There's the hard science that's [70:10] the that's the bedrock for this and then [70:13] there's the clinical person who has the [70:15] practice that practice does that. [70:17] Together, you get great success or [70:19] better I say success better than [70:20] anything that's out there today. The [70:22] American Cancer Society recently [70:23] released its latest projections for 25 [70:26] and 26, and the data paints a [70:28] fascinating dual-sided picture. More [70:30] people are getting diagnosed with [70:31] cancer. Um, new cases. The ACS projects [70:35] over 2.11 million new cancer diagnoses [70:38] in 2026. This translates roughly to [70:41] 5,800 new cases every single day. [70:44] >> Approximately 626,000 Americans are [70:47] expected to die from cancer in 2026. [70:50] >> Right. about 1,700 deaths per day. Lung [70:54] cancer remains the leading cause of [70:55] cancer death projected to cause more [70:57] fatalities than colurectal [71:00] >> colurectal and pancre pancreatic cancers [71:02] combined. I also just want wanted to [71:04] pick a point we were talking about [71:05] earlier which is about the metabolic [71:07] approach to cancers. [71:08] >> It says here and this is going to the [71:10] point about you know people telling you [71:11] to just eat whatever you want while [71:12] you're you know managing cancer. Um [71:15] because the primary goal of the hospital [71:16] dietitian is to prevent weight loss [71:18] during brutal chemotherapy regimes, [71:20] patients are frequently told to eat [71:22] whatever they can and eat whatever they [71:24] can keep down. It is incredibly common [71:25] for cancer patients to be handed meal [71:27] replacement shakes which are often [71:28] packed with corn syrups and refined [71:30] sugars, ice cream, and high carbohydrate [71:32] comfort foods just to keep their [71:34] calorific intake up. From a metabolic [71:37] perspective, this is a tragedy. While it [71:40] keeps weight on the patient, it [71:41] simultaneously floods the bloodstream [71:43] with glucose and insulin directly [71:44] feeding the tumor. Um, and while keto is [71:47] not the standard of care, the landscape [71:49] is beginning to slowly shift. There is a [71:52] growing minority of integrative [71:54] oncologists and specialized metabolic [71:56] clinicians worldwide that actively [71:57] prescribe therapeutic ketosis alongside [72:01] conventional treatments. Those doctors [72:03] use the keto diet and fasting protocols [72:05] to protect healthy cells and um and and [72:07] sanitize tumors before administering [72:09] lower more targeted doses of chemo. [72:12] Yeah, that's what we developed. That's [72:13] our that's our plan. That's that's what [72:14] we're doing. Okay. We we we do that [72:17] because we understand the biology and [72:18] biochemistry. And that's why we [72:20] developed we're developing the new [72:22] society called more the more alliance [72:24] metabolic oncology research and [72:27] education. This is bringing uh together [72:29] what you just mentioned there in a [72:32] logical approach to manage cancer. This [72:34] is a logical approach based on the hard [72:37] science of decades of research initiated [72:40] originally by Otter Werberg and then [72:42] continued by our group at Boston [72:44] College. The American Cancer Society [72:46] says that breast cancer is increasing, [72:48] prostate cancer is increasing, [72:49] pancreatic cancer, melanoma, HPV [72:51] associated oral cancers are steadily [72:54] increasing in the incidence of severe um [72:57] cancers. [72:58] >> Yeah, there has been no major advance in [73:01] managing glyopblast in 100 years. [73:04] >> What's glyobblasto? [73:05] >> That's the the the deadly brain cancer. [73:08] Okay, that killed uh Teddy Kennedy from [73:10] Massachusetts, Senator Kennedy, John [73:12] McCain, President Biden's son, Bo Biden. [73:16] It's killed a lot of various people and [73:18] it's considered a death sentence. No, [73:19] no, no, no. We we we're keeping these [73:21] guys alive. Okay, we're not saying we [73:23] cure the cancer, but we can certainly [73:25] keep them alive a lot longer. Pancreatic [73:27] cancer always considered so bad. We're [73:29] getting very excellent results in [73:31] managing pancreatic cancer using [73:33] metabolic therapies. We know what to do [73:35] and we know how to do it. I have [73:37] clinicians that work with me, dieticians [73:39] that know how to manage cancer [73:41] effectively. We can do it right now [73:44] today. If someone were to say, Seaf [73:46] Freed, get your get your group together. [73:48] Let me see what you can do. I will put [73:50] up our metabolic therapy against any [73:52] trial from any of these pharmaceutical [73:54] companies. We can keep these people [73:55] alive a hell of a lot longer to [73:57] participate in our society. We're not [73:59] doing that. [74:00] >> If you were made president today, [74:02] Thomas, [74:03] >> of the United States, [74:03] >> of the United States, [74:05] >> don't go there. I'm going to go there. [74:09] >> Those guys are [74:12] uh not, let's put it this way, they're [74:14] not scientifically literate. [laughter] [74:16] >> But I would have to be. Yeah. Right. [74:17] >> You, Professor Thomas, you're now [74:20] president of the United States, and your [74:21] primary objective is to bring down this [74:25] 1,700 Americans that are going to get [74:27] cancer a day. [74:30] >> Um, is it is it get cancer or die from [74:32] cancer? [74:32] >> No, they die from cancer. Okay. 1,700 a [74:35] day dying from cancer in the United 70 [74:37] an hour. Think about it. [74:39] >> You you can put in place policies to [74:41] stop this happening and to also help [74:43] people manage it better. What is it you [74:44] do? [74:44] >> First of all, we wouldn't throw out [74:46] everything. Just like I said, we have a [74:48] strategy now to manage cancer [74:50] effectively. [74:51] >> Okay. So, you we're not going to get rid [74:53] of the drugs that are making billions [74:55] and billions of dollars. We're just [74:56] going to use them at lower dosages in a [74:58] different different [74:59] >> But we also want to prevent it in the [75:00] first place. Well, preventing it that [75:02] comes back to our chart. [75:03] >> I'm going to write down the manifesto. [75:05] So, what what is what do we do to [75:06] prevent these 71 people an hour dying of [75:08] cancer? [75:09] >> Well, that has to come from government [75:10] policies. [75:11] >> Okay. You just got promotion. You're now [75:12] the king of the United States. So, you [75:13] don't even need to ask anybody. [75:15] >> What do you do to prevent the 71 people [75:17] a day dying of cancer? [75:19] >> It's going to be education. [75:20] >> Education number one. [75:22] >> Education number one. [75:23] >> Okay. [75:23] >> You have to let people know that those. [75:26] And now let me tell you another thing [75:28] that's really important. [75:30] It should not be any government or [75:32] government official telling anyone what [75:36] they should or should not eat. Okay? The [75:39] the power of this chart is um personal. [75:43] You're embolding the patient. They have [75:46] to know. We're not going to tell [75:48] somebody, "Oh, if you continue to eat [75:51] bad food, you're going to have you're at [75:53] high risk." And that person, I don't [75:55] care. I'll smoke cigarettes and I'm [75:56] going to Well, the government's not [75:57] going to come into this guy's house and [75:59] take away the bad food. No, no, no, no. [76:00] That should never happen. Those foods [76:02] are there because they give us pleasure, [76:05] but they should be the the knowledgeable [76:07] person would be to say, I'd like to have [76:10] it every now and then, but I can't live [76:12] in that environment. And the other thing [76:13] we do terribly in this country, the poor [76:16] people in these food deserts where you [76:19] only get crap food and and as a tragedy [76:23] in itself there they to go to whole uh [76:25] whole foods where they have the [76:27] expensive ribe eyes and all this stuff [76:29] that's much more expensive. A lot of [76:30] people can't afford the kinds of foods [76:33] that will put them in these better [76:34] healthy zones. [76:35] >> So we're going to make food healthy food [76:37] more cost cost effective cheaper. Those [76:40] are easy words to say, but in [76:42] practicality it's not. [76:44] >> Now, what kinds of foods should people [76:45] be eating? [76:46] >> Well, I I think they should just try to [76:47] avoid the highly processed carbs. Okay. [76:49] You don't listen to this. You and and [76:52] exercise. There's a lot of things we can [76:55] do that would mitigate the the [76:59] inflammatory conditions put on this [77:00] chart. The goal here is we know what [77:03] keeps us healthy. It's the efficiency of [77:06] that organel. We want to do everything [77:08] possible to keep that organel healthy. [77:11] We will reduce dementia. We will reduce [77:14] diabetes. We will reduce obesity. And [77:17] they say, "Well, GLP, why don't I why [77:19] don't do and human beings are are the [77:21] kind that I want a quick fix for [77:22] everything?" Right? [77:23] >> Ampeg. How about some ampeg? [77:25] >> Is this what is this GLP? [77:28] >> GLP1. [77:28] >> Okay. We don't, you know, first of all, [77:31] we haven't done any research yet to know [77:34] where a GLP would put you on the chart. [77:36] We do know one thing. It lowers blood [77:38] sugar. How level how high of a level [77:40] would it bring to ketone? Because it's [77:42] the ketones that keep the organel [77:44] healthy. So, I'm lowering blood sugar, [77:46] but am I raising the ketones that [77:48] enhance the bioenergetic efficiency of [77:50] the organel? I don't know what number [77:53] and hasn't been done yet. I don't I [77:54] haven't seen any papers coming out. [77:56] >> Okay. So, we'll keep the zen peek off [77:58] the table, but you're saying exercise [77:59] number three. So, I've got I've got [78:00] education, [78:02] kill the food deserts so people can get [78:04] healthy food. [78:04] >> Yeah. Um, stay away from the ultra [78:06] processed stuff. Number three, exercise. [78:08] We're going to give everybody free gym [78:09] memberships and whatever else they need. [78:10] >> Reduce stress, emotional stress. You got [78:12] to you got to do that. And there's a lot [78:14] of ways. Music therapy. There's a lot of [78:15] different ways you can meditation, [78:17] >> friends, happiness, all of those reduce [78:20] stress. So, I had I had a guy from uh [78:22] Korea. [78:24] I think it was Japan or Korea. We did a [78:26] big meeting one time and he he didn't [78:28] tell me what to do. He says, "Um, you [78:30] want to get cancer? If your job and if [78:32] your goal in life is to get cancer, you [78:34] got to eat crap food all the time, you [78:37] have to have terrible sleep, make sure [78:39] you never unass the couch, sit in front [78:41] of the TV all day, look at doom [78:42] scrolling, do all that kind of stuff. [78:44] Make sure you never exercise, and make [78:47] sure you don't have any friends or be [78:48] happy. He says, [laughter] [78:50] you're on a fast track for for not only [78:53] cancer, but all these other chronic [78:55] diseases. So, so that's the what I just [78:58] said is you need to not do that. [79:00] you're doing a great job. You know, [79:02] there's not many people are going to be [79:03] measuring their GKI every day, but there [79:06] are people who love to measure that kind [79:07] of stuff. Um, now I tell you another [79:10] thing. So, they put these things on your [79:12] arm, these continuous sugar monitors. [79:13] They're making continuous glucose ketone [79:15] monitors. So, apps are coming out now. [79:18] Believe me, there's apps. I have my [79:21] Lucas Lou and some others are making [79:22] these apps in my lab. and and um you can [79:25] take your cell phone and and photograph [79:29] a particular food item [laughter] [79:32] and and the food item immediate you put [79:35] places you're put the food item on the [79:37] chart so you'll know eating that will [79:39] give you what zone you'll be in if you [79:40] eat it. So um it's really interesting [79:43] and and these things are coming. We're [79:44] using AI to so but it's purely patient [79:48] empowerment. Okay. The patient [79:50] themselves, the person themselves make [79:53] the choices. No government president or [79:57] king or whatever you want to say should [79:58] ever tell people what and how they [80:01] should eat. The patients should be [80:03] familiar with this and have the [80:05] knowledge to know I'm going to test what [80:07] I think. So people say to me all the [80:09] time, "Well, just tell us what you can [80:12] eat." That's all they say to me. Okay, [80:14] eat whatever you want. You figure out [80:16] where on the chart you're going to be [80:17] and then you'll know. So people say, [80:19] "Well, I can't eat ketogenic diet." [80:20] Well, our our group in in Greece, now [80:22] you tell me. They got the brain cancer [80:24] tremendous success in keeping brain [80:26] glyopblastoma guys alive. What was the [80:29] diet? It was a calorierestricted [80:30] Mediterranean diet. salmon, [80:33] sardines, [80:35] olive oil, avocado, and exercise. That [80:39] is that like oh man, that that's the [80:41] worst diet. What about the carnivore [80:42] diet? What about the the ribeye with a [80:45] little sauce bernese on top of it? This [80:47] keeps your your blood sugar low and [80:49] elevates your ketone. If you want to do [80:51] it with plants, [80:53] everything you got fish, plants, you get [80:55] the vegans and all these kind of people. [80:58] This is a bioenergetic road map to [81:01] health. [81:01] >> Let me just give some specific. So this [81:03] is amazing. What about high fructose [81:05] corn syrups and refined? [81:06] >> Oh man, that's the worst kind of crap. [81:07] You don't take that. [81:08] >> What about What about industrial seed [81:10] oils? [81:11] >> Well, you know, people talk about seed [81:12] oils, [81:13] >> canola and soybeans. [81:14] >> I DON'T KNOW. BUT every there's another [81:16] thing too. [81:18] You and I are different. Uh we have an [81:20] individual metabolism. [81:22] uh age, race, sex, all all the religion, [81:26] all kinds of stuff determine what and [81:28] how you live. And I can't be sure uh [81:32] what you eat and what I eat or what you [81:34] exercise where it's going to put put us [81:36] on the chart. [81:36] >> Synthetic pesticides. I was reading here [81:38] that it's in increases the chance of [81:40] lymphoma by a staggering 41%. [81:42] >> They all damage the oxidative [81:44] phosphorilation, putting the cell at [81:46] risk for compensatory fermentation, [81:48] disregulated cell growth. Wow. The [81:50] problem, the problem. The field doesn't [81:52] understand what I'm saying with respect [81:55] to the origin of cancer, how it happens [81:57] mechanistically, how this organel [82:00] controls the life of the cell. They [82:03] don't know enough about the biology and [82:05] biochemistry of the mitochondria. You [82:07] ought to get guys on here like Nick [82:08] Lane, he he from England. I mean, these [82:10] guys like Doug Wallace and some of these [82:13] guys, they're mitochondrial biologists. [82:15] They they they understand this kind of [82:17] stuff. I want to give people actionable [82:18] things that they can think about. So, um [82:20] that's why I was asking you this [82:21] question about you becoming king. [82:23] Fasting protocols. [82:25] >> Well, intermittent fasting. [82:27] >> Let me let me talk about that just [82:28] briefly. Do you ever try it? [82:30] >> Yeah. [82:31] >> What do you think? You liked it? [82:32] >> It depends how long you're talking [82:34] about. [82:34] >> Okay, let's go a week. [82:36] >> Oh, I know. I've not fasted for a week [82:37] before. [82:38] >> Okay. You know what is the call the [82:39] wall? This guy, he just sent me his [82:40] book. It's coming out. Very nice guy. [82:42] Veral Simck. He say people share things [82:45] with me. The wall is after about three [82:48] days of not eating, just drinking water, [82:52] you hit this wall and it's like, "Oh [82:54] man, I'm just I can't deal with it [82:56] anymore. It's just a terrible feeling in [82:58] my body. I can't sleep at night. I got [83:00] the Jimmy legs. I got all kinds of [83:01] problems. Screw it. I'm not doing this." [83:03] He found out if you sip just tiny [83:05] amounts of a grape juice, you can get [83:07] get through the wall. What we do for the [83:08] cancer patients in the way we design our [83:11] clinical procedures with my clinical [83:13] friends, we do a zero carb diet for [83:16] about a week uh while the body is [83:18] readjusting getting getting bringing [83:20] them out of the red zone getting into [83:21] the yellow zone. You can't believe the [83:24] power of glucose as an addictive drug on [83:26] the brain. It's unbelievable. It's like [83:28] cocaine. It it's it's and you know that [83:30] when you start you start shaking and you [83:32] go. So, but if you don't eat carbs and [83:34] just eat meat or whatever to keep you in [83:36] a low GKI, um then when you jump off to [83:40] the water only fasting, it's much less [83:42] traumatic to the brain. You've gone [83:43] through the wall of the gate, so to [83:44] speak. So, once you know how to get [83:46] through the gate, you make this whole [83:48] process a lot a lot easier. And that [83:50] helps people enormously, especially [83:53] those people that want to get rid of [83:55] their chronic disease. Okay? Because or [83:57] some, you know, we have a lot of people [83:59] out there that just like to do all this [84:00] stuff. You know, you got these these [84:02] people that go overboard on everything. [84:03] But, you know, right now we have an [84:06] obesity, chronic epid cancer epidemic. [84:09] All of these epidemics are the result of [84:11] an abuse of that organel in one way or [84:13] another. And we have a pl a plan to [84:16] mitigate that abuse and at least people [84:18] have an at least they're empowered to do [84:20] it with the help of knowledgeable [84:22] physicians. [84:23] >> I want to just keep on this point of [84:24] actionable feedback. So, um Dr. Valter [84:26] Longos Dr. His extensive research [84:28] clinical trials prove that fasting [84:30] mimicking diets drastically lower IGF-1 [84:34] which triggers cellular autophagy and [84:36] actually makes standard cancer therapies [84:37] up to three times more effective by [84:39] removing the metabolic shield of cancer [84:42] cells. [84:42] >> Yeah. Which is the gluc the waste [84:44] [clears throat] products of of of gluc [84:45] which is the lactic acid and the suxenic [84:47] acid that all goes down. [84:49] >> Would you recommend again if you're king [84:51] would you recommend that [84:52] >> I would never recommend any I have to [84:54] just give them the knowledge. Then the [84:55] person has to make the decision [84:57] themselves. [84:57] >> Do you think it could be beneficial? [84:59] >> Of course, [84:59] >> if you were king to um have everybody [85:02] wear a CGM, one of those continuous [85:05] glucose monitors, at least once. [85:06] >> No. [85:07] >> Never. [85:08] >> No. I I think if you have cancer and you [85:11] really want to stay in this green zone [85:12] to know, right? Listen, I was down in [85:15] Mexico not long ago. I was talking to [85:16] one of the head physicians down there. [85:18] He wore one of these things, right? [85:20] >> He said, "Every time I wanted to go out [85:22] and have a party, have a good time, this [85:23] damn thing would be beeping." So what do [85:25] you ripped it off and threw it in the [85:26] trash? So [laughter] that you don't want [85:29] somebody barking in your ear when you're [85:31] having a good time. That's why what [85:32] you're doing right now with this, you're [85:34] choosing to prick your finger. [85:37] >> You're the one making that decision. [85:38] There's not something on your arm [85:40] saying, "Stephen, don't do that. Don't [85:41] do that." [85:42] >> But you know what? It was useful to wear [85:43] it once or twice because it even I could [85:46] I suddenly realized that things I put in [85:48] my mouth [85:49] >> had an impact on my blood sugar and my [85:51] blood which [clears throat] and also I [85:53] realized that it had an impact in 10 [85:54] minutes. [85:55] >> Yeah. [85:55] >> And I thought and then and then also [85:57] when my blood sugar came back down and [85:58] crashed [85:59] >> I thought oh gosh I feel [86:01] >> I could suddenly pair my behavior to my [86:04] feelings. [86:04] >> Yes. Well, that that now I'm not I I no [86:08] I I' I've seen that. And not only that, [86:10] uh Andrew Scarboro from England who who [86:12] has been doing this for for the stage [86:14] three go uh he's like 15 years out. He's [86:18] done this so many times with the finger [86:20] prick and all this. He knows now already [86:22] when his body is in these zones from the [86:24] feeling that you just described. But for [86:27] the people at the beginning and who are [86:29] given a terminal diagnosis, they want to [86:31] get into these green zones and they want [86:33] to use the things that are going to keep [86:34] them alive on the planet for a longer [86:36] period of time with a higher quality of [86:38] life. That is important. That thing on [86:41] your arm can help you stay in that zone [86:44] until you have this thing managed at [86:46] which time you can choose when to do [86:48] that. So there's flexibility in this [86:50] whole process. It's not one like for [86:52] example we have the standard of care [86:54] which is written in granite for crying [86:56] out loud. They get all they they if you [86:58] do anything different from the standard [86:59] of care you could lose your license as a [87:01] physician. Metabolic therapy is is [87:04] patient driven. It's driven on the [87:06] patient. [87:06] >> What about hyperbaric oxygen? Yeah. [87:08] There was a study in 2013 that [87:11] demonstrated that while the ketogenic [87:12] diet alone significantly slowed tumor [87:14] growth in systemic metastic cancer mouse [87:16] models, combining the diet with [87:18] hyperbaric oxygen therapy elicited a [87:20] profound synergetic decrease in tumor [87:23] growth and drastically increase survival [87:24] times. [87:25] >> Yeah, we published that paper with [87:26] Dominic D. Augustino. So we we put my So [87:29] uh listen, hyperbaric oxygen will create [87:32] oxidative stress in cells that do not [87:35] have efficient oxidative [87:36] phosphorilation. uh cancer cells. [87:38] >> Cancer cells. So you can kill cancer [87:40] cells by oxidative stress by irdiating [87:42] or poisoning them or you can put a [87:44] patient in in nutritional ketosis and [87:47] then put them in hyperbaric oxygen and [87:49] the cancer cells are selectively killed. [87:52] When you irdiate somebody, you're [87:54] damaging the whole body with all kinds [87:55] of stuff. And there's another thing, [87:57] Stephen, you got to listen to this and [87:58] you listen carefully. when you go to [88:00] these treat these standard of care [88:04] >> standard when you use standard of care [88:05] radiation chemo whatever they give [88:07] imunotherapies or whatever so the [88:09] patient comes in and he says I've been [88:10] really working hard on this the doctor [88:12] says oh no that doesn't work right gives [88:14] you some radiation or gives you [88:16] [laughter] flying up into the red zone [88:18] the treatment itself puts so much stress [88:20] on the body that the body itself starts [88:23] going you go into the red zone from the [88:24] very treatments that you're giving to [88:26] the patient which is making [88:28] strengthening the tumor else. [88:30] >> You're not against chemotherapy, though. [88:31] Are you? [88:32] >> No. I'm I'm I'm positive about it, but [88:34] it has to be used in the right context. [88:38] >> It has to be used when your body is in [88:40] this state of nutrition. And you can use [88:42] low doses so you don't force the tumor [88:45] cell to become even more resistant to [88:47] the treatment. [88:49] >> The next thing which is actionable is [88:51] what you talked about earlier, which is [88:52] these microplastics and forever [88:54] chemicals. In late 2023, the [88:55] International Agency of Research on [88:56] Cancer officially upgraded these forever [88:59] chemicals which are used in non-stick [89:00] pans and food packaging to a grade one [89:03] carcinogen [89:05] >> in humans, cancer causing in humans [89:07] based on strong mechanistic evidence [89:08] that it induces epigenetic which is gene [89:12] alterations and suppresses the immune [89:14] system. So you ban the forever [89:15] chemicals. [89:16] >> Okay, this is a beautiful paper. I went [89:19] back and I took what all of Otto Werberg [89:21] meticulously went through all of his [89:23] work showed where he was absolutely [89:25] correct and where he just didn't have [89:26] the the new information that would make [89:28] him I talked about the forever chemicals [89:30] microplastics guess what they damage the [89:34] organel they get into they break they [89:36] cause rosin damage they it reduce the [89:39] efficiency of oxidative phosphorilation [89:42] causing a compensatory increase in the [89:46] utilization of glucose and glutamine and [89:47] disregul related cell growth. Everything [89:49] comes back to this organel. Chron all [89:52] chronic diseases and cancer are the [89:53] result of damage to this organel. That's [89:56] why having this little thing here is so [89:58] important. It's a great prop. I got to [90:01] get one for my class. [90:02] >> You can keep it. Um the next thing is [90:05] purifying the water supply. Um heavy [90:07] metals are found in local water supplies [90:09] to run off and ultimately are [90:11] carcinogenic in some cases. The IARC [90:15] classifies arsenic and cacadium as group [90:18] one on carctogenics and they're [90:20] frequently found in unfiltered public [90:22] water infrastructure. So you clean out [90:25] the water supply as well. [90:26] >> Yeah. [90:27] >> You know all this stuff is coming into [90:29] our water supplies. People flushing down [90:31] all these chemicals into the into the [90:33] which then leech back into the water [90:35] supply. And every one of the chemicals [90:37] that we have looked at that has been [90:38] linked to oncology or disregulated cell [90:41] growth all damage the oxidative [90:43] phosphorilation chronically. So we're [90:45] bringing the entire focus back to things [90:49] what can I do to keep this organel [90:52] healthy uh even if I'm exposed to these [90:55] chemicals if I can do get into these [90:58] zones like you're trying to do. So even [91:00] if you are exposed to these, this [91:02] organel has an incredible healing power [91:04] in itself. [91:06] >> What is the most important thing we [91:07] haven't talked about that we should have [91:08] talked about, Professor Thomas? [91:09] >> Well, I mean, you've covered a lot. One [91:11] of the things I I want to talk about uh [91:13] is metastasis. [91:14] >> What's that? [91:15] >> That's the spread of the tumor [91:16] throughout the body. [91:18] >> Okay. So if you were to have a cancer [91:20] that's just localized in one spot, [91:23] >> you know, the probability of developing [91:25] a therapy that would be um long term is [91:29] highly increased. The problem that kills [91:32] people is the spread. So if the tumor is [91:35] in the breast and it spreads to the [91:36] liver and the lungs and the brain, you [91:38] know, you've got a problem. Lung cancer [91:40] spreads to the brain, the liver. Most of [91:42] these cancers that spread to the brain [91:44] or other organs become difficult and [91:47] that's why you use systemic chemotherapy [91:49] you're trying to stop. What we have [91:51] found is that you have a a stem cell [91:55] people love stem cells. If you ever hear [91:57] the term stem cell tumor wow stem cell [91:59] tumor stem cell tumors cannot [92:01] metastasize how do I know because I have [92:03] stem cell tumors diagnosed as stem cell [92:06] tumors with stem cell markers. I've [92:07] grown them. They grow very angry. They [92:09] get a lot of blood vessels, but they [92:11] can't spread. Okay, how do you get [92:14] spreading tumor cells in your body? The [92:16] immune system comes in, recognizes that [92:19] as an unhealed wound, and then fuses [92:21] with the stem cells, and then you have [92:23] these hybrid cells. They are programmed [92:26] to move around your body. So, they are a [92:29] macroofagage tumor cell hybrid. So, and [92:33] they're very hard to kill, but we found [92:35] they're remarkably sensitive. They're [92:37] glutamine driven. So we know they're [92:40] glutamine driven and they need the [92:42] glucose and that why that's why [92:44] metabolic therapy done the right way can [92:47] nail nail those metastatic cancer cells [92:50] purging them with a little little bit of [92:52] imunotherapy to go along with it. You [92:54] might be able to to get what we call [92:56] resolution. Don't forget my colleagues [92:58] and I do Diagto Joe Maroon we built the [93:01] press pulse therapeutic strategy. I [93:03] mentioned that on your previous show. [93:05] That's the way you you you press down [93:08] the glucose of the tumor and then you [93:10] pulse to kill the glutamine which will [93:11] which will target the metastatic cancer [93:13] cells enhancing the health and vitality [93:16] of the organs already infiltrated by the [93:18] tumor. [93:18] >> I looked on our previous conversation [93:20] doc professor Thomas and um it's quite [93:24] heartbreaking because the comments [93:25] sections are all people that are e [93:27] either struggling themselves with cancer [93:29] or a loved one of theirs their wife [93:31] their husband has just been diagnosed [93:33] with cancer. Is there anything for those [93:36] people that have clicked on this video [93:37] because I imagine they are in the [93:38] millions. [93:39] >> Yeah. [93:40] >> That you want them to hear. [93:41] >> Well, the thing of it is is why Well, [93:44] this is a bigger issue. When you have [93:46] the science and you have the strategy to [93:48] manage cancer effectively with minimal [93:51] toxicity, not to say we can cure, but to [93:53] say we can manage it. Why is it not [93:56] being done? [93:57] That's the question. But to them to them [94:00] who've tuned in. [94:01] >> Okay. So these kinds of conversations [94:04] that we have are allowing the [94:07] populations to realize that there is [94:11] their loved ones do not need to be [94:14] sacrificed [94:16] for the good of industries that are [94:19] generally considered profitable. They in [94:22] other words the profitability of the [94:24] industries are based on your sickness. [94:28] Uh and and a lot of those comments came, [94:30] oh, you can't you can't do anything. [94:31] Yes, you can do something about it. When [94:33] you're armed with the knowledge and [94:36] people ignore the knowledge, then [94:37] there's a problem. [94:38] >> Do people need to sort of self advocate [94:40] to some degree? [94:41] >> I think so. [94:42] >> With with uh care providers, what do [94:44] they [94:45] >> Yeah. I I think that's a very delicate [94:47] question. [94:47] >> Yeah. [94:48] >> That the oncologists never heard of this [94:49] stuff. [94:50] >> They have never read these papers. They [94:52] were never trained in medical school to [94:54] know the biology and biochemistry of [94:56] cancer. It was told to be a genetic [94:58] disease. Theories are so important in [95:01] science. For 1,800 years, people thought [95:05] the work of Aristotle, his comments and [95:07] the mathematics of Claudius Talami said [95:10] that the earth was the center of the [95:12] solar system and all the planets uh and [95:16] sun revolved around the earth. The [95:18] geocentric theory, right? Capernicus [95:21] struggled with the talami mathematics [95:23] and realized that if he put the the sun [95:26] in the center of the solar system and [95:28] made earth just another planet, a lot of [95:30] the mathematics made sense. Kepler comes [95:32] in and says these aren't circles, [95:34] they're ellipticals. Galileo takes the [95:36] telescope, sees the moon's interpreter [95:37] and was able to look at and quantify [95:40] where where predict where planets would [95:42] be at a certain period of time. Then [95:44] they took poor Gillodono Bruno. You know [95:47] about this guy Bruno? Oh, there Steven. [95:49] You got to know Bruno. Your job is to [95:50] know about the poor Bruno who was burned [95:52] alive by the Catholic Church for [95:54] challenging the the the geocentric [95:57] theory. And he became a martyr of [95:59] science. So when you have established [96:01] power structure, whether it's a religion [96:04] or whether it's an industry or whatever, [96:06] challenging that can be very very [96:07] hazardous. [96:08] >> Has it been hazardous for you? [96:10] >> Listen, no. I mean, I do what I do [96:13] because I like I just collect more and [96:15] more data to support. Hazardous for me [96:17] would be getting blindsided. Blindsided [96:19] would be somebody coming at me with a [96:21] piece of new data that I have never [96:23] considered. I don't sleep. I I think [96:25] about this stuff all the time to avoid [96:26] the blind side. My students are on the [96:29] on the alert for any paper that comes [96:31] out that says cancer oh cancer cells can [96:33] burn fatty acids and ketone bodies. Oh, [96:35] really? Let's go back through and [96:38] dissect out their control experiments [96:40] and you find in every case there was [96:41] always some glucose and glutamine in the [96:43] media making it look like the fatty [96:44] acids. So, so that's what bothers me. [96:47] What bothers me is getting hit with a [96:49] piece of data that undermines what we're [96:52] what we our knowledge base is. And so [96:54] far we haven't had that. Okay, it's [96:56] we're standing on the shoulders of Otto [96:58] Warberg, a giant in the field of [97:00] biochemistry. He was thrown under the [97:02] bus when everybody thought cancer was a [97:03] genetic disease. My this paper goes back [97:06] and shows exactly where Warberg made his [97:08] mistakes and where we have rectified [97:10] some of that. Bringing the whole field [97:11] back on where it should be. It is a [97:14] mitochondrial metabolic disorder and we [97:17] can account for all of the phenotypes [97:18] and characteristics of that disease [97:20] knowing that now with that knowledge [97:23] logical people and people interested in [97:25] helping others will will uh take [97:28] advantage of that. We're not throwing [97:30] out all these toxic chemicals. We're [97:32] learning how to use them in a different [97:33] way and that's where the success is [97:35] going to come. So let's con let's [97:37] conclude with a a actionable takeaway [97:40] for people who are suffering themselves [97:41] with with cancers um or have someone in [97:44] their family right now that is suffering [97:46] from cancers. What is the actionable [97:48] takeway? [97:49] >> Well, I think the action will take once [97:50] this paper comes out they can start [97:52] taking action if they are motivated [97:53] enough. [97:54] >> They can read about this. they can read [97:56] about it and then try to like just like [97:58] you're doing no different [97:59] >> get into these zones and then work with [98:03] their oncologists, knowledgeable people [98:05] to to to treat them with standards of [98:08] care. Yeah. As long as they can remain [98:10] and then we do non-invasive imaging, PET [98:13] scans, see MRIs. [98:14] >> Okay. So, specifically what what you're [98:16] saying is this paper, I will link it [98:18] below in the comment section for anyone [98:19] that wants to read it. This graph will [98:21] be on the screen throughout this episode [98:22] anyway, so people can screenshot it if [98:23] they want to have a look. And the way [98:25] that they test whe what what their GKI [98:28] index is is they can buy one of these [98:30] Keto Mojo things which you can get on [98:32] Amazon for $ 20 $30. [98:33] >> You prick your finger. It gives you the [98:36] glucose reading. Yeah. [98:37] >> You divide it by 18. [98:38] >> No, no. The new machines have the [98:40] button. You So even the people only have [98:42] to do that. [98:42] >> Okay. Fine. And as you can see on here, [98:44] this is an interesting way to sort of [98:48] increase your your management improve [98:51] your management of of some of these. [98:53] >> Yeah. And then there's a challenge [98:55] to get into those zones. Um, you know, [98:58] I'm not saying this is easy stuff. [99:01] GLP1 inhibitor, man, that's a hell of a [99:03] lot easier than than than doing this. [99:06] >> And I should probably say always consult [99:08] with a medical professional. [99:09] >> Yeah. Um, I I think uh because you know, [99:12] a lot of people they have a lot of [99:14] coorbidities. They have diabetes, high [99:17] blood pressure, hypertension, cancer. [99:19] They have a it's not a perfectly healthy [99:21] person with cancer. [99:22] >> Mhm. So before you go in to challenge [99:25] that, you need to have what you look [99:26] like you you might look, you know, you [99:28] might have to be adjusted in some way. [99:30] That's why the people who the physicians [99:32] that are working with this can do all [99:34] that. I I'm I'm not in the clinical [99:35] thing. [99:36] >> And there are some people who respond [99:37] poorly to the ketogenic diet is high [99:40] states of ketosis because I've I've [99:41] received DMs before from a woman who [99:44] said, "My my husband did ketosis and he [99:46] collapsed unconscious. He took him to [99:47] the hospital. He had some coorbidity." [99:49] >> Yeah. Yeah. Yeah. Oh, the other thing [99:50] too is you got to be some people have [99:52] carnitine deficiencies. Carnitine [99:54] prevents fatty acids from being made [99:55] into ketone bodies. [99:57] >> So, so, so they can be carnitine [99:59] supplementation can help them, but you [100:01] need a physician to know this. [100:04] >> We have a closing tradition where the [100:05] last leader question for the next and a [100:07] question left for you is on the subject [100:08] of energy. What in your life has brought [100:10] you the most energy and what was the [100:14] biggest energy drain you've ever [100:16] experienced? Well, this is bringing me [100:18] the biggest energy. This [laughter] [100:21] >> well not this the whole concept. The [100:23] idea that you have found [100:27] uh mother nature has allowed you to look [100:30] into the depths of of of what we [100:33] consider the biology and biochemistry of [100:36] how bodies work. and knowing how to take [100:39] that and apply it to people that are [100:41] suffering from all these different [100:43] chronic diseases and giving them the [100:45] opportunity to change that because [100:48] before that it was mysterious. Oh, I'm [100:51] do I'm in keto. What's your GK? I I [100:54] don't know. Well, now you have a [100:56] quantitative opportunity that gets us. [100:58] So, we have a lot of evidence. I think [101:00] people should be feel encouraged. I [101:03] think we have given hope to the hopeless [101:06] and and I think that's empowering and [101:08] the goal here is not to make a billion [101:11] dollars. It's just to know that you've [101:12] kept all these poor souls alive longer [101:14] than they were projected to be to be. [101:16] And I think this power and that keeps us [101:18] going because when we see more and more [101:20] people coming to me, I get emails back [101:22] from people three or four years ago and [101:23] I said, "Gee, I thought you were a [101:24] goner." And he says, "I'm doing really [101:26] well. Just came back from a vacation [101:28] with my wife." Well, that's empowering. [101:30] I said, "Well, that's good. And don't [101:31] forget, Stephen, all of our research [101:34] money comes from private foundations and [101:35] philanthropy. [101:37] >> So, [101:37] >> so is that a way that people can help? [101:39] >> Yeah. [101:39] >> And where do they go to help? [101:40] >> Oh, Travis Kristopherson's foundation. [101:43] So, we in my papers that we have the [101:46] foundations that support our work, [101:48] private foundations. So, I'll link [101:49] >> and there are occasionally, yes, please [101:51] link. There are occasionally people I [101:53] know and I when I give kits of [101:55] information to people uh I say please [101:58] consider making a donation only if it [102:00] works for you. Yeah. Don't charge them [102:02] anything or ask them to pay something if [102:05] it's not going to help them. If you were [102:07] told to be dead in 6 months and six [102:10] years later you're alive. Maybe you [102:11] throw us a few shekels into the private [102:13] found into the foundation supporting our [102:15] work. [102:15] >> I'll link that foundation below in the [102:17] comments section. Yeah, we have a couple [102:18] on breast cancer on on on general [102:20] general uh um support on the metabolic [102:23] approach that we have. So, we have a lot [102:25] going. We're very excited. You can see [102:27] all the papers we've published. Uh and [102:29] it's not like um uh some of these are in [102:32] top journals, some of them are in new [102:34] journals, but but the issue is we're [102:36] we're we're we're [102:38] publishing this. [102:39] >> My thing is, you know, I great great [102:41] great respect for science and doctors in [102:43] the medical profession. Go go go get [102:44] your information. Speak to your medical [102:46] provider. There's so many tools out [102:47] there now. Go and check for yourself. [102:48] >> Yeah. Well, I think in the oncology [102:50] field, that's where we have this vast [102:51] wasteland of misinformation or [102:53] misunderstanding, let's put it that way. [102:55] They don't understand these concepts [102:57] where, you know, people who have done [102:59] heart work and bone work and [103:00] replacements, those people are at the [103:01] state-of-the-art with this kind of [103:03] stuff. [103:03] >> Well, the last conversation we had, it's [103:04] reached about 15 million people. So, on [103:06] YouTube, it's got 10 million views and [103:08] then across audio platforms, it's got [103:09] another five or so million views. Yeah. [103:22] >> practitioner about, but also it actually [103:25] just creates a community of people in [103:26] the comment section where, you know, [103:28] this is a community of people that are [103:29] searching for hope. [103:30] >> Yeah. [103:31] >> And as some of them read through the [103:32] comment sections, they actually [103:33] commented saying, "It was so nice to to [103:35] speak to other people in the comment [103:36] sections about what I'm going through [103:38] and how it feels from an emotional [103:39] level." So, this is something I actually [103:41] wanted to say in this episode was if [103:42] you're if you're listening to this [103:44] conversation now and you've gotten to [103:45] this point, do feel free to go into the [103:47] comment section and just offer some [103:49] support and some love to other people um [103:52] who are struggling because you know it [103:54] can be a very lonely experience the [103:56] minute you find out you've got a [103:57] diagnosis and off you go into the [103:58] internet into podcasts into AI to try [104:00] and figure out what you can do. So, [104:02] yeah, do share things that have helped [104:03] you point at different resources that [104:05] are rigorous and offer emotional support [104:07] to those that are in the comments [104:08] section. and that would be a wonderful [104:09] thing. Thomas, thank you so much for all [104:12] that you do. Um, you're you're an [104:14] absolute worrier for pushing science, [104:16] the science into the world and for [104:19] fighting for these people that don't [104:20] have the tools. And if you I mean, I [104:22] don't think I've ever seen a comment [104:23] section quite like it in terms of the [104:25] gratitude that people have for the work [104:26] that you're doing. It is remarkable [104:28] work. Long may you continue to do it. [104:29] >> Well, thank you very much. and you you [104:31] know you play a very important part on [104:32] this because this information is not [104:34] disseminated to the the population and [104:37] it's the population of people that will [104:39] eventually make the change. So they're [104:41] going to want this especially when we [104:42] keep publishing more and more case [104:44] reports of successful cases and the ch [104:48] the system will change and we just have [104:50] to modify what we have to make it better [104:51] and I think that's what keeps us going. [104:53] So I have no plans of stopping this [104:55] anytime soon. My students are all [104:57] excited about this. they they're [104:58] learning about it at Boston College. So, [105:01] this is a big emphasis that we have and [105:03] we continue to do it. Again, scientific [105:05] literacy is so important uh for uh how [105:09] you um navigate through life and um [105:13] thank you very much for your show and [105:14] we'll we'll keep uh pushing this as as [105:17] hard as we can. [105:18] >> Thank you. YouTube have this new crazy [105:20] algorithm where they know exactly what [105:22] video you would like to watch next based [105:24] on AI and all of your viewing behavior. [105:26] And the algorithm says that this video [105:29] is the perfect video for you. It's [105:31] different for everybody looking right [105:32] now.